Professional Documents
Culture Documents
2010
1
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Holtz, Anders.
[Ryggmargsskador. English]
Spinal cord injury / Anders Holtz, Richard Levi.
p. ; cm.
Translated from Swedish.
Includes bibliographical references and index.
ISBN-13: 978-0-19-537276-2 (alk. paper)
ISBN-10: 0-19-537276-X (alk. paper)
1. Spinal cordWounds and injuries. I. Levi, Richard. II. Title.
[DNLM: 1. Spinal Cord Injuriestherapy. 2. Spinal Cord Injuriesrehabilitation. WL 400 H758s 2010a]
RD594.3.H6513 2010
617.40 82044dc22
2009011161
9 8 7 6 5 4 3 2 1
In your hands you are holding a translation of Definitive treatmentone that can restore
the first Swedish textbook on spinal cord injury neurologic deficits and return the patient to the
(SCI), a volume that illuminates this topic from same level of function that existed prior to the
the time of injury through long-term rehabilita- accidentdoes not yet exist. However, knowl-
tion. We had two reasons for writing. First, because edge about the acute mechanisms of injury,
we felt a need to document our experiences from emergent treatment at the scene of the accident
the past two decades, during which time we were and in the hospital, and long-term rehabilitation
involved in caring for this group of patients, and has increased significantly over the past few dec-
second, to help fill a void that has existed in the ades. This is also reflected in encouraging
literature up until now. advances in injury prevention, a decrease in
The theme of this book could justifiably be acute mortality, an increase in the number of
considered either extremely narrow or extremely incomplete (partial) versus complete injuries,
broad. Narrow, because spinal cord lesions and improvements in both prevention and treat-
irrespective of causeare uncommon, much ment of secondary and tertiary complications, as
more so than lesions in adjacent structures, well as more successful rehabilitation to an active
such as the brain or spinal column. Broad, lifestyle. Now it has become fully realistic for a
since SCI often have far-reaching effects on the person with a SCI to achieve a high degree of
function of all body organ systems. And also autonomy, have a family and a job, drive a car,
broad because the care of SCI involves not only actively pursue leisure activities, and enjoy a
a large number of medical specialties, but to a good quality of life for many decades after the
large degree also the allied medical professions, time of the injury.
as well as psychosocial and socioeconomic The purpose of this book is to present an over-
interventions. view of the fields of knowledge that are of central
Typically, SCI necessitates a dramatic read- importance to the care of patients with SCI. This
justment in lifestyle. From having been free to interdisciplinary approach equates to what is
engage in all activities associated with normal sometimes referred to as spinal cord medicine.
living, post injury even simple routine tasks However, readers in many languages have been
now become a challenge. In addition to more or relegated to individual subsections of diverse texts
less extensive paralysis and sensory deficits in fields such as neurology, neurosurgery, ortho-
below the level of lesion, patients often experi- pedics, rehabilitation medicine, internal medi-
ence significant impairments involving urina- cine, general surgery, and urology. The focus
tion, bowel movements, and sexual function. of this book is on our areas of specialization:
These deficits, often combined with problems neurology, neurosurgery, and rehabilitation med-
such as pain, spasticity, and pressure ulcers, icine. Those with special interests may supple-
become a heavy burden for both the individual ment their reading with specialized literature
with the SCI and for family and friends. primarily in urology, plastic surgery, hand sur-
Preventive measures and treatment of problems gery, andrology, gynecology, algology, psychiatry,
resulting from the injury therefore comprise a and, of course, the crucial areas for rehabilitation
natural theme for this book. outcome represented by the allied medical
vi PREFACE
professions of physical therapy, occupational for help with the content and Lena Lyons for
therapy, behavioral sciences, and the like. Largely creating the beautiful illustrations. Anders
for this reason, and in order to facilitate further Holtz would like to thank his entire family,
study, we have provided a fairly comprehensive from Adam to Britt Maria, for everything from
bibliography and reference section. photos to moral support. Richard Levi would like
We hope that a broad readership with a variety ke Seiger;
to extend his warmest thanks to Prof. A
of backgrounds will find this book to be useful Mr. Goran Lagerstrom and Dr. Claes Hultling; as
and that as a whole, it will serve as an introduc- well as to his family for their continual encour-
tion to the care of this challenging patient group. agement and support.
Our historical knowledge of spinal cord injury and ejaculation. The case report is concluded
(SCI) originates in ancient Egyptian society with a declaration of the treatment strategy of
(Third Dynasty, 30002500 years BC). During that timean ailment not to be treated. The
this relatively peaceful era, great resources were Egyptians refrained from surgical interventions
dedicated to construction work, and most of all to but relieved urinary retention by using bronze
the creation of the pyramids. It was possible, for catheters.
the first time, to describe a variety of injuries seen The next known reference to traumatic SCI is
within a relatively large population exposed to a dated to the time of the Trojan War (circa 1100 BC).
high incidence of trauma. In 1862, the Three immortal brothers, Zeus, Poseidon, and
Egyptologist Edwin Smith purchased documents Hades, ruled the sky and the living, the seas,
from this period describing different injuries to and the nether world, respectively. In the epic
the human body. These documents are regarded tale of the Odyssey, the youngest of Odysseus
as one of the worlds most valuable treasures of companions, Elpenor, fell from the palace
medical history. The documents, later named the roof, broke his neck, and his soul went down to
Edwin Smith Papyrus, contain 48 cases of trauma Hades.
including six cases of spine and/or SCI. The case Seven hundred years later, Hippocrates (circa
reports do not differentiate between injuries to the 460377 BC), the father of medicine, analyzed
spinal column and the spinal cord. Imhotep, an the relationship between vertebral injuries and
Egyptian official and architect responsible for the paralysis. He observed that if damage to the
step pyramid of Sakkara and a practicing surgeon, spinal cord only occurred on one side, a subse-
probably wrote the papyrus. The documents are quent paralysis always was located on the same
dated to approximately 2500 BC and clearly illus- side as the damage. Until the time of Hippocrates,
trate biomechanics, clinical evaluation and diag- Aesculapius, the sun-god Apollos son, was con-
nosis, treatment, and prognosis following sidered in the Greek mythology to be the god of
different injuries ranging in severity from mild medical healing, and the ancients believed that all
distortions without neurological impairment to such healing flowed from him. With his observa-
fractures leading to complete SCI. In the classical tions and practical application of basic medical
case report number 33 Instructions concerning a knowledge, however, Hippocrates succeeded in
crushed vertebra in his neck (here illustrated separating medicine from mythology. Because
with a modern magnetic resonance imaging of his efforts, medicine became a worldly and
[MRI] sequence in Fig. 12.16), a complete SCI rational endeavor. He is the main author of the
caused by a fracture in the cervical region is book Corpus Hippocraticum, which summarizes
described. A vertebral body has been crushed the medical knowledge of that time, and in it he
against an adjacent one as a result of the flexed describes for the first time the clinical condition
position of the head at the moment of injury. of chronic paralysis.
The clinical status includes paralysis of both Hippocrates presents the difficulties, such as
arms and legs (tetraplegia), loss of sensation constipation, painful urination, pressure sores,
below the level of injury, and loss of control of and leg swelling, associated with the aftermath
the urinary bladder. The patient also showed per- of traumatic SCI. He advocated a diet consisting
sistent involuntary painful erection (priapism) of four to nine pints of milk combined with honey
3
4 SPINAL CORD INJURY
and a special mild white wine from Mendez in downwards A medical orderly then either sat or
Egypt to mitigate these problems. stood on the deformity until reduction; alterna-
On Hippocrates advice, pressure sores were tively, a wooden board was placed crosswise over
treated with exposure to the air in combination the injured area to achieve a similar compression.
with the direct application of wine, juice, vinegar, Only few fragments of written documenta-
and oils, as well as aluminum salt and lead. He tion remain regarding SCI from the Greco-
recommended that the bandages be changed Roman era. Aulus Cornelius Celsus, working
every third day to avoid infections. during the 1st century BC, built upon the medical
The ancient Greeks frequently used spinal tradition of Hippocrates. He became aware of the
manipulations to manually reduce malforma- importance of the spinal cord itself, and he was
tions. Hippocrates introduced two devices, the probably the first to document rapid death as a
Hippocratic ladder and the Hippocratic board for consequence of a cervical SCI. Celsus introduced
this purpose (Fig. 1.1). The patient was placed in a the closing of small open pressure sores with
prone position and was stretched from the female hair as suture material. Within the field
shoulder area upward, and from the hips of medicine, the Greco-Roman era was
represented by two prominent figures, Galen spine, and he also suggested the importance of
and Paul of Aegina. the neck muscles in contributing to the stability
The Greek Galen (129199 AD), physician-in- of the cervical spine. His dissections of the
ordinary to the Emperor Marcus Aurelius and spine formed the basis for highly detailed draw-
also called the second Hippocrates, was the ings of the joints, vertebrae, muscles, and
first to report on the effect of experimental inci- tendons.
sions of the spinal cord. Galen noted that a After nearly a thousand years of medical
longitudinal incision to the spinal cord did not stagnation, in 1543, during the Renaissance,
result in any symptoms but a transverse inci- the Flemish anatomist and physician Andreas
sion at the level of the second and third cervical Vesalius published one of the greatest medical
vertebrae results in loss of motion and sensory books ever written (Fig. 1.2). This treatise of
functions below the level of the incision. He seven volumes entitled De Humani Corporis
also described the number of vertebrae com- Fabrica (The Fabric of the Human Body), contains
prising the different parts of the spinal for the first time drawings in which the human
column and introduced the terms scoliosis, nervous system is correctly illustrated. The illus-
lordosis, and kyphosis. trator Johann Stephan van Calcar produced all the
The famous surgeon Paul (625690), from drawings for Vesalius work. Because, until that
the Greek island of Aegina, described the impor- time, the anatomical conception of the human
tance of clinical examination. He concluded that body as presented by Galen had been based
a fracture of the vertebra should be suspected if on studies done on monkeys, not humans, the
the physician was unable to palpate the spinous work of Vesalius constitutes the first textbook to
process belonging to the damaged vertebra. He present human anatomy in a detailed and correct
proposed, on these occasions, the following treat- fashion.
ment: Make an incision of the skin externally The German surgeon Fabricius Hildanus in
and extract it (the fractured bone) and unite the 1646 described a method to reduce dislocations
wound with sutures. This is the first time that in the cervical region. A clamp was inserted
the removal of vertebral arches (i.e., a lami- through the spinous processes in the neck, after
nectomy) is described as a treatment for spinal which traction was applied. This closed reduction
fractures, and Paul of Aegina is considered the was supplemented by open reduction if necessary.
originator of this procedure. A very special event from a surgical point
Documents from India dated to the second of view, happened, during the battle of Amenen-
and third century mention immobilization as a burg in 1762. The surgeon Andre Louis success-
treatment option for fractures in the lumbar fully removed a bullet lodged in the lumbar
region. The Sushruta Samhita, a Sanskrit text spine, and the patient not only survived, but
on surgery, describes patients being laid on a also regained functional movement in the lower
table to which they were bound with ropes to extremities.
correct spinal deformities. Hindu descriptions During the 19th century, two famous persons
of treating spinal deformities with axial traction died following SCI. The first, Lord Nelson
precede Hippocrates by a millennium. (Fig. 1.3), flaunting his characteristic and highly
Medical science during the medieval period visible scarf, was shot in the thoracic spine during
was hampered by superstition and intellectual the battle of Trafalgar in 1805. He became paral-
stagnation. Western medicine during this yzed and died shortly after. Lord Nelson survived
period is regarded as primitive, and was predo- long enough to describe his paralysis to the
minantly practiced by monks. The most impor- ships surgeon, Dr. Beatty, as follows: That all
tant medical reference during this period, The power of motion and feeling below my chest are
Canon of Medicine, was written by the Persian gone and you very well know that I can live but a
astronomer and physician Avicenna (Ibn Seena). shorter time. Doctor Beatty replied: My Lord,
Leonardo da Vinci (14521519) was the first unhappily for our country, nothing can be done
to describe the physiological curvatures of the to you.
6 SPINAL CORD INJURY
The second celebrity, James Abram Garfield, In 1814, the English surgeon Henry Cline per-
the 20th president of the United States, became formed a laminectomy at the thoracic level. The
victim of an attempted assassination by a crazed patient, who suffered a fracture and a SCI, died
gunman in Washington D.C., in 1881. One nine days later. This resulted in a quite nihilistic
bullet lodged itself somewhere inside the attitude toward this type of surgical intervention,
Presidents body and was later found during as is illustrated by the following quotation from
autopsy a few inches from the spinal canal. The 1824: Laying a patient upon his belly and by inci-
famous scientist and inventor Alexander sions laying bare bones and exposing the spinal
Graham Bell devised a metal detector specifically marrow itself, exceeds all beliefs. However, a
for the purpose of finding the bullet, but the successful laminectomy performed following
metal bed frame on which Garfield was lying trauma was reported soon thereafter in 1829, by
made the instrument malfunction and the the American surgeon Gilpin Smith. The operation
bullet was not found. The president died a few resulted in improved sensibility and the pro-
months later as a result of internal bleeding and gressive neurological deterioration seen before
infection, the latter probably caused by insertion surgery was reduced. Charles Bell introduced
of unsterilized instruments into the wound. the clinically important concepts of spastic and
CHAPTER 1 HISTORY 7
flaccid paralysis in 1824, and he also described the group of patients by approximately 2000% since
concept of spinal shock. 1940.
During World War I, mortality following SCI Modern care of the SCI patient requires
was as high as 80% within the first two weeks knowledge within a variety of medical fields
following injury. Given these poor prognostic such as rehabilitation, urology, intensive care,
figures, a nihilistic attitude toward treatment algology, orthopedics, neurosurgery, fertility,
persisted during the 1920s and 1930s, until the and pharmacology, and also an interest in
modern era of rehabilitation began in 1943. In research and development. At present, the goal
that year, the Stoke Mandeville National Spinal of healing the injured spinal cord is still out of
Injuries Centre was opened in England by neu- reach. There exist, however, many therapeutic
rosurgeon Sir Ludwig Guttmann. A similar pio- measures to offer the SCI patient as to improve
neering work was conducted by Bors in the USA. his health and quality of life. Within the field of
The well-structured and comprehensive rehabi- SCI, the main focus of research is currently
litation at the center did not only help patients directed toward neuroprotection and, especially,
survive but also to readapt to society. The Stoke regeneration. Another ongoing challenge within
Mandeville Centre was, and is still, a model for the area of rehabilitation is to offer treatments in
many other rehabilitation units around the order to ensure a long, healthy, and fulfilling life.
world. The implementation of the treatment
model developed by Guttmann, together with Suggested Reading
concurrent progress within other fields of med- Lifshutz J, Colohan A. A brief history of therapy for
icine, has prolonged the survival time for this traumatic SCI. Neurosurg Focus 2004;16(1):18.
8 SPINAL CORD INJURY
9
10 SPINAL CORD INJURY
TABLE 2.1 Epidemiological data relating to Paresis refers to incomplete injury, which means
traumatic SCI in a European country that some degree of residual neurological func-
(Sweden). tion is present below the level of injury. Plegia
and Paralysis refer to complete injury. Tetra indi-
Incidence 1015
cates neurological involvement of both arms and
Prevalence 5,000
legs, whereas para indicates that only the lower
Age extremities are involved. The most common level
Mean age at injury 31 years of neurological injury in the cervical spine is C5.
Age at injury <30 years 5070% Among paraplegics, T12 is the most common
Age at injury >50 years 25% level of neurological injury.
Gender
male: female 4:1 ETIOLOGY
Completeness of lesion
Complete 45% Motor vehicle accidents are by far the most
(AIS A) common cause of acute SCI (44%). Accidents
related to acts of violence (24%), falls (22%),
Incomplete
sports (8%), and other factors (2%) are other
AIS B 15%
common causes. In Europe, falls are more com-
AIS C 10%
monly the cause of SCI, and in some countries
AIS D 30%
falls have become the dominant cause.
Level of lesion Additionally, the presence of acts of violence
Cervical spine 55% varies considerably between regions and over time.
Thoracic spine 15%
Thoracolumbar spine 15%
Relationship to Head Injuries
Lower lumbar spine and sacrum 15%
Ratio of paraplegia to tetraplegia 3:2 According to the U.S. Centers for Disease Control
Most common level of injury (CDC), for each case of traumatic SCI there occurs
Cervical C5 about 30 cases of moderate (Glasgow Coma Scale
[GCS] 913) to severe (GCS 38) traumatic brain
Thoracic Th12
injury.
Most common etiology In about 20% of cases, other severe injuries,
Motor vehicle accidents 4050% such as brain and thoracic injuries, also occur
Relationship to moderate/severe head among SCI patients. Only one-fifth of acutely
injury injured SCI patients have an isolated spinal
SCI: head injury 1:30 cord lesion.
Remaining life expectancy (injured at 20
years of age) SOCIOECONOMIC DATA
High tetraplegic 33 years
Low tetraplegic 39 years In addition to the personal tragedy associated with
Paraplegic 44 years SCI for the patient and family, society is also
burdened by massive costs resulting from these
injuries and their sequelae. The cost of medical
care for the first year for a patient with high tetra-
plegia is estimated at $800,000; for a patient with
The occurrence of SCI is further subdivided
low tetraplegia it is estimated at over $500,000;
by the AIS as:
and for a patient with paraplegia at $300,000. If a
Tetraplegia (complete) 20% person sustains a SCI at the age of 25, lifetime
Tetraparesis (incomplete) 30% medical costs are estimated at over $3.3 million in
Paraplegia (complete) 30% the case of high tetraplegia, $1.8 million for low
Paraparesis (incomplete) 20% tetraplegia, and $1.1 million for paraplegia. About
CHAPTER 2 EPIDEMIOLOGY 11
half of all acutely injured patients are single at the Suggested Reading
time of injury. The marriage rate is about 60% DeVivo MJ, Vogel LC. Epidemiology of spinal cord injury
lower and the divorce rate is about 2.5 times in children and adolescence. J Spinal Cord Med
higher than in the noninjured population. 2004;27(Suppl 1):S4S10.
Divanoglou A, Levi R. Incidence of traumatic spinal cord
injury in Thessaloniki, Greece and Stockholm,
MORTALITY AND LIFE EXPECTANCY Sweden: a prospective population-based study. Spinal
Cord April 2009. Epub ahead of print.
The immediate or early mortality for this patient Furlan JC, Krassioukov AV, Fehlings MG. The effects of
gender on clinical and neurological outcomes after
group is probably relatively high and largely acute cervical spinal cord injury. J Neurotrauma
dependent on other injuries such as head injury, 2005;22(3):368381.
multiple trauma, and/or respiratory arrest in Garrison A, Clifford K, Gleason SF, et al. Alcohol use
cases of high tetraplegia. However, mortality associated with cervical spinal cord injury. J Spinal
during subsequent hospital care is only 3% Cord Med 2004;27(2):111115.
Kirshblum S, Millis S, McKinley W, Tulsky D. Late neu-
during the acute phase. In the past, death over rological recovery after spinal cord injury. Arch Phys
the long term was mainly due to renal failure. Med Rehab 2004;85(11):18181825.
Advances in urinary tract management have led Kraus JF, Silberman TA, McArthur DL. Epidemiology of
to a significant reduction in renal failure as cause spinal cord injury. In: Menezes AH, Sonntag VKH,
of death. Instead, deaths today are predominantly eds., Principles of Spinal Surgery. New York: McGraw-
Hill, 1996:4158.
due to cardiovascular diseases, pneumonia, pul- Krause JS, Zhai Y, Saunders LL, Carter RE. Risk of mor-
monary emboli, and septicemia. tality after spinal cord injury: an 8-year prospective
The remaining life expectancy of individuals study. Arch Phys Med Rehabil 2009; 90(10):17081715.
injured at age 20 has been calculated to: Levi R. The Stockholm spinal cord injury study: medical,
economical and psycho-social outcomes in a preva-
33 years with high tetraplegia lence population (doctoral dissertation). Stockholm:
39 years with low tetraplegia Karolinska Institutet, 1996.
44 years with paraplegia National Spinal Cord Injury Data Base. Arch Phys Med
Rehab 1999;80(11):1363.
High tetraplegia usually refers to a neurological Tator C. Epidemiology and general characteristics of the
level of injury at C5 or higher (see Chapter 8). spinal cord-injured patient. In: Tator CH, Benzel CH,
eds., Contemporary Management of Spinal Cord Injury:
The prognosis for long-term survival is particu- From Impact to Rehabilitation. Park Ridge, IL:
larly unfavorable among ventilator-dependent American Association of Neurological Surgeons,
patients. 2000:7273.
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3 Anatomy and Physiology
A brief review of the spinal cord anatomy and lumbar enlargement (intumescentia lumbosa-
physiology is presented in this chapter. The cralis) gives rise to nervous structures forming
spinal cord transmits sensory information to the lumbar (L1L5) and sacral (SIS3) plexus,
the brain and also plays a crucial part in the which innervate the lower limbs.
regulation of motor and autonomic function. The terminal end of the spinal cord becomes
Knowledge of some basic anatomy and phy- narrower in shape and is denoted the conus
siology, will make it easier to understand the medullaris. It contains the sacral segments
clinical conditions presented later in this book. responsible for sensory information from the
We have deliberately omitted description of ver- lower part of the abdomen and genitals, for reg-
tebral column anatomy here; the anatomy of the ulation of motor sphincter functions and for
spinal column and adjacent supporting struc- parasympathetic innervation of the bladder wall
tures will be illustrated in Chapters 1015, in and distal part of the bowel (Fig. 3.1C; see same
association with the presentation of fracture figure in the Color Plate section).
classifications. The caudal extension of the conus medullaris
is called the filum terminale. It is enclosed in the
GROSS ANATOMY pia mater and extends down to the coccyx. The
filum terminale is finally attached, together with
The human spinal cord is cylindrical in appear- the dural sac extension (coccygeal ligament), to
ance and has a diameter of approximately 1 cm. It the coccygeal periosteum. The spinal cord is
is slightly flattened anteriorly as well as poster- localized centrally in the spinal canal by result
iorly. The spinal cord originates from the caudal of this attachment. Nerve roots originating from
part of the medulla oblongata. It leaves the skull the lumbar and sacral level surround the filum
through the foramen magnum and extends down terminale. The bundles of nerves resembles a
into the vertebral canal (Fig. 3.1A,B,C). Caudally, horses tail, and this structure is thus called the
in adults, it ends approximately at the disk level cauda equina. Horizontal extensions of the pia
between the first and second lumbar vertebrae mater are attached through the arachnoid to
(L1 and L2), and its length ranges between 42 the dural sac on each side of the spinal cord
and 45 cm. The spinal cord is divided, in the between the dorsal and ventral roots. These
craniocaudal direction, into the pars cervicalis, structures, the ligamenta denticulata, are located
pars thoracica, pars lumbalis, and pars sacralis. between the foramen magnum and the vertebral
The pars cervicalis, for example, corresponds to level of T 12 to L1 and prevent the spinal cord
that part of the spinal cord from which eight pairs from undesired movements.
of cervical spinal nerves emanate. The spinal cord The spinal cord contains 31 pairs of spinal
contains two thicker regions intumescentia cer- nerves (8 cervical, 12 thoracic, 5 lumbar, 5
vicalis and lumbalis. The cervical enlargement sacral and 1 coccygeal; Fig. 3.1A) and their corre-
(intumescentia cervicalis) is located between the sponding 31 segments. Each pair of nerve roots
fifth cervical (C5) and the first thoracic (T1) ver- exits the spinal canal through the intervertebral
tebrae. The spinal nerves originating from the foramina. The first seven pairs of cervical nerve
intumescentia cervicalis comprise the brachial roots exit through the intervertebral foramina
plexus that innervates the upper limbs. The above the correspondingly numbered vertebra.
13
14 SPINAL CORD INJURY
Spinal cord
Dura
mater
C1 2 Cervical
3 enlargement
Pars 4
cervicalis
5
6
C7
7
T1 8
Th1
2
3
4
Pars
thoracica 5
6
Lumbocsacral
7 enlargement
8
Conus medullaris
9
10
Pars 11
lumbalis T12
12
L1
Pars L1 Filum terminale
sacralis
Cauda equina
B)
3
4
L5
S1
5
d
c
S1 b
2
3 e
4
5
a
Nervus coccygis
A) Coccyx C)
Figure 3.1 Spinal cord topography. A: Side view. B: Front view C: Exposed spinal cord. a, dural sac; b, spinal
cord; c, conus medullaris; d, filum terminale; e, dorsal nerve root. See also Color Plate Fig. 3.1C.
CHAPTER 3 ANATOMY AND PHYSIOLOGY 15
However, the eighth pair of cervical nerve roots and below usually suffer from fractures located
leave the spinal canal between the C7 and T1 at the level of the T6 vertebra.
vertebra due to the existence of only seven cervical
vertebrae. The thoracic, lumbar, sacral and coccy- The Spinal Cord Meninges
geal nerve roots then exit through intervertebral
foramina located below the correspondingly num- Three layers of coverings (i.e., spinal meninges;
bered vertebra. The third thoracic pair of nerve Fig. 3.2A,B) surround the spinal cord. The outer-
roots, as an example, extends through the inter- most of these, the dura mater, consists of elastic
vertebral foramina between the third and fourth connective tissue and forms a sheath around the
vertebral bodies. spinal cord. The spinal dura is single-layered and
The lengths of the spinal column and spinal lacks the periosteal layer of the cranial dura. It is
cord are equal in the first trimester of fetal devel- therefore separated from the inner surface of the
opment. Connections are established during that bone forming the spinal canal, leaving a potential
period between the peripheral structures such as space between the dura and the bony surface, the
skeletal muscle fibers and spinal nerves, the epidural space. This space contains mainly fatty
latter extending through the intervertebral fora- tissue and venous plexuses. The spinal dura
mina almost horizontally. The vertebral column extends cranially to the level of foramen
then grows caudally during the second and third magnum and joins the inner meningeal layer of
trimester of development. The spinal cord, how- the cranial dura. Caudally, approximately at the
ever, does not extend to the same degree. level of the second sacral vertebra, the dural sac
Consequently, each part of the spinal cord is becomes narrower, in order to cover the filum
located more cranial to its corresponding ver- terminale, and is finally attached to the coccygeal
tebra. The length of each nerve root located in periosteum.
the spinal canal increases the more caudally the The arachnoid membrane, the middle cov-
pair of nerve root exits the spinal canal as a result ering, is attached to the inner surface of the
of this discrepancy in growth. The shortest dural sac. Normally, there is no space between
intraspinally located pair of nerve roots are thus these two coverings, and the arachnoid mem-
located within the cervical spine and the longest brane follows the dural sac caudally to the level
at the sacral level. of S2, where the cauda equina is finally enclosed.
The relation between vertebral spinous pro- The innermost layer, the pia mater, covers the
cesses and corresponding spinal cord segments spinal cord. The pia mater continues caudally
can be estimated as follows. As rule of thumb, as the filum terminale and attaches with the
add one to the number of the spinous processes dural sac to the coccygeal periosteum, thereby
of C2C5 to obtain the corresponding segment of preventing unnecessary movement of the
the spinal cord. Correspondingly, add two spinal cord.
between the spinous processes of C6T6, and The subarachnoid space, i.e., that space
finally add three in the interval between between the arachnoid membrane and pia
T7T10. The spinous process of the fifth thoracic mater, contains cerebrospinal fluid (CSF). The
vertebra is, for example, located at the level of the lumbar cistern, i.e., that area of the spinal canal
seventh thoracic segment of the spinal cord. containing the most CSF, is located between the
The spinous processes of T11T12 are located second lumbar and second sacral vertebral
at the level of the fifth lumbar spinal cord bodies (Fig. 3.3). This enlargement of the subar-
segment and the spinous process of LI is located achnoid space is routinely accessed for sampling
at the level of the fifth sacral spinal cord of CSF. Lumbar puncture (spinal tap) is per-
segment. This discrepancy between the num- formed with low risk despite the proximity of
bering of vertebrae and spinal cord segments multiple nerve roots in the cistern. These nerve
has important clinical implications. For roots, bathed in the CSF, slide away from the
example, patients exhibiting deteriorated sen- contact of the needle and are not injured during
sory function from the T9 segment (dermatome) the procedure.
16 SPINAL CORD INJURY
Anterolateral sulcus
Posterolateral sulcus
Pia mater
Arachnoid Subarachnoid
membrane space
Dura mater
A)
Subarachnoid
space
Ligamentum
Dorsal root
denticulatum Spinal nerve
Ramus dorsalis
Ramus ventralis
Ramii communicantes
B)
Figure 3.2 A: Spinal cord meninges. B: Nerve root anatomy in the vicinity of the spinal cord.
Canalis
centralis Posterior funiculus
Dorsal root
I Sulcus lateralis
II posterior
III
IV
V CP
VI
Lateral
VII funiculus
CA
X
VIII
IX
Sulcus lateralis
anterior
Figure 3.4 Neuroanatomic organization of the spinal cord. CP, cornu posterior; CA, cornu anterior. Roman
numerals indicate the cytoarchitectonic map according to Rexed.
18 SPINAL CORD INJURY
Funiculus Funiculus
gracilis Sulcus lateralis posterior
cuneatus
Lissauer's tract
Tractus
spinocerebellaris Tractus corticospinalis
posterior lateralis
Tractus rubrospinalis
Tractus
spinothalamicus Tractus reticulospinalis
lateralis lateralis
Tractus vestibulospinalis
lateralis
Figure 3.5 Cross-sectional illustration showing the distribution of the spinal cord pathways.
Gray Substance (Substantia Grisea) bodies located in the dorsal root ganglia, transmit
impulses to neurons in the posterior horns via
Both halves of the gray matter are connected at synapses. The sensory information is thereafter
the midline by a structure called the substantia either conveyed cranially to centers in the brain
intermedia centralis (Fig. 3.4). The anterior and or into the local spinal cord circuitry. The anterior
posterior part of the substantia intermedia horn contains mainly motor neurons innervating
centralis is also called the anterior and posterior skeletal muscles and interneurons. Lateral horns
commissure, respectively. The central canal (not illustrated) are found in the thoracic and
(canalis centralis) is located in the center of the upper two lumbar segments of the spinal cord
gray substance and serves as a CSF pathway only. They contain preganglionic sympathetic
between the fourth ventricle in the brainstem neurons which belong to the autonomic nervous
and the ventriculus terminalis, which constitutes system. The axons of the lateral horns exit the
the ventricular system termination in the conus spinal cord through the ventral roots together
medullaris. The H-shaped gray matter is further with the axons of the motor neurons.
divided, on the left as well as the right side, into
anterior and posterior horns, the cornu anterior White Substance (Substantia Alba)
and posterior, respectively. The entire gray sub-
stance is also divided into ten laminae named White matter is composed of, as previously men-
after the Swedish neuroanatomist, Bror Rexed. tioned, bundles of ascending and descending
The Rexed laminae IVI constitute the posterior myelinated and unmyelinated axons (fasciculi
horn, while the laminae VIIX are located in the or tracts) running in a craniocaudal direction. A
anterior horns and substantia intermedia bundle containing two or more tracts is called a
centralis. funiculus. The white matter contains three funi-
Nerve cells mediating sensory (afferent) infor- culi on each side of the midline, the anterior,
mation are, as previously mentioned, located in lateral, and posterior funiculi (Figs. 3.4 and
the posterior horns. Neurons, with their cell 3.5). The posterior funiculi from C1 to T6 are
CHAPTER 3 ANATOMY AND PHYSIOLOGY 19
subdivided into a medial (fasciculus gracilis) and gracilis after which they synapse, one or two
lateral part (fasciculus cuneatus). Axons cour- segments cranially, in nucleus dorsalis located
sing within the gray matter of one segment con- in Rexed lamina VII. Corresponding informa-
stitute the basis for the segmental reflex arc. tion above the level of C8 is transmitted via the
Bundles running just outside the gray matter fasciculus cuneatus to the medulla oblongata.
form intersegmental (propriospinal) tracts that The proprioceptive information is integrated
interconnect spinal cord segments. Finally, there with impulses from mechanoreceptors of the
are neurons connecting both the segmental and inner ear by the cerebellum, providing a basis
intersegmental tracts, with centers mainly for maintenance of body balance and position.
located in the brain.
The Anterolateral System
SPINAL CORD PATHWAYS
The anterolateral systems, which includes the
Ascending Tracts lateral spinothalamic tracts, constitutes one of
the most important clinical pathways in the
Posterior Funiculi spinal cord (Figs. 3.5 and 3.7). This pathway
transmits pain and temperature impulses from
The posterior funiculi are often referred to as the the skin, joint capsules, and skeletal muscle to the
dorsal (posterior) columns (Figs 3.5 and 3.6). The thalamus. Cell bodies of the peripheral sensory
heavily myelinated axons located in the posterior
columns are responsible for conscious proprio- Sensorimotor cortex
ception: kinesthesia (sense of position and move-
ment) and discriminative touch (ability to
separate two points and to localize touch stimuli).
Homunculus
Injuries to the dorsal columns lead to reduced or
lost ability for vibratory sense, stereognosis (the
capacity to identify the form and shape of various
objects), two-point tactile discrimination, touch,
Thalamus
and weight perception ipsilaterally caudally to
the level of injury. The sensory fibers entering
the spinal cord below the sixth thoracic segment Medial lemniscus
form the fasciculus gracilis, whereas those entering
above that level form the fasciculus cuneatus. The
vast majority of the sacral and cervical nerve cell Medulla oblongata
axons are located medially and laterally in these
pathways, respectively.
Complete damage to the dorsal columns
results in loss of position and movement ability,
Dorsal root
and this sensory loss leads to clumsy, poorly coor- ganglion Fasciculus gracilis
dinated movements. This condition is referred to
as dorsal column ataxia or sensory ataxia. Spinal cord
the diencephalon, through the brainstem, and movement. This tract is considered particularly
terminate within the spinal cord. The corticosp- important in regulating the precise movements
inal tract consists mainly of nerve cells that influ- of the fingers. About 1020% of the nerve fibers
ence spinal cord motor neurons. The overall of the corticospinal tract remain uncrossed as
function is consequently to mediate voluntary they descend to the spinal cord, and these fibers
movements in skeletal muscles. Between 80% form the anterior corticospinal tracts. This
and 90% of the nerve fibers cross to the contral- pathway contributes to the innervation of
ateral side at the transition between the medulla muscle located in the neck and trunk. It contains
oblongata and spinal cord (the pyramidal decus- consequently both uncrossed nerve fibers as well
sation), and the lateral corticospinal tract is as nerve fibers crossing the midline segmentally
formed (Figs. 3.5 and 3.8). The somatotopic orga- in the spinal cord before they synapse with
nization established in the cortex persists, and contralaterally located neurons.
cervical fibers are located medially and are The neurons forming the corticospinal tracts
followed in a lateral direction by the thoracic, are called upper motor neurons. The a-motor
lumbar, and sacral nerve fibers. The lateral corti- neurons located in the anterior horn of the
cospinal tract influences spinal cord motor spinal cord and their axons innervating the
neurons innervating the upper and lower skeletal muscles are the lower motor neurons.
limbs, and mediates skill and precision in Acute lesions affecting the upper motor neu-
rons result initially in a complete block of the
nervous activity below the lesion, since stimula-
tion of the segmental reflex activity ceases.
These patients present with a flaccid paralysis
of muscles, muscular hypotonia and, also, a loss
of bowel and urinary bladder reflexes (spinal
shock) as conduction activity is lost. If, the
lesion is located above T6, symptoms such as
bradycardia and hypotension will also appear.
This circulatory condition is called neurogenic
shock. The segmental reflex activity returns
within a few days or weeks following the acute
motor neuron lesion, due to activation of pre-
viously silent synapses and sprouting activity
Medulla oblongata of surviving axons finding new possibilities
for synaptic connections. Symptoms such as
spasticity, hyperactive bowel and bladder,
tendon reflex activity, and presence of the
Babinski sign indicate returning nervous
activity. However, a partial or complete
inability to perform voluntary motor activity
Spinal cord often remains also after the spinal shock has
resolved.
travel through the spinal cord in the lateral funi- consequence of injuries to this tract. The medial
culus. The function of this tract is, according to vestibulospinal tract cooperates with the labyrinths
the standard view, connected to the lateral corti- of the inner ear to control head position. The
cospinal tract and associated with mediation of reticulospinal tracts contain neurons originating
voluntary movements. The lateral vestibulospinal from the formatio reticularis located in the brain-
tract is an uncrossed tract originating from neu- stem at the level of the pons and medulla oblon-
rons located in the lateral vestibular nucleus situ- gata. The pathways are uncrossed and descend
ated in the borderland between the medulla down to the anterior and lateral funiculi of the
oblongata and the pons. It regulates extensor spinal cord. It has been demonstrated in animal
muscle tonus, in order to maintain the upright studies that this pathway modulates voluntary
position. The more devastating lesions to the lat- muscle movements, muscle tone, reflex activity,
eral spinothalamic tract often camouflage the and breathing capacity.
Sympathetic Parasympathetic
division division
III
Eye
Lacrimal VII
glands
IX
Salivary
glands
Bronchi
Heart
Upper
digestive
system
Liver
Adrenal
medulla
Lower
digestive
system
Urinary
bladder
Genitals
and sweat glands
To blood vessels
S2 - 4
Radicular Arteries
Vasocorona artery
Figure 3.12 Cross-sectional view showing the arterial supply of the spinal cord.
CHAPTER 3 ANATOMY AND PHYSIOLOGY 25
Flexor Reflex
Sensory
neuron
Inhibitory
interneuron
Inhibitory
interneuron
Inhibitory
motor neuron
Excitatory
motor neuron
Injuries to the spinal cord typically occur caused by a blow to the cord in the clinical setting.
following severe trauma, such as that caused by The device used in the experimental situation
vehicular accidents or falls. Extraspinal injuries consists of a cylinder, placed perpendicularly
and complications are often seen in several to the spinal cord, and a plastic impounder
organ systems both acutely, as well as in later that rests on the intact dura mater. A weight is
stages. This chapter addresses the posttraumatic then dropped from a predetermined height,
events that occur locally in the spinal cord. resulting in a kinetic impact to the spinal cord.
Our knowledge about the complex pathophy- The intensity of the injury is described in terms of
siological processes that are seen following gramcentimeterforce (GCF).
trauma to the spinal cord has increased during By contrast, static models, in which the spinal
the last decades, although crucial pieces of the cord is compressed but not impacted, represent
puzzle are still missing. A close cooperation yet another component of the real-life injury
between basic scientists and scientifically active mechanism. Here, the load is sustained for up to
clinicians has been established to map and better several minutes by a steady compression, thus
understand the various mechanisms that are reflecting an aspect of true trauma different
activated following an injury to the spinal cord. from the very transient and abrupt kinetic
However, most of our knowledge regarding impact caused by the weight-drop technique.
these processes has been obtained from experi- The compression model mimics a clinical situa-
mental animal studies (Table 4.1). tion in which sustained compression is caused by,
for example, bony fragments, extruded disk mate-
ANIMAL EXPERIMENTAL MODELS rial or epidural hematoma (Fig. 4.1).
29
30 SPINAL CORD INJURY
Crush injury
Extradural clip Modified aneurysm clips exerting various closing Initial millisecond impact to the spinal cord 1 Cord maceration
compression forces are applied extradurally around the
exposed spinal cord
Miscellanous
Transection The spinal cord is transected with a scalpel Laceration injury following knife wound 2 Laceration injury
and/or gunshot
Aortic occlusion The aorta is closed below the renal artery Ischemia 4 Solid cord injury
32 SPINAL CORD INJURY
VASCULAR MECHANISMS
Weight
A transient increase in systemic arterial blood
pressure, followed by hypotension, is seen in
immediate connection to the injury. These
cardiovascular alterations are caused by the
response of the sympathetic nervous system.
The sustained hypotension, together with the
damage to the spinal cord itself, results in a
decrease in spinal cord blood flow. It has
been proposed that this reduction in spinal
cord blood flow is the major contributing
factor behind most of the dynamic secondary
R
injury mechanisms. The term hypoperfusion
describes a situation with impaired or
reduced spinal cord blood flow without
reaching the critical threshold to result in
Figure 4.1 Static compression injury model. damage to the spinal cord tissue. Ischemia
R = exposed dural sac. occurs if the reduction of spinal cord blood
flow is severe enough and the duration of the
reduction persists long enough so that tissue
injury appears. Various secondary injury
mechanical damage results in tissue necrosis in
mechanisms are triggered as a consequence
contused areas; this damage seems to adversely
of ischemia, and those contribute to an ongoing
affect the gray matter earlier in the injury process
destruction (autodestruction) of spinal cord
than the white matter. A ring of preserved white
tissue.
matter surrounding the necrotic gray tissue thus
Changes in spinal cord blood flow may affect
remain in the post-acute period.
initially undamaged tissues of the gray
The injured nerve cells, during the first min-
and white matter in various ways. Local minor
utes following trauma, initiate increased firing of
bleeding and reduced spinal cord blood flow can
action potentials before impulse conduction
be observed in the gray matter after only 5 min-
ceases. An intracellular increase of sodium and
utes. A correlation exists between the degree of
calcium and an extracellular increase of potas-
spinal cord blood flow reduction and the
sium to toxic levels are examples of ionic
severity of spinal cord tissue damage. It has
derangements observed. These early changes
been shown in animal experiments that spinal
consequently result in a failure of normal
cord blood perfusion remains reduced for at
impulse transmission.
least 24 hours following the initial insult. The
blood flow in the white matter is simulta-
SECONDARY SPINAL CORD INJURY neously reduced after 5 minutes, but, conver-
sely to that in gray matter, resumes relatively
The secondary injury mechanisms begin within quickly, sometimes within 15 minutes of initial
minutes to days following injury. These mechan- insult, if permitted by the condition of the
isms include a variety of processes that, taken tissue. Vascular changes, such as damaged
individually or together, lead to cellular damage microcirculation and reduced or eliminated
and, ultimately, to cell death (see Table 4.2). autoregulation, are responsible for reduced
Vascular and biochemical changes, inflammation, spinal cord blood flow, subsequent ischemia,
edema, and apoptosis are examples of key and ultimate cell death.
CHAPTER 4 PATHOPHYSIOLOGY 33
A) B)
C)
Figure 4.2 Axial histological illustrations showing tissue changes at different times after injury. A: One hour
post-injury. Observe the small petechial bleedings mainly located in the gray matter. B: Twenty-four hours
post-injury. Extensive bleeding is seen in the gray matter. Blister-like vacuoles are seen within the white
matter. C: Nine days after injury. A necrotic area is seen in the posterior column region. The central canal is
indicated with an arrow.
Damage of nervous
tissue and vasculature Ionic derangements
Secondary
Injury
Mechanisms
Cell Death
the enzyme superoxide dismutase. The H2O2 is ultimately to cell death. This pathological lipid
eventually converted by the enzyme catalase to peroxidation is probably mediated by excitatory
water (H2O) and oxygen (O2). The protective effect amino acids and by a simultaneous increase in
of these enzymes on these reactive (toxic) free the intracellular calcium level.
oxygen radicals may, metaphorically, be compared
to that of a sponge which absorbs liberated free
Ionic Mechanisms
oxygen radicals and converts them to H2O and O2.
Changes in the oxidative mechanisms are seen The neurons of the spinal cord contain voltage-
following injury to the spinal cord. Iron (Fe2) is, regulating membranes responsible for neuronal
for instance, released from hemoglobin, and the impulse transmission (Fig. 4.5). The levels of
extremely powerful hydroxyl radical (.OH) is mainly extracellular sodium and chloride and
formed instead of H2O2 (Fig. 4.4). The hydroxyl intracellular potassium determine the membrane
radicals initiate an accelerated lipid peroxidation, potential. This membrane potential results from
a process somewhat similar to the growth of a an energy consuming transportation of ions across
snowball rolling downhill. This process begins the cell membrane and the permeability of the
only a few minutes after trauma. It results in the membrane to these ions. The voltage of an inactive
breakdown of the polydesaturated fatty acids cell remains close to a resting potential, with excess
in the lipid-containing cell membranes and of negative charge contained inside the cell. The
cell triggers an action potential when the mem-
Fentons reaction brane of an excitable cell becomes depolarized
beyond a threshold; that is, an impulse is trans-
Fe2+ + H2O2 Fe3+ + OH + OH mitted. The availability of energy, in the form of
Haber-Weiss reaction catalysed by iron ions adenosine diphosphate (ADP), is reduced when
spinal cord blood flow is decreased following
O2 + H2O2 ! OH + HO + O2 damage to the axons. The ionic equilibrium is
lost, and the membrane potential (depolariza-
Figure 4.4 The two most common mechanisms tion) is reduced. Sodium enters the intracellular
behind the formation of hydroxyl radicals (OH). space and remains there permanently.
Ca2+
Ion channel
Extracellular
Phospholipid
Cholesterol
Intracellular
Ca2+
Ca2+
This influx of sodium results in a corre- reduction of spinal cord blood flow in experi-
sponding influx of calcium, which further acceler- mental models. Introduction of receptor-binding
ates nerve cell breakdown. The increase of opioid receptor antagonists has been shown to
intracellular calcium is related to cell death, prevent peptides from attaching to the receptors
although the precise mechanism is unknown. and their effect on spinal cord blood flow is thus
Possibly, increased intracellular calcium influ- blocked. The postulated possible beneficial effect
ences enzymes, such as phospholipases and phos- of opioid receptor antagonists resulted in a clin-
phatases, to promote the breakdown of the cell ical trial using naloxone, although beneficial
membrane. These breakdowns results in the lib- effects could not be confirmed by these clinical
eration of free fatty acids, which are converted to, studies.
among other substances, prostaglandins. The pre-
sence of prostaglandins further increases the con- INFLAMMATION
striction of the blood vessels (vasospasm), which
in its turn also contributes to final cell death. The CNS is usually protected from inflammatory
reactions due to the ability of the bloodbrain
Excitatory Amino Acids barrier to keep immunologically active cells
away from brain and spinal cord. An invasion
Glutamate and other excitatory amino acids of immunologically active cells to the damaged
accumulate in the extracellular space within spinal cord is seen following the demolition of
15 minutes following injury. The concentration the bloodbrain barrier and results in an initia-
of these amino acids reaches toxic levels, with tion of the inflammatory response. Neutrophils,
concentrations about six to eight times above T-lymphocytes, and macrophages are cells
normal values. The precise destructive mecha- participating in this inflammatory response.
nism of the excitatory amino acids is still The invading T-lymphocytes release cytokines,
unknown. However, calcium and the excitatory proteins, and peptides with signalling properties
amino acids pass into dendrites and cell bodies that act like hormones and neurotransmitters.
when sodium channels are opened at the time of These cytokines are of great interest in research
injury. Various receptors are affected by the because of their cytotoxic effects. The cellular
released glutamates, resulting in an additional process of phagocytosis is the most important
influx of calcium and other positive ions. property of the macrophages, but these cells
Accumulation of calcium in the intracellular also release substances with cytotoxic proper-
space is probably the most likely mechanism ties. Inflammatory mediators are consequently
behind the neurotoxic action of the excitatory responsible for an increase in spinal cord tissue
amino acids. damage, and many inflammatory mediators
such as prostaglandins, serotonins, and leuko-
Opioid Receptors trienes contribute to this tissue destruction.
slightly opened if energy access in the damaged peak 23 days after injury and regresses at the
tissue is restricted to 6070% of normal levels. end of the first posttraumatic week. Spinal cord
Injurious molecules enter into the cells and edema often extends one to two levels above
initiate a chain reaction of molecular events. injury level and probably contributes to the neu-
The enzyme caspase is one of these injurious rological deterioration seen immediately fol-
molecules, promoting cutting and breaking lowing injury. Aggravation of edema formation
down of other proteins. The final stage of apop- occur with excessive administration of i.v. fluids
tosis includes a caspase-dependent activation of in the acute stage (see Chapter 6). Excessive infu-
enzymes, which cleaves DNA. The DNA of the sions of fluid constitute a threat to the function
cells is thus reduced to fragments, leading to cell of the spinal cord in the first 23 days following
death. Apoptosis is morphologically character- injury. The accumulation of edema initiates, pre-
ized by cell shrinkage, chromatin condensation, serves, and prolongs most of the other secondary
and chromosomal fragmentation. The macro- injury processes, and this eventually contributes
phages absorb dead cells without initiating an to increased cell death in the early posttraumatic
inflammatory response. The cellular content is stage. The tissue destruction continues to pro-
not transported to the extracellular space, and gress both rostrally and caudally from the injury
the disposal of cellular debris does not damage site during the final chronic stage. This chronic
the organism. Apoptosis strikes the oligoden- stage may persist for many years. Various recep-
drocytes most frequently. Demyelinization tors and ionic channels change their degree of
occurs if oligodendrocytes die, since these cell activity, and macrophages as well as neutrophil
provide myelin to the surviving axons (see also polymorphs remove devitalized tissue. A conti-
Chapter 34). nuing demyelinization of the white matter
Necrosis, by contrast, is a less energy-dependent results in a progressive transmission failure of
process. The mitochondria are activated if the nervous impulses. The axons degenerate
energy access in the tissue is reduced to less (Wallerian degeneration, i.e., breakdown of axons
than 30% of normal levels. The ionic pumps distal to the lesion), and the spinal cord shows
lose their function, and lysis of all cell structures signs of atrophy. Cavities, with or without fluid,
begins. Cellular edema and damage to the mito- develop. Adhesion of the spinal cord to adjacent
chondria, disruption of the cellular membranes, structures (e.g., the spinal meninges) is seen in
and an inflammatory response morphologically areas subjected to infiltration of connective
characterize necrosis. This results in a release tissue, as when there is damage to the outer sur-
of intracellular contents to the extracellular face of the spinal cord. The diameter of the cen-
surroundings and, finally, cell lysis. tral canal increases, and the continuing
accumulation of cerebrospinal fluid results in
EDEMA the formation of cyst cavities in about 50% of
spinal cord injured patients.
Normally, intra- and extracellular fluid diffuses
through the semipermeable endothelium in a CONCLUSION
balanced ebb and flow. However, the largest
volume of fluid is accumulated in the intercel- The pathophysiological events following an
lular space following trauma to the spinal cord. injury to the spinal cord can be divided into
Signs of edema (an increased accumulation of primary, secondary, and chronic phases. The
fluid) occur shortly after injury, and this edema primary injury comprises direct mechanical
is mainly located in the border zone between destruction of nervous tissue and vascular struc-
gray and white matter. Damage to the endothe- tures. The effects of the primary trauma are
lium constitutes the prerequisite for edema for- considered irreversibleno known treatments
mation and results in fluid leakage into the can repair these damages and improve neurolo-
extracellular space. Arachidonic acid and its gical function. A transformation from primary to
metabolites mediate the progressive edema secondary injury mechanisms occurs gradually,
accumulation. Edema formation reaches its during a period ranging from minutes to days
38 SPINAL CORD INJURY
after injury. A cascade of vascular mechanisms, Beattie MS, Hermann GE, Rogers RC, Bresnahan JC. Cell
biochemical alterations, inflammation, edema, death in models of spinal cord injury. Prog Brain Res
2002;137:3747. Review.
and apoptosis contributes to an ongoing auto-
Bramlett HM, Dietrich WD. Progressive damage after
destruction of the spinal cord tissue. The apop- brain and spinal cord injury: pathomechanisms and
tosis progresses in both cranial and caudal treatment strategies. Prog Brain Res 2007;161:125141.
direction during the chronic stage. This stage Carlson GD, Gorden C. Current developments in spinal
ranges from days to years. Receptors, ion chan- cord injury research. Spine J 2002;2(2):116128. Review.
Choo AM, Liu J, Dvorak M, et al. Secondary pathology
nels, and other structures try to restore func-
following contusion, dislocation, and distraction
tions, and damaged spinal cord tissue is spinal cord injuries. Exp Neurol 2008;212(2):490506.
removed from the site of injury. The demyelini- Epub 2008 May 14.
zation of the white matter continues, leading to Dumont RJ, Okonkwo DO, Verma S, et al. Acute spinal
an atrophy of the spinal cord. Cyst formation cord injury, part I: pathophysiologic mechanisms. Clin
Neuropharmacol 2001; 24(5):254264. Review.
located in previously injured areas of the spinal
Fehlings MG, Agrawal S. Role of sodium in the pathophy-
cord and/or a widening of the central canal siology of secondary spinal cord injury. Spine 1995;
appears (syringomyelia) during this chronic 20(20):21872191.
stage. The spinal cord is often tethered or Fehlings MMG, Sekhon LSH. Cellular, ionic, and biomo-
attached to the dural sac (see Chapter 30). The lecular mechanisms of the injury process. In: Tator
CH, Benzel CH, eds., Contemporary Management of
primary injury cannot be treated, but only avoided
Spinal Cord Injury: From Impact to Rehabilitation.
by prevention. An adequate and acutely initiated Park Ridge, IL: American Association of Neurological
intensive care and careful rehabilitation may, Surgeons, 2000: 3350.
however, minimize the consequences of sec- Kim DH, Vaccaro AR, Henderson FC, Benzel EC.
ondary injury mechanisms. Active rehabilitation Molecular biology of cervical myelopathy and spinal
cord injury: role of oligodendrocyte apoptosis. Spine J
and, in some selected cases, surgical treatment
2003; 3(6):510519. Review.
may relieve some of the negative consequences Kwon BK, Tetzlaff W, Grauer JN, et al. Pathophysiology
of SCI during the chronic stage. and pharmacologic treatment of acute spinal cord
injury. Spine J 2004;4(4):451464.
ACKNOWLEDGMENTS Park E, Velumian AA, Fehlings MG. The role of excito-
toxicity in secondary mechanisms of spinal cord
injury: a review with an emphasis on the implications
The authors wish to express their gratitude to for white matter degeneration. J Neurotrauma 2004;
assistent professor Anders Lewen, 21(6):754774. Review.
Department of Neuroscience, Neurosurgery, Pouw MH, Hosman AJ, van Middendorp JJ, et al.
University of Uppsala, Sweden, for his valu- Biomarkers in spinal cord injury. Spinal Cord
able contribution and support in the creation 2009;47(7):51925. Epub 2009 January 20. Review.
Sekhon LH, Fehlings MG. Epidemiology, demographics,
of this chapter. and pathophysiology of acute spinal cord injury. Spine
2001;26(24 Suppl):S212. Review.
Suggested Reading Swartz KR, Scheff NN, Roberts KN, Fee DB. Exacerbation
Agrawal SK, Fehlings MG. Mechanisms of secondary of spinal cord injury due to static compression occur-
injury to spinal cord axons in vitro: role of Na, ring early after onset. J Neurosurg Spine 2009;11
Na()-K()-ATPase, the Na()-H exchanger, and the (5):570574.
Na()-Ca2 exchanger. J Neurosci 1996;16(2): 545 Tator CH. Experimental and clinical studies of the patho-
552. physiology and management of acute spinal cord
Agrawal SK, Theriault E, Fehlings MG. Role of group I injury. J Spinal Cord Med 1996;19(4):206214. Review.
metabotropic glutamate receptors in traumatic spinal Tator CH, Koyanagi I. Vascular mechanisms in the
cord white matter injury. J Neurotrauma 1998;15(11): pathophysiology of human spinal cord injury. 1997.
929941. Available online at www.aans.org.
5 Clinical Examination
The spinal cord connects the brain with the rest involves only a part of the cord cross-section. The
of the body with respect to motor, sensory, and spectrum of symptoms of incomplete injuries
autonomic functions. In addition, the spinal cord varies depending on whether the spinal cord is
contains several neural networks (minibrains) injured anteriorly, posteriorly, centrally, or later-
that participate in both simple reflexes, as well as ally. Finally, symptoms will vary according to
in more complex events (such as gait, bladder, whether the injury is focal, multifocal, or diffuse.
bowel, and sexual functions). Knowledge of spinal cord anatomy will allow
The ascending and descending pathways run the location and extent of injury to be deduced
longitudinally along the periphery of the spinal from the spectrum of symptoms. Such a topo-
cord. For example, axons to or from the lower graphic diagnosis (i.e., Where?) is the first step
extremities travel nearly the entire length of the in making the diagnosis. The second step is to
spinal cord, and an injury anywhere along its ascertain the cause of injury (i.e., What?).
length can result in motor and/or sensory deficit History and physical exam remain the most
in the legs. important diagnostic tools. Of course, the clinical
In addition, the spinal cord demonstrates a diagnosis typically must be confirmed or refuted
segmental arrangement, in which the spinal through additional laboratory, radiologic, and/or
nerves exit from the stem of the spinal cord neurophysiologic diagnostic methods. These
in an organized fashion, like the branches of a methods are described in Chapter 8, as well as
tree. This stem with its numerous transverse in conjunction with discussions of specific
branches forms the anatomical basis for symp- injuries.
toms relating to spinal cord lesions. The patient
will experience symptoms below a particular HISTORY
level on the body that corresponds to the injured
spinal cord segment. The history in acute trauma cases focuses heavily
As a result, motor, sensory, and/or autonomic on the circumstances surrounding the trauma
symptoms may occur. Such symptoms may and on the symptoms that indicate neurological
be due to neural deficit (such as paralysis and involvement (see Chapter 7). Preexisting spinal
sensory loss) or to neural irritation (such as pain disease involving the back, such as spinal
and paresthesias). Sometimes, interruption of an stenosis or ankylosing spondylitis, increases the
inhibitory supraspinal influence on the spinal probability of neurological involvement in
cords intrinsic structure may lead to what is trauma cases.
known as a release phenomenon, with increased History taking in cases of suspected nontrau-
muscular tension and increased deep tendon matic spinal cord disease is appropriately
reflexes (spasticity). initiated by discussing the patients current com-
A sudden injury, such as acute spinal cord plaints. Each symptom is noted and analyzed
compression, results in a constellation of symp- separately in regard to onset and progression.
toms somewhat different from that of a slowly Common symptoms in cases of spinal cord
progressive disorder. A complete injury that disease include localized back pain, radiating or
involves a transection of the spinal cord results in diffuse pain, impaired gait due to muscle weak-
different symptoms than an incomplete injury that ness and/or sensory disturbance, stiffness,
39
40 SPINAL CORD INJURY
impaired fine motor function/clumsiness, secondary importance in lesions that are limited
sensory disturbance, increased urinary urgency to the spinal cord. However, a screening exam-
and/or impaired bladder function, incontinence, ination of these functions should generally be
and erectile dysfunction. The symptoms may carried out. With respect to the cranial nerves,
involve one or both arms and legs, as well as high cervical spinal cord lesions may sometimes
the trunk. The distribution of sensorimotor impair function of the accessory and trigeminal
symptoms may indicate either para (both nerves, as well as the sympathetic innervation to
legs) or tetra (both arms and both legs) involve- the eye and face (Horner syndrome). Please refer
ment. In other words, the symptoms indicate a to neurology textbooks for a description of a
horizontal levelwhich is most commonor, general neuro exam.
in rare cases, a hemi involvement, or vertical A complete neurological examination is time
level. Information about previous and current consuming; that which may be considered a rea-
known disorders may provide important etiolo- sonably comprehensive physical examination
gical clues. Examples of diseases that may affect varies according to circumstances. Time is of
the spinal cord include cancer, multiple sclerosis the essence when examining patients in emer-
(MS), amyotrophic lateral sclerosis (ALS), gency situations and, understandably, the neuro
herniated disk, rheumatoid arthritis, acquired exam in such instances must therefore be more
immunodeficiency syndrome (AIDS), malnutri- cursive. In emergency situations, repeated exam-
tion, and arteriosclerosis. As regards past inations (to detect changes, such as worsening
medical history, it is particularly important to paralysis or deteriorating level of consciousness)
inquire about previous back and tumor diseases. are given priority over a single highly detailed
A prior history of meningitis, subarachnoid examination.
hemorrhage, back surgery, or myelography In the case of acute trauma to the spine it is of
with intrathecal contrast injection may lead to fundamental importance to verify whether neu-
scarring of the meninges, with subsequent rological signs are present. If so, the level of neu-
spinal cord involvement. Social history should rological injury must be identified (the most
include questions about alcohol and drug caudal level of the spinal cord with normal func-
abuse. Intravenous drug users comprise a risk tion) and the degree of neurological involvement
group for spinal epidural abscess. The clinician must be assessed (whether all sensory function
should obtain the patients family history of and voluntary motor function is absent below the
neurological disease, since several hereditary level of injurya complete injury; or if any sen-
diseases may be associated with spinal cord sory and/or voluntary motor function remains
involvement. an incomplete injury). In traumatic SCI, we use a
standardized method of examination based on
PHYSICAL EXAM the American Spinal Injury Association (ASIA)
classification system (see Chapter 2). The
Generally, the focus of the neurological exam minimum emergency examination also includes
varies depending on the suspected area of an assessment of the stability of the vertebral
injury as indicated by the history (e.g., the column, and every suspected case of spinal
brain, spinal cord, nerve roots, peripheral trauma should be treated as if the vertebral
nerves, or muscles), and depending on whether column were unstable until proven otherwise.
a unifocal, multifocal, or diffuse pathologic Additional radiologic examinations are carried
process is contemplated. out in regular order on such occasions, typically
The neuro exam for suspected spinal cord including plain x-ray, magnetic resonance ima-
involvement should include sensation, motor ging (MRI) and/or computed tomography (CT);
function, deep tendon reflexes (DTRs), and see also Chapter 6.
muscle tone of the arms, legs, and trunk. For rapidly progressing nontraumatic cases
Higher functions such as cognition, speech, involving the spine, the clinician must consider
and memory, of course, reflect brain rather several possible etiologies (e.g., herniated disk,
than spinal function and are therefore of abscess, infarction, hemorrhage, or myelitis),
CHAPTER 5 CLINICAL EXAMINATION 41
necessitating a thorough analysis of the history. neurons does not occur until at least 50% of the
Here, too, the neurological examination should motor neuron pool has been destroyed.
primarily focus on establishing whether neuro- As the segmental a-motor neurons are
logical involvement is present and if so, the injured, the descending motor tracts passing
probable level of injury should be ascertained. through the area of injury along the longitudinal
In cases of para- or tetraparesis, spinal cord axis of the spinal cord are typically also injured.
compression must be either ruled out or treated These are known as the upper motor neurons. The
emergently. a-motor neurons in the spinal cord below the
For slowly progressing nontraumatic cases level of injury thus lose their supraspinal con-
involving the spine, the differential diagnoses nection, and the muscles innervated by intact a-
are even more numerous, and the clinician motor neurons are therefore also affected by
must carry out a comprehensive review of paresis, although this type of paresis is instead
the history and physical examination. Here, the characterized by muscular hypertonia (spastic
time element is not as critical as in emergency paresis), only a slight degree of atrophy, increased
situations, and workup can often be done deep tendon reflexes, and absence of fasciculations.
electively on an outpatient basis (see also Clinically manifest paresis typically does not
Chapter 19). occur until at least 50% of the upper motor
neurons have ceased functioning, and total
paralysis does not occur until more than 90% of
SEGMENTAL AND LONG-TRACT SYMPTOMS the neurons cease to function.
It is easy to be confused by the fact that lower
For a more comprehensive review, please refer to motor neuron paresis can be present above upper
Chapter 3, including its illustrations. In cases of motor neuron paresis. Also note that in the case
focal (circumscribed) spinal cord lesions, regard- of acute injuries, also paresis related to upper
less of etiology, we expect to find a segmental, motor neuron damage will at first be flaccid,
roughly horizontal level on the body, with with decreased or absent reflexes. This transient
normal function cranial to this level, and condition is known as spinal shock and is
impaired or absent function caudal to this level. described in greater detail later.
The segmental level is a reflection of the skin A spectrum of symptoms with segmental
innervation (dermatome) and muscle innervation flaccid paresis at the level of injury and spastic
(myotome). Knowledge about the bodys seg- paresis below the level of injury thus typify focal
mental innervation is required to correctly diag- spinal cord lesions. Such lesions may be seen
nose levels. with trauma, transverse myelitis, spinal cord
Establishing the sensory level is an important tumors, spinal epidural abscess, and cervical
component of the neurological examination in spinal stenosis. However, symptoms may be
cases of suspected spinal cord involvement. The more complex in cases of diffuse or multifocal
sensory examination should include at least the spinal cord involvement along the longitudinal
modalities light touch and pain. and/or transverse axes, and a definite level of
In the myotomes innervated from the injured injury may then be lacking or difficult to define.
spinal cord segment(s), signs of what is known
as a lower motor neuron injury may be demon- SENSORY FUNCTION
strated. This is caused by injury to the segmental
a-motor neurons in the anterior horns of the Assessment of sensory function requires patient
spinal cord. When these lower motor neurons cooperation. Granted, expressions such as grima-
are injured, a paralysis occurs characterized by cing and other nonverbal behavioral pain reac-
muscular hypotonia (flaccid paresis), pronounced tions may indicate that the patient perceives a
atrophy, decreased or absent deep tendon reflexes, painful stimulus but, to a large extent, testing
and fasciculations (involuntary contractions in sensory function is reliant upon the patients
individual muscle fiber bundles). Clinically ability to adequately report his perceptions. In
manifest paresis due to injury of the a-motor the case of sensory deficit, stimulation may also
42 SPINAL CORD INJURY
elicit reflex motor responses, such as a flexor not lost until about 75% of the dorsal column
reflex. It is not unusual that a patient may very axons are nonfunctional.
well experience pain in an area of the body com- Vibration stimuli are also mainly mediated
pletely devoid of sensation. On the trunk of the through the dorsal columns. Testing vibration
body, sensory testing is the primary method of is of great value in cases where polyneuropathy
establishing the neurological lesion level. It is is suspected (diffuse disease of the peripheral
also important to underscore that sensation nerves), in which impairment of vibration
includes not just one, but several distinct modal- sense is often one of the earliest signs. A
ities (pain, temperature, light touch, deep pres- vibrating tuning fork is first placed on top of
sure, vibration), and that sensory loss may very the patients large toe. If the patient does not
well be selective for one modality or another. sense vibration here, the tuning fork is serially
A more detailed discussion is found in the next applied more proximally and cranially to the
sections. medial malleolus, proximal tibia, anterior
superior iliac spine, the costal arch, and finally
Light Touch the clavicle.
Pathology affecting the dorsal columns may
Light touch, including two-point discrimination lead to sensory ataxia, in which impaired sensory
(the ability to distinguish between two simulta- feedback in regard to position of the extremities
neous, closely spaced sensory stimuli as sepa- leads to clumsy, imprecise movements. In addi-
rate), is mediated in part through the dorsal tion, paresthesias often occur, and are probably
columns and in part via the ventral spinotha- due to spontaneous impulses arising from
lamic fasciculus on the contralateral side. Since within the injured axons. Common descriptions
the impulses travel through the spinal cord in include pins and needles, perception of vibra-
not one, but two anatomically distinct pathways, tion, sensation of a tightly drawn band, and/or
a total loss of light touch sensation below the hypersensitivity to touch (hyperesthesia) below
neurological level generally implies a total or the level of injury. One distinct type of par-
near-total transverse lesion. esthesia elicited from the dorsal column is
known as the Lhermittes sign, which involves
Dorsal Columns an unpleasant sensationsimilar to electrical
shocksshooting down the back when the
Proprioception provides information about joint neck is flexed.
position and movements. Conscious propriocep-
tion is initially transmitted through the dorsal Pain and Temperature
columns of the spinal cord to reach conscious
awareness at the cortical level. Unconscious pro- Pain is mediated via several spinal pathways, the
prioception is transmitted through the dorsal most important of which is the lateral spinotha-
and ventral spinocerebellar tracts to the cere- lamic tract. An injury to this pathway system
bellum. Impaired proprioception is an important causes decreased sensitivity to pain and tempera-
sign of dorsal column lesions. Generally, we ture stimuli from the contralateral side of the
begin testing in the most distal parts of the extre- body starting one or two dermatomes below the
mity. The examiner fixes the distal interphalan- level of the lesion. Lesions of the pain pathways
geal joint of the finger or toe (usually the thumb may also result in irritative symptoms that man-
or large toe) from the sides with one hand, and ifest as a perception of pain below the level of
then flexes or extends the distal phalanx by grip- lesion. Such pain may be described as dull or
ping the sides of the finger/toe between the more distinctly as burning or lancinating. When
thumb and index finger of the examiners other testing sensitivity to pain, the patient should be
hand. Patients should be able to perceive a instructed to indicate the presence or absence of
couple of millimeters of movement. In the case pain when pricked with a pin. Even when sensi-
of a distal deficit, proprioception should also be tivity to pain is absent, the patient may still
tested in more proximal joints. Proprioception is have intact sensation to touch, and may thus
CHAPTER 5 CLINICAL EXAMINATION 43
experience being pricked. Therefore asking activating their muscles, and a true paresis
patients whether they feel the pinprick is not may not actually be present. The concept of
enough; it is necessary to specifically ask normal strength varies greatly among different
whether pain is present. people. The normal strength of a 20-year-old
Temperature, like pain, is mediated via the male body-builder is of course extremely exceed-
lateral spinothalamic tract. When lesions are ing that of an 80-year-old woman. A helpful sug-
centrally located in the spinal cord (such as syr- gestion is thus to use the patient as his own point
ingomyelia), the fibers that cross over and convey of reference, by comparing strength on the left
pain and temperature are those mainly affected. and right sides and between arms and legs. It
Clinically, this manifests as loss of sensation for furthermore should be remembered that not all
these modalities within a band-shaped area motor function is voluntary. During voluntary
reflecting the affected spinal cord segments. In activation, a spastic muscle may react with a
the case of complete spinal cord lesions, tem- superimposed involuntary contraction, which
perature sensitivity is lost below the level of may distort the assessment of volitional strength.
injury. A change in perception of temperature Motor function testing in cases of suspected
sensitivity may be an early sign of a lesion in the spinal cord lesions focuses on the extremities,
spinothalamic tract. The patient may note an as it is difficult or impossible to evaluate seg-
absence of sensitivity to heat and/or cold within mental motor function in the trunk.
the affected area of skin, for example while show- Muscle strength is conventionally assessed
ering or bathing. Since neural impulses for pain according to a 6-point scale, where 0 total
and temperature travel in the same pathways, it paralysis and 5 normal function (see Chapter 8).
is usually sufficient to test only sensitivity to If the injury is at the level of the cervical spine,
pain. If nevertheless temperature sensitivity is the paralysis will encompass both arms and legs
being tested, it is convenient to do this by (i.e., tetraplegia). If the level of injury is below the
touching the patients skin with a metal tuning cervical spine, the paralysis will encompass the
fork. The patient should be able to discern varia- legs and possibly the trunk, (i.e., paraplegia).
tions in skin temperature of just a few degrees in Even if these concepts are used in everyday clin-
either a hot or cold direction. ical practice to describe both complete and
Particular care should be exercised when the incomplete injuries, it is more accurate to speak
patient uses the descriptor numb. This may of tetra- or paraparesis in cases of incomplete loss
denote a sensation of heaviness in a partially of motor function (where a degree of voluntary
paralyzed extremity (even in the absence of any motor function remains below the level of
sensory loss!), paresthesias (indicating irrita- injury), and to reserve the terms tetra- or para-
tion), or a de facto sensory deficit or complete plegia for total loss of motor function (where no
absence of sensation. voluntary motor function remains below the
Patients may often detect discrete sensory level of injury). The term paralysis is also used,
disturbances even when the examiner is unable and generally refers to cases of complete loss of
to discover any pathology during the examina- function.
tion. In particular, this applies to irritative symp- The clinical picture seen when motor path-
toms such as pain and paresthesias. ways are affected varies, as mentioned earlier,
depending on whether the upper or lower
MOTOR FUNCTION motor neurons are involved. In the case of early
involvement of the upper motor neurons a subtle
Motor function testing has the advantage over sensation of stiffness in the affected extremity is
sensory testing in that examiners can directly the first symptom, often combined with a ten-
use their own senses to verify the findings. dency to stumble and problems negotiating
However, patients may intentionally choose not stairs. Patients often drag or shuffle their feet
to fully exert themselves (or perhaps not even in a characteristic manner. Muscular atrophy is
try to volitionally activate the muscle at all). In slight in the case of upper motor neuron lesions.
addition, pain may inhibit patients from fully (Injuries to the lower motor neuron may result
44 SPINAL CORD INJURY
in loss of up to 80% of muscle volume, whereas area of stimulus. In older and/or overweight
lesions of the upper motor neurons entail no persons, abdominal reflexes are often difficult
more than about a 20% loss of muscle volume). to demonstrate.
Muscle tone and deep tendon reflexes are Babinski sign is a pathological reflex response
increased. In general, upper motor neuron expressed by dorsal extension of the big toe in
lesions first lead to impairment of distal fine response to a stimulus exerted along the lateral
motor function and subsequently to impairment edge of the foot in a proximal to distal direction
of gross motor strength. Distal motor function and then turning in toward the medial side of the
can be tested by having patients play the piano forefoot, proximal to the base of the toes. This
with their fingers in the air, or by wiggling their maneuver is often accompanied by a simulta-
toes. A subtle sign of upper motor neuron invol- neous fanning out or spreading of the other
vement is that such movements are carried out toes. The presence of the Babinski sign indicates
more slowly and clumsily. upper motor neuron damage in the brain or
Patients are often able to notice symptoms spinal cord.
of discrete upper motor neuron injury earlier
than the examiner can detect them. Conversely, Muscle Tone and Spasticity
in lower motor neuron injury, the examiner often
notes findings in the physical exam before the Muscle tonethe involuntary basal tension
patient subjectively experiences any symptoms. of a musclemay be normal, decreased, or
increased. Decreased muscle tone accompanies
Reflexes paralysis due to a lower motor neuron injury
and is also seen in the acute phase following an
Testing of deep tendon reflexes is a key part upper motor neuron injury (i.e., during spinal
of the neurological examination. Increased shock). Increased muscle tone accompanies the
deep tendon reflexes are signs of upper motor post acute and chronic phases following an
neuron damage, whereas weakened or absent upper motor neuron injury. This is known as
reflexes suggest damage to the afferent or spasticity (spastic increase in muscle tone) and
efferent fibers of the segmental reflex arc. The should be distinguished from other types of mus-
reflexes that are routinely tested include the cular hypertonia, especially rigidity, which char-
biceps, brachioradial, triceps, patellar, and acterizes conditions such as Parkinsons disease.
Achilles. There is considerable individual varia- Spasticity in turn is a complex and multifa-
tion in regard to how easily reflexes can be eli- ceted aspect of a phenomenon known as the
cited. The most important sign of pathology is a upper motor neuron syndrome. SCI is often accom-
discrepancy in reflex response between different panied by pronounced and sometimes proble-
muscle groups in the same patient, rather than matic spasticity.
the overall briskness in reflex response per se. An acute spinal cord lesion initially results in
In focal spinal cord lesions, normal deep flaccid paralysis below the level of injury, with
tendon reflexes are typically noted above the muscular hypotonia and loss of deep tendon and
level of injury, impaired or absent reflexes are superficial reflexes. This is assumed to be the
found at the level of injury, and increased result of a conduction block of electrical trans-
reflexes are elicited below the level of injury. mission in the spinal cord. This transient phase
Unlike deep tendon reflexes, which are mono- is called spinal shock. After a period of time span-
synaptic, the abdominal reflexes are polysynaptic. ning days to weeks, muscle tone and reflexes
These latter reflexes are abolished by both upper below the level of injury return and become
and segmental lower motor neuron lesions. The increased, likely due to activation of so-called
abdominal reflexes are most easily examined by silent synapses (i.e., previously inactive synapses in
gently scratching the skin in the four quadrants motor neurons linked to segmental reflex activity).
of the abdomen surrounding the umbilicus and In addition, afferent fibers in the dorsal root grow
observing the resultant muscle contraction, out and establish new synapses (sprouting). Taken
which normally pulls the umbilicus toward the together, these two mechanisms cause the paresis
CHAPTER 5 CLINICAL EXAMINATION 45
to convert from flaccid to spastic, with hypertonia extremities with the patient in a supine position,
and increased deep tendon reflexes. the examiner may place one arm under the
In cases of a more gradual onset of the patients knees and begin by carefully rolling
spinal cord lesion, these plastic mechanisms the patients legs from side to side to help the
have time to offset the loss of descending stimuli. patient relax. Next, the examiner may quickly lift
Spinal shock with transient muscular hypotonia the patients legs by raising the arm under the
thus will not occur. Instead, we will note a patients knees. If the lower leg stiffly follows
gradually increasing spasticity accompanying along, the exam suggests an increase in muscle
the paresis. tone, because normally this maneuver only
Spasticity among patients with SCI may vary causes knee flexion and the patients heel
in severity. An assessment of muscle tone is remains in contact with the examination table.
important in choosing appropriate therapy. For the upper extremities, the examiner may
Muscular hypertonicity in SCI can manifest instead hold the patients hand, as when shaking
clinically at least in three different ways: hands, and carry out a maneuver that results in
gentle flexion and extension of the patients
1. Spasticity: A rapid monosynaptic reaction.
elbow and wrist. Once the patient relaxes, the
Clonus is a repetitive phenomenon of this
examiner adds a maneuver to rotate the forearm.
type.
If muscle tone is increased, a distinct catch
2. Flexor spasms: A contraction reflex in the
(sudden increased resistance) is noted during
lower extremities in which a Babinski sign
passive supination of the patients forearm.
comprises part of this reflex. Sustained
In addition to an increase in tonic reflexes, which
flexor spasms may result in muscle
can be documented with assessment scales such
contractures and joint subluxation, such
as the Ashworth scale, spastic muscle contractions
as in the hip joint.
may also lead to involuntary movements, known
3. Spastic rigidity: A slow, polysynaptic,
as spasms. Spasm frequency can be documented
extensive reaction in which the increased
with the Penn Spasm Frequency Score or similar
muscular tone may persist over a long
instruments.
period of time.
Briskness of the deep tendon reflexes, in
Functional impairment caused by increased which heightened reflexes indicate an increase
muscle tone may also be classified according to in phasic reflex activity, can be clinically graded
its severity. Thus, severity may vary from mild according to the following scale:
gait disturbances in patients with incomplete
0 absent reflex
injury, to painful and disabling spastic rigidity.
decreased reflex
In the past, severe spasticity was treated surgi-
normal reflex
cally by cutting tendons, nerve roots, and mus-
pathologically increased reflex
cles, but such methods are now rarely used.
Other types of therapy include nerve blocks In spastic paresis, muscular hypertonia is
(botulinum toxin, phenol) and administration strongest in those muscles that have best-
of oral medications (baclofen, benzodiazepines, preserved strength. In the arms, these muscles
clonidine, dantrolene). Baclofen is usually admi- include the shoulder adductors, elbow flexors,
nistered orally, but is associated with limiting wrist flexors, and finger flexors. In contrast,
side effects such as fatigue, headache, nausea, in the legs, the hip extensors, knee extensors,
confusion, and respiratory depression. These and plantar flexors dominate. However, the
side effects are dose dependent and most pro- dominance of extensor muscles in the legs
nounced early in the course of treatment. The (paraplegia-in-extension) may convert into a
sedative properties of the drug limit the max- dominance of flexors (paraplegia-in-flexion) in
imum daily dose, which is about 100120 mg response to chronic nociceptive stimuli (e.g., as
(see Chapter 30). a result of pressure ulcers).
Muscle tone can be tested in many ways. In addition to spasticity, the upper motor
When checking muscle tone in the lower neuron syndrome also includes pathologically
46 SPINAL CORD INJURY
increased flexor reflexes in the lower extremities incomplete injuries vary depending on whether
and impaired distal fine motor function and they involve the anterior, posterior, central, or lat-
decreased gross muscle strength. Stimulation eral portions of the spinal cord cross-section.
of the foot may elicit flexor reflexes, expressed Certain patterns of injury are sufficiently
as an involuntary dorsal extension of the big common to justify specific syndrome nomencla-
toe and simultaneous flexion of the ankle, knee, ture. We briefly describe these syndromes here.
and hip joints. Other spasticity-related phe- Note that the syndrome designations in and of
nomena include spread (irradiation) of extensor themselves only describe the extent and/or location
reflexes in response to percussion, as well as of an injury within the spinal cord. They say
repetitive flexor contractions (clonus) in response nothing about the cause of injury, even though
to a sustained extensor stimulus. The upper certain syndromes are typically associated with
motor neuron syndrome is also accompanied specific etiologies.
by certain changes in the physical properties of
the tissues that further increase resistance to Total Cord Syndrome
movements. These changes include decreased
elasticity, fibrosis, and contractures. Total cord syndrome (Fig. 5.1), or total transverse
In summary, several factors interact to lesion, occurs when conductivity is interrupted
impede or preclude a particular movement in in all ascending and descending pathways of the
the setting of an upper motor neuron syndrome: spinal cord, leading to loss of all sensation and all
agonist muscle paresis, antagonist co-contrac- voluntary motor function below the level of the
tion (simultaneous, and thereby movement- lesion. Bladder and bowel control is also lost.
impeding contraction) and antagonist muscle Sexual function is affected, with impairment of
spasticity, joint contractures, and physical the ability to have an erection, ejaculate, and
changes in the antagonist muscles. experience orgasm in men, and decreased
vaginal lubrication and impaired ability to
SPINAL CORD SYNDROMES experience orgasm in women.
Paralysis
Paralysis
Right Left
Paralysis
Figure 5.3 Lateral cord syndrome (Brown-Sequard syndrome), exemplified here by a left-sided injury to the
spinal cord.
48 SPINAL CORD INJURY
or bowel function. These patients typically have a segmental reflex arcs are disrupted as they pass
better prognosis for both restoration of function from the dorsal to the ventral spinal cord horns,
and ADL. which also causes loss of deep tendon reflexes
within the affected segments.
Central Cord Syndrome The most common cause is traumatic injury
to the cervical spinal cord, usually the result of
Central cord syndrome results from lesions of the hyperextension trauma in association with some
central portion of the spinal cord cross-section degree of preexisting spinal stenosis. Patients
(Fig. 5.4). Clinically, the syndrome is character- with central cord syndrome due to a lesion of
ized by loss of pain and temperature sensation the cervical spinal cord will have more severe
within one or more adjacent dermatomes (corre- impairment of function in the arms than in the
sponding to the level[s] of the lesion) due to legs. Bladder, bowel, and sexual function, as well
disruption of the crossing spinothalamic tracts. as gait, may be relatively well preserved.
Should this central lesion expand, it may also
come to involve the medial portions of the corti- Posterior Cord Syndrome
cospinal tracts and/or the gray matter in the
anterior horns, which would then cause paresis Posterior cord syndrome arises as a result of bilat-
within the affected myotomes. Fibers in the eral involvement of the dorsal columns (Fig. 5.5).
This syndrome is rare. Clinically, it is character- Pure Motor Spinal Cord Syndrome
ized by a loss of proprioception and vibration
sense, with preserved motor function as well A nontraumatic pure motor spinal cord syndrome
as preserved pain and temperature sensation. may involve only the upper motor neurons,
only the lower motor neurons, or a combination
Mixed Syndrome of upper and lower motor neurons (Fig. 5.7). An
example of the latter can be seen in motor neuron
In most traumatic cases, damage has a patchy disease, in which paralysis, spasticity, hyper-
distribution in the cross-section of the spinal reflexia, Babinski sign, pronounced muscle
cord, and the clinical picture fails to fit neatly into atrophy, and fasciculations may all occur simul-
any of the syndromes just described (Fig. 5.6). In taneously. In such cases, sensory function
such cases, we refer to a mixed syndrome. remains intact, as do bladder and bowel control.
Paralysis
Paralysis
Motor Sens.
Cauda Equina Syndrome the medial thighs. The motor deficit is character-
istically of the lower motor neuron type.
In addition to these syndromes involving the
spinal cord proper, we somewhat illogically also
Suggested Reading
include cauda equina syndrome (Fig. 5.8). This
syndrome does not entail injury to the spinal McKinley W, Santos K, Meade M, Brooke K. Incidence
and outcomes of spinal cord injury clinical syndromes.
cord itself, but is caused by a loss of function
J Spinal Cord Med 2007;30(3):215224.
in two or more of the 18 lumbosacral nerve roots Nielsen JB, Crone C, Hultborn H. The spinal pathophy-
that form the cauda equina. The deficit typically siology of spasticityfrom a basic science point of
involves the perineal and gluteal areas, as well as view. Acta Physiol (Oxf ) 2007;189(2):171180. Review.
6 Management at the Accident Scene
The management of the acutely spinal cord prerequisites to reduce the impact of secondary
injured patients has, in addition to the funda- injury and give the injured individual the best
mental life-saving goal, three main objectives: hope of regaining at least some neurological
to minimize neurological deterioration, to mobi- function.
lize the patient as soon as possible, and to imple-
ment an adequate rehabilitation. The early care MANAGEMENT AT THE ACCIDENT SCENE
of the injured patient starts immediately, at the
site of accident. It has previously been shown Up to 60% of all patients with acute traumatic
that up to 25% of spinal cord injured patients SCI prove to have injuries to other organ systems
suffer further neurological deterioration before as well. Head trauma associated with uncon-
arriving at the hospital. In some instances, this sciousness, injuries to the chest and abdomen,
could be avoided. and multiple fractures occur frequently
Adequate management immediately after (Table 6.1). Identification of trauma patients at
injury is vital and will optimize survival in the risk is the first step in the evaluation and man-
short term and the ultimate neurological out- agement at the site of an accident. The circum-
come in the long term. The proportion of stances indicating an increased risk of SCI are
patients with complete lesions has diminished described in Table 6.2. It is sometimes easy to
from 65% during the 1970s to approximately overlook SCI, especially among patients with
45% in later studies. The number of patients impaired consciousness. Therefore, it is a great
with deteriorating neurological function during advantage to establish a dialogue, at the site of
prehospital transfers has also been reduced. the accident, with the injured patient. Tables 6.3
Improved care at the site of the accident is one through 6.5 present those circumstances that
reason for this improved neurological outcome. may indicate that a person has suffered an SCI,
The importance of secondary injury mechan- but also and of equal importance, conditions
isms has been clearly shown in animal experi- indicating that an injury to the spine and/or
ments (see Chapter 4), and improved clinical spinal cord is very unlikely.
outcomes likely reflect a reduction in secondary
injury through proper management. ADVANCED TRAUMA LIFE SUPPORT
In cases of incomplete SCI, which results
in subtotal loss of function below the level of The management of vital functions such as
injury, the prognosis is better and the conse- breathing and circulation, as well as controlling
quences less devastating as compared to those extensive blood loss (fractures, chest or abdom-
associated with a complete lesion, which results inal hemorrhage) always has the highest priority.
in total loss of function below the level of injury. Most professionals treating patients at the site of
Since most traumas result in incomplete SCI, accident use the Advanced Trauma Life Support
careful and adequate care at the site of the (ATLS) guidelines developed and continuously
accident in combination with qualified medical revised (every fourth year) by the American
management at the emergency hospital are vital College of Surgeons.
51
52 SPINAL CORD INJURY
TABLE 6.2 Circumstances indicating risk of TABLE 6.5 Circumstances speaking against a
injury to the spinal cord. Patients lesion of cervical spine/spinal cord.
presenting with one or several of Such lesions may be excluded if all
these symptoms should be treated criteria are present.
as if suffering from SCI until The patient is awake and shows no signs of
proven contrarywise. disorientation
All high-energy trauma No signs of head injury
Depressed/clouded consciousness No signs of alcohol and drug intoxication
High speed traffic or motorcycle accidents No pain from the cervical region
Falls >5 meters (>15 feet) No signs of neurological deficits
Severe facial injury No distracting pain that may divert the patients
Severe pain at the site of the seat belt attention from pain localized in the neck
region
TABLE 6.3 Circumstances, in awake patients, Five main tasks of pre-hospital management
indicating an injury to the spinal (i.e., at the scene of the accident) take precedence
cord. Patients presenting with according to the ATLS guidelines:
one or several of these symptoms
should be treated as if
suffering from SCI until proven Evaluation
contrarywise. Resuscitation
Vertebral column pain Immobilization
Extrication
Reduced strength in arms and/or legs
Transportation
Lack of movement in arms and/or legs
Numbness and loss of sensory function
Pain in arms (burning hands syndrome)
These responsibilities are presented separately
and legs
here, but are, of course, often performed simul-
Signs of urinary leakage and incontinence
taneously in view of the needs of each individual.
CHAPTER 6 MANAGEMENT AT THE ACCIDENT SCENE 53
of the cervical spine, which secondarily may other injuries above the level of the clavicle are
reduce the effect of existing compression of the diagnosed. If fractures to the skull base have not
spinal cord by vertebral fragments. been excluded, nasopharyngeal intubation is
Oropharyngeal airway insertion, suction of the consequently contraindicated, and orotracheal
airways, and/or removal of foreign bodies consti- intubation is usually preferred if an injury to
tute the next step in airway management, in cases of the spinal cord is suspected. The inflated orotra-
inadequate oxygenation. Endotracheal intubation cheal cuff serves two functions: It prevents
is required only if a free airway is still at risk. It is reflow of gas during assisted ventilation, and it
of greatest importance that cervical alignment and prevents aspiration of blood, gastric contents,
immobilization be maintained during these proce- and/or cerebrospinal fluid. The neck must be
dures, and it has been shown that neurological kept in a neutral position, and this is achieved
function does not deteriorate if an orotracheal inser- by a second person stabilizing the neck during
tion is performed correctly. It is thus vital that, the intubation procedure. It is highly recom-
during the intubation procedure, neutral position mended that the anterior part of the rigid cervical
remains unchanged (see Immobilization). collar be opened during the intubation man-
Patients with a suspected SCI should receive euver, to facilitate opening the patients mouth
supplemental oxygen during transport to the without hyperextending the neck. It has been
hospital. Oxygen can be given by nasal cannula shown that intubation while using hard cervical
or face mask if the patient is awake. The jaw collar immobilization induced significant move-
thrust maneuver and insertion of an oropharyn- ment of the cervical spine, whereas intubation in
geal tube may facilitate oxygenation if the patient neutral position did not produce a corresponding
is not fully awake and endotracheal intubation is movement of the vertebrae.
not considered necessary.
Circulation
Breathing
Control of the hemodynamics is the next impor-
The patient must always be guaranteed adequate tant step in the management of the traumatized
ventilation. Airway management is concentrated patient. The heart rate and blood pressure
on breathing (ventilation) as soon as the airway is is measured repeatedly. Active bleeding is
secured. The respiratory rate and pattern is stopped, usually by direct local pressure, and
observed, since ventilation is affected by intravenous lines are inserted. There is some
paralysis of the diaphragm and respiratory acces- controversy regarding the choice of the initially
sory muscles following SCI. The ventilation may administered fluid. The standard procedure is to
also be hampered following multitrauma by a administer Ringers lactate since hypovolemia,
flail chest (due to multiple rib fractures), and/or caused by excessive bleeding, is the most
open pneumothorax. common cause of shock, and all patients in
The patient must be intubated if ventilation is shock are considered to have a hemorrhagic
impaired. This means logistically a return to shock until proven otherwise. The hypotension
Airway in order to secure the airway. associated with shock may, however, among
Intubation is necessary if the patient is uncon- patients with cervical and high thoracic SCI
scious or suffers from impaired consciousness, (above the level of T4-T6) be caused by the SCI
has reduced ventilatory capacity, or if an obstruc- itself, a condition known as neurogenic shock.
tion of the airway is suspected. The ATLS guide- These high-level injuries to the spinal cord
lines point out that experience rather than result in a loss of sympathetically induced regu-
technique decides whether orotracheal or naso- lation of peripheral vascular tone, thus an accu-
pharyngeal intubation is to be performed. The mulation of blood in the extremities, and a
latter requires, however, that the patient exhibit reduced central venous return. This altered
adequate spontaneous respiration. distribution of blood leads to a reduced cardiac
According to ATLS guidelines, fractures to preload and secondarily to a decreased cardiovas-
the skull base must be suspected if facial or cular function. Hypotension (usually a systolic
CHAPTER 6 MANAGEMENT AT THE ACCIDENT SCENE 55
TABLE 6.6 Characteristics of neurogenic versus secondary mechanical injury to the spinal cord
hemorrhagic shock. and further deterioration of neurological symp-
toms. Up to 20% of spinal cord injured patients
Neurogenic Hemorrhagic
present with more than one fracture to the spinal
Shock Shock
column. The entire body must, therefore, be
Hypotension Yes Yes immobilized and secured in order to prevent
Pulse Bradycardia Tachycardia unnecessary movement of the spinal column.
Skin Warm and Cool and Consequently, a rigid cervical collar, sandbags
dry clammy placed to each side of the head, and taping the
Mental status Normal Affected forehead down to the board secures the neck
Urine Normal Low while the rest of the body is fully immobilized
production using foam blocks and tape on a long
spineboard.
Figure 6.2 A hard cervical collar is applied. Figure 6.4 Log-rolling maneuvers second phase.
cervical collar should be applied before any other extremities. Signs such as local tenderness, focal
part of the body is moved. hematomas, and an increased distance between
spinal processes (Fig. 6.4), indicate skeletal,
Log-roll Maneuver and Placement on the Spine Board muscle, and/or ligament injury. The patient is
turned back to the supine position, using a
The patient is rotated to one side using the log- reverse log-roll maneuver, after the examination
roll maneuver with spine precautions in order to is finished and is simultaneously placed on a
examine the spinal column (Figs. 6.3 and 6.4). spine board (backboard; Fig. 6.5).
The technique demands at least four individuals The cervical collar alone does not completely
and aims to avoid movement in the spinal immobilize the cervical spine. The head must be
column during the rotation, thus making it pos- secured using adhesive tape or its equivalent
sible to investigate the spine while it remains in a after the patients body has been placed on the
straight position. Person 1 is responsible for spine board; this prevents rotational movement
maintaining the neutral in-line position of the and achieves complete immobilization (Fig. 6.6).
head and neck and coordinates the subsequent The spine board is an excellent means of trans-
log-roll maneuver and placement of the patient portation for immobilized patients, but because of
on the spine board. The remaining three indivi- the risk of pressure ulcers (especially in the sacral
duals simultaneously turn the chest, pelvis, and region), patients should not be immobilized thus
for more than 2 hours. Protective padding, such
Figure 6.3 Log-rolling maneuver, first phase. Figure 6.5 The patient is placed on the spine board.
CHAPTER 6 MANAGEMENT AT THE ACCIDENT SCENE 57
Motorcycle Accident
ACKNOWLEDGMENTS
Dyson-Hudson TA, Stein AB. Acute management of trau- Tator CH, Benzel CH, eds., Contemporary Management
matic cervical spinal cord injuries. Mt Sinai J Med of Spinal Cord Injury: From Impact to Rehabilitation.
1999;66(3):170178. Park Ridge, IL: American Association of Neurological
Fehlings MG, Louw D. Initial stabilization and medical Surgeons, 2000:6171.
management of acute spinal cord injury. Am Fam Sheerin F. Spinal cord injury: acute care management.
Physician 1996;54(1):155162. J Bone Joint Surg Am 2009;91(11):25682576.
Hadley MN, ed. Cervical spine immobilization before Tator CH, Duncan EG, Edmonds VE, et al. Changes in
admission to hospital. Neurosurgery 2002;50(3): epidemiology of acute spinal cord injury from 1947 to
S7S17. 1981. Surg Neurol 1994;40:207215.
Hadley MN, ed. Transportation of patients with acute Tator CH, Duncan EG, Edmonds VE, et al. Neurological
traumatic cervical spine injuries. Neurosurgery 2002; recovery, mortality and length of stay after acute spinal
50(3):S18S20. cord injury associated with changes in management.
Rabinovici R, Ovadia P, Mathiak G, Abdullah F. Paraplegia 1995; 33(5):254262.
Abdominal injuries associated with lumbar spine frac- Whetstone W. Prehospital management of spinal cord
tures in blunt trauma. Injury 1999;30(7): 471474. injured patients. In: VW Lin, ed., Spinal Cord
Rengacharry SS, Alton SM. Resuscitation and early med- Medicine: Principles and Practice. New York: Demos
ical management of the spinal cord injury patient. In: Medical Publishing, 1996:107111.
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7 Management at the Hospital
Patients having sustained a SCI are treated intensive care treatment in the acute stage fol-
according to similar general principles as indivi- lowing SCI.
duals with multiple trauma. The focus of this In 1984, Tator and coworkers presented the
chapter is, however, directed toward the specific results of administering volume expanders
aspects of treatment related to SCI, assuming that (using crystalloid solutions, plasma, and whole
all facilities needed to optimize the treatment of blood) to avoid hypotension; the use of adequate
this patient group are available at the receiving ventilation, including endotracheal intubation
hospital. It is not possible to describe all treatment and assisted ventilation if required; and routines
routines in detail, so only general principles are to avoid sepsis and urological complications to
presented in this chapter. reduce the consequences of secondary injury in
Patients having sustained an acute, severe SCI patients, versus a comparable group not
injury to the spinal cord, especially at the cervical receiving similar therapy. These measures
level, may quite often exhibit hypotension, hypoxia, resulted in a reduced mortality and morbidity,
and pulmonary dysfunction. This may result in shorter in-hospital stays, and reduced overall
hemodynamic instability and insufficient ventila- costs. At the time, this study set the gold stan-
tion even if circulation and breathing capacity dard for the intensive care treatment of SCI
is considered normal during the initial period patients.
following injury. A risk always exists for further The treatment protocol of the NASCIS II study
neurological deterioration upon and immediately (see Chapter 9) represents the introduction of
after arrival to the hospital. The incidence of neuro- modern intensive care, equal to that given to multi-
logical deterioration in such instances is not well trauma patients, also to this group of patients.
surveyed; neurological deterioration was observed The necessity for rapid and active treatment of
in 5% of patients after arrival to hospitals in the the SCI patient is based on the theory of primary
National Acute SCI Study (NASCIS II) published and secondary injury mechanisms. Every patient,
in 1990. This is an improved rate compared to regardless of severity of neurological deficits,
those reported by previously performed retrospec- should be treated as if he had a potential of
tive studies. regaining function on a spinal cord and/or a
NASCIS patients were treated at intensive spinal root level. Therefore, the goal of therapy is
care units during the acute stage following to preserve neurological function by preventing
injury. Monitoring of ventilation and circulation secondary injury mechanisms through the correc-
parameters revealed hemodynamic instability, tion of hypoxia and/or hypotension, the treatment
heart rhythm disturbances, and insufficient ven- of associated injuries, and an ongoing monitoring
tilation resulting in hypoxia. The identification of the neurological status. These goals are reached
and treatment of these complications is of crucial through active intensive care that focus on venti-
importance to minimize morbidity and mor- lation, circulation, pharmacological treatment,
tality. Avoiding further neurological deteriora- repeated neurological examinations, adequate
tion and optimizing the chances for recovery of radiological investigations and, if needed, surgical
neurological function is the goal of aggressive repair.
61
62 SPINAL CORD INJURY
The patient should be placed in the remain within the blood vessels and help to
Trendelenburg position, regardless of the type draw back extravasated fluid, thus resulting in
of shock, in order to increase the reflow of the improved cardiovascular function and spinal
peripherally distributed blood and improve the cord blood flow.
circulation. The Trendelenburg position is espe- Bradycardia triggered by neurogenic shock is
cially effective if the patient suffers from neuro- initially treated with atropine, whereas hypoten-
genic shock. sion associated with this condition is usually
The standard treatment for shock is to treated with vasopressors, such as dopamine,
deliver crystalloid (isotonic) solutions, such as and if needed, dobutamine.
Ringers lactate, although some controversy
exists regarding the choice of fluid replacement. Neurological Examination
The presence of neurogenic shock should be
suspected as soon as all relevant investigations A detailed neurological examination is vital
have been performed and injuries to other organ following initial resuscitation. The neurological
systems have been excluded, and especially if evaluation should be performed repeatedly
fluid replacement with crystalloid solutions is throughout the early posttraumatic phase,
ineffective in restoring systemic blood pressure. in order to detect alterations in neurological
It is of utmost importance to identify neurogenic status.
shock as soon as possible, since the continued The American Spinal Injury Association
administration of crystalloid solutions to these (ASIA) standards of neurological and functional
patients will result in an accumulation of fluid in classification of SCI are considered the most
the extracellular space. A risk of a rapid, over- accepted guidelines for assessment of neurolo-
compensating fluid delivery exists since, as a gical function (a detailed description is presented
rule, crystalloid solutions are administered in a in Chapter 8). Examination according to ASIA
volume approximately four times exceeding a standards makes it possible to determine the
suspected blood loss. This fluid overload may neurological level of injury, characterize
lead to spinal cord as well as pulmonary edema. remaining neurological function below the
Thus, the principles of fluid replacement in level of injury, and evaluate for the complete-
SCI follow those for brain injury as soon as ness of the lesion (including the various neu-
neurogenic shock has been diagnosed. The total roanatomical syndromes of incomplete injury).
fluid volume delivery must be maintained at a The possibility of detecting changes in neuro-
maximum of 2.5 L during the first 24-hour logical function is considered especially impor-
period. Colloid solutions, such as albumin, tant. The examination is easy to repeat, and
dextran, or starch- and gelatin-based prepara- enables a reliable prognosis in the early stage
tions, are administrated as needed. These solu- following injury. The ASIA uniform standards
tions contain larger molecules compared to also facilitate communication between all units
isotonic solutions. These larger molecules treating the SCI patient. The standards are
CHAPTER 7 MANAGEMENT AT THE HOSPITAL 65
also of substantial value in the field of future dens, a so-called type 2 odontoid fracture. The
research. three figures illustrate a similar injury as visua-
The neurological evaluation is hampered by lized by plain radiographs, CT including recon-
factors such as concurrent brain injury or altered struction images, and MRI. The MRI
degree of consciousness due to drugs or excessive demonstrates spinal cord edema as a sign of a
intake of alcohol. In addition, the prognostic pos- severe injury to the spinal cord.
sibility for regaining function may be hidden by
the presence of spinal shock. Peripheral nerve Pharmacological Treatment
injuries or damage to the brachial plexus, as well
as immobilized extremities due to fractures, The use of drugs in the treatment of the spinal
may further complicate the interpretation of the cord lesion is a relatively recent phenomenon.
neurological examination. Nonetheless, the value As we learn more about the mechanisms of
of performing a careful neurological examination secondary injury in SCI, pharmacotherapy con-
of sensory and motor function, especially tinues to be refined to the acute stage following
at sacral levels, cannot be overemphasized. It injury. These so-called neuroprotective pharma-
is not unusual to detect spared sacral function cological treatments aim to reduce or reverse
among signs of an otherwise complete injury. the actions of secondary pathophysiological
This finding may result in an altered treatment events (see the section Biochemical
strategy, since the lesion is, in such cases, Changes, in Chapter 4 and see Chapter 9 for
regarded as incomplete and the prognosis is more details of the pharmacological treatment
considered better than that for complete lesions. of SCI).
Once the initial goal of optimal respiratory and The final cornerstone in the management of
cardiovascular management is achieved, radiolo- the SCI patient is surgical decision-making.
gical investigations may be directed toward areas The choice between surgical intervention or
of interest, guided by the findings of the clinical conservative (nonsurgical) treatment in the man-
neurological evaluation. In the acute stage, how- agement of fractures and/or ligamentous inju-
ever, most imaging studies will encompass the ries must be evaluated carefully, and a detailed
entire spinal column. review of possible treatment approaches for the
The purpose of the neurological examination cervical, thoracic, and lumbar spine is presented
is to not only localize the level of lesion, but in Chapters 10 through 15. Here, we describe
most importantly to detect signs of deteriora- treatment options assuming a hypothetical SCI
tion or improvement in function. In the face of with a simultaneous fracture and/or ligamen-
multiple vertebral injuries, the neurological tous injury.
examination serves to determine the level of In deciding on a treatment plan, it is impor-
the SCI. New developments in the field of radi- tant to distinguish between injuries that result
ology have improved the ability to visualize only in fractures and/or ligamentous damage
posttraumatic changes to both the spinal and those that also primarily involve the spinal
column and the spinal cord, and optimal treat- cord. The indications for surgery, depending on
ment depends strongly on a precise radio- the severity of the injury, may be either ortho-
graphic assessment of the injured area. The pedic, neurosurgical, or both.
available techniques are plain radiographs, Orthopedic treatment of the skeletal and/or
computed tomography (CT), and magnetic ligamentous injury is focused on reposition
resonance imaging (MRI). The indications, and stabilization of the injured segment.
advantages, and disadvantages using these Neurosurgical interventions are undertaken to
methods are presented in Chapter 8. The three reduce compression of the spinal cord caused
techniques are exemplified in Figure 7.1AC, by fracture fragments, blood, disk material,
illustrating a fracture through the base of the and/or ligamentous tissue.
66 SPINAL CORD INJURY
A) B)
C)
Figure 7.1 Imaging techniques illustrating a fracture through the base of dens. Arrows indicate the fracture
line. A: Plain radiographs B: Magnetic resonance imaging (MRI); a, spinal cord edema C: Computed
tomography (CT) scan.
General Considerations: Conservative Versus Surgical instances of the central cord syndrome, occur
Treatment among elderly patients with spinal stenosis and
a mild hyperextension trauma. Ligamentous
Impairment of neurological function usually injuries in the upper part of the cervical spine
indicates the presence of a concomittant severe without a concomitant fracture, on the other
injury to the spinal column and/or ligaments. hand, may occur in tandem with a lesion to
Such lesions are typically regarded as mechani- the spinal cord, thus indicating instability in
cally unstable if they occur simultaneously with the affected spinal column segment(s). As
a spinal cord lesion. Exceptions, such as in many has been discussed extensively elsewhere in
CHAPTER 7 MANAGEMENT AT THE HOSPITAL 67
this book, controversy exists as to whether inju- increase in surgical interventions and less
ries to the spinal column and ligamentous interest in conservative approaches.
structures should be treated surgically or
conservatively. Guidelines for Surgical Intervention
Conservative treatment of SCI, still com-
monly used in for example in Great Britain, is Certain trends regarding surgical decision-
based on Sir Ludwig Guttmanns principles of making can be discerned in the literature despite
postural reduction. According to these princi- considerable disagreement. The indications for
ples, patients are treated with bed rest, with or surgical treatment are presented in Table 7.4,
without traction, until pain is relieved. This is although the choice of treatment for any parti-
followed by the use of various cervical collars for cular patient is heavily influenced by a variety of
612 weeks. Surgical treatment may be consid- circumstances. Because, by strict scientific cri-
ered in later stages, if a remaining spinal defor- teria, neither surgical nor nonsurgical treatment
mity proves to be unstable and/or a progressive has been shown to be preferable regarding neu-
neurological deterioration is detected. The rological restoration following SCI, the authors
conservative treatment of injuries to the upper present, in Table 7.5 their interpretation of the
cervical spine includes an external orthosis recommendations found in the literature.
such as the Halo-vest (see Chapter 15). The Surgical intervention is indicated if the patient
Halo approach is currently used in the treat- exhibits an ongoing neurological deterioration
ment of over 60% of cervical spine injuries. As in combination with radiologically verified
long as the fracture is kept in acceptable align- compression of the spinal cord. Early surgical
ment, this treatment is preferable if no concur- decompression of the spinal cord is most often
rent SCI is present. However, the Halo recommended if the patient suffers from an
treatment may, according to some authors, incomplete lesion and the radiological examina-
delay rehabilitation among patients with an tion reveals a concomitant compression of the
injury to the spinal cord. Among patients spinal cord caused by bony fragments, blood,
without a simultaneous injury to the spinal and/or disk material. Consensus is lacking
cord, orthoses are also used in 75% of thoraco- regarding surgical intervention in patients with
lumbar injuries. complete lesions showing radiologically verified
Controversies persist regarding the benefits compression of the spinal cord.
of surgical decompression of the spinal cord There are additional relative indications for
and restoration of spinal column alignment surgical intervention. Patients with fractures
following trauma, as well as regarding the and/or ligamentous injuries at the cervical level,
timing of surgery. Animal experimental studies in combination with a SCI and a concurrent
show that continuing compression from bone, compression of the cervical roots, could serve as
blood, or intervertebral disk material increases an example of such an indication. In such cases,
the severity of neurological deterioration, and the primary goal of the surgical intervention is not
this increase is time-dependent. It has also to restore spinal cord function per se, but rather to
been shown that early removal of the foreign save nerve root function. An improved nerve root
material results in less ultimate neurological
deficits. Similar circumstances should logically
apply to humans, but no scientific data exists TABLE 7.4 Goals of surgical treatment in SCI
proving that early decompression and stabiliza- patients.
tion is preferable to nonsurgical treatment in
Restore spinal column alignment and stability
humans. On the other hand, neither has it
Facilitate early mobilization
strictly been scientifically proven that conserva-
Reduce pain from spinal column lesions
tive treatment is more efficacious. Given the
Minimize hospital length of stay
nature of the disorder, such studies are difficult
Prevent secondary complications (e.g. pain,
to undertake. Current trends in the treatment of
deformity, and neurological deterioration)
SCI patients, however, tend to involve an
68 SPINAL CORD INJURY
TABLE 7.5 Guidelines for surgical and conservative (non-surgical) treatment of SCI patients.
Surgical Treatment Conservative Treatment
Neurological deterioration Yes No
Neurological improvement No Yes
Neurological level of lesion Caudal Cranial
Radiological evaluation Instability No instability
Spinal cord compression Yes No
evident on CT/MRI
Spinal cord changes on MRI Contusion Edema
Age Younger Older
Attitudes of the surgeon I Believer in the relevance of Non-believer in the relevance of
secondary injury mechanisms secondary injury mechanisms
Attitudes of the surgeon II Judges the risk for surgical Judges the risk for surgical
complications as acceptable complications as unacceptably
Gastrointestinal and Nutritional Measures basis since constipation will delay post injury
return of bowel peristalsis.
Acute disturbance of autonomic control of
intestinal function, in combination with the hor- Bladder Care
monal response to stress and the possible presence
of abdominal trauma, result in digestive dysfunc- The nerve supply of the bladder is blocked during
tion and a reduced uptake of nutrients. Acute, the period of spinal shock, and the bladder is thus
paralytic ileus and gastroparesis results in an accu- unable to empty by reflex. An urethral catheter
mulation of large volumes of intestinal fluid. must be inserted within the first 23 hours after
This accumulation of fluid contributes to injury. Bladder distension must be avoided due to
hypovolemia and electrolyte disturbances, and the risk of autonomic dysreflexia. Permanent
reflux of gastric content may lead to aspiration bladder dysfunction (e.g., detrusor damage and
pneumonia. It is therefore of great importance to reflux) may occur if the bladder remains dis-
relieve the stomach of excess fluid, especially if tended. The indwelling catheter is replaced
the patient exhibits paralytic ileus, using naso/ by intermittent catheterization as soon as
orogastric tubes. Many authorities also advocate the patients general condition is stabilized.
continuous drainage of the stomach in order Intermittent catheterization will reduce the rate
to counteract reflux and pneumonia. The symp- of bacteriuria, which is important since urinary
toms of paralytic ileus usually resolve within 23 tract infection is probably the most frequent com-
weeks. plication of the post acute period.
Stress- and steroid-mediated gastric ulcers occur
frequently in the acute stage. Symptoms such as Pressure Ulcer Prevention
hematemesis, referred pain to the shoulder
region, tachycardia, and diffuse abdominal dis- Skin care is an early priority and should start
comfort may indicate the presence of gastric immediately following injury. The patient must
ulcers. These symptoms are sometimes be turned every 2 hours during the acute stage.
masked among SCI patients, and one must be Areas of bony prominence vulnerable to pres-
vigilant for the presence of gastric ulcers. sure ulcers, such as the sacral and trochanter
Monitoring the acid level of gastric contents is regions, must be particularly protected from
used in some institutions, and prophylactic unnecessary pressure. Mattresses containing
therapy, usually antacids or H2-blockers, is air, water, or foam should be used to minimize
given. Treatment of verified gastric ulcers fol- pressure to sensitive areas.
lows current routines.
Total parenteral nutrition (TPN) and/or ent- Contracture Prevention
eral nutrition should be initiated as soon as pos-
sible following injury. TPN, preferably through a A contracture denotes a shortening of a muscle,
central venous catheter, should replace the peri- tendon, or ligament. The prevention of wrist
pheral administration of fluids as soon as pos- contractures is especially important following
sible, with the administration of TPN usually injury. Patients should be offered range-of-
starting within 2448 hours following injury. motion exercise programs and orthotic devices.
Enteral nutrition is initiated as soon as bowel
sounds are audible and the patient starts to ACKNOWLEDGMENTS
pass gas. Pancreatitis is often associated with
paralytic ileus, probably caused by an unba- The authors would like to express their gratitude
lanced parasympathetic stimulation resulting in to our colleague Staffan Palsson, Department of
spasm of the sphincter of Oddi and an increase Anesthesiology, Norrtalje Hospital, Sweden,
in amylase production. Among patients and ATLS nurse Ragnhild Klum, Department
suffering from pancreatitis, TPN is continued of Anesthesiology, Akademiska Sjukhuset,
until amylase values are normalized. Evacuation Uppsala, Sweden, for valuable contributions in
of the bowels should be performed on a regular the creation of this chapter.
CHAPTER 7 MANAGEMENT AT THE HOSPITAL 71
Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardio- cord injury: results of a prospective pilot study to
vascular consequences of loss of supraspinal control of assess the merits of aggressive medical resuscitation
the sympathetic nervous system after spinal cord injury. and blood pressure management. J Neurosurg 1997;87
Arch Phys Med Rehabil 2000;81(4):506516. Review. (2):239246.
Urdaneta F, Layon AJ. Respiratory complications in patients Wilberger JE. Diagnosis and management of spinal cord
with traumatic cervical spine injuries: case report and trauma. J Neurotrauma 1991;(8) Suppl 1:S2128.
review of the literature. J Clin Anesth 2003;15(5):398405. Winslow C, Rozovsky J. Effect of spinal cord injury on the
Vale FL, Burns J, Jackson AB, Hadley MN. Combined respiratory system. Am J Phys Med Rehabil 2003;82
medical and surgical treatment after acute spinal (10):803814. Review.
8 Diagnostic Methods
CLINICAL ASSESSMENT AND CLASSIFICATION (with a cotton tip applicator or similar object) and
ACCORDING TO ASIA pain (using a pin or similar object). Sensory func-
tion is graded as follows: normal 2; impaired/
The International Standards for Neurological and distorted 1; absent 0; not testable NT. The
Functional Classification of SCI, developed by latter may be due to amputation or a cast covering
the American Spinal Injury Association (ASIA) the area. In most cases, testing of sensory function
(Fig. 8.1), are often used for clinical neurological is not too difficult. However, some pitfalls may be
classification of focal spinal cord lesions, especially mentioned:
traumatic myelopathies. They provide a standar-
dized quantitative description of the neurolo- During pain testing with a pin, should the
gical level of injury and sensorimotor function patient perceive touch without any pain
above and below this level. However, an exam- component, the pain sensation should
ination conducted according to ASIA only fur- be graded as absent within the relevant
nishes part of the clinically relevant information dermatome.
and therefore is not intended to replace a com- Should a painful stimulus be perceived as
plete neurological exam. Moreover, assessment stronger when testing a specific dermatome
conducted according to ASIA is not designed compared with testing a dermatome with
to address diffuse, multifocal, and/or pathway- normal sensation (such as on the face or
specific lesions. Conventional neurological other location well above the level of
examination is preferable in such cases. This injury), sensitivity to pain should be
chapter presents an overview of the ASIA classi- graded as impaired/distorted within the
fication system. For further details please refer relevant dermatome.
to the specific manuals available. If during sensory testing of a dermatome
the patient should perceive stimulation
Assessment with both light touch and pin-prick as
painful, thus lacking the ability to differ-
Sensory Function entiate a blunt from a sharp stimulus,
sensation to pain should be graded as
Sensory examination comprises testing of what distorted or absent in the relevant
are known as key points in each of the 28 derma- dermatome.
tomes on both the left and right sides of the body Should the patient experience any sensory
(Fig. 8.2). The key points correspond with a perception, regardless of type, in response
defined area of skin in each dermatome where to light touch and pin-prick in the anal
overlapping innervation to adjacent dermatomes region, the injury should be classified as
is at a minimum, thereby making these areas incomplete; otherwise as complete.
most suitable for testing the function of each spe- The definition of complete versus incomplete
cific dermatome. The dermatomes extend from injury is based solely on the presence or absence
level C2 to S5, where S4 and S5 are considered as of sensory function (and/or motor function
one dermatome. Each key point, including the voluntary sphincter contraction) in the anal region,
anal/perianal region, is tested for light touch regardless of the presence or absence otherwise of
73
74 SPINAL CORD INJURY
5 Active movement through full range The most difficult key muscle to assess in the
of motion against full (normal) upper extremities is the triceps (Fig. 8.3).
resistance When testing this muscle, it is essential
5* The patient succeeds in overcoming to maintain a horizontal forearm position
sufficient resistance to movement for across the chest (with patient lying supine).
muscle strength to be considered Patients with weak or absent triceps function
normal, assuming that simultaneous often unintentionally cheat by externally
mobility-inhibiting factors could be rotating the shoulder in order to passively
eliminated (e.g., pain inhibition)
extend the elbow.
NT Not testable; the muscle cannot be
When testing the deep finger flexors, the
assessed due to amputation, casting,
ankylosis or simultaneous plexus wrist and proximal phalanges must be stabi-
injury, or peripheral nerve damage lized in order to isolate the muscle. Finger
flexion may otherwise result passively from a
C2 C2
C3
C3
C4
C4 Th2
Th2
C4
Th4
Th4
Th6
Th6 Th2
C5 Th8
Th8
Th10
Th10
Th1 Th12
Th1
Th12
C6
L1
L1 C6
C8 L2
L2
C8 S3
L3
C7
C7
L3
S2
L3
L4
L5
L4
L5
S1
Figure 8.2 Segmental skin innervation (dermatome chart) on the front and back of the body.
76 SPINAL CORD INJURY
tenodesis effect; in other words, by passive ten- The sum of motor function points is given
sion on the flexor tendon with wrist extension. for the left and right side (maximum of 50,
Special care must also be given to exam- respectively) and as a total (maximum of 100).
ining the finger abductors. Among patients
A) B)
Figure 8.4 Testing of finger abductors for the purpose of isolating muscle activity while spreading the
fingers.
CHAPTER 8 DIAGNOSTIC METHODS 77
level of lesion where sensory and/or motor resi- movements are avoided in a patient with a poten-
dual function is present in a patient with a com- tially unstable neck injury. The CT examination
plete lesion, by definition. also provides superior imaging, compared with
conventional x-ray. The disadvantage is a larger
RADIOLOGIC WORKUP FOR SPINAL radiation dose, but this is justifiable on condition
COLUMN TRAUMA that the indication for the radiographic examina-
tion is correct. In patients exposed to high-
The purpose of the neurological examination is energy trauma with or without head injury or
to record the current neurological status and any suspicion of an injury to some other vital part
deterioration or improvement over time, as well of the body, such as the thorax or abdomen, a
as to locate the level of lesion so that radiologic cervical spine examination is included in the
workup can be aimed at the suspected level of trauma CT protocol used routinely for this
lesion. As diagnostic imaging is undergoing patient group. The trauma CT examination
rapid development, of all chapters in this book, includes the head, cervical spine, thorax, and
the description of radiologic workup is likely to abdomen, as well as the thoracic and lumbar
become outdated first. spine down to and including the symphysis
To ensure that the patient with a SCI receives (i.e., the pelvis is included in the examination).
optimal treatment, we depend on an accurate Consequently, no conventional x-ray of the thor-
radiologic diagnosis of the injured area. A large acic and lumbar spine is necessary in trauma
number of techniques are available, and in this patients.
chapter we discuss the most common diagnostic
imaging methods currently available: conven- Conventional X-ray
tional x-ray, computed tomography (CT), and
magnetic resonance imaging (MRI), where the The conventional radiographic examination
latter does not involve ionizing radiation. See includes four projections, starting with a lateral
Figure 7.1, which compares the use of these view of the cervical spine (Fig. 8.5). The prin-
three techniques. ciple governing assessment of this examination
Following trauma, many conceivable sce- is that all seven cervical vertebrae must be visua-
narios can arise that may influence the choice lized, along with the upper portion of the T1
of diagnostic procedure. Spinal column trauma vertebral body. If the transition between the C7
must be considered in relation to other injuries, and T1 vertebral bodies cannot be adequately
which may mean that the radiologic workup visualized, a so-called swimmers view is obtai-
varies, even if spinal status is similar from ned, which entails lifting one arm up over the
patient to patient. head (on the same side as the x-ray cassette)
For example, in acute minimal cervical spine while pulling the opposite arm down and simul-
trauma with no medical history of head injury, taneously gently rotating the shoulders to elim-
where the patient is alert and neurologically inate them from the field of view. This method
intact, and suspicion of fracture is low, a conven- significantly improves visualization of the rele-
tional cervical spine x-ray is recommended as an vant level.
initial screening method. When reviewing the lateral cervical spine,
However, in a patient who by history has four lordotic lines are of importance (Fig. 8.6).
suffered a concussion and has neck pain, the The anterior vertebral body line, which corre-
recommendation is to analyze possible injury to sponds to the anterior longitudinal ligament,
the cervical spine with a CT, on condition that a follows the anterior margin of the vertebral
CT scanner with spiral technology is available. In bodies in a relatively soft, flowing line. In addi-
patients with concussion, a CT of both the head tion, there are two similar lines behind the
and cervical spine is preferable to a plain x-ray vertebral bodies, of which the anterior line corre-
of the cervical spine and CT of the head. The sponds to the posterior longitudinal ligament
advantage of this strategy is faster patient and simultaneously to the anterior wall of the
management, since unnecessary transfers and spinal canal, while the other corresponds to the
CHAPTER 8 DIAGNOSTIC METHODS 79
2
1
4
3
2
1
Figure 8.13 Sagittal reconstruction image in which Figure 8.14 Sagittal magnetic resonance image
the facet joints are clearly visible. (MRI). Image clearly shows the contents of the
spinal canal. In this T2-weighted sequence, the
spinal cord is depicted as gray and the spinal fluid
as white.
technique. However, the main advantage of MRI
is the ability to visualize hemorrhages and
edema, as well as other changes within spinal
cord tissue. Even excellent visualization of the
skeleton is now possible, and luxations of the
facet joints can be demonstrated using this
3
technique.
MRI is usually carried out with sagittal and 4
axial projections (Figs. 8.14 and 8.15). T2-
weighted and proton densityweighted images 5 7
are best suited to demonstrate soft-tissue injuries
in and around the spinal cord. In T2-weighted 6
studies, the most commonly used sequence, the
spinal fluid is depicted as white, as is acute spinal
cord edema (see Fig. 7.2). The appearance of
hemorrhages is time-dependent following
2
trauma, since different hemoglobin metabolites
show different attenuation. 1
The extent of bleeding and edema also pro-
vides some indication of the severity of injury
and therefore also about prognosis. Schaefer
and coworkers presented a classification system Figure 8.15 T2-weighted axial magnetic resonance
to elucidate the appearance of T2-weighted image (MRI). Image showing multiple structures
images in SCI and how they relate to prognosis apart from the spinal cord (1), cerebrospinal fluid
(Table 8.1). (2), and vertebral body (3). The carotid (4) and ver-
In summary, MRI examination is now the tebral (5) arteries, as well as the nerve root (6) are
best option for answering most questions clearly visualized. The posterior longitudinal liga-
about spinal column and spinal cord anatomy ment (7), resembling the wings of a bird, is attached
and pathophysiology. The need for CT to at the midline.
CHAPTER 8 DIAGNOSTIC METHODS 83
TABLE 8.1 Relationship between MRI appearance (T2-weighted) and prognosis according to Schaefer.
Appearance Prognosis
Type 1 Hypointense (dark) changes in the spinal cord Associated with severe neurological
corresponding to intramedullary hematoma. deficits and poor prognosis
Type 2 Hyperintense (light) changes within the spinal cord Motor recovery possible
corresponding to edema without focal
hemorrhage. The edema extends beyond the
height of one vertebral body from the level of
injury.
Type 3 Same as type 2, but the edema extends less than This patient group has the least
the height of one vertebral body from the level neurologic deficit and the best
of injury. prognosis.
image details within the actual area of problems associated with monitoring respiratory
injury continues to decrease as the quality and cardiovascular function while the examina-
of MRI imaging improves, as is illustrated tion is being conducted.
by this MRI sequence of the facet joints
(Fig. 8.16). ACKNOWLEDGMENTS
MRI cannot be carried out on patients who
have magnetically active implants, such as pace- The authors wish to extend their thanks to
makers and older osteosynthesis materials. Dr. Marten Annertz, Neuroradiology section,
Otherwise, the only disadvantages of MRI are University Hospital in Lund, for his invalu-
the lack of round-the-clock availability in able help in providing and describing the
some facilities, time requirements, and practical radiographic material presented in this
chapter.
Suggested Reading
Anderson K, Aito S, Atkins M, et al. Functional recovery
outcome measures work group. Functional recovery
measures for spinal cord injury: an evidence-based
review for clinical practice and research. J Spinal
Cord Med 2008;31(2):133144.
Bono CM, Vaccaro AR, Fehlings M, et al. Measurement
techniques for lower cervical spine injuries: consensus
statement of the Spine Trauma Study Group. Spine
(Phila Pa 1976 ) 2006;1;31(5):603609.
Bono CM, Vaccaro AR, Fehlings M, et al. Measurement
techniques for upper cervical spine injuries: con-
sensus statement of the Spine Trauma Study Group.
Spine (Phila Pa 1976 ) 2007;1;32(5):593600.
Flander AE, Croul SE. Spinal trauma. In: Atlas SW, ed.,
Magnetic Resonance Imaging of the Brain and Spine
Philadelphia: Lippincott, Williams and Wilkins,
2002:17691825.
Furlan JC, Noonan V, Singh A, Fehlings M. Assessment
of impairment in patients with acute traumatic spinal
cord injury: a systematic review of the literature.
J Neurotrauma 2009;December 23.
Figure 8.16 Sagittal magnetic resonance image Grauer JN, Vaccaro AR, Lee JY, et al. The timing and
(MRI). Image illustrating the normal position of influence of MRI on the management of patients
the facet joints (red ring). with cervical facet dislocations remains highly
84 SPINAL CORD INJURY
variable: a survey of members of the Spine Trauma Tator C. Epidemiology and general characteristics of the
Study Group. J Spinal Disord Tech 2009;22(2):9699. spinal cord-injured patient. In: Tator CH, Benzel CH,
Comment in: Surg Neurol 2009 July;72(1):45. eds., Contemporary Management of Spinal Cord Injury:
Harris JH, Mirvis SE. The Radiology of Acute Cervical From Impact to Rehabilitation. Park Ridge, IL:
Spine Trauma, 3rd ed. Baltimore: Williams & American Association of Neurological Surgeons,
Willkins, 1996. 2000:1519.
Lammertse D, Dungan D, Dreisbach J, et al. Neuroimaging
in traumatic spinal cord injury: an evidence-based Internet
review for clinical practice and research. J Spinal Cord
www.internetmedicin.se Search by specialty at the upper
Med 2007;30(3):205214. Review.
left. Click on Neurokirurgi [Neurosurgery] and then
Levi R. The Stockholm spinal cord injury study: medical,
Halsryggsskador (med eller utan ryggmargsskador)
economical and psycho-social outcomes in a preva-
[Cervical spine injuries (with or without spinal cord
lence population (doctoral dissertation). Stockholm:
injuries)].
Karolinska Institutet, 1996.
Model SCI Care Systems report statistics from
McGraw JK. Interventional Radiology of the Spine. New
15% of the spinal cord injury population. Via
York: Humana Press, 2004.
search engine: National Spinal Cord Injury
Miyanji F, Furlan JC, Aarabi B, et al. Acute cervical trau-
Statistical Center. The first hit describes UABs
matic spinal cord injury: MR imaging findings corre-
National Spinal Cord Injury Statistical Center. Go
lated with neurologic outcomeprospective study
to the Model Spinal Cord Injury Care Systems site
with 100 consecutive patients. Radiology 2007;243(3):
for a wealth of interesting statistics.
820827. Epub 2007 April 12.
Parizel PM, van der Zijden T, Gaudino S, et al. Trauma of
Other
the spine and spinal cord: imaging strategies. Eur
Spine J 2009;2. Epub ahead of print. National Spinal Cord Injury Database. The best reference
Ross JS, M Brant-Zawadzki, Chen MZ, Moore KR. is the November 1999 issue of Archives of Physical
Diagnostic Imaging: Spine. New York: Elsevier, 2004. Medicine and Rehabilitation. See Archives of Physical
Swischuk LE. Imaging of the Cervical Spine in Children. Medicine and Rehabilitation November 1999;80(11):
New York: Springer-Verlag, 2002. 1363.
9 Pharmacological Treatment
85
86 SPINAL CORD INJURY
patients who demonstrated motor improvement with fewer side effects. Since these patients
were given MPSS within 8 hours following injury. received a bolus of MPSS, the effect of tirilazad
Strong criticism, both methodological and statis- as such was difficult to assess and therefore no
tical in nature, was aimed at the NASCIS 2 study. definite conclusion about the effect of this drug
The major criticism was that NASCIS 2 only could be drawn.
assessed gains in motor score according to ASIA, In summary, the NASCIS study authors
but not in abilities according to, e.g., Functional recommend continuing treatment for 24
Independent Measure (FIM). hours if treatment is initiated within 3 hours
Patients who sustained bullet wounds and of the injury and continuing treatment for 48
were treated with intravenous steroids demon- hours if treatment is initiated within 38
strated no neurological improvement compared hours of the injury. The recommendation of
with the placebo group. the authors to use methylprednisolone for 48
In the third NASCIS study, which was hours is based solely on the motor score
published in 1997, FIM was added. In NASCIS according to ASIA, since no significant
3, patients in all three groups were adminis- improvement in FIM could be demonstrated.
tered the same bolus dose of methylpredniso- NASCIS 3 was also the target of much criti-
lone as in NASCIS 2. The patients were then cism (from Hugenholtz and colleagues [2002],
divided into three groups. One group received among others). Reviewers expressed a
the same dose of MPSS infusion as in NASCIS number of critical viewpoints on how the
2 for 23 hours, another group for 48 hours, study was conducted and interpreted, and
and the third group received the lazaroid tiri- their criticism was directed at the same prin-
lazad for 48 hours (2.5 mg/kg bolus every ciples as in NASCIS 2. Despite the NASCIS
6 hours). studies, there is still no consensus on
Lazaroids are synthetic nonglucocorticoid whether methylprednisolone has a significant
steroids. Experimentally, they have been found benefit on neurological recovery. Also of rele-
to be more potent than methylprednisolone vance to this discussion is the fact that
in counter-acting iron-dependent lipid peroxida- administration of cortisone for 48 hours is
tion. Animal experiments have also shown associated with a higher risk of side effects
that the lazaroid tirilazad has an effect on neuro- such as pneumonia, sepsis, and respiratory
logical recovery, and the hypothesis is that tiri- complications than is treatment for
lazad not only counteracts lipid peroxidation on 24 hours, even though the difference in the
the microvascular level, but also decreases post- complication rate did not reach statistical sig-
traumatic ischemia. Nor does Tirilazad have the nificance. Other side effects associated with
negative effects of methylprednisolone, such as administration of methylprednisolone include
immunosuppression and hyperglycemia. aggravation of diabetes, immunosuppression,
The 1-year follow-up of NASCIS 3 was increased risk of infections, impaired wound
published in 1998, and the authors concluded healing, and increased risk of bleeding ulcers.
that if treatment began within 3 hours of injury, According to Hugenholtz, the use of ster-
a similar motor improvement was obtained 1 year oids in SCI can be summarized by stating
after the trauma, regardless of whether the patient that high-dose infusion with methylpredniso-
was treated for 24 or 48 hours. If treatment began lone that begins within 8 hours of injury is
within 38 hours of the trauma, outcome was not to be considered as standard therapy or
better when treatment continued for 48 hours. If as a treatment guideline, but rather as a
treatment was initiated more than 8 hours after possible optional treatment. This reflects
the injury, improvement in motor function was the general opinion about steroid therapy,
less than that seen in the placebo group in the which is also in line with the scientific
NASCIS 2 study. The group of patients who review published in the journal Neurosurgery
received tirilazad for 48 hours demonstrated the in 2002. Table 9.1 shows the treatment pro-
same pattern of improvement as those patients tocol at one Swedish center using Solu-
who received MPSS infusion for 24 hours, but MedrolR in the acute phase.
CHAPTER 9 PHARMACOLOGICAL TREATMENT 87
Indications:
Acute spinal cord trauma.
Properties:
Animal experiments studies have shown that the substance counteracted several of the secondary mechanisms of injury that arise
after trauma. According to the National Acute SCI clinical studies 2 and 3 (NASCIS 2 and NASCIS 3), the drug has a beneficial
effect on motor recovery after SCI.
Duration of treatment
If the treatment/bolus dose is initiated within 3 hours post injury, then treatment should continue for 24 hours.
If the treatment/bolus dose is initiated within 38 hours post injury the treating physician will decide whether an additional
24 hours of treatment (total of 48 hours) is indicated.
Contraindications:
Cauda equina syndrome, penetrating injuries, presence of serious life-threatening disease, pregnancy, drug abuse, and
ongoing steroid therapy.
Patients younger than 13 years should not be treated with Solu-Medrol.
Dissolve the required amount of Solu-Medrol for 12 hours in the benzyl alcohol that comes with it. Use a 100 mL
infusion solution of normal saline (9 mg/mL) (contents in soft plastic bag).
Then aspirate the corresponding volume of normal saline (9 mg/mL) infusion solution given by the table above.
Next add the volume of Solu-Medrol solution given in the table above to the remaining normal saline solution.
The total volume of the infusion, regardless of weight, will be 125 mL (appropriate volume even for overweight patients)
Infusion rate: 11 mL per hour
From Bracken MB:, Shepard MJ, Collins WF and coworkers: A randomized controlled trial of methylprednisolone or naloxone
in the treatment of acute SCI. New England Journal of Medicine 1990;322:14051411.Bracken MB, Shepard MJ, Holford TR,
Leo-Summers L, Aldrich E, Fazl M, et al. Administration of methyl prednisolone for 24 or 48 hours or tirilazad mesylate for 48
hours in the treatment of acute SCI. Results of the Third National Acute SCI Randomized Controlled Trial. National Acute
SCI Study. JAMA 1997;277(20):1597604, with permission.
88 SPINAL CORD INJURY
The incidence of spinal column fractures the spinal column. (All references relating to
and/or ligamentous injuries is estimated at Chapters 1015 are shown at the end of this
25 per 1,000 individuals. The number of chapter.)
individuals treated for a spinal column
injury is thus at least 100 times higher than
MOTION SEGMENT
the number of individuals afflicted by trau-
matic SCI. A motion segment contains two adjacent vertebral
Chapters 1015 present detailed surveys bodies including their facet joints, ligamentous
of injuries to the spinal column and liga- structures, and the interposed intervertebral disk
ments. Fractures and ligamentous injuries of (Fig. 10.1).
the upper and lower cervical spinal column
are described in Chapters 11 and 12, respec-
tively. These chapters also contain an over- ANATOMICAL PLANE
view of the treatment options in injuries to
the cervical spine. The surgical techniques Anatomical or reference planes are used to
used to treat these injuries are described in illustrate the extent of an injury. Three anato-
Chapter 13. mical planes are illustrated in Figure 10.2. The
Classification and treatment of thoraco- frontal or coronal plane divides the body into
lumbar fractures is presented in Chapter 14. an anterior and posterior part. The sagittal
Nonsurgical treatment is presented in Chapter plane splits the body vertically into a left and a
15. We have chosen to present the use of orthoses right side; consequently, sagittal images contain
in one chapter since the principles of such treat- sequences viewed from the side. The transversal
ment are, in many respects, similar for the entire plane divides the body into an upper (rostral)
spinal column. and a lower (caudal) part. Transverse images
Our review of surgical and nonsurgical are also called axial images. The anatomical
treatments is based on the literature and dis- planes cross each other at 90-degree angles
cussions with colleagues within this field. and can thus be used as a coordinate system
We are well aware of differing treatment prin- to describe the direction of movements in
ciples among various countries and trauma spinal cord trauma.
centers. The text thus should be viewed as
merely presenting options rather than defini- BIOMECHANICS
tive guidelines.
Initially, we wish to introduce the terms The nomenclature presented here is often
motion segment and anatomic plane, and also used when injuries to the spinal column
briefly review some biomechanical aspects of and ligaments are described. The right-handed
91
92 SPINAL CORD INJURY
Axial Axial
rotation rotation
Mz
Mz Fz
Z-axis
Compression Z-axis Distraction
Fz Mediolateral
translation force
My Fy
Flexion
Mediolateral
translation force Y-axis
Anteroposterior Fy Posteroanterior
shear force My shear force
Fx
Extension Fx
Mx
Y-axis
X-axis X-axis
Lateral Lateral
bending Mx bending
A) B)
Figure 10.3 A,B: Schematic overview of the three-dimensional axes/coordinates and the different loads that
may occur in a trauma to the spinal column.
Inferior
A) (lower) B)
Figure 10.4 A,B: Description of moments located inside and outside of the sagittal plane.
TABLE 10.1 Forces and moments involved in trauma to the spinal column.
Forces Moments
Translation force along the x-axis (anteriorly or Lateral bending moment around the x-axis
posteriorly)
Compressiondistraction force along the z-axis (axial) Rotation moment around z-axis
Translation force along the y-axis (medially or laterally) Flexionextension bending moment around the
y-axis
94 SPINAL CORD INJURY
Holdsworth FW. Fractures and dislocations of the spine. Omeis I, Duggal N, Rubano J, et al. Surgical treatment
J Bone Joint Surg 1963;45-B:620. of C2 fractures in the elderly: a multicenter retro-
Hostler D, Colburn D, Seitz SR. A comparison of three spective analysis. J Spinal Disord Tech 2009;22(2):
cervical immobilization devices. Prehosp Emerg Care 9195.
2009;13(2):256260. Panjabi MM, White III AA. Basic biomechanics of the
Levine AM, Edwards CC. The management of traumatic spine. Neurosurg 1980;7(1):7693.
spondylolisthesis of the axis. J Bone Joint Surg Am Patel AA, Dailey A, Brodke DS, et al. Spine trauma
1985;67:217226. study group. Subaxial cervical spine trauma clas-
Lind B, Sihlbom H, Nordwall A. Forces and motions sification: the subaxial injury classification
across the neck in patients treated with halo-vest. system and case examples. Neurosurg Focus 2008;
Spine 1988;13:162167. 25(5):E8.
Magerl F, Aebi M, Gertzbein SD, Harms J, Nazarian Patel AA, Dailey A, Brodke DS, et al. Spine Trauma Study
S. A comprehensive classification of thoracic and Group. Thoracolumbar spine trauma classification:
lumbar injuries. Eur Spine J 1994;3:184201. the thoracolumbar injury classification and severity
Magerl F, Seemn P-S. Stable posterior fusion of the atlas and score system and case examples. J Neurosurg Spine
axis by transarticular screw fixation. In: Kehr P, Werdner 2009;10(3):201206.
PA, eds., Cervical Spine I. New York: Springer-Verlag, Smith HE, Vaccaro AR, Maltenfort M, et al. Trends in
1987:322327. surgical management for type II odontoid fracture:
Menezes AH, Sonntag VKH. Principles of Spinal Surgery. 20 years of experience at a regional spinal cord injury
New York: McGraw-Hill, 1996. center. Orthopedics 2008;31(7):650.
Nassr A, Lee JY, Dvorak MF, et al. Variations in surgical Traynelis VC, Marano GD, Dunker RO, et al. Traumatic
treatment of cervical facet dislocations. Spine 2008; atlantooccipital dislocation. Case report. J Neurosurg
33(7):E188E193, Eur Spine J 2009;September 2 (Epub 1986;65:863870.
ahead of print). White AA, Panjabi MM. Clinical Biomechanics of
Nicoll EA. Fractures of the dorso-lumbar spine. J Bone the Spine, 2nd ed. Philadelphia: JB Lippincott,
Joint Surg 1949;31-B:376394. 1990.
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11 Upper Cervical Spine Fractures and Ligament
Injuries (C0C2)
Injuries to the upper cervical spine (or the occipi- (Figs. 11.111.4). The principal stabilizing struc-
toatlantoaxial [C0C2] joints) occur following tures in the craniovertebral junction are the facet
trauma to the head and neck region. A broad joint capsules of C0C1, the anterior and posterior
variety of neurological complications are seen as a atlantooccipital membranes, and the two lateral
result of fractures and ligamentous injuries in atlantooccipital membranes (not illustrated). The
this area. Death may occur due to respiratory transverse ligament is the strongest stabilizing
insufficiency in cases with concomitant injury to ligament of C1 and holds C1 to the skull base
the cervical spinal cord. However, most injuries in through the ascending part of the cruciform liga-
the upper cervical spine do not result in any neu- ment. The skull base is stabilized to C2 mainly by
rological deficits because of the relatively large the tectorial membrane (occipitoaxial ligament)
diameter of the spinal canal and also because and the paired alar ligaments. The tectorial mem-
most of the fractures in this region expand rather brane prevents hyperextension in the upper cer-
than narrow the spinal canal. vical region, and the paired alar ligaments prevent
C0C2 fractures represent about 1015% of excessive rotation and lateral bending between
all cervical spine fractures. An isolated axis C0 and C1.
fracture is the most common type of injury of the The atlas is a unique vertebra in that it has
upper cervical spine. In one large epidemiological neither a vertebral body nor intervertebral disks
study, isolated axis fractures constituted 71% in contact with the adjacent occiput and axis
(294 patients) of 414 patients presenting with frac- (Fig. 11.4). The muscles are attached at the tuber-
tures to this region. Seventeen percent (70 patients) cles located in the middle of the cylindrically
in the same study were fractures of the atlas and shaped arches. The ovally shaped lateral masses,
the remaining 12% (50 patients) involved both viewed from above, articulate with the occipital
C1 and C2 vertebrae. It should be observed that condyles in a ball-and-socket configuration
50% of atlas fractures are associated with a fracture (Figs. 11.1, 11.4). The tops of the lateral masses
of the axis. Fractures of the atlas represent only are concave, and fit well with the oval occipital
13% of all fractures of the spinal column, but condyles. The ball-and-socket configuration
they are responsible for 20% of all fatal injuries. results in virtually no axial rotation in the C0C1
These deaths usually occur at the scene of the joints, and in a limited degree of flexion, extension,
accident, before any prehospital care is available. and lateral bending. The articulating surfaces
between atlas and axis are biconvex, resulting in
ANATOMICAL OVERVIEW the opposite pattern of movement when compared
to the C0C1 joints. The axial rotatory capacity is
The occiput, atlas, and axis form a biomechanical extensive whereas flexion, extension, and lateral
unit in which the atlas serves as a sort of bending movements are very limited.
washer to buffer the forces between the stiff Two principal stabilizing ligaments lay between
occipital condyles (i.e., the skull base) and the C1 and C2. The strongest stabilizer, the transverse
mobile axis vertebra (i.e., the cervical spine). ligament, runs between the medially located tuber-
Several ligaments and other structures cles of the lateral masses. This ligament acts as a
maintain stability of the upper cervical spine seat belt by attaching the dens to the posterior
97
98 SPINAL CORD INJURY
C0
C0
C1
C2 C1
C2
C3
A) B)
C2
C)
Figure 11.1 Spiral CT scans showing the cervical spine. A: Coronal reconstruction illustrating the
occipito-atlantal-axial unit. The relationships between C0C1, C1C2, and most importantly, C2C3
are shown in this image. The red arrow indicates the uncinate process (processus uncinatus). B:
Sagittal view through the articulating joints a few centimeters from the midline (paramedian view)
demonstrating the ball-and-socket configuration between the C0 and C1 joint and the biconvex C1
C2 joint. Observe the C2C3 joint that is considered a normal joint in the cervical column. The
structure between the C1C2 and C2C3 joints (arrow) is the pars interarticularis. C: Midline sagittal
section illustrating the relationship between the top of dens (C2), foramen magnum (double arrow),
and the anterior and posterior arches of C1 (single arrows).
surface of the anterior arch of the atlas. The alar No universally accepted classification of
ligaments extend between occiput and the tip of fractures and ligamentous injuries exists in
the dens and surround C1 between the occiput and this region. Classifications similar to those
C2 (Figs. 11.111.3). The ligament prevents wide of the thoracic and lumbar spine are not applic-
rotation and lateral bending of CI. able because of the very specific anatomical
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 99
Alar ligament
CO-CI
Dens Facet joint capsule
Cruciform
ligament and
transverse
ligament
Tectorial membrane
Tectorial membrane
Apical ligament
Transverse ligament
Anterior longitudinal
ligament
Posterior longitudinal
ligament
and biomechanical conditions and the great broad overview of injuries in this region and
variety of injuries. The loading mechanisms their standards of treatment (Table 11.1).
behind many of the fractures and ligament Specific surgical and nonsurgical treatments
injuries in this region are complex and diffi- for these injuries are presented in Chapters 13
cult to reconstruct. Here we present a and 15, respectively.
100 SPINAL CORD INJURY
Transverse ligament
C1 lateral mass
Tectorial membrane
Posterior arch
TABLE 11.1 Injuries to the upper cervical spine: classification and treatment options.
Reducing the Non-surgical treatment Surgical treatment
malalignement
Occipital condyle
fractures
Type I and II Soft or hard cervical
collars
Type III Hard cervical collar or Occipito-cervical fusion if
Halo vest instability is present
Atlanto-occipital Avoid traction but Halo vest Occipito-cervical fusion if
dislocation try to reponate significant malalignment
the dislocation
Atlas fractures
Isolated ring Soft or hard cervical
fractures collar for 68 weeks
Jefferson fracture
Minor dislocation Cervical collar, cervico- Fusion C0CII if ongoing
<7 mm thoracic orthosis or dislocation despite
Halo-vest non-surgical treatment
Major dislocation Halo-vest Fusion C0CII if ongoing
>7 mm dislocation despite
non-surgical treatment
Lateral mass fracture
Non-dislocated Cervical collar 68 weeks
Comminute Halo-vest
Transverse ligament Fusion CICII
rupture
Axis fractures
Odontoid fractures
Type I Hard cervical collar if
atlanto-axial instability
has been excluded
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 101
OCCIPITAL CONDYLE FRACTURES when the cervical column is pressed toward the
stiff and fixed cranium.
Occipital condyle fractures are rare. They usually
occur as isolated fractures following compression Diagnosis and Classification
force, axial rotation, and lateral bending moment.
Occipital condyle fractures are associated with Plain radiographs rarely capture these fractures.
blunt head injuries as a result of the axial force Computed tomography (CT) imaging is
running from the crown to the mandible. The required, and the visualization of the fractures
risk of sustaining a fracture of the skull base is enhanced by two- and three-dimensional
including the occipital condyles increases, thus, reconstruction. The radiological investigation
102 SPINAL CORD INJURY
Apical ligament
Alar ligament
Type I
Type II
A) Type III B)
Figure 11.5 Occipital condyle fractures. A: Occipital condyle fractures type IIII. B: Computed tomography
(CT) reconstruction of a right-sided type II fracture (arrow describes the fracture line).
regarding instability is focused on the alar liga- base fracture; and type III is an avulsion fracture
ment and the tectorial membrane (Fig. 11.5). of the occipital condyle as a result of the tension
Anderson and Montesano have classified occi- force of the alar ligament.
pital condyle fractures into three types. Type I
refers to a comminute fracture (i.e., containing Treatment
several fragments) with neither significant dis-
placement of bone into the foramen magnum The choice of treatment depends on circum-
nor signs of avulsion of the alar ligament. The stances, such as the presence of a uni- or bilateral
type II fracture is an extension of a linear skull- occipital condyle fracture, other fractures/
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 103
ligamentous injuries in the upper cervical spine, measures the distance between the basion and
and/or the presence of neurological impairment. the posterior arch of the atlas (BC); the second
Typically, there is no need for surgical treat- line describes the distance between the opisthion
ment of occipital condyle fractures, since they and the anterior arch of the atlas (OC). The mean
usually heal without complications. Types I and ratio (BC/OC) in normal individuals is 0.77.
II are considered stable and are treated with Values of 1.0 or greater suggest an atlantoocci-
external immobilization (e.g., 812 weeks in a pital dislocation.
cervical soft or hard collar). Halo-vest treatment According to Traynelis and coworkers, atlan-
may be an alternative in the type III injuries, tooccipital dislocations are divided into type I
because of an increased risk of instability. (anterior dislocation), type II (vertical disloca-
Unstable type III fractures may be part of an tion), and type III (posterior dislocation;
occipitocervical instability and are then treated Fig. 11.9). Atlantooccipital dislocations are, as
by occipitalcervical fusion. previously mentioned, associated with injuries
to the cranium and face. Concomitant damage
to the brainstem may explain the relatively high
ATLANTOOCCIPITAL DISLOCATION mortality associated with this type of injury.
Atlantooccipital dislocations are most frequently
Atlantooccipital dislocation constitutes approxi-
seen in child pedestrians who have been struck
mately 1% of all injuries to the upper cervical
by cars. The horizontal placement of the articu-
spine. They are typically fatal and are most
lating joints between C0 and C1 in children
common among children. The injury
facilitates the gliding of these joints.
mechanism involves multiple components such
as hyperextension and hyperflexion bending
moments. The pattern of decelerationaccelera- Treatment
tion as a cause of this type of injury resembles
the injury mechanism associated with whiplash The choice of treatment of atlantooccipital
injuries. Most of the supportive structures stabi- dislocations depends on the severity of the
lizing the craniocervical junction are damaged, ligamentous injuries. Traction is generally con-
particularly the alar ligaments and tectorial traindicated. The spinal cord may be stretched
membrane, resulting in forward dislocation of during this procedure, resulting in further risk of
the occipital condyles in relation to the lateral cord injury. A hard cervical collar should be used
masses of atlas (Fig. 11.6). until final treatment is decided. Minor
dislocations, also among children, are treated
with a halo-vest orthosis. Gross misalignments
Diagnosis and Classification
and injuries that are considered ligamentous are
Atlantooccipital dislocations may not be visua- usually managed with an occipitalcervical
lized on plain radiographs. Indirect signs, such fusion.
as retropharyngeal hematoma and emphysema
located anterior to the spinal column, indicate ATLAS FRACTURES
concomitant damage to the posterior pharyngeal
wall. Magnetic resonance imaging (MRI) reveals Atlas fractures occur following axial force or
clival hematoma and changed signals in, for vertical compression acting on the vertex of
instance, the alar ligament (Fig. 11.7). The dis- the skull. The force is transmitted caudally,
tance and degree of displacement between the and the occipital condyles become pressed
foramen magnum and atlas can be assessed by against the lateral masses of atlas. The most
two- and three-dimensional CT reconstructions famous type of atlas fractures is the Jefferson
(Fig. 11.8). The relationship between the cra- fracture, after the researcher who classified these
nium and upper cervical spine can be assessed fractures based on their appearance and the
using the Powers index. The Powers index is the degree of involvement of the alar and transverse
ratio between the length of two lines. One line ligaments.
104 SPINAL CORD INJURY
CI
A) B)
Figure 11.6 Spiral computed tomography (CT) scan. Frontal reconstruction illustrating a displacement at
the level of C0 and C1 (particularly on the right side). The reconstruction is performed exactly in a straight
position in relation to C2. A: A bilateral displacement of the joints is seen at the level of C1 and CII. The
appearance of the right and left lateral masses differs and these findings show that C1 is rotated in relation to
C1 (compare to Figure 11.4). B: The axial view also shows that C1 is rotated in relation to ramus mandibulae
(arrow). The vertebral body of C2 is uninjured (compare to Figure 11.1A).
Figure 11.7 T2-weighted magnetic resonance image (MRI). Image illustrates a hematoma with high-density
signals in the C0C1 region. The thin white arrow indicates clivus, the thin red horizontal arrow points to the
hematoma, and the thick vertical red arrow shows the tectorial membrane. The membrane is disconnected
from the caudal part of the clivus by the hematoma. The hematoma reaches to the front of atlas (the thick
white arrow points out the arch of atlas).
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 105
BC
Isolated ring fractures (arch fractures)
OC Jefferson fracture:
With minor dislocation
With severe dislocation (Spence distance
>7 mm indicate ligament injuries)
Lateral mass fracture without dislocation
Comminute lateral mass fractures
Figure 11.8 Computed tomography (CT) recon- Transverse ligament rupture
struction used to calculate the Powers index.
Treatment
A) B)
Figure 11.12 A: Axial computed tomography (CT) of C1 illustrating a Jefferson fracture. Multiple fractures
of the atlas ring are seen but only a minor dislocation occurs. The white arrow in the middle points at the dens
axis. The posterior arch of atlas is not included in this view. B: A classical Jefferson fracture with altogether
four fracture lines.
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 107
Transverse ligament
X X+Y 7 mm Y
Figure 11.13 The distances x and y shows a dislocation between the inferior articular surface of C1 and the
superior articular surface of C2. The vertebral body of C1 is increased in width, and the transverse ligament is
considered ruptured if the Spence distance (the sum of x and y) is equal to or exceeds 7 mm.
located knot, placed below the angle of the jaw and examination of the skulls revealed no disruptions
mastoid process, resulted in a force through the of the skull base but fractures of the cervical spine.
skull base as the victim was dropped. This mode of The submental knot position was used from then
knot placement had been used since the Roman on, because it produced a quick and thus
era and resulted in disruptions of the cranial base humane death. Biomechanically, the use of the
but no fractures of the cervical spine. The submen- submental knot resulted in a distraction force and
tally placed knot, however, resulted in instant hyperextension, leading morphologically to a
death, as demonstrated by Captain C. F. Fraser, separation of the arch of axis from the vertebral
superintendent at the Rangoon Central Jail. He body (i.e., a traumatic spondylolisthesis). The
donated five skeletons to Wood-Jones, and the hangmans fracture, according to current
CI
C1 lateral mass
CII
CIII
Odontoid Fractures
Type III
Diagnosis and Classification
Figure 11.16 Odontoid fractures types I, II, and III.
Odontoid fractures may be overlooked easily,
especially if nondislocated, and where plain
radiographs are used in the acute setting. CT,
using thin slices and reconstruction images, bone is very limited at the fracture site and the
better demonstrates these fractures, which are presence of soft-tissue material may, by becoming
subdivided according to Anderson and interposed at the fracture surfaces, also contribute
dAlonzo into three types (Fig. 11.16). to nonunion. Type III fractures engage the
Type I fractures are uncommon. They are vertebral body itself. The fracture area is large,
usually oblique and located at the tip of the dens. and this fracture type usually heals without
They are considered avulsion injuries located at problems (Fig. 11.19).
the attachment of the alar ligament to the odon-
toid process. This type of fracture may be asso- Treatment
ciated with craniocervical instability because of
the damage to the alar ligament. Type II fractures Almost all type I odontoid fractures heal without
are the most common. They are located at the problems. However, one must consider the possi-
junction of the odontoid process and the vertebra bility of a coexisting atlantooccipital dislocation
of C2 (Figs. 11.17 and 11.18). This fracture has a before choosing treatment for this stable type of
high incidence of nonunion (65% if dislocation is fracture. The standard treatment is, after injuries
>6 mm) probably caused by stoppage of the blood to the alar ligament have been excluded, a hard
supply. The cross-sectional area of cancellous cervical collar for 6 weeks. Surgical fusion of
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 109
Figure 11.17 A nondislocated fracture at the junction of the vertebral body and the odontoid process.
A) B)
Figure 11.18 A: A type II fracture with approximately 5 mm anterior dislocation of the odontoid process/
atlas complex in relation to the vertebral body of C2. Observe the anterior dislocation of the posterior arch of
CI in relation to the vertebral body of CII. B: The same type of fracture. The dislocation here, however, is
considerably more substantial. The posterior arch of C1 is also displaced anteriorly, resulting in a further
narrowing of the spinal canal (the double arrow shows the distance between the posterior arch of C1 and the
posterior superior edge of C2).
C1C2 may be performed if a ligamentous injury is collar (in dislocations of <6 mm) or a Halo-
detected. vest, whereas surgical treatment is required in
Treatment of type II fractures is based on the some cases. Some studies indicate a high fre-
patients age, the appearance of the fracture, and quency of nonunion among patients treated
the presence of concurrent injuries. There is an with Halo-vest. Two possibilities of surgical
increased risk of nonunion (pseudarthrosis) if the treatment for this fracture type are available if
dislocation between the odontoid process and the the fractures do not heal, anterior or posterior
vertebral body of C2 is equal to or exceeds 6 mm. internal fixation. The disadvantage of posterior
Stabilizing treatment for type II fractures is internal fixation is the abolishment of all move-
considered necessary. The stabilizing measures ment between C1 and C2. This results in a rota-
are either nonoperative using a hard cervical tional reduction of about 50% in the cervical
110 SPINAL CORD INJURY
A) B)
Figure 11.19 Odontoid fracture type III. Computed tomography (CT) axial (A) and frontal (B) reconstruction
images are obtained through the vertebral body of C2 (the arrow in B shows the fracture line).
spine. The advantage of the anterior internal is a treatment option in rare cases. Surgical
fixation is the preservation of the full ability to management with internal fixation may be
rotate. used if the Halo-vest treatment fails. These rare
Noncomminuted type II fractures dislocated cases are treated with a posterior fusion between
less than 5 mm and located perpendicular to the C1 and C2.
odontoid process are usually treated with a
Halo-vest for 1012 weeks. Plain radiographs Traumatic Spondylolisthesis (Hangmans
or CT scans are regularly performed during Fracture)
this period. Anterior fixation, using odontoid
screws, is a common alternative. The screws This type of fracture usually results from an axial
offer instant rigid fixation, allow healing, and force and hyperextension bending moment.
preserve rotation between atlas and axis. A hard The pars interarticularis of C2, also known as the
cervical collar offers an additional treatment pedicle or isthmus, is one of the weakest structures
possibility among very old osteoporotic of the cervical spine (Fig. 11.1B). A bilateral frac-
patients. ture through the pars interarticularis constitutes
Patients exhibiting fractures with a high risk the prerequisite for Hangmans fractures.
for nonunion may be considered candidates for
surgical intervention. Fractures dislocated 6 mm Diagnosis and Classification
or more with an oblique fracture line in the
anteroposterior view or with a comminute Sagittal plain radiographs may capture a hang-
appearance are usually treated by internal fixa- mans fracture, although CT gives a more exact
tion. Patients showing signs of SCI and/or chest depiction of the fracture morphology. Traumatic
injury are also usually candidates for surgical spondylolisthesis is classified, according to
intervention. Levine and Rhyne, into four subgroups. This
Type III fractures almost always heal if classification is based on the morphology of the
treated with a Halo-vest. A hard cervical collar fracture, as well as on the angulation and
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 111
Treatment
A) B)
in avulsion of the anterior inferior corner of bony or ligamentous damage. AAI is defined as
the C2 vertebral body. Type II resembles the an atlantodens interval (ADI; i.e., the distance
type III odontoid fracture (Fig. 11.16) but is between the odontoid process and the posterior
localized further back on the C2 body. Type border of the anterior arch of the atlas) of more
III is a burst fracture of the C2 body, and type than 3 mm in adults and of more than 5 mm in
IV is a sagittally oriented vertical split fracture children, as measured by plain radiographs.
through the body of C2. This fracture is con- Instability may result in displacement in all direc-
sidered unstable. tions. Translation of the vertebral arch of the atlas
in relation to the dens (anteroposterior transla-
Treatment tion) and rotation of the atlas relative to the axis
(rotatory displacement) are the most common
Treatment of this fracture group is based on the types of atlantoaxial instability. The strong trans-
degree of dislocation between the atlas and axis. verse ligament and the facet capsules normally
Fractures considered stable are treated with a maintain the integrity of the atlantoaxial articula-
hard cervical collar, whereas unstable fractures tion. A rupture of the transverse ligament results
are initially managed with a Halo-vest. The frac- in the most common types of AAI mentioned.
ture area of spongy bone is large, which results The most severe types of instability, such as a
in a high percentage of healing. Surgical treat- vertical displacement, also require disruption of
ment is required in the management of the type I the alar ligament and tectorial membrane,
fracture and also if alignment is impossible to resulting in a widening of the C1C2 facet joints.
obtain in the other types of fractures treated
nonsurgically. A posterior fusion is then usually Diagnosis and Treatment
performed between C2 and C3.
AAI is typically seen on plain lateral flexion-
Atlantoaxial Instability extension radiographs, although the interpreta-
tion of atlantoaxial rotatory displacement is
Atlantoaxial instability (AAI) is characterized by more difficult using this technique. An atlan-
an excessive (i.e., nonphysiological) movement at toaxial distance of greater than 45 mm, as
the junction between atlas and axis as a result of demonstrated by lateral radiographs, is
CHAPTER 11 UPPER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C0C2) 113
indicative of anteroposterior instability. Two- A hard cervical collar is used if there are no
and three-dimensional CT reconstructions, signs of fracture of C1 or C2 and if the transverse
however, detect avulsion fractures engaging ligament is intact. Lateral flexion-extension
the transverse ligament. An increased distance radiographs are performed at the end of the
between the lateral mass and the dens of more treatment period. Internal fixation must be
than 2 mm indicates instability. MRI may reveal considered if signs of instability remain.
hematoma and ligamentous damage. Patients with ruptures of the transverse ligament
The most common causes of AAI are: require surgical treatment.
Rotatory displacements are extremely rare. The
Anteroposterior instability:
type I rotatory displacement only requires a hard
Rupture of the transverse ligament
cervical collar if the displacement is corrected and
Odontoid fractures
remains in alignment during a treatment period of
Unstable Jefferson fractures
46 weeks. Surgical treatment is indicated if a
Associated occipitocervical instability
redislocation occurs during the period of conserva-
(rupture of the alar ligament)
tive treatment. Rotatory displacement of type II
Rotatory displacement:
and III generally requires surgical treatment
Facet subluxation (type I)
(i.e., fusion of C1 and C2).
Rupture of the transverse ligament
115
116 SPINAL CORD INJURY
Interspinal Anterior
ligament longitudinal The Two-column Spine Concept
ligament
Supraspinous
ligament This concept is based on the following principles
Spinous process (Fig. 12.4):
Intervertebral disk
The anterior column consists of the pos-
Figure 12.2 Major support structures of the spinal terior longitudinal ligament and all struc-
column. tures located anterior to this ligament,
CHAPTER 12 LOWER CERVICAL SPINE FRACTURES AND LIGAMENT INJURIES (C3C7) 117
A) B)
Figure 12.3 Imaging of (A) the vertebral artery and (B) the vertebral foramina.
including the vertebral body. The soft- Instability is operationalized according to the
tissue components (the so-called anterior White and Panjabis checklist (Table 12.1). A frac-
ligament complex) comprise the anterior ture is considered unstable if the totla score >5.
longitudinal ligament, the intervertebral
disk, and the posterior longitudinal liga-
ment in each motion segment of two adja-
cent vertebrae. TABLE 12.1 Diagnostic checklist of clinical
The posterior column consists of all structures instability in the middle and lower
behind the posterior longitudinal ligament, cervical spine (scoring points within
including the vertebral arches, facet joints, parenthesis).
and posterior ligamentous complex. Anterior elements damaged or unable to
function (2)
Posterior Posterior elements damaged or unable to
Anterior longitudinal function (2)
longitudinal ligament
ligament Sagittal plane translation (flexion/
Facets extension x-rays) >3.5 mm (4)
Relative sagittal plane angulation (resting
x-rays) >11 degrees (2)
Abnormal disk narrowing (1)
Developmentally narrow spinal canal (1)
Posterior Spinal cord damage (2)
ligament
complex Nerve root damage (1)
Dangerous loading anticipated (1)
A) B)
The Three-column Spine Concept
Figure 12.4 The two-column spine concept. A: The three-column spine concept offers an alter-
anterior column; B: posterior column. native classification. This concept was initially
118 SPINAL CORD INJURY
designed by Denis to classify fractures in the thor- intervertebral disk, and the vertebral body. The
acic and lumbar spine. It is, however, also quite middle column is formed by the posterior part of
frequently used when instability in the lower cer- the intervertebral disk, the vertebral body, and
vical spine is discussed (Fig. 12.5). According to the posterior longitudinal ligament. Thus, the
this concept, the anterior column contains the ante- anterior and middle column in Denis classifica-
rior longitudinal ligament, the anterior part of the tion corresponds to the anterior column in the
concept of White and Panjabi. The posterior
column is identical in both of these concepts.
Anterior Instability is, according to the three-column
longitudinal spine concept, operationalized as a failure of two
ligament
or three of the three columns.
A fracture is always instable if the middle
column is damaged, since damage to this column
always involves additional failure, either of the
anterior or posterior column or both. Neither
classification has been evaluated scientifically, so
should therefore only be considered as heuristic
means to facilitate the choice of treatment.
Posterior
longitudinal FRACTURE CLASSIFICATION
A)
ligament
Closed fractures in the lower cervical spine may,
as previously mentioned, be divided into four
subgroups: flexion-dislocation injuries, flexion-
compression injuries, compression-burst inju-
ries, and extension injuries.
IV
III
II
Figure 12.6 Flexion-dislocation injuries. The empty square behind the facet joint in type II illustrates a
unilateral facet dislocation.
Facet subluxation
TABLE 12.2 Treatment guidelines following injuries to the lower cervical spine.
Narrowing Posterior Treatment
of the Spinal Ligament
Cord Injuries
Flexion-dislocation injuries
Flexion-sprain injury No Yes Hard cervical collar; Halo-vest treatment;
surgery
Unilateral facet dislocation Yes Yes Halo-vest treatment; surgery
Bilateral facet dislocation Yes Yes Surgery
Floating vertebra Yes Yes Surgery
Flexion-compression injuries
Reduction of vertebral
body height
<30% No No Hard cervical collar
>30% No No Hard cervical collar; Halo-vest; surgery
>30% Yes Yes Anterior (if necessary) posterior
internal fixation
>30% No Yes Anterior or posterior internal fixation
Compression-burst fractures
Type I No Hard cervical collar
Type II No Hard cervical collar
Type III Yes Surgery
No Halo-vest treatment
Extension injuries
Distraction-extension
Type I Hard cervical collar/surgery
Type II Surgery
Compression-extension
Type I Hard cervical collar
Type II Hard cervical collar/surgery
Type V Surgery
Mb Bechterew Yes Yes a) Anterior internal fixation and fusion
followed by
b) optional treatment with posterior
internal fixation and fusion or Halo-vest
however, internal fixation performed to pre- complete (Figs. 12.6; II, 12.8 and 12.9). The
vent uni- or bilateral facet dislocations, as well articulating surfaces are exposed completely if a
as to prevent development of chronic pain unilateral facet dislocation occurs. This is known
and neurological sequelae. as the nude facet or inverted hamburger sign.
C5
C5
IV
III
II
Grad 4
C4
Figure 12.13 Flexion-compression injury grade IV without and with arrow and fracture line. The
double-arrow shows the prevertebral soft-tissue shadow. The red line indicates the course of a flexion
teardrop fracture involving C3 and C4. The teardrop fragment is attached to the C5 vertebral body via the
anterior longitudinal ligament. An additional ligamentous injury must be present at the level of C3 and
C4. The fracture traverses the posterior two-thirds of the intervertebral disk, through the posterior part of
the spinal canal and finally between the spinous processes of C4 and C5. The vertebral body of C4 is
dislocated a few millimeters in relation to CV.
vertebral body is dislocated into the spinal canal presence of ligamentous injuries, and the
in the most severe type of injury, grade V, and the severity of the neurological deterioration is of
distance between the articulating facet joint sur- importance in fracture management if the ver-
faces is increased. Locked facets, a characteristic tebral body height is reduced by more than one-
sign of flexion-dislocation injuries, are not third.
observed in flexion-compression injuries. Surgical treatment is the method of choice in
the presence of posterior ligament injuries and/or
Treatment significant bony compression of the spinal cord.
Treatment
III
II
Extension Injuries
C3
Extension injuries are seen following distraction
(Fig. 12.17) or compression (Figs. 12.19 and
12.20). Elderly people with spondylosis are parti-
cularly vulnerable to this type of injury, and a
high incidence of spinal cord involvement is
observed in this group (Fig. 12.18). Avulsion of
an anteriorly located fragment is seen in younger
individuals, in addition to damage to either the
anterior or posterior structures.
Distraction-Extension
Figure 12.19 Left axial CT scan. Image illustrates a unilateral fracture and the right image a bilateral
vertebral arch fracture, most obvious seen on the left side.
those cases. Surgical treatment is usually indi- the injured vertebra and the vertebra located
cated for severe grade II injuries. above and anteriorly between the injured ver-
tebra and the vertebra located below (arrows in
Fig. 12.20).
Compression-Extension
Treatment. Unilateral compression-extension inj-
The two least complicated levels in a five-level
ury (grade I) is treated conservatively using a hard
scale of compression-extension injuries include
cervical collar. A bilateral fracture of the vertebral
fractures at one (unilateral; grade I) or two (bilat-
arch (grade II) is usually treated in the same
eral; grade II) locations on the vertebral arch, as
fashion. However, it is highly recommended
illustrated by the axial CT images in Figure 12.19.
that an additional CT scan be performed after 8
The most severe type of injury (grade V) includes
weeks, at the end of the conservative treatment
fractures at two locations on the vertebral arch and
period. Surgical treatment is required if the CT
an anterior dislocation of the vertebral body.
reveals a dislocation of the vertebral body, and
Ligamentous injuries occur posteriorly between
should be considered initially in those cases in
which the fracture lines extend through the facet
joints on both sides. The most severe compres-
sion-extension fractures are managed surgically.
Bechterew Disease
FUSION AND INTERNAL FIXATION The paraspinal muscle groups are then loosened
TECHNIQUES from the vertebral arches and retracted as later-
ally as possible without involving or damaging
The goals of surgical management following the vertebral arteries (see Chapter 12; Fig. 12.3).
traumatic injuries to the cervical spine are to The paraspinal muscles are held laterally using
decompress the spinal cord, restore cervical self-retaining retractors and an adequate expo-
column deformities, and achieve acute and sure of the vertebral arches is achieved. Removal
long-term stability of the motion segment. The of the vertebral arch (laminectomy) is the first
use of instrumentation offers immediate stabi- step of the decompression and/or instrumenta-
lity to the injured spine, and is further main- tion procedure. Presence of vertebral arch frac-
tained until bony fusion is established or the tures and suspected damage to the dura
healing process of the ligamentous structures is motivates this procedure (Fig. 13.4; also see
completed. The vertebral bodies of the cervical same figure in Color Plate section). The dura is
spine resembles ring-shaped objects that must visualized after removal of the vertebral arches,
be reattached to form an aligned column again and this step precedes fusion and instrumenta-
following damage. Spinal fixation devices may tion. Bone chips are usually harvested from the
be placed at one, two, or three locations on each posterior iliac crest but the bone collected from
vertebra in the damaged motion segment (i.e., the laminectomy may, in some cases, yield suffi-
one-, two-, or three point fixation; Fig. 13.1). cient bone material to perform the fusion.
The anterior and posterior approaches to Tricortical bone (three of four sides of the trans-
explore the cervical spine will also be illustrated plant consist of cortical bone; Fig. 13.5A) is most
in connection with presentation of the spinal frequently collected from the posterior iliac crest.
stabilization techniques. The transplant is usually 34 cm in length. Before
starting the internal instrumentation procedure,
this transplant is shaped to fit the space between
UPPER CERVICAL SPINE
the vertebral arches of the injured motion seg-
ment, usually C1 and C2.
Posterior Approach to the Cervical Spine
129
130 SPINAL CORD INJURY
Figure 13.1 One-, two-, and three-point fixation. (Courtesy of T. Henriques, M.D.)
Wire Techniques
CI
CII
A) B)
Figure 13.5 A: Wire technique according to Brooks and Jenkins. Tricortical bone is used as fusion material.
B: Plain radiograph obtained sagittally showing the location of the wire following fixation according to
Gallie.
Combination Techniques
A variety of metal implants for occipitocervical Odontoid screw insertion is performed for the
fixation are available (Fig. 13.9). Devices such fixation of odontoid fractures. The compression
as plates and rods are most often used, while technique, using one or two screws, to stabilize
wiring techniques are rarely applied. Bony fractures of the odontoid process equals that of
material is used to fuse the occiput to the transarticular screw fixation (Fig. 13.10A,B). This
cervical spine. technique is not suitable for oblique fractures, and
posterior internal instrumentation is required in
those cases. Access to odontoid screw fixation is
achieved through an anterior approach, described
later.
A) B)
traumatic and provides better control over the fascia, is identified. The fascia and the anterior
disk space. The incidence of postoperative longitudinal ligament are divided. The longus
kyphosis and secondary neck pain is reduced. colli muscles are elevated laterally using self-
The anterior plate is considered a simpler device retaining retractors, after which the anterior
to handle, compared to posterior fixation instru- aspects of the vertebral bodies and interver-
mentation, and the fusion rate is higher with tebral disks are accessible to decompression,
this technique. fusion, and internal fixation.
The patient is placed in a supine position
and the neck is stabilized in extension using Internal Instrumentation Techniques
either Gardner-Wells traction with 23 kg or a
horseshoe-shaped support. The cervical spine Traditionally, internal fixation of the lower cer-
adopts a natural lordosis as a result of this vical spine was obtained by a posterior approach
positioning. The position of the shoulders is if the injury was localized to the posterior
corrected to maximize the C-arm view. The column using the two-column classification.
skin incision is either performed transversally The anterior approach and corresponding fixa-
through a skin crease at the level of approxi- tion were used if the injury was localized predo-
mately C5 or parallel and anteriorly to the ster- minantly to the anterior column. However,
nocleidomastoid muscle (Fig. 13.11AH; also numerous recent studies shows that anterior
see same figure in the Color Plate section). fixation is sufficient even if the posterior
The platysma muscle is divided, and the fascia column is damaged, and presently most injuries
of the sternocleidomastoid muscle is opened. to the lower cervical spine are fixed via an ante-
The carotid artery is now identified, and blunt rior approach. A combination of both anterior
dissection passes medial to the carotid sheath, and posterior approaches is used if instability is
the jugular vein, and the vagus nerve severe, for instance, in cases with bilateral facet
and lateral to esophagus and trachea. The joint dislocation (see Fig. 13.11AH; also see
longus colli muscle, covered by the prevertebral same figure in Color Plate Section).
134 SPINAL CORD INJURY
d
c
b
a
a
b
A) B)
C) D)
E) F)
Figure 13.11 Guidelines for anterior and posterior decompression, fixation and fusion (AH) of bilateral
facet dislocation. A: The arrow indicates direction of skin incision along the left medial border of the
sternocleidomastoid muscle. a, collar bone; b, incisura jugularis sternalis (the V-shaped notch at the top of
sternum). B: a, sternocleidomastoid muscle; b, carotic sheath; c, disk; d, medial attachment of the longus
colli muscle. C: The dural sac is exposed following removal of the disk (decompression of the dural sac). D:
Tricortical bone (a) is harvested from the left iliac crest. E: The adjusted graft replaces the removed disk. F:
Anterior cervical plate fixation. G: Intraoperative photo showing a posterior exposure of the dural sac. The
screws and rods are in place. H: Postoperative plain radiography illustrating the location of the anterior
cervical plate and posterior instrumentation. See also Color Plates Fig. 13.11AH.
CHAPTER 13 SURGICAL MANAGEMENT OF INJURIES TO THE CERVICAL SPINE 135
G) H)
Posterior Instrumentation
A) B) C)
Figure 13.13 One-, two- and three-point fixation corresponding to figure A, B, and C, respectively. (Courtesy
of T. Henriques, M.D.)
the upper cervical spine. A few examples are Intralaminar Clamps (Hooks)
presented here.
The use of intralaminar hooks is similar in both
Wire Techniques the upper and lower cervical spine.
Various straight plates can be bent and adjusted Various types of rods have lately been intro-
to fit the configuration of the cervical spine. The duced. These rods are adjustable to the config-
posterior plating techniques do not need intact uration of the cervical column. The fixation
lamina and can therefore be used in patients system comprises either bone screws or hooks
with multiple fractures to the posterior columns, that are implanted into the cervical vertebrae of
in addition to injuries of the facet joints and the spine. A rod can be applied across the cervical
vertebral body fractures (Fig. 13.15). The length column to counteract rotational movement in
of the plates depends on the severity of the the motion segment (see Fig. 13.11G,H; also
injury. see same figure in Color Plate section).
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14 Thoracolumbar Fractures and Ligament Injuries
Stability of the thoracic and lumbar spine is, as in important role in providing stability to the thor-
the lower cervical spine, maintained by the inter- acic spine by preventing hyperextension move-
vertebral disks, vertebrae (vertebral bodies and ments in the motion segments (Fig. 14.1). The
arches), and ligamentous structures. Stability in posterior ligamentous complex consists of sev-
the thoracolumbar region is much more pro- eral structures. The posterior longitudinal liga-
nounced, due to the stronger posteriorly located ment is much thinner compared to the anterior
ligamentous structures and larger facet joints. one, and it thus lacks biomechanical properties
The articulating surfaces of the facet joints have of importance. The inter- and supraspinous
an increased concavity and convexity, resulting ligaments and the articular capsule enveloping
in increased contact between these components the facet joint also contribute to stability by
(Fig. 14.1). The ribs, sternum, ligaments, and minimizing flexion in the motion segment.
large vertebrae also contribute to the greater The combination of flexion bending moments
stability of this part of the spinal column. This and compression forces is the most common
results in a different injury profile in the thora- traumatic load to the thoracic spine. For
columbar region as compared to the cervical example, in the abrupt transfer of motion that
spine. As a rule, fractures rather than disloca- occurs in a motor vehicle accident, the upper
tions are seen. part of the body and the head continue to move
Most of the body weight is carried by the inter- forward while the lower part of the body comes
vertebral disks and vertebral bodies. The ability of to a halt. This results in hyperflexion of the
the vertebral bodies to bear weight decreases with thoracic and lumbar spine, with the load con-
age as a result of diminished water content in the centrated on the anterior part of the vertebral
disks and osteoporosis in the vertebrae. This body. A collapse of the vertebral body may occur
results in an increased vulnerability to trauma, if the load is severe enough, with the spongiotic
and fractures as a result of low-energy trauma bone either compressed or crushed. The pos-
are seen quite commonly among patients with terior ligamentous complex may also be
osteoporosis. The most important task of the damaged as a result of distraction forces
intervertebral disks is to absorb and distribute toward these posterior structures. Fractures
loads as equally as possible between adjacent ver- occur most frequently at the junction of the
tebral bodies. The facet joints have no weight- rigid thoracic spine and the more mobile
bearing capacity except in the middle and lower lumbar spine. Sixty percent of fractures in the
lumbar spine; because of the physiological thoracolumbar region are located between the
lumbar lordosis, the center of load is located levels of T12 and L2. The L1 vertebra is the most
more posteriorly in that region, giving the facet affected vertebral body (30%).
joints there some weight-bearing ability. The con-
struction and dimension of the lumbar facet THE CONCEPT OF INSTABILITY
joints contribute to their stability. The joints func-
tion as bony barriers is to prevent translational The incidence of posttraumatic neurological
and rotational displacement (see Chapter 10). deterioration, kyphotic deformity, and pain
The anterior longitudinal ligament is one of increases in unstable fractures, so classification
the strongest ligaments in the body, playing an of these injuries should reflect their relative
139
140 SPINAL CORD INJURY
Ligamentum flavum
Intertransverse
ligament
Spinous process
Supraspinous
ligament Posterior
longitudinal
Interspinous ligament
ligament
Anterior
Facet joint longitudinal
capsule ligament
Intervertebral
disk
Rib Vertebral body
stability and also help to determine prognosis, to evaluate whether a fracture is stable or
especially since the risk of future complications unstable and to direct treatment according to
could be decisive in the choice of treatment. this conclusion.
Here, we present two frequently used classifica-
tions, after which some general principles The Three-column Concept of Fracture
regarding available treatment options will be Classification
discussed.
In Denis three-column model, the anterior and
FRACTURE CLASSIFICATIONS middle columns correspond to the anterior
right left
A) B) C)
Figure 14.8 Chance fracture. A: Observe the vertical fracture through the spinous process (arrow) demon-
strated in a spiral computed tomography (CT) with (B) sagittal reconstruction and (C) the corresponding
fracture illustrated using magnetic resonance imaging (MRI).
144 SPINAL CORD INJURY
A) B)
Figure 14.9 Fracture-dislocation type of injury. The plain radiograph shows (A) a lateral and (B) anteropos-
terior displacement as illustrated by this magnetic resonance image (MRI) obtained sagittal view (arrow).
fractures; or (e) the degree of spinal canal compro- that instability occurs if at least two of the three
mise is equal to or exceeds 50%. columns are damaged. The table shows which
The presence of three or more individually columns are considered stable or unstable fol-
stable compression or burst fractures in a row lowing different types of injuries. The table also
is, according to some authors, considered an illustrates which type of further load may
unstable situation. increase the risk of additional injury to an already
unstable/damaged column.
Seat-belt and Fracture-Dislocation Injuries. In these Compression fractures are typically regarded
types of injuries, failure occurs to at least two as stable. The spinal column should, following
columns; thus, these two fracture types are a compression injury, be protected against flexion
always regarded as unstable. bending moment that further increases compres-
sive force. Burst fractures may be either stable
Guidelines to Determine Stability or unstable under compressive forces, resulting
in the same restriction toward flexion bending
Guidelines to determine stability on the basis of moments. Seat-belt and fracture-dislocation
Denis classification are suggested in Table 14.2. injuries are always unstable under distractive
These guidelines are based on the assumption forces and all types of loads.
TABLE 14.5 Type C injuries: anterior and posterior spinal column of more than 5 degrees (Cobb
element injury with rotation. angle >5 degrees; Fig. 14.11).
A1.3 occurs most often among patients with
C1 Type A injuries with rotation (compression
osteoporosis. The fracture is called fish ver-
injuries with rotation)
tebra if the compression is seen predominantly
C1.1 Rotational wedge fracture in the central part (Fig. 14.12).
C1.2 Rotational split fracture
C2 Type B injuries with rotation A2 or Split Fractures. A2 fractures denote cases in
C2.1 B1 injuries with rotation (flexion- which compression results in a splitting of the
distraction injuries with rotation) entire vertebral body. This splitting may occur in
C2.2 B2 injuries with rotation (flexion- three different fashions (A2.1A2.3). The so-
distraction injuries with rotation) called pincer fractures are characterized by a cen-
C2.3 injuries with rotation (hyperextension- trally located splitting, and the defect is filled
shear injuries with rotation) with intervertebral disk material (Fig. 14.13).
Both the end plates and the anterior wall are
C3 Rotational shear injuries
damaged, but the posterior wall is intact. This
C3.1 Slice fracture type of fracture is typically located in the lumbar
C3.2 Oblique fracture region but is usually not associated with the
development of kyphosis.
are not associated with spinal canal compromise A3 or Burst Fractures. A3 or burst fractures
caused by retropulsed fracture fragments. (fragmentation of bone) correspond to burst frac-
A1.2 corresponds with Denis compression tures in Denis classification and constitute
group. The transition between A1.1 to A1.2 the most severe type of compression fractures.
(Fig. 14.10) occurs if the reduced vertebral body The spinal canal is, as a rule, narrowed by
height (wedge shape) results in an angle to the retropulsed fragments. The A3 fractures range in
A) B)
Figure 14.10 A,B: Vertebral body impaction with a clear wedge formation. The degree of impaction is
calculated by comparing the vertebral body height of the damaged vertebra to the corresponding height of
the adjacent vertebral bodies.
CHAPTER 14 THORACOLUMBAR FRACTURES AND LIGAMENT INJURIES 147
Figure 14.11 Cobb angle a. severity from partial (failure of either the upper or
lower end plate via burst-split involving fragmen-
tation of one end plate while the rest of the ver-
tebra is split sagittally [Fig. 14.14]) to complete
burst fractures, in which the entire vertebral body
has been fragmented. An increased distance
between the pedicles and fractures of the vertebral
lamina is, identically with Denis burst fractures,
seen in the A3 group.
TABLE 14.8 Scale of instability from the fracture classified as unstable, but the necessity
AO-perspective. of surgical management may still be question-
able because conservative treatment constitutes
Type Stable Unstable
an equally good alternative.
A A1/A2 A2/A3 The type B injuries serve as an example.
B (B1/B2) B1/B2 Conservative treatment is proposed principally
B3 if the bony structures are injured, whereas sur-
C All gical management is suggested if the damage
involves the intervertebral disk and ligamentous
structures, since conservative treatment usually
with severe displacement in several planes is fails to heal soft-tissue injuries. The importance
regarded as unstable (C3.3). in these cases of clinical investigation must be
Stable type-A fractures (A1/A2) transform emphasized. The clinician must not forget to
gradually into unstable fractures (A2/A3) palpate the spinal processes if a burst fracture
(Table 14.8). Increased vertebral body compres- (according to Denis) or an A3 group injury
sion is seen at radiological examination, and (according to Magerl) is discovered at the initial
resistance against compressive forces is likewise radiological investigation. Soreness, pain, or a
gradually decreased. The fracture becomes gra- suspected defect during palpation of the spinous
dually unstable against additional compressive processes indicates failure of the posterior liga-
forces. The B1 and B2 fractures are considered ment complex. MRI should then be performed to
unstable under additional flexion bending confirm or exclude such an injury. The mode of
moment and, naturally, under compression in treatment may change if the MRI reveals an
the presence of a significant vertebral body injury to the posterior ligamentous structures.
injury. C-type fractures are always considered A fracture that initially was considered for con-
unstable under all types of load. servative treatment (some A3 fractures) may
now, due to clinical and MRI findings, be reclas-
Treatment. Both Denis and Magerls classifica- sified as a B-type of injury, because both the
tions are used in the choice of management anterior and posterior columns are engaged
following thoracolumbar fractures. The choice and the patient should receive surgical treat-
of treatment, irrespective of the presence of ment. This approach is in accordance with the
SCI, is still under debate, although the number modern view of fracture classifications, which
of patients receiving surgical management gra- emphasizes the importance of posterior liga-
dually increases, a result of rapid developments mentous structures.
in the field of instrumentation and the wish to The next sections briefly review some aspects of
reduce the length of hospital stay. conservative treatment, followed by the most
Unproblematic compression fractures invol- common surgical interventions for thoracolumbar
ving only the anterior column are treated con- fractures. Conservative alternatives are presented
servatively, whereas burst fractures with an in more detail in the next chapter. We have delib-
increased distance between the pedicles and erately chosen to describe treatment options in
with posteriorly dislocated fragments resulting general terms, considering how difficult it is to
in a narrowing of the spinal canal are treated evaluate the relative stability or instability of a frac-
surgically, since these fractures are assessed as ture and in light of varying regional traditions of
being stable and unstable, respectively. Deciding management for these types of injuries.
on surgical versus conservative management in
both these fractures is usually easily made. The CONSERVATIVE TREATMENT
remaining fractures, however, are treated on the
basis of a more complicated assessment as Conservative (nonsurgical) treatment encompasses
regards stability or instability. three components: bedrest, pain management, and
Particular difficulties regarding choice of orthotic devices. Varying guidelines exist regarding
treatment arise when the patient exhibits a the length of conservative treatment; most authors
150 SPINAL CORD INJURY
3. Which internal fixation devices should be excellent. However, this method requires more
used to achieve an immediate, rigid surgical skill, and the complication rate exceeds
immobilization of the spinal column? that of the posterior approach. The anterior
approach can be especially troublesome at the
Various points of view regarding the answers to
thoracolumbar junction. Symptoms associated
these questions will be presented in the
with irritation of the sympathetic nervous
upcoming sections, and some surgical principles
system are difficult to avoid since this method
related to injury classification will also be
includes manipulation of the diaphragm. An
illustrated.
insufficient posterior decompression, involving
a situation in which a significant and unaccep-
Anterior Approach table compression of the spinal cord remains
following the initial procedure, may constitute
The anterior approach is preferred if the purpose
an absolute indication to perform this procedure.
of exploration is to access the anterior and lateral
An anterior approach and subsequent fusion and
aspects of the spine. This is achieved either trans-
fixation may also be indicated following severe
peritoneally (i.e., straight in from the front), or
intervertebral disk and vertebral body damage if
using an anterolateral approach. The latter
posterior fusion is regarded as insufficient to
method is performed through a retroperitoneal
prevent the future development of kyphosis.
approach to the lumbar and thoracic spine at the
level of T11 or below, or through a transthoracic
access above the level of T11 (Fig. 14.16). The Fusion and Instrumentation
anterior approach may appear attractive because
Tricortical bone harvested from the anterior
it allows good exposure of the spine, and the
superior iliac crest replaces the damaged bone
technical conditions to perform the decompres-
removed during the decompression procedure.
sion and subsequent fusion and fixation are
The purpose of the transplant is to reconstruct
the stabilizing and weight-bearing functions of
the vertebral body. Artificial transplants filled
with spongiotic bone have been used in a
similar fashion (Fig. 14.17). The aim of the
fusion is to create a long-lasting, stable homo-
genous bony block involving the replaced
vertebra, as well as the vertebral body above
and below the level of injury. The Kaneda
device can serve as an example of an instrumen-
tation used subsequent to an anterior approach.
The very thin plate reaches from the level above
to the level below the injury, and the thinness of
the plate counteracts pressure on the vessels
located adjacent to the vertebral body. The
instrumentation provides a rigid fixation of the
spinal column, allowing the patients unrest-
ricted mobilization.
POSTERIOR APPROACH
A) B)
Figure 14.20 Instrumentation. A: Using pedicle screws, longitudinally directed rods, and rods directed at a
right angle in relation to the longitudinal rods (arrow). B: Posterior instrumentation using pedicle screws
and rods. See also Color Plate Fig. 14.20B.
154 SPINAL CORD INJURY
solution to all types of injury in this region. The forces (B3 injuries) if the patient sustains a type
adjacent levels, historically fixed by Harrington B, distraction fracture. A transverse disruption of
rods, are not involved in the instrumentation. the posterior column is seen in the B1 and B2
Pedicle screws do not require intact vertebral groups, and the spinal column is consequently
lamina, as do hooks and wires. As an example, always unstable under flexion forces. Stability
these screws are normally placed in the pedi- under extension remains, since the anterior
cles belonging to T12 and L2 if the fracture is longitudinal ligament is intact. This is of great
located at the level of L1. It is important to importance in planning surgical procedures:
emphasize that the stability of the damaged Increased flexion must be avoided if instru-
spinal column in the long term is accomplished mentation is used to stabilize the motion
by bony fusion as such, while the immediate segment, in order to avoid future kyphosis.
and short-term stability is achieved by the The B3 group is unstable under extension
instruments applied. since the anterior longitudinal ligament is
damaged, whereas this group of fractures is
stable under flexion. Pedicle screws or hooks
GUIDELINES RELATED TO VARIOUS TYPES OF are currently the most widely used fixation
FRACTURES devices; their purpose is to replace
the function of posterior structures. Pedicle
Type A, Compression Fractures screws are used in a manner similar to that
used during the fixation of compression frac-
Instability in type A fractures is principally related tures, and hooks placed in a claw position (i.e.,
to compressive forces (Table 14.2). Distraction of bilaterally) have the same properties as pedicle
the anterior part of vertebral body (the posterior screws. Both techniques enable repositioning
wall is uninjured) is therefore the most important of the fracture and a rigid stabilization of the
maneuvre to correct and restore vertebral height posterior structures, which is of greatest impor-
and minimize kyphosis, by restricting the mobility tance in the treatment of distraction fractures.
of the vertebral body. The correction of a vertebral The tendency to use hooks increases the higher
body using fixation instruments is called ligamen- up the thoracic spine the fracture is located,
totaxis (see discussion in the preceding section). due to the gradual decrease in pedicle diameter
The restoration of the vertebral body to an anato- in the upper thoracic spine.
mically acceptable appearance usually results in
normal vertebral body height, and the pressure of
retropulsed bony fragments toward the anterior Type C, Rotation Injuries
part of the dura is reduced. The fixation device
relieves pressure from the restored fracture and Instability under axial rotation always occurs
protects the injured motion segment from displa- following type C injuries, in addition to the
cement movements during the healing period, those types of instability associated with type
since it guaranties stability of the injured A and B injuries. Type C represents the most
motion segment until fusion is accomplished. unstable type of injuries, with an increased risk
The weight-bearing duties of the vertebral body for horizontal displacement in all directions
are shifted from the spinal column to the instru- (anteroposterior and lateral). (All three col-
ment as a result of the pedicle screw placement. umns have failed according to Denis
This also counteracts additional compressive classification; and both columns have failed
forces on the fractured area and further devel- under the A0 classification scheme.) All
opment of kyphosis. type C injuries are, as a rule, treated surgically
due to the high risk of instability. This type
Type B, Distraction Fractures of injury shares the poor healing properties
of other injuries involving disks and other
The spinal column is partially or totally unstable soft tissues such as ligaments. A posterior
against flexion (B1 and B2 injuries) or extension approach is considered sufficient, since the
CHAPTER 14 THORACOLUMBAR FRACTURES AND LIGAMENT INJURIES 155
Orthoses are devices applied externally to support restriction of movement, since both the neck and
weakened parts of the body. Following an injury to the head are fixed to the chest. Thus, the Halo
the spinal column, the aim of spinal orthoses is to device is a suitable option in the treatment of
minimize movements in the injured motion seg- unstable fractures, preferably of the upper cervical
ment, restore spinal alignment, and contribute to spine (see treatment guidelines in Chapter 11).
trunk stability. The efficacy of spinal bracing is Contraindications to the Halo-vest are infec-
inversely proportional to the volume of tissue that tions in the scalp and skull bone, and skull frac-
separates the brace from the spine. The use of tures that may hamper screw fixation, as well as
longer orthoses is usually preferable compared to some patient-related factors (age, abuse). The
shorter ones. This circumstance is of importance, device consists of a crown or ring (available in
especially in the treatment of lumbar fractures (see different sizes) with adherent screws that are
later in this chapter). As an example, four to five attached to the skull bone, a vest, and connecting
levels above and below the level of injury is rods. The single frontal and diagonally located
included in bracing of thoracolumbar fractures. dorsal pins are tightened simultaneously using a
The so-called three-point supporting devices fulfill torque screw, after which the two remaining
these demands when used in the thoracolumbar screws are applied in the same manner. Injury
region, because they offer biomechanical stability to the supraorbital nerve must be avoided when
despite the localization of injury in this region. applying the frontal screws (see references and
Braces that are equipped with several points of Fig. 15.2). The use of the device reduces head
contact with the torso and/or those providing a flexion and the extension-bending moment sig-
longer contact surface are thus more efficacious. nificantly, and the extension of the fixation to the
Most stable and some unstable fractures may be chest results in a three-point supporting device.
successfully treated by an external splinting tech- Misalignments, as a result of fractures and/or
nique (i.e., spinal bracing), but there are several ligamentous injuries, can be corrected by
alternatives in the conservative treatment of adjusting the tilt of the ring prior to the fixation
spinal fractures. Here, we review the most fre- of the chest part of the device.
quently used orthotic models. We have chosen to Although the device is the most frequently used
describe their application only briefly, since local external fixation device and provides the best avail-
traditions and other factors finally decide the indi- able external stability, it does not provide 100%
cations (fracture type and injury level) for each fixation. Bengt Lind and coworkers showed that
individual orthosis. significant flexion and extension is seen in every
motion segment in the cervical spine despite the
CRANIOTHORACIC STABILIZING use of a Halo device. They also found that the motion
TECHNIQUES is most extensive in the upper cervical spine, but
decreases further down. The position of the body
The Halo-vest (Fig. 15.1) remains the most and the type of patient-related movements causes
frequently used device for external splinting of great variability of load to the cervical spine. Despite
the cervical spine. This device offers significant these findings, craniothoracic external fixation
157
158 SPINAL CORD INJURY
Supraorbital
nerve
A)
B) C)
Figure 15.1 Halo-vest. Illustrated version (A). Patient application (B,C). It is of great importance to avoid
penetrating the supraorbital nerve and frontal sinus medially, as well as the thin temporal bone and the
temporal muscles located laterally.
remains an attractive option following some injuries, the smaller tissue volume separating the
especially those to the upper cervical spine. The treat- cervical spine from the brace and the possi-
ment period is most often around 12 weeks, and bility of using the skull and chest as contact
radiological examinations are performed repeatedly areas.
during and after treatment. Cervical orthoses (COs) provide limited
restriction of rotation and lateral bending;
CERVICAL ORTHOSIS luckily, these motions are of less importance
than sagittal movement (i.e., from maximal
External fixation using orthoses offers accep- flexion to maximal extension), and flexion-
table stability to the cervical spine because of extension movement is well prevented by COs.
CHAPTER 15 CONSERVATIVE TREATMENT FOLLOWING INJURIES TO THE SPINAL COLUMN 159
A) B)
Figure 15.4 Hard cervical collars. Aspen model (A). Philadelphia type (B).
160 SPINAL CORD INJURY
movement in the C1C7 region. However, the lumbar spine. Lumbar bracing offers most pro-
achieved restriction of sagittal motion may be clini- blems, since four or five levels above and below
cally insufficient. These collars are used in the the fracture must be splinted in order to achieve
treatment of certain fractures considered as acceptable stability. The use of orthoses that
stable, and in some cases as a complementary immobilize one leg is one solution to this pro-
treatment following surgery. blem. However, this extension of the bracing
results in an inability to sit, and this type of
CERVICOTHORACIC ORTHOSIS orthoses is seldom accepted by patients. Many
lumbar fractures are, as a consequence of such
A three-point bending support is achieved by difficulties, managed surgically. A variety of
lengthening the cervical orthosis in a caudal direc- orthoses to be used for thoracolumbar external
tion and by including the chest (Fig. 15.5A,B). splinting are available. The lid-and-box and the
The aim of the prefabricated cervicothoracic three-point corset are two examples of techni-
orthosis (CTO) is to prevent flexion and rotational ques used to splint the thoracolumbar region.
motion following injuries ranging from C1 to T7.
These braces include the sternal-occipital-man- Lid-and-Box
dibular immobilizer (SOMI) brace, and they
offer substantial limitation of movement in This model is suitable in the treatment of frac-
lower parts of the cervical spine. tures located between T7 and L5. The aim is to
prevent flexion, local bending, and rotation. The
LUMBOTHORACIC ORTHOSES term lid-and-box is used to describe a solid
torso corset produced and adapted for individual
Scarce data are available regarding the efficacy of purposes. The first step in this procedure is to
attempts to externally stabilize the thoracic and make a plaster cast of the torso. This plaster-cast
A) B)
positive is used as a model to produce the final are either prefabricated/customized or hand-
thermoplastic corset. Polyethylene, a high-tem- made to adapt to individual requirements.
perature thermoplastic, is the most frequently
used material in the lid-and-box brace. The poly- Prefabricated Models
ethylene thermoplastic layer is thicker in this
model compared to other braces and thus offers The supporting areas of the three-point corset
a more rigid stabilization of the thoracolumbar are located in front of the sternum and pubic
region. The lid-and-box model encases the entire regions, while the posterior plate is aligned
torso, with openings located on each side and the with the fracture (Fig. 15.6AC). The sternal-
anterior part fashioned as a removable lid. This symphyseal distance, as well as the location of
model has been developed to facilitate the treat- the posterior plate, is adjustable, which allows
ment of painful fractures, and it may also be used the three-point corset (with some limits), to be
in the initial period following injury, when adapted to each individual.
assisted rotation in the bed is the only movement
that is allowed without the use of a corset. The Individually Adapted Plaster-cast Models
lid-and-box is removed while the patient in a side-
lying position and, thus, the braces are removed The plaster-cast model of the three-point corset is
only when the patient is lying down. This brace is used in the treatment of fractures when a high
also used in the treatment of fractures above risk of posttraumatic kyphosis is anticipated. The
the level of T7, since the lid can be extended aim of this model is to more sufficiently prevent
cranially. A cervical orthosis can be attached to flexion in the fractured area, as compared to that
the lid-and-box, which further extends the possi- achievable with prefabricated models. The con-
bility of treating more cranially located fractures. tact area in this model is broader and larger, and
Such a model is called a cervicothoracicolumbar this model also prevents strong lateral bending
orthosis (CTLO). moment in addition to its antiflexion properties.
Three-point corsets are used to treat fractures The Boston overlap brace (BOB) is the most
located between the levels of T8 and L5. They frequently used model of lumbar orthosis
A) B) C)
Figure 15.6 Corsets. Customized three-point corset (A,B). A fracture treated conservatively using this type
of corset (C).
162 SPINAL CORD INJURY
A) B)
(Fig. 15.7A,B). The purpose of the BOB is, as from the front. Because its purpose is to prevent
with all other corsets, to prevent flexion, lateral hyperflexion, and the impact on the posterior
bending, and rotational moments. This model is part of the BOB in considerably less compared
used in the treatment of fractures located to the front side, the model does not need to
between the levels of L1 and L5. Both standard reach very far below the level of L1.
and customized BOBs consist of a 3-mm poly-
ethylene layer over interior cell thermofoam, ACKNOWLEDGMENT
which is added to improve patient comfort.
Customized lumbar orthoses are available in 0, The authors would like to express their warm
15, or 30 degrees of lordosis in order to fixate the gratitude to orthotic engineering technician
pelvis and prevent flexion. The BOB normally Charlotta Hubner for introducing us, with a cau-
reaches T10 anteriorly and is opened and closed tious hand, into the world of orthotics.
16 Children with Spinal Cord Injury
This chapter addresses only those conditions likelihood of sustaining an SCI in early childhood
relating to pediatric traumatic SCI that differ is low, the injuries are typically more severe than
significantly from those of adults with trau- those seen in adults. Traumatic brain injury
matic SCI. In addition to certain differences occurs in about 40% of children with SCI and,
in anatomy and biomechanics, we present cer- as in adults, constitutes the most commonly
tain types of fractures and ligamentous injuries associated injury.
seen solely or predominantly in children. Table 16.1 presents data from a study of 179
Generally speaking, pediatric SCI is typically children (110 boys and 69 girls) with spinal
more severe. Parents and family obviously column injuries (Osenbach & Menezes 1992).
become more involved in both the acute and Young children, especially infants, show an
long-term care of children with SCI than in increased propensity for injuries to the upper
adults in a similar situation; and special med- cervical spine, due to a disproportionately large
ical and psychosocial considerations must be head in relation to the body, as well as to un-
addressed to help children with SCI mature developed neck muscles (Fig. 16.1). Among teen-
into adulthood in a way that is as normal and agers, the mechanisms of injury are mainly
harmonious as possible. related to risk-taking behaviors such as motor
There are no universally accepted guidelines vehicle-, fall-, and sports-related accidents. A
for the acute medical care of children with SCI. trend seems to indicate that the younger the
In part this may be due to the fact that older patient, the higher the level of injury on the
children (810 years of age) begin to demonstrate spinal column.
a spectrum of injuries similar to that of adults. The Osenbach and Menezes study also
Among young children the differences in shows that 93 of the 179 patients had complete
injury patterns are significant, but SCI in that (42) or incomplete (51) SCI. Children with
age group is extremely rare. However, several Downs syndrome, rheumatoid arthritis, and
articles provide excellent summaries of current skeletal dysplasias are at increased risk of sus-
medical guidelines (see the section Suggested taining spinal cord lesions.
Reading).
PROGNOSIS
EPIDEMIOLOGY
In a study involving 20 children with complete
It is very uncommon for young children to sustain injury, Wang and colleagues showed that neu-
a SCI; the incidence increases dramatically, how- rological improvement was recorded in 30% of
ever, from the mid-teen years onward. According the patient group, which is significantly better
to current statistics the overall incidence of pedia- than in adults. The neurological improvement
tric SCI in the United States is approximately 2 occurred over a long period of time post injury.
cases per 100,000 children. The incidence of SCI However, cervical dislocations with severe neu-
among children younger than 5 years is rological deficit were associated with a low rate
extremely low. Among children with SCI who of neurological improvement, and atlantoocci-
are age 2 or younger, the C1C2 segment is pital injuries were often associated with early
involved in almost 80% of cases. Although the death.
163
164 SPINAL CORD INJURY
TABLE 16.1 The causes and localizations of skeletal injuries* presented with the percentage
of patients with neurological involvement in relation to level of injury**
Children Children Percentage of patients with
08 years 916 years SCI in relation to level of injury
Cause
Motor vehicle accidents 28 (45%) 72 (61%)
Falls 15 (24%) 15 (13%)
Sports 1 (2%) 23 (20%)
Birth injuries 10 (16%)
Other 8 (13%) 7 (6%)
Total 62 (100%) 117 (100%)
Distribution
C0C3 33 (53%) 31 (26%) 36%
C4C7 16 (26%) 32 (27%) 73%
Th ThL 9 (14%) 33 (29%) 67%
Lumbar 4 (7%) 21 (18%) 28%
Total 62 (100%) 117 (100%)
*
Expressed in absolute numbers, with percentages in brackets.
**
C cervical, Th thoracic, ThL thoracolumbar.
TABLE 16.2 Differences between principles of care of children and adults in the hospital.
Children Adults
Head large and difficult to control, in part due to Head smaller, fully developed neck
un-developed neck muscles muscles
Skeletal structures still growing and developing Mature skeleton
Thin skull, sutures open Thick skull, sutures closed
Use of steroids untested Steroid treatment is an option in adults
Respiratory problems indicated by hypercapnia Respiratory problems indicated by hypoxia
Crying may camouflage respiratory problems
Fluid balance highly sensitive Fluid balance usually easier to regulate
Calorie requirements high Calorie requirements essentially follow
normal metabolic demands
Rapid metabolism Slow metabolism
Rehabilitation focus to teach the child various Rehabilitation focus relearning
steps of development
Latex allergy: greatly increased risk Latex allergy: moderately increased risk
Complains about neck pain dens (the atlas-dens interval, ADI; Fig. 16.4)
Is assessed to have other painful injuries may be up to 2.5 mm, according to some authors.
that may distract attention from a neck In children, the ADI changes with age, and
injury various distances are specified in the literature.
Shows signs of intoxication The ADI may be up to 4.5 mm, especially in
Radiologic workup is not indicated if the child has young children, due to loose ligaments and
undergone trauma but remains alert, has a normal incomplete ossification. Consequently, varia-
neurological examination, has no neck pain or stiff- tions in ADI occur that that may complicate
ness, has no distracting injury, and shows no signs assessment of problems such as atlantoaxial
of intoxication. Recommendations for the radi- instability.
ologic workup of children follow.
Computed Tomography Scan. Computed tomo-
Conventional X-ray. If an isolated cervical spine graphy (CT) is always the diagnostic procedure
injury is suspected, radiologic workup begins of choice for the workup of high-energy trauma,
with a conventional radiograph of the cervical since CT is the superior method for imaging the
spine. If the child is unable to open the mouth, skeleton. Modern CT scanners create imaging
a rubber tongue blade may be inserted to facil- slices less than 1 mm thick through the entire
itate imaging of the dens in the frontal cervical spine, with an acceptable radiation dose,
projection. and then convert the images into three-dimen-
Plain films may show indirect signs of liga- sional reconstructions.
mentous injury. If conventional x-rays are
normal, but the childs clinical status raises sus- Magnetic Resonance Imaging. Only magnetic reso-
picion of ligamentous injury, flexion-extension nance imaging (MRI) provides direct informa-
radiographs should be carried out about 1 week tion about ligamentous injury, disk herniation,
post injury. and hemorrhages in and around the spinal cord.
Considerable difficulties may be associated MRI can also provide guidance for how long
with the interpretation of plain films in children. immobilization should continue, when return
For example, in adult patients, the distance to activity is acceptable, and aid in prognostica-
between the posterior arch of the atlas and the tion in the presence of spinal cord changes.
CHAPTER 16 CHILDREN WITH SPINAL CORD INJURY 167
Thoracolumbar Injuries
Burst fractures tend to occur in the lower Pharmacological treatment with steroids
thoracic and lumbar spine, where axial forces in children under age 13 lacks sufficient
are large. Many burst fractures may be treated scientific evidence; methylprednisolone
conservatively, but severe dislocation requires thus is usually not given in this age group.
surgical treatment. The principles for stabilizing
these fractures are similar to those for compres- SPINAL CORD INJURY-RELATED SEQUELAE IN
sion fractures. THE PEDIATRIC GROUP
Treatment of seat-belt injuries and fracture-
dislocation injuries follows essentially the same Hypercalcemia
guidelines as those for the adult population.
Hypercalcemia related to increased bone resorp-
SUMMARY OF EMERGENCY CARE tion (as reflected in elevated serum calcium) is
particularly common in teenage boys. In typical
Although a review of the literature on the treat- cases, onset of symptoms is insidious, with
ment of children with acute cervical SCI pre- abdominal pain, nausea, vomiting, malaise,
sented in Neurosurgery (Apuzzo 2002) fatigue, polyuria (i.e., large urine volumes), poly-
concluded that the available literature only dipsia (i.e., large fluid intake), and dehydration. In
offers diagnostic guidelines and treatment some cases, behavioral changes are also present,
options, but no conclusive treatment protocols, and psychotic symptoms can occur. The condition
there appears to be consensus regarding certain may also be asymptomatic. Hypercalcemia may
aspects of workup and treatment: lead to conditions such as renal failure and stone
formation in the urinary tract. Treatment
It is difficult to achieve a neutral position includes intravenous fluid administration, diure-
for the cervical spine during transport on a tics, and bisphosphonates.
spineboard.
It is possible to rule out spinal column
Autonomic Dysreflexia
and/or SCI solely on clinical grounds (see
also Chapter 6). Autonomic dysreflexia in small children often
Conventional radiographs of the cervical presents atypically as vague malaise, rather
spine should include frontal and lateral than the classic description with severe pulsating
views, open mouth (dens frontal), and headache. An increase in blood pressure of
oblique projections. 20 mmHg or more above baseline should
Most pediatric spinal column injuries arouse suspicion of this condition.
can be treated conservatively, and Halo-vest
treatment is the most effective immobiliza- Disturbance of Temperature Regulation
tion method. This treatment is associated
with acceptable risks, including some Poikilothermiathe tendency for body tempera-
increase of morbidity due to infections and ture to passively adjust to ambient tempera-
loosening of pins. tureis particularly pronounced among young
The only specific pediatric injury for which children with SCI, in part due to a disproportio-
there is solid evidence for choosing a spe- nately large surface area in relation to body
cific treatment is epiphysiolysis of C2 in weight, and in part because the youngest chil-
children under 7 years. First-line treatment dren cannot adequately communicate that they
for this injury involves closed reduction and feel too cold or too hot.
immobilization. Children typically react more readily with fever
Isolated ligamentous injuries of the upper than do adults, and this also applies to children
cervical spine may heal with external fixa- with SCI. Common causes of fever include
tion alone. If the injury is associated with respiratory infections, deep vein thrombosis, het-
deformity, surgical treatment may be erotopic ossification, fractures, pressure ulcers,
considered. wound infections, and various intraabdominal
172 SPINAL CORD INJURY
has a later onset (on average more than 1 year after Hadley MN, ed. Management of pediatric cervical spine
the injury, compared with only a few months in and spinal cord injuries. Neurorsurgery 2002;50(3):
S85S99.
adults).
Hadley MN, ed. Spinal cord injury without radiographic
abnormality. Neurosurgery 2002;50(3):S100S104.
Fractures Kochanek PM, Tasker RC. Pediatric neurointensive care:
2008 update for the rogers textbook of pediatric inten-
As in adults, children with SCI are at increased sive care. Pediatr Crit Care Med 2009;10(4):517523.
Lennarson PJ, Menezes AH. Pediatric spinal cord injury.
risk of sustaining fractures in paralyzed limbs.
In: Tator CH, Benzel CH, eds., Contemporary
Fractures, often seen in conjunction with osteo- Management of Spinal Cord Injury: From Impact to
porosis, should be suspected if local swelling is Rehabilitation. Park Ridge, IL: American Association
present in an extremity, especially swelling of the of Neurological Surgeons, 2000:209229.
supracondylar portion of the femur and the prox- Lyon RM. Pediatric spine injuries. In: Frymoyer JW,
Wiesel SW, eds., The Adult and Pediatric Spine, 3rd
imal tibia. Fractures may also manifest as fever
ed. Philadelphia: Lippincott, Williams & Wilkins,
of unknown origin. 2004:425444.
Osenbach RK, Menezes AH. Pediatric spinal cord and
ACKNOWLEDGMENTS vertebral column injury. Neurosurgery 1992;30
(3):385390.
Pang D, Wilberger JE Jr. Spinal cord injury without radi-
The authors would like to warmly thank
ological abnormalities in children. J Neurosurg 1982;
Associate Professor Peter Pech, Radiology Unit, 57(1):114129.
Uppsala University, for his assistance in the Puisto V, Kaariainen S, Impinen A, et al. Incidence of
creation of this chapter. spinal and spinal cord injuries and their surgical treat-
ment in children and adolescents: a population-based
study. Spine (Phila Pa 1976) 2010;1;35(1):104107.
Suggested Reading
Vogel LC, Anderson CJ. Spinal cord injuries in children
Bosch PP, Vogt MT, Ward WT. Pediatric spinal cord injury and adolescents: a review. J Spinal Cord Med 2003;26
without radiographic abnormality (SCIWORA): the (3):193203.
absence of occult instability and lack of indication for Vogel LC, Krajci KA, Anderson CJ. Adults with pediatric-
bracing. Spine 2002;27(24):27882800. onset spinal cord injuries: part 3: impact of medical
Bilston LE, Brown J. Pediatric spinal injury type and complications. J Spinal Cord Med 2002;25(4):297305.
severity are age and mechanism dependent. Spine Wang MY, Hoh DJ, Leary SP, Griffith P, McComb JG.
(Phila Pa 1976) 2007;1;32(21):23392347. High rates of neurological improvement following
Cirak B, Ziegfeld S, Knight VM, et al. Spinal injuries in severe traumatic pediatric spinal cord injury. Spine
children. J Pediatr Surg 2004;39(4):607612. 2004;29(13):14931497.
Goetz E. Neonatal spinal cord injury after an uncompli- Yucesoy K, Yuksel KZ. SCIWORA in MRI era. Clin Neurol
cated vaginal delivery. Pediatr Neurol 2010;42(1):6971. Neurosurg 2008;110(5):429433. Epub 2008 March 19.
This page intentionally left blank
17 Cervical Spinal Column and Spinal Cord Injuries
in Athletes
Injuries to the spinal column, with or without combination of axial compression and flexion to
spinal cord involvement, account for 23% of which the individual is exposed when the depth of
all sports-related injuries. Fracture-dislocation the water is misjudged and the head hits a rock,
injuries are seen in one-third of all cases, mainly the ocean floor, or the bottom of a pool. By
in conjunction with American football, rugby, providing information to avoid diving into water
wrestling, ice hockey, and diving accidents. C5 is of unknown depth (shallow water), avoiding
the most common level of injury, probably because alcohol in conjunction with diving, and being cer-
mobility is greatest at this level, and these activities tain about pool depth, the number of diving acci-
involve axial compression with a component of dents with this tragic outcome could be reduced.
flexion at the time of the injury. Although few
injured individuals sustain severe fractures and Skiing
SCI, those who do so in conjunction with elite-
level sports receive considerable publicity. This Trauma resulting in SCI, for obvious reasons, is
chapter describes injuries related to a number of more common in downhill than in cross-country
sports, as well as various forms of spinal cord skiing. The helmets that many people wear today
involvement resulting from athletic activity. reduce the risk of head injury, but not of SCI, and
Finally, we present two algorithms on the various information on the slopes should point out the
aspects to consider when deciding whether to importance of always skiing in groomed areas.
allow players to return to contact sports following
serious injury to the spinal column, with or American Football
without spinal cord involvement.
This sport is associated with a relatively high risk
HIGH-RISK ATHLETIC ACTIVITIES of incurring SCI, compared with other contact
sports. The incidence of tetraplegia in organized
Diving American football is estimated at about 1 case per
100,000 registered athletes, which corresponds
Diving accidents account for 75% of patients with about 1015 new cases annually among
who sustain a SCI during athletic activities 1.5 million active football players. Most of these
(Fig. 17.1), although they only account for SCI occur in high school athletes. The explanation
about 10% of all SCI. Those individuals who may lie in differences in size, age, strength, and
sustain a SCI are usually males diving into maturity among players in this age group. Most
lakes or the open sea, and injury to the spinal injuries are related to tackling; players with long
column and/or spinal cord is usually the sole slender necks appear to be most vulnerable. Most
high-energy injury found. Diving accidents that SCI occur to the tackler when he hits his opponent
entail a fracture of the fifth vertebra are in 70% of with the crown of his head while his neck is bent
cases associated with a simultaneous SCI, and it slightly forward, producing axial compression in
is not uncommon for more than one vertebra combination with mild flexion at the moment of
to be fractured. The mechanism of injury is a impact (Fig. 17.2).
175
176 SPINAL CORD INJURY
Rugby
Figure 17.1 Diving accident with axial compression Rugby is the most common sport related to
and flexion as the mechanism of injury. SCI in some countries, such as South Africa.
Certain phases of play are deemed particularly
dangerous. Players are particularly vulnerable
to trauma when forming a scrum(the forma-
tion players make when they group in a cluster
at the start of play). The player who gets the ball
and has the misfortune to have the cluster pile
on top of him after falling with his head against
the surface could then be exposed to hyper-
flexion trauma combined with a rotational
component, and the injury that usually arises
is a unilateral facet dislocation. Tackling in
rugby is also dangerous, especially when the
tackler uses his outstretched arms to fell the
opponent with a headlock-like grip, which sub-
jects the tackled player to hyperextension,
often combined with a rotational component.
In a sandwich tackle, a player is hit by two
tacklers, one of whom tackles the legs and the
other the upper body. A particularly dangerous
type of tackle is similar to that seen in
Figure 17.2 Tackling with axial compression and American football, with flexion and axial
flexion. compression.
CHAPTER 17 CERVICAL SPINAL COLUMN AND SPINAL CORD INJURIES IN ATHLETES 177
cord is compressed at the moment of the injury. Isolated Radiographic Signs of Spinal Column
The pincer mechanism, as described by Injury (Type 4)
Penning, is considered to be an accurate descrip-
tive model. According to this theory, the spinal Type 4 injuries includes posttraumatic cases that
cord is compressed between the lower posterior only demonstrate radiographic changes such as
corner of the upper vertebral body and the base fractures, herniated disks, or ligamentous injury
of the spinous process of the lower vertebra (Fig. at the cervical spine level, but demonstrate no
17.3). Given these circumstances, a differential neurological involvement (Table 17.2).
diagnostic cause of burning hands syndrome
should also be considered. GUIDELINES FOR RETURN TO ATHLETIC
Burners or stingers correspond to brief ACTIVITY
episodes of paresthesias or motor weakness in
the upper extremities. This spectrum of symp- Tables 17.1 and 17.2 present guidelines for
toms is caused by a traction or compression returning to or termination of athletic activity
injury to the brachial plexus or to the 5th or 6th after the various types of injuries just described.
cervical nerve roots (Fig. 17.4).
Type 1, 2, and 3 Injuries
Type 4 Injuries
TABLE 17.1 Algorithm for return to athletic activity after various types of
neurological involvement.
Neurological Injury Number of Injury Return to Activity
(Type 1, 2, 3) Incidents
Type 1 One or more No
Type 2 and 3 One episode Yes
Two episodes Recommendations
vary/no consensus
Three or more No
episodes
TABLE 17.2 Algorithm for return to athletic activity following type 4 injury and cervical
spinal stenosis.
Radiological injury Stability Aspects Return to Activity
(Type 4)
Fracture, Unstable No
ligamentous injury
Injury treated with either Halo-vest No
or surgery
Stable under load Yes
Spear tacklers spine No
Cervical spinal Clinical assessment more important Recommendations based on
stenosis than radiological finding injury type 1, 2, and 3
Athletes who sustained a fracture deemed neurologic symptoms and essentially follow
stable under load, that did not require Halo- the recommendations for type 13 injuries. An
vest treatment or surgical stabilization, and incidental finding of cervical spinal stenosis
who have a normal neurological examination probably poses very little risk for athletes who
may return to athletic activity. Laminar frac- engage in contact sports.
tures, spinous process fractures, and minor
vertebral compression fractures are examples Suggested Reading
of fractures in which the athlete may resume Bailes JE. Spinal injuries in athletes. In: Menezes AH,
activity. Sonnntag VK, eds. Principles of Spinal Surgery.
Athletes meeting Torgs definition of spear New York: McGraw-Hill Companies, 1996:465492.
tacklers spine may not return to activity. Boden BP, Jarvis CG. Spinal injuries in sports. Neurol Clin
2008;26(1):6378; viii. Review.
Recommendations are difficult to make in Chao S, Pacella MJ, Torg JS. The pathomechanics, patho-
cases of cervical spinal stenosis, and there are physiology and prevention of cervical spinal cord and
no truly effective screening methods for asses- brachial plexus injuries in athletics. Sports Med
sing the risk of active participation in sports in 2010;40(1):5975.
Giovanini MA, Day AL. Spinal injuries in athletes with cervical
cervical spinal stenosis (defined as an antero-
stenosis. Techniques Neurosurg 1999;5(2): 185193.
posterior diameter of less than 12 mm). The Kuhlman GS, McKeag DB. The burner: a common
recommendations for cervical spinal stenosis nerve injury in contact sports. Am Fam Physician
mainly take into account the presence of 1999;60:20352042.
180 SPINAL CORD INJURY
Maroon JC, Bailes JE. Athletes with cervical spine injury. expose the cervical spine to axial energy inputs. Am J
Spine 1996;21(19):22942299. Sports Med 1993; 21(5):640649.
Rihn JA, Anderson DT, Lamb K, et al. Cervical spine injuries Torg JS, Ramsey-Emrheim JA. Management guidelines
in American football. Sports Med 2009;39(9):697708. for participation in collision activities with conge-
Tator CH. Recognition and management of spinal cord nital, developmental, or post-injury lesions involving
injuries in sports and recreation. Neurol Clin 2008;26 the cervical spine. Clin Sports Med 1997;16(3):
(1):7988; viii. Review. 501530.
Torg JS, Sennett B, Pavlov H, Leventhal MR, Glasgow SG. Wilberger JE Jr. Athletic spinal cord and spine injuries.
Spear tacklers spine. An entity precluding participa- Guidelines for initial management. Clin Sports Med
tion in tackle football and collision activities that 1998;17(1):111120.
18 Penetrating Injuries
Spinal cord injuries caused by projectiles (e.g., to motor vehicle accidents as the most
bullets) are among the severest types of injury common cause of trauma-induced paraplegia.
an individual can endure (Fig. 18.1). One of the Of cases caused by shooting, 40% were due to
great pioneers in neurosurgery, Dr. Harvey shots entering from behind and about 20%
Cushing, who was active during World War I, were caused by shots that entered from the
was of the opinion that only patients with front. Half of these SCI involve the thoracic
incomplete injuries could survive. He esti- spine and, not surprisingly, young men were
mated mortality at about 80% among soldiers typical victims. Many of those persons have
who sustained any type of SCI. The general substance abuse problems, which may be a
rule of thumb at that time was that surgery contributing factor to their often poor rehabi-
was not indicated for patients with a complete litation outcomes. In all, bullet wounds
injury unless that injury was below the level of account for about 15% of all SCI in the
the spinal cord; that is, caudal to L1, in which United States (data from 1980s), and 1 in 20
case this patient group was treated with super- bullet wounds involves an SCI. Knife wounds,
ficial wound debridement, just as those with the other type of penetrating injury, appear to
incomplete SCI. During the interval between be particularly common in South Africa, pos-
the world wars, treatment strategy was to carry sibly because firearms are not yet commonly
out debridement of only the entry and exit available.
wounds. A relatively dramatic improvement
of medical care for bullet wounds with spinal BULLET WOUNDS
cord involvement occurred during World War
II with the introduction of sulfa drugs and Ballistic Aspects
penicillin, improved transportation from the
scene of injury, and because appropriate reha- Ballistics is the study of the motion of unguided
bilitation row could be offered. Modern prin- projectiles. The wound caused by a bullet is a
ciples of war surgery were first employed function of its shape, mass, and velocity. The
on a large scale during the Vietnam War, kinetic energy (energy of motion) of a bullet,
including those principles that apply today Ek, can be calculated from the formula E k 1/
with respect to debridement and closure of 2 mv2, where m is bullet mass (kg) and v is
dural defects. bullet velocity (m/s). Factors such as the bul-
lets shape (round, pointed, or flat) and con-
EPIDEMIOLOGY sistency (solid or hollow) also influence the
effect of the energy. In addition to kinetic
In contemporary civilian life, low-caliber pistols energy, the path of the projectile to the tissue is
and rifles with bullet speeds of less than 700 m/s also of significance. The appearance of the tissue
give rise to most SCI. Few epidemiological wound is dependent on whether the bullet has
studies are available, but one frequently cited a straight track, an element of torque, or if a tum-
report from Rancho Los Amigos Hospital in bling effect influenced the path of the bullet
California reflects the spectrum of injuries in toward the body. The severity of a wound
that state, where bullet wounds are second only can also vary at the same velocity depending on
181
182 SPINAL CORD INJURY
A) B)
C) D)
Figure 18.1 Gunshot wound. Illustration of (A) skin entry wound and a computed tomography (CT) collage
of a bullet located at the C1 and C2 level. Lateral view (B). Frontal view (C). Axial projection (D).
the type of tissue hit. Thicker and thus more with secondary projectiles such as bone frag-
resistant bone slows the kinetic energy of the ments that may penetrate the spinal cord. It is
bullet, although secondary missiles in the form indeed entirely conceivable that contusion
of bone fragments may cause significant tissue injuries to the spinal cord and nerve roots may
damage. In summary, the severity of the wound occur without penetration of these tissues by the
varies with the velocity of the projectile, the bullet.
density of the tissue, and the characteristics of
the projectile, such as shape, mass, and pattern Local and Systemic Pathophysiology
of movement.
Each bullet creates a path through the tissue Acute Phase
and, in conjunction with this path, a cavity is
formed. The size of the cavity is directly propor- Bullet wounds in the thoracic spine between
tional to the kinetic energy. The spinal cord may T1 and T10 thus often result in complete inju-
become injured by the projectile itself, but the ries, probably because of the narrow diameter of
shock wave or pressure wave generated is the the spinal canal, which amplifies the effect of the
most common mechanism of injury, combined shock wave. It is uncommon for bullet wounds at
CHAPTER 18 PENETRATING INJURIES 183
the lumbar level to cause complete injuries, since column to the intestines, bladder, or pleura.
injuries at the L1 and L2 level and further caud- Arteriovenous fistulae may form adjacent to
ally involve peripheral nerves that belong to injuries involving the vertebral artery.
cauda equina rather than central nervous
system tissue. Chronic Phase
Twenty-five percent of all bullet wounds at the
thoracic level have at least one associated sys- Among the complications arising after pene-
temic injury. The most common thoracic inju- trating bullet wounds is the development of
ries include hemopneumothorax, as well as cysts in the spinal cord. These cysts are usually
pleural and parenchymal hemorrhage. multilobular. The unique pathophysiologic pat-
The severity of the SCI thus is related to the tern following bullet wounds is for these cysts to
kinetic energy of the bullet and on the other fac- assume the form of microcysts, rather than
tors mentioned earlier. Additional factors that forming one single cyst centrally located in the
may influence the pathophysiologic processes spinal cord. Arachnoiditis, causing scar tissue
are whether or not a direct mechanical trauma formation and tethering of the spinal cord, may
(direct hit by the bullet) afflicts the spinal cord, often precede cyst formation.
whether the trauma was caused by the recoil effect Pain is very common after bullet wounds.
of fragments, or if a contusion wound occurred Pain is usually dysesthetic and amplified by
because of a shock wave. Epidural and subdural light touch. According to some authors, this
hematomas are relatively rare compared with pain is worse at night, but otherwise remains
intramedullary hemorrhage. The pathophysio- relatively constant.
logic chain of events, with a primary and sec- Patients with SCI caused by penetrating
ondary phase followed by a chronic phase, is trauma demonstrate a higher incidence of neu-
similar to that of other contusion and crush rological deterioration in late stages than do
wounds. Penetrating injuries below the conus those with other types of SCI, especially if the
are not infrequently associated with injury to the bullet is allowed to remain in the spinal canal.
lumbosacral plexus. Fragments from clothing, Development of pain may indicate neurological
skin, and other debris that accompany the bullet deterioration as a result of inflammatory pro-
in its track constitute a special pathophysiologic cesses. Otherwise, patients with penetrating
process. Bullets may also be mobile and shift wounds manifest similar late complications as
around in the spinal canal, which entails a those with SCI of nonpenetrating etiology (see
dynamic pathophysiologic process over time. Chapter 30).
The material of which the bullet is made also
appears to be significant. For example, bullets Management
made of lead are not as toxic to the local tissues
as are copper bullets. General Guidelines During the Acute Phase. Treatment
The presence of a foreign body may also entail of any systemic effects resulting from the trauma
a rejection process around the bullet. If the bullet (thorax, abdomen, etc.) must be given priority
is located near the spinal cord, a compression of before addressing the actual injury to the spinal
the spinal cord may arise, but there is also an cord and its consequences. Immobilization,
increased risk of various infectious processes, attention to breathing and circulation, neurolo-
such as meningitis, epidural and intramedullary gical assessment, and transport to the hospital
abscesses, and osteomyelitis. follow the same principles that govern manage-
In the abdominal region, colonic injuries in ment of patients with SCI in general.
particular are associated with osteomyelitis and Particular note should be given to the fact that a
meningitis. Penetrating wounds through the patient with SCI and simultaneous injury to the
ventricle and small intestine are far less likely thorax and/or abdomen often cannot experience
to cause infection. infralesional pain, which may mask serious condi-
Fistulae occur late in the course of events after tions such as active intraabdominal bleeding.
a bullet wound, and may extend from the spinal The ability to distinguish between neurogenic
184 SPINAL CORD INJURY
shock and hypovolemic shock due to bleeding is that the prognosis is probably not as dire as
very important (Table 6.6). It is also important previously believed and is comparable to the
to initiate treatment with antibiotics as soon as prognosis after motor vehicle accidents.
possible post trauma. Consequently, surgical intervention for such
For radiologic workup, conventional x-ray and injuries has increased.
computed tomography (CT) are most commonly In cases of progressive neurological deteriora-
employed. Workup of penetrating trauma tion caused by fragments that put pressure
should include the probable trajectory of the on the spinal cord, surgical treatment with
bullet with a good margin if only the entry decompression is typically recommended. Such
wound is detected. Magnetic resonance imaging surgery entails relieving the pressure on the
(MRI) has its limitations, especially if the bullet spinal cord by removing the bullet or other
contains iron, in which case there is a risk that tissue that presses against the spinal cord.
the bullet may move in response to the magnetic Penetrating wounds to the spinal cord that
field, which may enlarge the area of tissue cause an immediate complete injury are not,
damage. The risk of MRI workup should there- per se, an indication for surgical exploration.
fore be avoided. The risks of infection, development of fistulae,
Vascular injury to the carotid artery or jugular and anesthesia-related complications are too
vein must be suspected if hematoma is palpable high in relation to the marginal potential for
around entry wounds in the cervical spine. Some improvement of neurologic function through
authors suggest radiographic assessment of the surgical intervention. Surgery is usually done
cervical vessels in order to diagnose possible for incomplete myelopathy with persistent
fistulae. Injuries to the throat and esophagus significant spinal cord compression, and com-
can be evaluated through the use of contrast plete cervical injuries may be explored if surgical
x-ray imaging; this is important, since an injury decompression may improve function in one or
to the esophagus that remains undiagnosed two nerve roots; in other words, if surgical inter-
after 24 hours is associated with high mortality. vention focuses on the nerve roots, rather than
In the presence of visceral damage within the spinal cord.
the abdomen, neurosurgical procedures are Cauda equina injuries with small intraspinal
associated with a high risk of complications. metal or bone fragments are not usually oper-
Therefore, repair of visceral damage combined ated. However, if a largely intact bullet or large
with initiation of antibiotics should precede bone fragment compresses the spinal cord or
neurosurgery aimed at decompressing the nerve root, surgical exploration is generally car-
spinal cord and stabilizing the spinal column. ried out, since large fragments remaining in this
In summary, exploration of injuries to the region cause an increased incidence of posttrau-
skull, cervical region, chest, and abdomen, as matic pain.
well as other fractures outside the spinal Most surgeons agree that surgical intervention
column, should be given higher priority than to close cerebrospinal fluid fistulae is indicated. In
the radiologic diagnosis of SCI and neurosur- highly unusual cases where spinal fluid leakage
gical intervention in patients with multi- occurs and the point is to prevent infection,
system trauma and SCI after a penetrating patients with both complete and incomplete inju-
trauma. ries may be explored. Initially, however, a 57-day
trial of lumbar drainage may be tried in combina-
Surgical Treatment tion with 1 week of antibiotic treatment. These
measures are typically sufficient to close fistulae.
Indications for Surgery. Indications for surgical Research presented by colleagues at Louisiana
intervention following penetrating trauma are State University Medical Center reflects generally
subject to endless discussion, but only a few accepted opinion regarding indications for
scientific studies have addressed the prognosis surgical intervention for such injuries. Their
in penetrating injuries. The authors conclude study, encompassing 15 cases, including 10
CHAPTER 18 PENETRATING INJURIES 185
involving the thoracic level and 5 at the lumbar Instability. Instability is extremely uncommon
level, shows that none of the patients with com- after a bullet wound. However, if instability
plete injury demonstrated any meaningful neuro- should be present, the stabilizing procedure is
logical recovery, regardless of whether bullets or not carried out during the acute phase. Instead,
bone fragments compressing the spinal cord were the patient is treated with traction or orthosis
removed or not. By contrast, all patients with until such time that surgery is appropriate.
incomplete cauda equina injury improved after
decompression of the spinal cord. None of the Conclusion
patients in this material suffered from complica-
tions such as fistulae, spinal fluid leakage, infec- The prognosis for recovery of neurological func-
tion, or progressive neurologic dysfunction. All tion is very poor for complete acute SCI
patients who experienced hyperesthesia prior to following gunshot wounds. Management is
surgery showed significant improvement after essentially similar as for other high-energy
removal of the bullet or bone fragment. trauma in which SCI has occurred. However,
SCI is given low priority if the trauma has given
Goals for Surgical Intervention. The goal of surgical rise to systemic effects such as in injuries to the
treatment is to: thorax and abdomen.
Surgical measures for bullet wounds of the
Prevent progressive neurologic dysfunction spinal column and the spinal cord play a limited
Prevent cerebrospinal fluid fistulae role. Surgical treatment is indicated for progres-
Debride devitalized tissue to minimize the sive neurological deficits and to close cerebrosp-
risk of infection inal fluid fistulae. In patients with preserved
Remove projectiles that contain lead or neurological function who have a significant
copper to reduce the inflammatory simultaneous residual compression of the
response conus and cauda region, surgery may be consid-
Relieve the spinal cord and nerve roots ered to counter the increased risk of posttrau-
from pressure resulting from hematoma, matic pain. Late complications such as pain are
bone, and bullet fragments common after penetrating trauma.
Nontraumatic myelopathies refer to spinal cord and preferentially involve the cervical and upper
disorders that are not caused by external trauma. thoracic levels rather than more caudal seg-
However, from a rehabilitation standpoint, certain ments. MS plaques tend to have a symmetric
nontraumatic myelopathies bear close resem- and bilateral distribution. Diagnosis is con-
blance to trauma cases, especially those character- firmed by magnetic resonance imaging (MRI) of
ized by focal involvement (i.e., in which the lesion the brain and spinal cord, which may demon-
affects only a limited portion of the spinal cord) strate scattered plaques within the central nervous
and in those where disease progression after onset system (CNS) (Fig. 19.1). During the acute phase,
of illness is essentially stationary. Even patients with active inflammatory lesions, MS plaques will
with progressive myelopathy (i.e., conditions in enhance with intravenous contrast. Cerebrospinal
which underlying disease entails progressive wor- fluid (CSF) examination may demonstrate
sening) may in some cases benefit from treat- oligoclonal banding in electrophoresis and selec-
ment at spinal centers. An overview of the tive g-globulin elevation.
most important nontraumatic myelopathies is Three main variants of MS have been described
presented in this chapter. For details please at the spinal cord level: neuropathic, subacute
refer to general neurology textbooks. spinal cord compression, and acute transverse
myelitis.
In the neuropathic variant, sensory symptoms
INFLAMMATORY CONDITIONS dominate, such as peripheral paresthesias,
which may either be spontaneous or provoked
Multiple Sclerosis by touch. Sensory impairment is minimal, and is
often felt as if a thin layer of fabric was located
In Europe and North America, multiple between the skin and the stimulus. Often the
sclerosis (MS) is the most common cause of patient experiences Lhermittes phenomena, char-
nontraumatic neurological impairment among acterized by electric shock-like sensations that
persons between the ages of 15 and 50. Spinal radiate down along the spine and sometimes
cordrelated symptoms are the first manifesta- out into the extremities in response to neck
tion in 1030% of cases. The disease can be flexion. However, this phenomenon is not
relapsing-remitting or chronically progressive pathognomonic of MS, as it may occur in several
(primary-progressive). It is not uncommon for other spinal cord disorders. In general, reflexes
a disease course that is initially relapsing- are increased, abdominal reflexes may be absent,
remitting to become chronically progressive and Babinskis sign is present.
after a number of years. This is referred to as The subacute spinal cord compression variant
secondary-progressive MS. The disease is char- most closely mimicks the medical history
acterized by autoimmune inflammatory lesions of cervical spondylotic myelopathy (see below).
in the white substance of the brain and spinal MRI workup is here necessary to rule out condi-
cord. These lesions lead to demyelinization and tions causing spinal cord compression. However,
the subsequent formation of scar tissue, known careful history may reveal that many of these
as plaques. Spinal plaques in MS are most com- patients have also had previous flare-ups with tran-
monly found in the dorsal half of the spinal cord sient neurological symptoms from other parts of
187
188 SPINAL CORD INJURY
artery, also known as the great radicular artery Treatment is surgical for circumscribed spinal
of Adamkiewicz (Fig. 3.10), which is typically hematomas that compress the spinal cord, and
located in the lower thoracic or upper lumbar comprises removal of the hematoma.
spine, a massive infarction often occurs that is About half of patients with total sensorimotor
equivalent to an anterior cord syndrome at the deficit at the time of surgery will achieve some
spinal cord level. About half of patients with degree of functional recovery, and about 10%
spinal cord infarction achieve significant will experience total functional recovery.
motor functional recovery after the injury.
Typically, these are young patients with incom- Intraspinal Vascular Malformations
plete paresis.
Extramedullary vascular malformations within
Intraspinal Bleeding the spinal cord are typically caused by a fistula
between the feeding artery and the draining vein.
Hemorrhage within the spinal canal may be epi- The resultant increase in pressure within the
dural (Fig. 19.3), subdural, subarachnoid, or venous system leads to a serpentine dilatation
intramedullary, involving the substance of the of the vessels. The cause of the spinal cord symp-
spinal cord itself (hematomyelia). About 25% of toms may be either compression from a mass
hemorrhages occur in patients with ongoing effect from these vascular tangles, or due to
anticoagulant therapy or coagulopathy (i.e., dis- shunting of the blood past spinal cord tissue,
eases with increased bleeding diathesis); trauma resulting in local hypoxia. A vascular malforma-
accounts for 10% of cases, and hemorrhage tion may also become manifest, with acute onset
from vascular malformations or tumor account of clinical symptoms due to hemorrhage or
for another 5%. No demonstrable cause can be infarction in the spinal cord (see earlier discus-
found in the remaining 60% of cases. The spec- sion). Most of these patients are middle-aged or
trum of symptoms is characterized by acute back older men who experience slowly progressive
pain, rapidly followed by progressive paresis and symptoms.
sensory deficits below the level of the lesion. Intramedullary vascular malformations typi-
cally have their onset earlier than those that are
extramedullary, usually in childhood or in early
adulthood.
Diagnosis of intraspinal vascular malforma-
tion is confirmed by MRI (Fig. 19.4A), MR angio-
graphy, and/or spinal angiography. Treatment
is determined on a case-by-case basis and con-
sists either of some type of surgical intervention
and/or embolization (Fig. 19.4B; also see same
figure in Color Plate section).
INFECTIOUS CONDITIONS
A) B)
Figure 19.4 Intramedullary vascular malformation. A: Intramedullary vascular malformation at the level of
the T8T9 disk. B: Intraoperative photo showing a vascular abnormality (cavernoma) located in the spinal
cord. See also Color Plate Fig. 19.4B.
recover completely, in contrast to patients who pain sensation, areflexia, and muscular hypo-
have become paraplegic more than a day or so tonia. Moreover, there is loss of proprioception
before initiation of treatment, who will typically leading to a positive Romberg test (i.e., patients
suffer permanent paralysis. The treatment con- lose their balance when asked to stand up
sists of urgent surgical decompression and anti- with their eyes closed). In addition, neurological
biotics. Intraoperatively, abscesses are often examination may reveal Argyll-Robertson pupils
found to be relatively firm in consistency rather (i.e., pupils are unequal in size, irregular, and
than in a liquefied state. react to convergence but not to light), optic
nerve atrophy with peripheral visual field loss,
Epidemic Poliomyelitis and Post-polio and sometimes also signs of upper motor
Syndrome neuron injury including the presence of a bilat-
eral Babinski sign.
Immunization has essentially eradicated this
disease in the developed world, but many per- AIDS-related Myelopathy
sons who have survived the disease still live
with the sequelae. The neurotrophic polio virus Myelopathy may signal the onset of acquired
attacks the anterior horn motor neurons in the immune deficiency syndrome (AIDS), with
spinal cord, leading to more or less widespread spastic paraplegia, often in combination with
and pronounced paresis and muscle atrophy. peripheral neuropathy. The condition may also
Some persons previously afflicted with polio appear in the late stages of the course of the
have experienced progressive symptoms after a disease.
stable period of 2530 years. This condition is
sometimes referred to as post-polio syndrome. The HTLV-1associated Myelopathy
cause of this condition has not been established.
The fact that patients with a past history of This condition, also known as tropical spastic
polio have spent some of their neuronal reserve paraplegia, is caused by infection with the
capacity may lead to disproportionate progres- human T-lymphotropic virus type 1 (HTLV-1)
sive functional deficits when additional neuronal and mainly occurs in the West Indies, equatorial
death, as part of physiological aging, occurs. regions of Africa, and in Japan. The virus is
Immunological mechanisms have also been transferred sexually or by blood. Clinically
proposed. This diagnosis should be considered and on MRI, the condition may resemble the
in patients with a past history of poliomyelitis, findings of MS, but it occurs in an Afro-Asian
although other possible causes must also be population where MS is rare. The condition is
ruled out. characterized by chronic inflammation of the
spinal meninges and perivascular regions of
Tabes Dorsalis (Tertiary Syphilis) the spinal cord. Severe demyelination of the cor-
ticospinal tract, and in the thoracic spinal cord in
Syphilis (lues) is a sexually transmitted infection particular, may be noted. Lymphocytic pleocy-
with a shifting spectrum of symptoms during tosis and elevated proteins may be seen in the
the protracted course of the untreated disease. cerebrospinal fluid. HTLV-1 antibody serology
During what is known as the tertiary stage is positive.
of syphilis, which is usually reached 1020
years after primary infection, the spinal cord DEGENERATIVE CONDITIONS
may become involved. At this point, progressive
scar tissue formation of the spinal meninges Herniated Disk
may secondarily impact the dorsal columns
and other neural structures. Typical symptoms Disk herniation of the cervical and thoracic spine
include attacks of sudden electric shock-like may lead to compressive myelopathy (Fig. 19.6).
pains, known as tabetic crises. Interruption of The herniation may arise suddenly or gradually.
the sensory reflex arc causes loss of deep Usually, some local pain is present, combined
CHAPTER 19 NONTRAUMATIC MYELOPATHIES 193
Impinged
nerve roots
Herniation
Intervertebral
disk
A) B)
C) D)
Figure 19.9 Intradural tumor. A: The tumor is located inside the dura but outside the spinal cord.
B: Magnetic resonance image (MRI) showing a spinal meningioma at the level of the foramen magnum.
C,D: Intradural tumor. C: Intraoperative image corresponding to B. D: Neurinoma located adjacent to the
conus medullaris. The nerve roots (a) are subjected to compression. See also Color Plate Fig. 19.9C,D.
regards neurological deficits depends on how cured by surgical removal. Common types of
soon treatment is initiated after onset of symp- tumors include meningioma and neurinoma
toms. In cases of rapidly progressive paraparesis, (Fig. 19.9AD; also see Fig. 19.9C,D in Color
surgery should be performed immediately if there Plate section). Symptoms are similar to those
is to be any chance of neurological recovery. produced by spinal epidural tumors, but the
Prognosis for survival depends on the biological course of disease is usually longer.
properties of the tumor and the degree of spread.
Intramedullary
Intradural Extramedullary
Intramedullary tumors typically comprise epen-
Intradural extramedullary tumors are usually dymomas and astrocytomas (Fig. 19.10AC).
benign, with very slow growth, and can often be An ependymoma is often localized in the lower
196 SPINAL CORD INJURY
A)
B) C)
Figure 19.10 Intramedullary tumor. A: Tumor location within the spinal cord. B: Magnetic resonance image
(MRI) showing a tumor in the upper spinal cord (arrow). C: Intraoperative image showing an intramedullary
spinal cord tumor (arrow, tumor; double arrow, spinal cord). See also Color Plate Fig. 19.10C.
portion of the spinal cord and the cauda equina, later stage, when the tumor has expanded far
whereas an astrocytoma arises mainly in the out into the periphery of the spinal cord, will
upper spinal cord. Ependymomas and benign the long pathways be affected. In these cases,
(i.e., low grade of malignancy) astrocytomas are bilateral signs of injury to the pyramidal tracts
associated with a postoperative 10-year survival with progressive spastic paraparesis are noted.
of about 80%, whereas the corresponding figure The dorsal columns appear to be relatively resis-
for malignant astrocytomas is 15%. tant to infiltration or distortion, and any mani-
Intramedullary tumors are often associated festations from these pathways are late signs
with a clinical course with initial neuronal irrita- in intramedullary lesions. In the final stages
tion and subsequently a breakdown of crossing of this process, only the most peripheral fibers
pain and temperature fibers within the affected that conduct sacral sensory nerve impulses will
segment. As the tumor expands laterally, the function (sacral sparing).
segmental reflex arcs will be interrupted.
Disease affecting the sympathetic pathways of MYELOMENINGOCELE
the cervical spinal cord may produce a unilateral
or bilateral Horner syndrome (i.e., ptosis, miosis, Myelomeningocele (MMC) is caused by a defec-
and enophthalmos). If the lesion extends toward tive closure of the neural tube and occurs in about
the anterior horn cells, segmental muscle 3/10,000 births (Fig. 19.11). Etiologically, the
atrophy and paresis will also arise. Only at a condition is associated with hereditary factors,
CHAPTER 19 NONTRAUMATIC MYELOPATHIES 197
neuron lesions), and progressive bulbar paralysis months following radiation therapy, in contrast
(muscles innervated from the brainstem are to so-called acute transient radiation myelopathy
preferentially affected). The different variants fre- which has a clinical picture characterized by
quently overlap. Clinically, patients often present early onset a prominent Lhermitte sign.
a mixed picture of upper and lower motor neuron
damage. Bladder and bowel function, as well as Cystic Myelopathy/Syringomyelia
sensory function, are unaffected. The disease
often leads to death due to respiratory insuffi- This condition is characterized by fluid-filled
ciency within 35 years. Typically, the hands are expansive cavities within the spinal cord caused
involved first with progressive paresis and muscle by a disturbance in CSF circulation. This
atrophy, followed by insidiously increasing spastic obstruction to the normal flow of CSF may be
paraparesis. This clinical syndrome may resemble due to a congenital malformation such as an
that seen in cervical spondylotic myelopathy (see Arnold-Chiari syndrome (Fig. 19.12). In this con-
earlier discussion), which thus is an important and dition, the cerebellar tonsils are pulled down
treatable differential diagnosis. MRI should there- to the level of the C2 arch, instead of being at
fore always be done. Neurophysiological investiga- the level of the foramen magnum (Arnold-Chiari
tions are also often carried out, mainly to rule out type II). An obstruction of CSF circulation may
treatable motor polyneuropathy, which constitutes also arise secondary to prior arachnoiditis.
another differential diagnosis. Electromyography Early symptoms include dissociated sensory
(EMG) typically demonstrates widespread mus- loss and pain due to damage of the crossing
cular denervation. spinothalamic fibers. As the cavity expands in a
We should also briefly mention some
other rare diseases characterized by progressive
muscle atrophy due to involvement of the ante-
rior horn motor neurons. Werdnig-Hoffman
disease (spinal muscular atrophy type I) is usually
fatal in early childhood. Kugelberg-Welander
disease (spinal muscular atrophy type III) is a
juvenile and more benign variant of Werdnig-
Hoffman disease, and Duchenne-Aran disease is
an adult form of this condition. Please refer to
specialist literature for further details.
OTHER CONDITIONS
Radiation-induced Myelopathy
craniocaudal direction, additional spinal cord seg- and may be less pronounced. Significant bladder
ments successively become involved. During involvement is uncommon until the late stages of
expansion from the central spinal cord to the the disease. Spasticity strongly dominates the
periphery, progressive paresis and impairment clinical picture. Deep tendon reflexes are highly
of other sensory modalities also occur. MRI increased, and in some patients muscular hyper-
confirms the diagnosis. The course of this disease tonia is so pronounced that reflexes cannot be
is rather unpredictable. Treatment is surgical in elicited because the muscles are constantly in
cases where syringomyelia produces significant maximum contraction. Sensory involvement
symptoms (see Chapter 30). may occur. A recessive hereditary form usually
has its onset at age 710 and is associated with a
Subacute Combined Degeneration poorer prognosis, while a dominant hereditary
form usually begins after age 20 years and has a
This condition is due to vitamin B12 deficiency. more benign course.
Most patients are elderly. Degenerative changes
occur in both central and peripheral nervous Friedreich Ataxia
system myelin. The earliest symptoms are
related to peripheral nerve damage and include Friedreich ataxia is autosomal (i.e., nonsex-
paresthesias, areflexia, and gait ataxia. Within linked) recessive (i.e., both parents must carry
the spinal cord, the posterior columns become the trait). Pathologic changes, usually degenera-
involved first, followed by the lateral columns tive in nature, involve structures such as the
(thus combined degeneration). Neurological dorsal root ganglia, dorsal columns, lateral corti-
examination shows decreased vibration sense cospinal tract, and the dorsal spinocerebellar
and proprioception in the lower extremities. tract. Onset of symptoms is usually before age
Deep tendon reflexes may be hyperactive (due 20. Signs of myelopathy are prominent. Patients
to pyramidal tract involvement) or weak (due to demonstrate progressive gait ataxia, decreased
peripheral nerve involvement). This condition deep tendon reflexes in the lower extremities,
may also be accompanied by dementia and presence of Babinski sign, diminished proprio-
optical nerve atrophy. One-quarter of patients ception and vibration sense in the lower extre-
with this condition do not demonstrate the mities, and dysarthria. Many patients exhibit
megaloblastic (pernicious) anemia, which other- cardiomyopathy and 1020% develop diabetes
wise usually accompanies this condition. Most mellitus. The diagnosis is confirmed through
cases involve an underlying deficiency of demonstration of a characteristic chromosomal
intrinsic factor, which is required for B12 defect.
absorption from the small intestine. Further
tests may show depressed serum levels of High-voltage Electric Shock
vitamin B12 and high levels of homocysteine
and methylmalonic acid. Antibodies to intrinsic Electricity, passing through the spinal cord as
factor are also present. It is important to diag- in lightning strikes or accidents involving
nose this condition, since vitamin B12 substitu- high voltage may result in a progressive
tion may lead to complete cure of symptoms. myelopathy.
Hereditary spastic paraplegia is a rare condition Decompression illness, also known as the
with variable heredity and a protracted course. bends, is caused by rapidly moving from a
The pathology involves the lateral corticospinal high atmospheric pressure environment to one
tracts, and sometimes the dorsal columns. The with low pressure, and results in the formation
course of disease is progressive, and onset is of intra- or extravascular bubbles from inert dis-
characterized by progressive stiffness of the legs. solved gases within the blood and tissues. These
Involvement of the upper extremities comes later bubbles may cause symptoms by directly
200 SPINAL CORD INJURY
ACUTE STRESS REACTIONS AND the patient handles the situation) will come to
PSYCHOLOGICAL DEFENSE MECHANISMS play a major role. Usually, it is more difficult
for introverts to cope with the situation than for
Sustaining an acute SCI always entails a major extroverts. Persons with poor self-confidence and/
psychological trauma for victim and family alike. or self-esteem who previously were highly con-
The course of the stress reaction may span many cerned with physical appearance and achieve-
years. During the early stages, both patient and ment will experience the injury as particularly
family protect themselves against the scope of frustrating. Persons with an external locus of
the event through several more or less subcon- control will consider their chances of affecting
scious defense mechanisms. Common psycholo- their life situation as negligible and will thereby
gical defense mechanisms include denial, experience problems in the rehabilitation setting.
projection, intellectualization, and avoidance. Conversely, an internal locus of control is asso-
Denial means that the patient simply does ciated with a feeling of ability to impact personal
not accept that she is the victim of a severe destiny, something which significantly facilitates
injury with probably irreversible consequences. the rehabilitation process. Moreover, the presence
As long as denial dominates the psychological or absence of a well-developed social network will
picture, it is extremely difficult to convey to the affect the rehabilitation process. Persons who live
patient information and insight that requires an in relative isolation will, as a rule, require more
adequate perception of reality. support from staff than will those who are more
Projection may sometimes entail aggressive gregarious.
outbursts toward healthcare staff and others as The adaptation process following SCI may
a reaction to the frustration caused by the injury. last several years. This is particularly important
In such cases, it is important to understand the to bear in mind in the current healthcare setting,
underlying cause of the patients behavior and as hospital stays become successively shorter for
avoid direct confrontation. economic reasons. A significant portion of the
Intellectualization may be expressed as a psychological reactions to the injury will often
purely cognitive (intellectual) acceptance of the first become manifest after the patient has been
injury, such as by focusing on all available factual discharged home, due in part to the short length
information, but without any emotional of stay in the hospital, the early presence
reaction. of insight-blocking defense mechanisms, and
Avoidance is reflected by various ways of sometimes heavy sedation with drugs during
defending oneself from reminders of the dis- the early rehab phase. This underscores the sig-
ability, for example by avoiding looking in the nificance of a well-structured outpatient follow-
mirror and/or by avoiding contact with other up post trauma.
people with disabilities.
MENTAL DISORDERS
ADAPTATION
Several studies suggest that mental disorders are
To handle the crisis that an SCI entails, the more common among persons with SCI than in
patients coping strategies (i.e., the ways in which the general population. It has been reported that
201
202 SPINAL CORD INJURY
depression or significant depressive symptoms family members, and coping with sexual
occur in about 25% of men and 50% of women dysfunction.
during the post-acute phase. Differentiation The risk of substance abuse and self-
from a normal grief reaction to trauma is destructive behavior must be considered. Suicide
sometimes difficult, and treatment with antide- is reported to be the most common cause of death
pressants often should be initiated in unclear in the post-acute phase following discharge from
cases. the hospital; the suicide rate among patients with
Sleep disturbances are common (see later SCI is five to ten times greater than that in the
discussion) and may be both a reason for and population at large.
effect of mental problems. Disturbed sleep When considering long-term satisfaction and
results in a number of adverse psychological quality of life after SCI, the degree of neurolo-
and physical effects, and a short course of gical deficits appears to play a lesser role than
hypnotics is often indicated. factors such as presence of pain, incontinence,
In some cases, a patient may suffer from and spasticity.
posttraumatic stress disorder (PTSD). Typically, in
this condition, a person who has been exposed to MANAGEMENT
a traumatic event continually relives the experi-
ence in thoughts or nightmares, avoids stimuli All patients with SCI should be met with an
associated with the trauma, and suffers from a open, optimistic, and affirming attitude. They
decrease in vitality and an increase in irritability. should be encouraged to express their feelings,
Studies have shown that up to one-third of and time must be allotted to listen to what they
patients demonstrate this condition. have to say. It is essential to be understanding of
Other emotional sequelae may relate to aggressive behavior and poor compliance, espe-
clinical or subclinical traumatic brain injury sus- cially during the early post-injury stages. Respect
tained at the same time as the SCI. In suspected for the patients personal dignity is paramount.
cases, a neuroradiological and neuropsycholo- This approach is reflected in how the caregiver
gical workup may help define the degree of handles sensitive issues in the rehabilitative pro-
organic brain damage. cess, such as bladder and bowel management,
Poor mental health has a negative impact on personal hygiene, and incontinence. Many
the rehabilitation process. For example, depres- patients need formal counseling. Such coun-
sion increases the risk of urinary tract infections seling should be part of the rehabilitation plan.
and pressure ulcers, and also contributes to It is important for each patient to have the oppor-
general poor health. The tendency for such tunity for assessment by a psychologist or psy-
patients to engage in substance abuse and other chiatrist in order to determine whether
self-destructive behavior increases. All things psychopharmacological treatment, psy-
considered, well-structured psychological man- chotherapy, and/or additional psychiatric and
agement becomes an essential component of neuropsychological testing are needed. Among
both the initial and long-term rehabilitation of psychotherapeutic treatment options, cognitive
persons with SCI. It is important not to view the psychotherapy has made significant inroads in
psychologist or psychiatrist as someone to con- recent years. Not only patients, but also family
sult only in the presence of overt psychiatric and friends, need to be made aware of their
disease; instead, they should be considered as psychological reactions in conjunction with an
integral to the rehabilitation team as the physical injury.
or occupational therapist.
Many of the psychological challenges of SCI SOCIAL IMPACT
will first manifest after patients are discharged
home and confront a new reality. A few of the The nuclear family is the social unit most
many challenges to be met include the ability to strongly affected by SCI. In many cases, the
clearly communicate need for assistance, an social roles within the family change radically.
increased dependence on partners and other With respect to the relationship between man
CHAPTER 20 PSYCHOSOCIAL FACTORS 203
and woman, there is a risk that the caregiver role initial care period. It is reasonable to assume that
outcompetes the partner role. The divorce rate is a rehabilitation outcome resulting in optimal
higher in relationships in which one party has a functional capacity and a high degree of
SCI. This is mainly true when the injury afflicts autonomy is preferable to dependence on assis-
one of the partners in an already established tance and subsidies.
relationship. In cases where the relationship
was formed after the SCI occurred, divorce rates Suggested Reading
are not elevated. Several textbooks are available for further study as
With respect to parenting, several studies regards long-term management of SCI. The fol-
have shown that persons with SCI are neither lowing selection includes the major classic text-
better nor worse in this role than able-bodied books on the subject (e.g., Guttman, Bedbrook,
parents. Physical disability in and of itself does Rossier), which are perhaps mostly of historic
not preclude being a good parent. interest. In addition, the list includes some
In most cases, the SCI clearly has a negative recommended comprehensive current textbooks.
impact on personal finances. However, on the
contrary, in some cases there may actually be a Bedbrook GM. The Care and Management of Spinal Cord
Injuries. New York: Springer-Verlag, 1981.
negative economic incentive for returning to
Guttmann L. Spinal Cord Injuries: Comprehensive Manage-
work. This is unfortunate, since employment, ment and Research. Oxford: Blackwell Scientific Public-
in addition to its financial value, also serves to ations, 1973, 1976.
improve quality of life and promote health. In Illis LS. Spinal Cord Dysfunction, Vol. II. Intervention and
general, the ability to return to work should Treatment. Oxford: Oxford University Press, 1992.
Kirshblum S, Campagnolo DI, DeLisa JA, eds. Spinal Cord
command greater attention in the rehabilitation
Medicine. Philadelphia, Pa.: Lippincott Williams &
process than what is currently the case. Routine Wilkins, 2002.
approval of disability retirement is to be avoided, Lee BY, Ostrander LE, Cochran GVB, Shaw WW. The Spinal
and a majority of patients with SCI regrettably Cord Injured Patient: Comprehensive Management.
fail to return to the work force. Philadelphia: W.B. Saunders Company, 1991.
Lin VW, ed. Spinal Cord Medicine: Principles and Practice.
Thanks to legal reforms involving service sup-
New York: Demos Publishing Medical, 2003.
port and assistance for people with disabilities, Mathias CJ, Bannister R. Autonomic Failure. A Textbook
many SCI patients in several countries are now of Clinical Disorders of the Autonomic Nervous System,
entitled to personal assistance. The law contains 4th ed. New York: Oxford University Press,
provisions for monetary compensation to certain 1999:494513.
Randal R, Betz MJ. The Child with a Spinal Cord Injury.
people with disabilities, to cover the cost of such
Shriners Hospitals for Crippled Children Symposium.
assistance. In many cases, such acts have allowed American Academy of Orthopaedic Surgeons, 1996.
persons with SCI to engage in work, leisure, and Randolph W, Evans MD. Neurology and Trauma. Philadelphia:
community activities to a much greater extent W.B. Saunders Company, 1996:276322.
than previously. However, such reforms also Rossier AB. Rehabilitation of the Spinal Cord Injury Patient.
Zurich: University Medical Clinic, Cantonal Hospital
entail a risk of becoming a substitute for optimal
Zurich.
rehabilitation interventions. The option to Somers MF. Spinal Cord Injury: Functional Rehabilitation.
become self-sufficient is always preferable to New Jersey: Prentice Hall. Inc., 2001.
remain being dependent on assistance, even if Zejdlik CP. Management of Spinal Cord Injury, 2nd ed.
this will require a greater investment during the Jones and Bartlett Publishers, Inc. 1992.
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21 Pain
Pain receptors, also called nociceptors, are struc- condition characterized by hyperactivity (hyper-
tures that become stimulated when there is a sensitivity) within the receptor neurons of
threat of tissue damage. Such receptors consist the dorsal horn. This hyperactivity may be due
of free nerve endings, of thin myelinated A-d to either an increase in C-fiber activity or an
fibers or unmyelinated C fibers (Fig. 21.1). increase in demyelination. Intracellular bio-
A-d and C fibers convey different types of pain chemical changes, especially within Rexed
sensations. The A-d fibers have higher conduction lamina II (substantia gelatinosa), also contri-
velocity and give rise to a fast, distinct, well- bute to hyperreactivity. Substances involved in
localized pain. Pain conveyed through the C fibers nociceptive transmission include peptides like
is dull, diffuse, more difficult to localize. The pain substance P, excitatory amino acids (e.g., gluta-
fibers enter the spinal cord via the dorsal root entry mate and aspartate), inhibitory neurotransmit-
zone (DREZ), and usually terminate in Rexed ters (e.g., glycine and g-aminobutyric acid
laminae I, II, and V (Fig. 21.2). At the first synapse [GABA]), opioids, and nitric oxides. GABA and
located in the dorsal column or dorsal horn, the the opioids are of particular interest in the con-
signal is received and modified via interneurons text of surgical treatment. GABA has been iden-
and descending pathways before continuing to the tified as an inhibitory amino acid for impulse
supraspinal levels via the second neuron. transmission in the spinal cord. Animal studies
Certain primary afferents branch along the have shown that release of GABA decreases in
longitudinal axis of the posterior horn in the response to peripheral injury and the presence
Lissauer tract (Fig. 21.2), which means that these of neuropathic pain.
primary afferents are connected at several levels in Pain is a major problem in the aftermath of
the spinal cord. According to convergence theory, SCI. More than two-thirds of all SCI patients
an individual neuron within the dorsal horn suffer from chronic pain, and in about one-
may communicate with several neurons from third the pain is so severe that it interferes with
one type of tissue and/or with several neurons daily activities and reduces quality of life.
from different tissues. This complicates the task According to the International Association
of the brain to adequately localize the origin of for the Study of Pain (IASP), pain is defined as
the pain. an unpleasant sensory and emotional experi-
The posterior horn of the spinal cord contains ence associated with actual or potential tissue
various types of nociceptive neurons. In part, damage, or described in terms of such damage.
there are specific neurons that only receive a This definition emphasizes the subjectivity of
small number of primary nociceptive afferents; pain, and that pain can be both a physiological
these neurons only cover a small area of the phenomenon as well as an emotional and cogni-
body, such as one foot. In part, multireceptive tive reaction.
or wide-dynamic-range neurons (WDR neurons) The pain system encompasses peripheral
with large receptor fields receive impulses from receptors; afferent neural pathways; connecting
different A and C fibers (Fig. 21.3). and modulating centers in the spinal cord;
When the spinal cord is injured, anatomical ascending pathways; centers in the brainstem,
and neurochemical changes occur within its thalamus, cerebral cortex, and other areas; and
tissue, the end result of which is an excitatory descending pathways.
205
206 SPINAL CORD INJURY
Dorsal root
entry zone (DREZ)
Lissauer's
tract
Lamina I and II
Lamina V
A-delta fiber
C-fiber
WDR
NS
Large myelinated
A-delta fibers
anterior shoulder muscles, in order to restore rhomboids, levator scapulae, and supra- and
muscular balance in the joint. The sitting posi- infraspinatus muscles. The pain is triggered by
tion in the wheelchair should be optimized. In an imbalance of the rotator cuff muscles, with
addition, the patient should avoid using the arm disproportionately more power for scapular
in positions that provoke impingement, espe- retraction (pulling back) than for protraction
cially abduction/flexion of the arm in excess of (pushing forward). To avoid shoulder problems,
90 degrees in combination with inward rotation. an adequate sitting position in the wheelchair is
Symptoms may be alleviated by avoiding important; in particular, the arms should be sup-
overuse, by prescription of anti-inflammatory ported by the armrests, so that the weight of the
drugs, and/or by corticosteroid injection of the humerus does not pull the humeral head from its
bursa or joint (see also the section Shoulder socket. When performing range-of-motion exer-
Problems in Chapter 22). cises, the shoulder joint should not be flexed or
abducted more than 90 degrees. Excessive
loading of a shoulder joint with weak dynamic
Neuropathic Pain
stabilizing musculature stresses the capsular liga-
Carpal tunnel syndrome (with median nerve com- ments, ultimately resulting in joint instability.
pression) is common among persons with para- Pain from internal organs located at the level of
plegia and low-level tetraplegia; prevalence injury mainly occurs when the neurological level
increases with time. Contributing factors to this of injury is below the midthoracic spinal cord.
problem include repetitive trauma from wheel- Nociceptive stimuli arising from the abdominal
chair propulsion and repetitious increases in and pelvic organs are conveyed rostrally through
pressure within the carpal tunnel, such as visceral afferents that follow the sympathetic
during transfers. neural pathways. This kind of pain is often
Ulnar nerve neuropathy with site of compres- characterized as vague, diffuse, and difficult to
sion in the wrist is also common. Preventive localize. In these patients, it is necessary to be
measures include padded gloves to protect the vigilant for diseases affecting internal organs,
palmar aspect of the wrist and avoidance of since the clinical presentation will be atypical.
weight-bearing on an extended wrist, by instead
using a neutral wrist position. For more discus- Neuropathic Pain
sion please refer to Chapter 23.
Pain of this type may be either peripheral or
central in origin. The former may be caused by
PAIN AT THE LEVEL OF INJURY a segmental nerve root injury. Such pain is often
unilateral and paroxysmal (episodic), and distrib-
Nociceptive Pain uted along a single dermatome. The latter, so-
called central neuropathic pain, is often bilateral,
Spinal posttraumatic instability may cause pain at with a band-shaped distribution and usually per-
the level of injury. This pain is often aggravated sisting. It is denoted as transitional zone pain,
by movement and weight-bearing. since it occurs at the border between normal
The prevalence of musculoskeletal shoulder pain and impaired or absent sensitivity. The cause is
among persons with tetraplegia (for whom this usually a direct lesion to the pain pathways in the
condition will be classified as being pain at the spinal cord, with onset immediately after injury.
level of injury, in contrast to persons Should onset of pain occur more than 612
with paraplegia where it is classified as pain months after injury, underlying progressive post-
above the level of injury) is, as for persons with traumatic myelopathy (PPM) have to be ruled out.
paraplegia, 4060%. The causes are similar. In That condition is believed to be precipitated by
addition, a specific type of shoulder pain in tetra- scar tissue formation between the spinal cord
plegics may occur, known as scapular pain, and the meninges, which impairs cerebrospinal
located along the medial border of the scapula. fluid circulation. It occurs in 25% of patients
Tenderness to palpation can be found over the with traumatic SCI, and pain is the most
CHAPTER 21 PAIN 209
Invasive
treatment /
surgery
Opioids
Antidepressants
Non-narcotic analgesics
Non-steroidal anti-inflammatory drugs
(NSAID)
Patient information
Physical and Psychological rehab programs
common presenting symptom. If the condition pain is not distributed along a single peripheral
progresses, the pain may sometimes decrease nerve or nerve root, but has a more diffuse
concomitantly with loss of sensation in the regional distribution. Frequent signs include
affected segment. This corresponds to an local swelling, a change in skin circulation, and
ascending sensory level. Progressive paresis and increased sweating. Bone scan may show a dif-
other symptoms may also occur, see Chapter 30. fuse increase in uptake.
Spinal cord MRI is the study of choice when PPM
is suspected. PAIN BELOW THE LEVEL OF INJURY
Patients with tetraplegia may display a com-
plex regional pain syndrome (CRPS), producing Nociceptive Pain
neuropathic pain involving the upper extremi-
ties. This chronic pain is believed to be precipi- Nociceptive pain below the neurological lesion
tated by impaired autonomic innervation. The level may occur persons with incomplete SCI, or
CRPS concept has replaced the earlier terms in patients with complete injuries but with a zone
sympathetic reflex dystrophy and causalgia. Such of partial preservation (segments below the level of
210 SPINAL CORD INJURY
Musculoskeletal problems are very common increased demands on use of the upper extremi-
after SCI and may give rise to added chronic ties in daily life.
disability. Several studies have shown the preva- Skeletal components of the shoulder
lence of musculoskeletal pain to be between 50% (Fig. 22.1) include the scapula, the clavicle,
and 75%, and many factors contribute to this and the humerus. The humeroscapular joint is
situation. Osteoporosis (i.e., loss of bone mass) is constructed to allow for movement, and is ill-
extensive below the level of lesion and the risk suited for weight-bearing. The glenoid cavity is
of fractures is high. Paralysis in itself causes small and shallow in relation to the head of the
ergonomic problems, in part due to poor trunk joint. This joint has been likened to a golf ball
stability. The load on remaining functioning resting on a peg; consequently the humeroscap-
muscles increases, and normally nonweight- ular joint is dependent on a well-developed
bearing joints are forced to support considerable muscular cuff for its stability. The tendons
body weight during transfers, pressure relieving of the muscles comprising this cuffteres
maneuvers, and wheelchair propulsion. The list minor, subscapularis, infraspinatus, and
of factors contributing to musculoskeletal pro- supraspinatusare gathered into a shared
blems is lengthy. In addition to negative impact common tendon aponeurosis. This structure,
on the ability to perform activities of daily living known as the rotator cuff, is readily subject to
(ADL), pain in itself often have a markedly nega- injury, both from acute trauma and from
tive effect on quality of life. Chronic pain chronic repetitive overuse. The approach to
is probably the major cause of diminished workup of shoulder problems includes a thor-
quality of life in the long-term after SCI (see ough history and clinical examination. Skeletal
also Chapter 21). changes may be seen on plain x-ray. Soft-tissue
changes can be visualized by magnetic reso-
NECK AND BACK PROBLEMS nance imaging (MRI) or with arthroscopy.
Rotator cuff ruptures, aseptic necrosis of the
A number of factors contribute to pain in the humeral head, and osteolysis of the distal clavicle
neck and back. Individuals with traumatic SCI are more common in persons with SCI than in
by default have various degrees of damage to the the general population, especially among wheel-
spinal column. Spinal paralysis typically leads to chair-bound patients with paraplegia. Repetitive
impaired muscle function in the trunk and trauma to the upper extremities in conjunction
thereby frequently to the development of with activities such as transfers and wheelchair
kyphoscoliosis. propulsion is responsible for the damage.
Among persons who manually propel their
SHOULDER PROBLEMS wheelchair, the space under the ceiling
formed by the acromion, coracoid process, and
The most common causes of musculoskeletal ligaments will be narrowed. This situation pre-
pain after SCI involves pathology in and around disposes to impingement of the rotator cuff.
the shoulder joints. The shoulder joint is Mild shoulder problems may be alleviated
designed for flexibility, rather than for weight- with anti-inflammatory drugs and possibly local
bearing, but SCI typically necessitates such corticosteroid injections. It is not settled whether
211
212 SPINAL CORD INJURY
Area of M. supraspinatus
impingement
Clavicle
Acromion
Bursa
Cavitas
glenoidalis
M. deltoideus
Scapula
Humerus Parts of
rotator cuff
Figure 22.1 Anatomy of the shoulder. The picture illustrates the shallow joint socket, the
basic construction of the joint that prioritizes mobility over stability, and the cuff surrounding
the joint (rotator cuff). These anatomical conditions predispose the joint to impingement and
overuse injuries resulting from the excessive loads placed upon the shoulder joint after SCI.
indications for surgical treatment of shoulder muscles. Due to chronic inflammation of the
problems among SCI patients should be more extensor muscle attachments, distinct palpatory
liberal than those applied to the general popula- tenderness may be elicited just distal to the epi-
tion. However, it is clear that most surgical condyle. Treatment options include anti-inflam-
shoulder interventions in SCI patients require matory medications, support strap, local steroid
intense postoperative rehabilitation often in an injection and, in therapy-resistant cases, surgical
in-patient setting. As long as postoperative release of the extensor tendons from the
immobilization is required for the shoulder epicondyle.
joint, many persons with SCI will essentially be
completely ADL-dependent.
PREVENTATIVE AND REHABILITATIVE
MEASURES
ARM PROBLEMS
If musculoskeletal problems arise following SCI,
Not only the shoulders, but the entirety of upper the resultant impairment will become dispropor-
extremities will typically be chronically over- tionately great. Wheelchair-bound individuals
loaded after SCI, resulting in tendonitis and with SCI have no opportunity to rest the upper
compression neuropathies. A correlation has extremities without becoming completely immo-
been noted between such problems, and obesity bilized and ADL-dependent. Preventative exer-
and/or poor wheelchair handling technique. cises, appropriate trials of assistive devices, and
The prevalence of elbow pain has been shown early diagnosis and treatment are thus of great
to be about 15%. A common maneuver that importance. In the shoulder joints, the external
provokes such pain is pronation of the forearm, rotators are usually weaker than the internal rota-
extension of the elbow, and simultaneous wrist tors. Since the external rotators also help to hold
extension while grasping grip rings as the person the shoulder joint down, these muscles are impor-
manually propels the wheelchair. The loads tant for preventing impingement. Exercise pro-
incurred during this maneuver put the patient grams must therefore focus on restoring
at risk for lateral epicondylitis (tennis elbow). muscular balance around the shoulder joints. If
This condition is characterized by radial pain, chronic shoulder problems do arise, it becomes
especially with activation of the extensor important to motivate the patient to accept an
CHAPTER 22 MUSCULOSKELETAL PROBLEMS 213
HETEROTOPIC OSSIFICATION
Heterotopic ossification (HO) was first described Figure 22.2 Heterotopic ossification. The process is
in 1918. HO is characterized by the formation of characteristically located around the hip and
bone in tissues adjacent to joints (Fig. 22.2). The knee joint.
newly formed bone tissue is histologically iden-
tical to normal bone. This process usually begins during the
This condition may arise secondary to direct first few weeks following trauma. The earliest
muscle trauma (so-called traumatic myositis ossi- symptom is progressive limitation in the range
ficans), as a sequel of fracture or surgery in the hip of motion within the afflicted joint, followed
joint, and in response to paralysis after central by swelling, erythema, increased local tissue tem-
nervous system (CNS) injuries. HO has been perature, and pain. Differential diagnosis
described after both traumatic SCI and brain inju- includes deep vein thrombosis, erysipelas,
ries. In the latter instances, the condition is always osteomyelitis, and septic arthritis. In 60% of
localized to a neurologically afflicted area; thus, in cases, the abnormal ossification occurs
SCI, HO occurs below the level of lesion. The con- around the hips, typically anteromedial to the
dition is more common among patients with joint, and in 30% of cases around the knee
complete lesions and with pronounced spasticity. joints, especially medially. In individuals with
The incidence is 2030%, but only in about half of tetraplegia, bone may form around the
these patients does the condition pose clinically shoulder or elbow joint in rare cases.
significant consequences. Large-scale HO may
preclude a good sitting position in the wheelchair,
contribute to the occurrence of pressure ulcers, The Brooker classification divides HO into
and may worsen spasticity. Its cause is unknown. four groups:
Probably both local and systemic inflammatory
Class 1: Isolated islands of bone
factors play a role, the latter referred to as systemic Class 2: More than 1 cm separates
inflammatory response syndrome (SIRS). opposing ossification centers
Ossification is a three-stage process: in the Class 3: Less than 1 cm separates
first stage, an extracellular matrix called osteoid opposing ossification centers
is formed, next the osteoid is mineralized, and Class 4: Total bony ankylosis
finally, mature bone tissue is formed.
214 SPINAL CORD INJURY
patients who completely lack voluntary muscle In summary, a realistic hand surgical outcome
function distal to the elbow. At the other end of is often said to be that the patient will be able to
the spectrum are those patients with preserved carry out those same activities that he could already
function of all muscles, with the exception of the achieve prior to surgery, only more easily and effec-
intrinsic muscles of the hand. tively. Reconstructive hand surgery thus rarely
Elbow extension can be achieved through a enables the patient to develop brand new skills.
deltoid-to-triceps transfer, or a biceps-to-triceps
transfer. Wrist extension can be improved in cer- Functional Neuromuscular Stimulation
tain patients by transferring contractile function
from the brachioradialis to the extensor carpi Functional neuromuscular stimulation (FNS) is
radialis brevis tendon. A key grip can be created sometimes an alternative or complement to
in patients who have retained at least some ability reconstructive hand surgery. The method,
for active wrist extension. An active key grip can mainly developed in the United States, uses
be achieved by fusing the carpometacarpal joint both transcutaneous nerve stimulation and
of the thumb, anchoring the extensor pollicis implantable electrodes. For example, the
longus tendon to the back of the wrist, and trans- NeuroControl Freehand System is an implantable
ferring the brachioradialis tendon to the flexor system that is controlled by movements of the
pollicis longus tendon. A number of alternative opposite shoulder. The technique enables a
strategies may be used, and the more functioning patient with high SCI to activate and control a
muscles that remain below elbow level, the more preprogrammed sequence of muscle contrac-
alternatives are available. tions and thereby achieve a usable grasp.
23 Compression Neuropathies
217
218 SPINAL CORD INJURY
Lig. carpi
tranzsversum
Treatment
Vagotonia
When an attack of AD is suspected, the patient
One major cardiovascular complication seen
should be placed in an upright position and tight
during the acute stage after traumatic tetraplegia
clothing should be loosened. Urinary retention
is episodes of bradycardia or even cardiac arrest
must be ruled out and/or treated (catheteriza-
caused by autonomic imbalance with relative
tion, irrigation of indwelling catheter). The next
dominance of parasympathetic activity. The
step is to rule out and/or treat rectal fecal impac-
precipitating factor may be vagal stimulation
tion as the cause of elevated blood pressure
caused by intubation and/or suction of the
(digital rectal exam and, when needed, stool
airways. In high SCI, vagal impulses cannot be
removal after lubrication with local anesthetic
adequately counter-balanced due to interruption
ointment). Should a systolic blood pressure ele-
of the sympathetic innervation of the heart.
vation above 150 mm Hg persist, the blood pres-
sure should be lowered using a rapid-acting
Autonomic Dysreflexia antihypertensive drug such as a calcium channel
blocker. Other precipitating causes should
SCI at the T6 level or rostrally (i.e., above the then be explored, such as abdominal disorders,
sympathetic splanchnic outflow) predispose to infection, fracture/soft-tissue injury, paronychia,
autonomic dysreflexia (AD). Nociceptive stimuli thrombosed hemorrhoid, or anal fissure.
normally lead to sympathetic activation, but with
SCI and its associated interruption of the fibers to Arterial Hypotension
the cerebral vasomotor centers, such activation
becomes exaggerated due to loss of supraspinal Systemic blood pressure is typically low in per-
inhibition. Plasma levels of norepinephrine sons with SCI in the upper thoracic or cervical
immediately rise and correlate with symptoms cord. Sitting and resting systolic blood pres-
and blood pressure elevation. sure for a person with tetraplegia is typically
AD is characterized by attacks of blood pres- 90110 mm Hg. Such low blood pressure is
sure elevation with severe headache. Other symp- due to decreased sympathetic activity and conse-
toms include malaise, nausea, facial flushing, quently correspondingly decreased vasomotor
sweats, and goosebumps (Fig. 24.1). The combi- tone below the level of lesion. Low systemic
nation of headache attacks with sweating and blood pressure, assuming that it does not fall
219
220 SPINAL CORD INJURY
Headache
Flushing
Sympathetic
Perspiration activation
Level of
Elevated BP
spinal cord
lesion
Figure 24.1 Autonomic dysreflexia (AD). In persons with a neurological level of lesion of T6 or higher,
infralesional nociceptive stimuli may lead to attacks of blood pressure elevation with symptoms such as
headache, sweats, and facial flushing.
below a critical level and becomes symptomatic, is blood pools in the lower extremities and, in the
not necessarily disadvantageous from a health absence of compensatory vasoconstriction, a fall
standpoint. On the contrary, hypertension rather in blood pressure occurs. Blood flow returning to
than hypotension is a significant pathogenic the heart decreases, leading to a drop in filling
factor. It is thus postulated that low blood pres- pressure, end-diastolic volume, and stroke
sure among tetraplegic patients even might volume. This may result in cerebral hypoperfu-
provide some protection against cardiovascular sion with symptoms such as dizziness, visual
diseases. disturbances (black-out), weakness, faintness,
and possibly loss of consciousness. Precipitating
Orthostatic Hypotension or aggravating factors include standing or sitting
up too quickly, rising abruptly on waking in the
Orthostatic hypotension is defined as a drop in morning, heavy meals (due to shunting of blood
systolic blood pressure of more than 20 mm Hg from the systemic to the splanchnic circulation),
and/or a symptomatic (dizziness, faintness, etc.) physical exertion, alcohol consumption, high
drop in blood pressure when the patient sits up ambient temperature, fever/infection, dehydra-
or stands up. Orthostatic problems are common tion, and certain medications (e.g., tricyclic
in complete injuries at or above the T6 level, antidepressants, antihypertensives, diuretics,
especially during the first weeks and months opioids). Neurogenic orthostatic hypotension
following SCI. The cause is impaired or absent usually resolves gradually during the rehabilita-
sympathetically mediated peripheral vasocon- tion period. Possible explanations for this
striction. When standing or sitting up, venous physiological adaptation include compensatory
CHAPTER 24 CIRCULATORY AND RESPIRATORY DISORDERS 221
changes in other vascular beds, stimulation of the decreases by 1025% compared with the popula-
reninangiotensinaldosterone system, compen- tion at large, and the ideal weight should thus be
satory receptor hypersensitivity in the vascular 510 kg lower. In addition, these patients cannot
walls (as a consequence of sympathetic denerva- respond with sympathetically mediated vasocon-
tion), spontaneous return of the spinal postural striction (which increases venous return) or sym-
reflexes, increasing spasticity, and/or adaptive pathetically mediated elevation of heart rate and
autoregulation of blood flow to the brain. myocardial contractility, which further limits
their work capacity.
Treatment Aerobic exercise is an important component
of the rehabilitation process, both initially and
Treatment should focus on alleviating symp- in the long-term. Physical activity associated
toms rather than on normalizing blood pressure. with activities of daily living (ADL) is insuffi-
The following measures constitute first-line cient in itself to achieve an aerobic effect. The
treatment: benefits of exercise include increased func-
During early phases of rehabilitation, gra- tional reserve capacity in daily life, as well as
dual mobilization on the slant board to con- long-term prevention of cardiovascular disease.
dition postural reflexes The more caudal the neurological level of
Distribution of food intake into small, fre- injury and the more incomplete the injury,
quent meals the greater the potential for improving aerobic
Elevation of head at night to reduce nocturia fitness.
(i.e.,. large nocturnal urine volumes) and
thereby reduce hypovolemia and orthostatic Coronary Heart Disease
hypotension in the morning
Avoidance of rapid changes in position Atherosclerotic coronary heart disease has in
(sitting, standing, lying) recent years become one of the leading causes
Avoidance of strenuous physical activity of death among SCI patients. Several risk fac-
in high ambient temperatures tors are overrepresented: decreased physical
Discontinuation of antihypertensive medi- activity, low high-density lipoprotein (HDL)
cation cholesterol (the good cholesterol), impaired
Increased salt and fluid intake glucose tolerance, increased insulin resistance,
Use of compression hosiery and/or abdom- increased proportion of body fat, hypertension
inal girdle (in paraplegics), smoking, and psychosocial fac-
tors such as depression and social isolation. In
In addition, in rare cases, pharmacological treat- addition, it has been proposed that recurrent
ment may be indicated, such as dihydroergota- chronic infections (such as urinary tract infec-
mine, etilefrine, or fludrocortisone. The latter tions and infected pressure ulcers) may increase
medication is a mineralocorticoid, in which the cardiovascular risk via inflammatory mediators
mechanism of action involves some fluid such as C-reactive protein (CRP). Several of
retention. these factors are amenable to preventive mea-
sures. Health-promoting interventions such as
Reduction in Cardiovascular Fitness smoking cessation, physical exercise, dietary
modification, stress management, and regular
There are several causes for fitness to decline health check-ups are obviously important for
following SCI. Patients are immobilized by rehabilitation and long-term follow-up of per-
paresis and many become overweight. Calorie sons with SCI.
expenditure decreases and persons with SCI From a diagnostic point of view, patients with
especially tetraplegicsexperience a decline in a lesion level at or above T5T6 pose a special
muscle and bone mass, while their body fat problem, since the sensory loss in these cases
increases relatively or absolutely. Depending may mask the pain of angina pectoris and
on level of injury, the basic energy requirement myocardial infarction.
222 SPINAL CORD INJURY
Respiratory function may be further compro- (see Chapter 30), respiratory function should be
mised by SCI due to spasticity in the trunk mus- reassessed by spirometry and similar tests.
cles, spinal deformity such as kyphoscoliosis,
chronic constipation, and side effects of various
Pneumonia
drugs that may depress respiratory function.
Three major complications may result from Pneumonia remains an important cause of
impaired respiratory muscle function: death in tetraplegia. Patients with tetraplegia
or high paraplegia are at increased risk of infec-
tion due to paresis of the diaphragm and/or
Chronic ventilatory insufficiency/hypoven- intercostal muscles, which impairs the ability
tilation to dispose of secretions. Tracheostomy or endo-
Impaired ability to cough with risk of tracheal intubation further increases the risk of
choking, stagnation of secretions, and infection. The risk of aspiration pneumonia is
atelectasis also increased, especially in the acute phase,
Lower respiratory infections and pneumonia, with decreased level of consciousness, gastro-
that may lead to an acute and serious aggra- paresis, and paralytic ileus. Patients with high
vation of ventilatory insufficiency SCI should be immunized against pneumo-
coccal infection and influenza.
The clinical picture of pneumonia may
be atypical in high tetraplegia. Sensation of
Patients with high SCI should routinely be pain from the thorax may be absent. The ability
assessed for ventilatory function while under to cough may be weak or absent due to wea-
emergency care and during the early rehabilita- kened respiratory muscles. Dominant vagal
tion phase. These patients should be strongly tone in the acute phase leads to an increase in
advised not to smoke. In cases of esablished mucous secretions within the airways. The clin-
hypoventilation, the patient should be provided ical picture is characterized by malaise, fever,
respiratory support such as continuous positive tachypnea, and tachycardia, as well as elevated
airway pressure (CPAP; see Sleep Apnea, in indicators of infection in the blood, hypoxemia,
Chapter 28) or should be placed on a ventilator. and pulmonary infiltrates on chest x-ray. Among
During long-term follow-up, and especially in the differential diagnoses, it is especially impor-
the case of progressive neurologic deterioration tant to always consider pulmonary embolism.
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25 Gastrointestinal Problems
Gastrointestinal problems following SCI fall into addition to direct neurologic reasons for this,
two main categories: (1) direct neurologic conse- problems may arise due to frequent use of the
quences of injury, such as changes in gastrointest- Valsalva maneuver (bearing down) or external
inal motility and loss of sphincter control; and (2) abdominal pressure during bowel evacuation,
indirect effects secondary to immobilization, life- as well as due to a greater proportion of time
style factors, medications, and the like. As has been spent in a reclining or semireclining position.
pointed out repeatedly in this book, diagnosis of In tetraplegia, retrosternal burning pain as a
gastrointestinal problems may often be obscured symptom of esophagitis may be absent. The
by the absence of nociception below the neurologic sole expression of this problem may then be a
level of injury. A strict bowel regimen with regular, recurring sour taste in the mouth due to acid
controlled emptying while avoiding leakage is of reflux and/or symptoms related to complicating
great significance for rehabilitation outcome and disorders, such as dysphagia (swallowing
quality of life. This chapter covers common con- difficulties) or bleeding. Treatment is similar
sequences and complications, as well as recom- as for the population at large. It is especially
mendations for bowel management programs for important to recommend cutting back on
patients with upper and lower motor neuron tobacco, caffeine, and alcohol; to have patients
injuries. sit up after meals; and to avoid eating right
before going to bed.
ORAL HYGIENE PROBLEMS
Gastroesophageal Reflux The risk of peptic ulcer is high during the acute
phase after SCI, in part due to the acute physio-
Patients with tetraplegia in particular are at logical and psychological stress, and in part to
increased risk of gastroesophageal reflux. In the frequent use of high-dose steroid treatment.
225
226 SPINAL CORD INJURY
Consequently, prophylactic treatment with chronic phase following SCI involve the colon.
proton-pump inhibitors or H2-blockers is often Its principal function is to reabsorb fluid.
recommended. During the chronic phase, long- Peristaltic contractions of the colon are coordi-
term use of nonsteroidal anti-inflammatory nated with respect to both segmental and for-
drugs (NSAIDs) is the main contributing factor ward-propelling waves. The intestines have a
to the risk of gastritis and/or ulcer. highly developed intrinsic nervous system,
known as the enteric nervous system, which is
Superior Mesenteric Artery Syndrome largely embedded in the intestinal wall and
consists of the Meissner plexus (submucosal
An uncommon but nevertheless noteworthy plexus), the Auerbach plexus (intramuscular
condition is superior mesenteric artery syndrome. plexus), and interneurons. Because the system
Here, the distal duodenum is intermittently is highly autonomous, colon physiology
compressed between the superior mesenteric remains partially intact following SCI.
artery and the aorta. The duodenum will then Normal defecation entails an interplay between
be strangulated between these two arterial struc- involuntary and voluntary activities. Involuntary
tures. Symptoms include epigastric fullness and activities include the gastrocolic reflex, which is
sometimes pain after food intake, followed by triggered by food intake. Giant migratory contrac-
nausea and vomiting. A sharp drop in weight, tions (GMCs) arise within the colon in response to
which is common in the early stages after SCI, a full stomach and propel the intestinal contents
predisposes for this syndrome. through the colon toward the rectum. The stool
distends the rectum and puborectalis muscle,
PANCREATITIS which causes the internal sphincter to relax.
This is called the rectoanal inhibitory reflex.
The risk of pancreatitis mainly increases in the Simultaneously, contraction of the external anal
early stages following SCI. Possibly, autonomic sphincter and the puborectalis muscle will retain
imbalance may lead to increased tone in the the feces (known as holding reflex).
sphincter of Oddi, resulting in congestion and The activities related to defecation include
inflammatory irritation. Signs of pancreatitis voluntary relaxation of the external anal sphincter
include anorexia, tachycardia, fever, arterial and puborectalis muscle and an increase of the
hypotension, and/or paralytic ileus. The diag- intraabdominal pressure through the Valsalva
nosis is confirmed by elevated serum amylase maneuver, which facilitates expulsion of feces.
and lipase, as well as signs of pancreatitis on SCI often interfere with the normal physiolo-
abdominal computed tomography (CT). gical process just described. The resulting
malfunction is referred to as neurogenic bowel
GALL BLADDER DISEASE dysfunction. The cardinal symptoms that charac-
terize this condition include constipation and
The incidence of gallstone formation and cholecys- incontinence. From a pathophysiological stand-
titis is also increased following SCI. Diagnosis point, one or more of the following phenomena
and treatment follow the usual guidelines. As play a role: absent sensory function, loss of
with other diseases in SCI patients, the pain voluntary sphincter control, flaccid or spastic
component will be masked when the source is sphincter paresis, impaired peristaltic activity
located below the neurologic level of injury. and coordination, and/or inadequate synchrony
between peristalsis and sphincter activity.
NEUROGENIC INTESTINAL PROBLEMS
Constipation
Pathophysiology
Constipation is the rule after SCI. Paralytic ileus is
For an overview of the innervation of the gastro- present during the acute phase and transiently
intestinal tract, see Figure 25.1A,B. Most of the leads to an inability to pass stool (this problem is
gastrointestinal problems that arise in the addressed in Chapter 7). Constipation may be
CHAPTER 25 GASTROINTESTINAL PROBLEMS 227
operationally defined as fewer than three bowel Lower motor neuron injuries occur as a result of
movements per week and/or incomplete evacua- lesions in the conus and/or cauda equina, leading
tion and/or chronic abdominal distension. to decreased tone within the descending colon and
According to this definition, about two-thirds of extinction of the peristaltic reflex. The time
all persons with SCI suffer from constipation in required for the intestinal contents to pass through
the chronic phase. The underlying pathophy- the gastrointestinal tract becomes prolonged, thus
siology differs between upper and lower motor too much liquid is resorbed from the feces, causing
neuron injuries. the stool to become hard. The external anal
Frontal cortex
Pons
L1-L2
S2-S4
Nervi
Nervus pelvici
hypogastricus
Nervus
pudendalis
Levator ani
External sphincter
Internal sphincter
Symp.
Parasymp.
Somatic
Sens.
A)
Figure 25.1 A: Nerve supply of digestive system. Schematic of the nerve supply to the distal portion of
the colon. As can be seen, both voluntary (somatic) and involuntary (autonomic) neural components are
present, which ensures functions such as continence.
228 SPINAL CORD INJURY
N. Vagus
Colon
Ganglion
celiacum
Auerbach's
Ganglion plexus
mesenterica
superior
Ganglion
mesenterica
inferior
Meissner's
plexus
Plexus
S2 - S4 hypogastricus
Preganglionic fiber
Postganglionic fiber
B)
Figure 25.1 B: Nerve supply to the colon. The vagal nerve (cranial nerve X) innervates the proximal portion of
the intestine. Also note the intestines intrinsic nerve supply from Meissner and Auerbach plexus.
Consequently, the prospects for preserved intestinal function remain despite SCI, although both incon-
tinence and constipation are common.
sphincter becomes totally or partially denervated Among the many possible underlying causes, diar-
and thereby flaccid, preventing both reflex and rhea as a side effect from treatment with broad
voluntary contraction, thus increasing the risk of spectrum antibiotics deserves special mention.
incontinence. Other factors contributing to incon- Such treatment is commonplace among SCI
tinence include paresis of the pelvic floor muscles patients mainly due to frequent urinary tract infec-
and decreased tone in the puborectalis muscle. tions. Long-term or recurrent antibiotics treatment
Spinal cord lesions above the level of the conus increases the risk of Clostridium difficile enteroco-
lead to upper motor neuron lesions. Such lesions litis. It is likewise important to consider the
will also prolong transit time through the colon, possibility of stercoral diarrhea, in which fecal
but in contrast to the situation seen in lower impaction in the form of a solid fecaloma irritates
motor neuron lesions, spasticity increases the the rectal wall, paradoxically causing diarrhea.
tone of both the colon wall and the external anal
sphincter. The net effect of overactive segmental WORKUP
peristalsis, underactive propulsive peristalsis,
overactive holding reflex, and spastic contraction In accordance with the particulars of the case, the
of the external anal sphincter is a clear tendency clinician should review diet, fluid intake, medica-
toward constipation. tions, and bowel regimen including bowel evacua-
tion technique, frequency, and duration, as well as
Diarrhea incontinence (when, how often, precipitating
factors, etc.). The situation should be assessed as
In addition to constipation, diarrhea may also to gain understanding of how the current bowel
cause severe problems, since continence by volun- regimen is working in relation to the patients
tary sphincter contraction is often lost in SCI. The lifestyle in general. Abdominal and digital rectal
risk of bowel incontinence is thus very high if the exam should be included in the physical examina-
stool becomes too loose for whatever reason. tion. Note should be taken of resting tone of the
CHAPTER 25 GASTROINTESTINAL PROBLEMS 229
anal sphincter and puborectalis, as well as the external anal sphincter tone is weak, stool
presence or absence of the anocutaneous reflex should be evacuated from the rectum one or
(i.e., contraction of the external anal sphincter in more times daily in order to prevent inconti-
response to stimulation of the perianal skin), nence. The patient must be taught to insert a
voluntary sphincter contraction, and the bulboca- finger into the rectum to manually remove
vernosus reflex (i.e., reflex contraction of the anal feces. Stool evacuation can be further facilitated
sphincter in response to compression of the glans through deep breathing, Valsalva maneuver,
penis or clitoris). contraction of abdominal muscles, and/or clock-
Depending on symptoms and physical find- wise abdominal massage through the abdominal
ings, various additional tests may be indicated, wall.
including fecal hemoglobin, stool culture, deter- In upper motor neuron lesions, the emphasis
mination of C. difficile toxin in the stool and is on activating reflexes. Bowel reflexes may be
presence of cysts, ova, and parasites. Blood tests stimulated through abdominal massage, suppo-
often include complete blood count (CBC), liver sitories, and/or enema combined with digital
function tests, serum amylase, and electrolytes. stretching and manipulation of the rectum.
Radiographic examinations to be considered One problem that may be encountered is anor-
include plain abdominal films, possibly ectal dyssynergy (i.e., paradoxical anal contrac-
including computed tomography (CT) and/or tion), which means that the external anal
magnetic resonance imaging (MRI). sphincter fails to relax as the rectum contracts.
However, the sphincter can be made to relax by
TREATMENT inserting one finger into the anus to decrease
resistance to evacuation. Such rectal stretching
After carrying out the relevant workup and ruling and stimulation also activates the rectoanal inhi-
out or correcting underlying pathology, emphasis bitory reflex, which relaxes the internal
should be placed on establishing a strict bowel sphincter, and activates the rectocolic reflex as
regimen. The purpose of this regimen is to well as the local intestinal peristalsis. Digital
eliminate incontinence, achieve effective bowel manipulation reportedly is most effective if
evacuation, and prevent secondary complications. stimulation occurs for about one minute and is
An overarching goal is to achieve regular bowel repeated every 510 minutes during the evacua-
evacuation at least three times a week. Regular, tion process. The bowel should be emptied daily
frequent, and complete evacuation of the bowel and at a minimum every 3 days.
reduces the risk of bowel leakage. Implementing Newer treatment options include pulsed irriga-
a good bowel regimen often requires a significant tion enhanced evacuation (PIEE). Functional elec-
educational, multidisciplinary effort. Practical trical stimulation of sacral roots (Chapter 26) can
dietary counseling should be provided, with also lead to improved bowel evacuation. In recent
emphasis on adequate fluid intake (23 liters/ years, surgical treatment has become more
day). Regular physical activity improves intestinal common. In addition to colostomy, we should
motility and should be encouraged. Microenemas also mention appendicocecostomy (Malone proce-
are often useful, but irritant laxatives should be dure) as an alternative treatment option, in
avoided if possible. which the appendix vermiformis is used to
In lower motor neuron lesions, spinal cord- create a connection between the abdominal wall
mediated reflexogenic intestinal peristalsis is and the proximal colon. By catheterizing this
reduced or absent. Therefore, bowel evacuation stoma, 200500 mL of isotonic saline solution
should be coordinated with meals in order to can be infused to flush the colon, thereby
take advantage of the gastrocolic reflex. Since providing an anterograde enema.
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26 Urogenital Sequelae Including Sexual Dysfunction
Up until the mid-twentieth century, renal failure Sympathetic innervation occurs via the hypo-
was one of the main causes of death among SCI gastric nerve, which originates in the T11L2
patients due to the adverse combination of recur- spinal cord segments and mainly supplies mus-
rent urinary tract infection (UTI), urolithiasis, cles in the bladder neck and proximal urethra.
elevated pressure in the urinary tract, and urinary Sympathetic activation chiefly supports the
reflux. Chronically infected pressure ulcers also reservoir function of the bladder by increasing
contributed to renal failure through the develop- the degree of contraction in the bladder neck
ment of amyloidosis. Fortunately, antibiotics, muscles.
improved bladder management programs, and Somatic innervation, which comes from the
regular monitoring have substantially reduced pudendal nerve and originates from the S2S4
both mortality and morbidity. spinal cord segments, innervates the external
In addition to the medical risks associated striated-muscle sphincter. The somatic nervous
with urologic dysfunction following SCI, incon- system also mainly supports the reservoir func-
tinence comprises an important psychosocial tion of the bladder by increasing flow resistance
problem. Neurourology thus continues to play a through the urethra.
central role in the short- and long-term manage- Sensory innervation, which is chiefly acti-
ment of SCI patients. vated by stretching of the bladder wall by bladder
fullness, is mediated via the pelvic nerve, while
PHYSIOLOGY OF MICTURITION pain and temperature stimuli from the bladder
mucosa are mainly conveyed through sensory
The urinary bladder acts as a reservoir for urine, fibers within the hypogastric nerve.
which is produced by the kidneys, then flows Voluntary control of the detrusor is initiated
through the ureters to reach the bladder. The by impulses from the frontal cortex, which are
ureters run obliquely through the bladder wall, conveyed through the pons and the reticulosp-
which reduces the risk of reflux (backflow). As inal tract. The frontal cortex is also directly
the bladder empties, the urine passes through connected to the pudendal nucleus by the corti-
the urethra. This flow of urine is blocked by cospinal tract, and impulses through this
two sphincters: an internal smooth muscle and system support voluntary control of the external
an external striated muscle sphincter. The lower urethral sphincter. Supraspinal control of mic-
urinary tract has both autonomic (involuntary) turition is mainly inhibitory.
innervation from parasympathetic and sympa- When a certain threshold bladder pressure
thetic nerves, as well as somatic (voluntary) is reached, corresponding to a certain bladder
innervation. volume, continence is ensured by an increase
Parasympathetic innervation is conveyed in sympathetic activation that results in contrac-
via the pelvic nerves, which originate from the tion of the internal urethral sphincter. To further
S2S4 segments of the spinal cord (Fig. 26.1). ensure continence, contraction of the external
Parasympathetic activation leads to contraction urethral sphincter increases as a result of
of the bladder muscle (detrusor) and results in both voluntary and reflex activity. When it is
bladder emptying. time for micturition, voluntary relaxation of the
231
232 SPINAL CORD INJURY
Frontal cortex
Pons
Th 11-12
S2-S4
Nervus
hypogastricus
Nervi
pelvici
Symp.
Parasymp.
Somatic
Sens.
Figure 26.1 Schematic of nerve supply to the lower urinary tract. As shown, both voluntary (somatic) and
involuntary (autonomic) neural components are involved.
external urethral sphincter reduces resistance A micturition center located in the pons is
to urinary flow. Sympathetic activity decreases, responsible for synchronizing bladder contrac-
which results in relaxation of the bladder neck, tion and sphincter relaxation, provided that the
while increased parasympathetic activity leads to neural pathways between this pontine center and
bladder contraction. the sacral cord are intact.
CHAPTER 26 UROGENITAL SEQUELAE INCLUDING SEXUAL DYSFUNCTION 233
Rhizotomy
Dorsal root
Ventral root
Electrodes
Abdominal
wall
creation of an artificial bladder, e.g., from a part significant part of the effect of the procedure is
of intestine, with a urostomy on the abdominal thus due to the conversion of a spastic bladder
wall (Fig. 26.7). Please refer to the literature for into a flaccid one by rhizotomy. The electrical
further details. stimulation as such causes micturition through
so-called post stimulus voiding. The mechanism
Sacral Root Stimulation involves stimulation that initially produces
concomitant contraction of the sphincter and
This method is based on electrical stimulation detrusor, after which, as electrical stimulation
of the ventral sacral nerve roots to empty the ceases, the external sphincter relaxes earlier
bladder. The electrodes are surgically placed on than the bladder, and urine is discharged.
the ventral roots, and the dorsal sacral roots are
usually severed (rhizotomy; Fig. 26.8). Rhizotomy, DETRUSORSPHINCTER DYSSYNERGIA
as such leads to a deafferentation of the bladder,
which will abolish reflex incontinence, while Physiologically, the activity of the detrusor and
increasing bladder capacity (bladder volume) and the urethral sphincter is coordinated, so that
bladder compliance. micturition takes place in the presence of low
Rhizotomy unfortunately also extinguishes intravesical pressure. Inadequate coordination
reflex erection and ejaculation, as well as any results in simultaneous contraction of the
remaining sensation in the perineal region. A detrusor and sphincter, accompanied by an
CHAPTER 26 UROGENITAL SEQUELAE INCLUDING SEXUAL DYSFUNCTION 237
increase in intravesical pressure. This condition complexity is the frequent presence of asympto-
arises in the presence of suprasacral SCI; in matic bacteriuria in patients with SCI. Presence
other words, with upper motor neuron lesions of pyuria (i.e., white blood cells in the urine)
and a spastic bladder. Detrusorsphincter dyssy- indicates mucosal involvement and increases
nergia produces high intravesical pressure the probability that the bacteriuria reflects a clini-
during micturition, as well as increased residual cally significant infection. However, pyuria may
urine, and therefore predisposes for infection, also occur in various noninfectious conditions
vesicoureteral reflux, hydronephrosis, and renal such as stone formation and catheter-induced
damage. Choice of method for emptying the trauma of the mucous membranes.
bladder influences the consequences of the con-
dition. For example, intermittent catheterization
will eliminate the pressure consequences of A common definition of symptomatic UTI
detrusorsphincter dyssynergia in conjunction in SCI patients is bacteriuria with >105 CFU/mL,
with micturition, in contrast to the situation pyuria, fever, and one or more of the following
with reflex voiding/tapping. symptoms: suprapubic tenderness or flank
tenderness, bladder spasm, changes in
The fact that the dyssynergia in itself is often
micturition pattern, increased spasticity, and/
asymptomatic, while at the same time is an
or increased dysreflexia (in the absence of
important pathogenic factor for urinary tract other causes). The presence of high fever,
complications is a strong argument for per- chills, and pronounced malaise suggests
forming routine neurourological workup in involvement of the upper urinary tract, i.e.,
SCI rehabilitation and follow-up. pyelonephritis or urosepsis.
The purpose of pharmacological treatment
of detrusorsphincter dyssynergia is to reduce
detrusor pressure. This can be achieved with Selection of antibiotics for treatment of sympto-
anticholinergics, such as oxybutynin (DitropanR). matic UTI should preferably be based on prior
In addition, a-blockers such as prazosin urine culture. In some cases, treatment must
(MinipressR, VasoflexR, HypoaseR) may reduce be initiated based on clinical experience while
outflow resistance. awaiting test results. Most UTIs in patients with
The goal of surgical treatment is to reduce SCI are caused by bacteria from the intestinal
outflow resistance by transurethral sphincter- flora, primarily gram-negatives and enterococci.
otomy or insertion of a urethral stent. Another Antibiotics are usually not indicated in case of
treatment option is rhizotomy of the dorsal sacral asymptomatic bacteriuria. An exception is made
roots (see Sacral Root Stimulation). Surgical for patients infected with urea-splitting organ-
treatment is rarely used today. isms such as Proteus mirabilis, which predisposes
for the formation of struvite stones (see next sec-
URINARY TRACT INFECTION tion). Another exception is made for pregnancy,
wherein bacteriuria predisposes for prematurity.
UTI is the most common type of infection In patients with therapy-resistant or fre-
among SCI patients. Inefficient emptying of quently recurring UTI, the urinary tract should
the bladder, leaving residual urine, and bacteria be worked up for anatomical abnormalities such
being introduced by catheterization constitute as abscess, urolithiasis, obstruction, or strictures,
specific risk factors. UTI symptomatology may as well as for occurrence of functional disorders
differ in SCI patients compared with the popula- such as vesicoureteral reflux and/or high resi-
tion at large. Classic symptoms such as dysuria dual post-voiding urine volumes in the bladder.
(i.e., painful urination), painful urgency, and
suprapubic or flank pain will be absent in patients UROLITHIASIS
with sensory deficits. In these patients, UTI
instead commonly manifests through fever, Urolithiasis (urinary tract stones) is signifi-
autonomic dysreflexia, increased spasticity, cantly more common in SCI patients than in
and/or incontinence. Adding to the diagnostic the population at large. As in the general
238 SPINAL CORD INJURY
population, the incidence of urolithiasis is and/or ultrasound can demonstrate stone size,
higher among men. SCI is followed by two location, and possible obstruction.
phases during which formation of stones is par- From a treatment standpoint, a distinction is
ticularly common. The first phase occurs from sometimes made between medical and sur-
about 12 months to about 12 years after injury. gical stones. Medical stones occur without con-
It is typically associated with formation of cal- current signs of infection, obstruction, or
cium stones. Such stone formation relates to the progressive renal impairment, and show no ten-
recent onset of paralysis and immobilization, dency for growth as demonstrated on repeated
which causes demineralization of bone and x-ray examinations.
thus increased metabolism and excretion of Surgical stones are stones that gradually
calcium. A second phase of stone formation typi- increase in size on repeated x-ray examinations,
cally occurs about 1015 years after injury, and and/or result in obstruction, macroscopic hema-
relates to deterioration of bladder function with turia, recurrent UTI, pain, and/or progressive
urinary obstruction, high residual volumes, high renal failure. UTIs associated with obstructive
intravesical micturition pressure, vesicoureteral urolithiasis are to be considered emergent and
reflux, and/or recurrent UTI. This stage is asso- require surgical intervention, primarily to
ciated with struvite stones. These stones are remove the obstruction. This may be accom-
strongly correlated with UTI with urease-produ- plished through percutaneous nephrostomy.
cing bacteria, such as Proteus, Pseudomonas, Once flow is reestablished and the infection
Klebsiella, and E. coli. Such bacteria cause alkali- adequately treated with antibiotics, stones may
nization of the urine, usually to a pH >7.2. In be removed by endoscopic extraction, percuta-
this alkaline environment, in which UTI also neous nephrostolithotomy, or lithotripsy (extra-
leads to mucosal damage and inflammatory exu- corporeal shock wave lithotripsy, ESWL). Open
date, a vicious circle with accelerating stone surgery is seldom needed.
formation easily arises. Moreover, matrix stones,
consisting of mucosal debris with low crystal- RENAL FAILURE
line content occur more often in patients with
recurrent UTI caused by urease-producing Several factors predispose to renal failure in SCI
microorganisms. patients. They include diminished renal perfu-
Stone classification can also be based on the sion, urinary flow obstruction, vesicoureteral
appearance and/or location of the stones. For reflux, urinary tract infections, urolithiasis, and
example, stones known as staghorn calculi can urosepsis. In earlier times the leading cause of
follow and fill up the anatomy of the renal death, renal failure has now become a relatively
pelvis. These are typically struvite stones. Stones rare complication thanks to improved urological
in the bladder are also usually composed of stru- management.
vite and may constitute a treatment-resistant Acute renal failure in SCI patients mainly
haven for bacteria that may also predispose to occurs during the acute post-injury phase, as a
stone formation in the upper urinary tract. consequence of neurogenic, hemorrhagic, or
A classic symptom of urinary tract obstruc- septic shock. The toxic effects of medications or
tion due to stones is pain, which, however, may rhabdomyolysis associated with massive soft-
be absent in SCI patients. Other symptoms of tissue trauma may also result in renal failure.
stones in the urinary tract include fever, nausea, Pathophysiologically, acute renal failure is classi-
vomiting, tachycardia, tachypnea, palpatory ten- fied as prerenal, renal, or postrenal (obstructive).
derness over the abdomen and flank, and/or In chronic SCI, acute renal failure is pri-
frequent recurrent or treatment-resistant UTI. marily caused by urinary tract obstruction due
Laboratory workup includes electrolytes, to stone formation.
urea, creatinine, cystatin, complete blood count, Chronic renal failure is no longer a leading
urine sediment, and urine culture. Radiologic cause of death following SCI, but still poses
workup with plain abdominal films, pyelo- a potential threat and is an important reason
graphy, spiral computed tomography (CT), for providing lifelong medical follow-up.
CHAPTER 26 UROGENITAL SEQUELAE INCLUDING SEXUAL DYSFUNCTION 239
Underlying factors include chronic pyelone- artery and its branches. There are three venous
phritis, urolithiasis with obstructive nephro- systems: superficial, intermediate, and deep.
pathy, vesicoureteral reflux, and hypertension Erection arises by means of afferent input
with nephrosclerosis. Amyloidosis (increased from widely differing sources such as the imagi-
deposition of protein in renal tissue that nation, emotions, memories, smells, visual
impairs kidney function) secondary to chronic impressions, and somatosensory stimuli. These
infections also occurs. Laboratory findings may diverse impulses are integrated within the
include elevated urea and serum creatinine hypothalamus. Efferent pathways pass through
levels (even though serum creatinine may be the mesencephalon and brainstem down to the
unreliable due to decreased muscle mass in spinal cord level. The brainstem mainly plays an
individuals with SCI), decreased creatinine inhibitory role with respect to spinal sexual
clearance, anemia due to low erythropoietin reflexes.
levels, platelet dysfunction with bleeding ten- The penis is innervated by three systems: the
dency, and secondary hyperparathyroidism. sacral parasympathetic (pelvic nerve), the thora-
Clinical symptoms of overt chronic renal insuf- columbar sympathetic (hypogastric nerve and
ficiency include disruption of higher cerebral lumbar portion of the sympathetic trunk), and
functions, peripheral neuropathy, fluid reten- the somatic (pudendal nerve; Fig. 26.9). The
tion, uremic pericarditis, and osteomalacia. autonomic interaction involved in the erectile
For a detailed discussion please refer to specia- process is complex. However, the dominant
lized literature. autonomic influence in this process is parasym-
pathetic. Nitric oxide (NO) is the most important
SEXUALITY AND FERTILITY PROBLEMS neurotransmitter for erection. The mode of
IN MEN actions of androgens also involves the nitric
oxide system.
Very few areas in the realm of SCI care have There are two main types of erection: psycho-
undergone such positive developments as the genic and reflexogenic. These are mediated in part
opportunities for the treatment of sexual disor- through different pathways. Erection occurs
ders and infertility. From the previous state of through relaxation of the smooth muscles of
virtual neglect, this field is now recognized for the penile vessels, which facilitates filling the
the great importance it deserves, while at the erectile tissues with blood, thereby leading to
same time therapeutic options have substantially an increase in size and rigidity of the penis,
improved. which in turn increases venous occlusion that
Since 80% of traumatic SCI occurs in men, further enhances tumescence.
and since sexual function is also most affected in The male sexual climax includes two phases:
men, we will devote more space to the problems emission and ejaculation. Emission is sympatheti-
faced by men with SCI. For the equivalent dis- cally mediated by the hypogastric nerve. In
cussion about SCI in women, see Chapter 29. addition to the forward propulsion of sperm, this
phase includes stimulation of a-adrenergic recep-
Sexual Physiology and Anatomy tors to close the bladder neck and prevent retro-
grade ejaculation. During the ejaculation phase
The penis contains two dorsal tube-like cham- that follows, there is intermittent relaxation of the
bers, the corpora cavernosa, and a third narrower external urethral sphincter and spasmodic con-
ventral chamber, the corpus spongiosum. These tractions of the seminal vesicles, prostate, and
chambers contain sinusoids capable of being urethra, which discharges sperm. Propulsion is
filled with blood. A membrane known as the strengthened by involuntary rhythmic contrac-
tunica albuginea surrounds the corpora caver- tions of bulbospongiosus, ischiocavernosus,
nosa. All three chambers are also surrounded levator ani, and related muscles. Ejaculation
by what is known as Bucks fascia. The blood is followed by a refractory period of varying
supply to the penis comes from the internal length, during which time a second ejaculation
pudendal artery through the common penile is impossible.
240 SPINAL CORD INJURY
T11 - L2
Plexus L
hypo- S1 - S5
gastricus S
Urinary
bladder
Plexus
presacralis
Nervus
pudendalis
(motor)
Nervus
Pelvicus
Nervus
pudendalis
(sensory)
Figure 26.9 Innervation of male genitalia (left) and female genitalia (right). Note especially the thoraco-
lumbar sympathetic innervation and the sacral parasympathetic innervation. In addition to this, somatic
innervation occurs via the pudendal nerve. Overriding control from the brain and brainstem requires intact
spinal cord connections.
sexual issues in the context of the total with partner and social network, and other
situation, which includes self-perception, issues. It is also advisable to include the
bladder/bowel management, sensory function patients partner when discussing the various
(including erogenous zones), concomitant med- available treatment options, as well as ED and
ical problems, psychological status, relationship infertility.
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27 Pressure Ulcers
245
246 SPINAL CORD INJURY
MANAGEMENT
Grade 4
Grade 1 persisting erythema in intact skin
Grade 2 partial skin damage involving the Figure 27.1 Pressure ulcers. The sequence of illus-
epidermis, but not penetrating the dermis trations shows successively more extensive ulcera-
Grade 3 full skin thickness lesion pene- tion. Grade 1 is characterized by an erythema that
trating into subcutis fails to blanch. Grade 2 involves a superficial ulcer.
Grade 4 also involvement of muscles, Grade 3 entails a full skin lesion penetrating into
connective tissue, joint capsules and/or subcutaneous tissue, and grade 4 also involves
underlying bone (Fig. 27.1). deeper tissues.
CHAPTER 27 PRESSURE ULCERS 247
Necrotic tissue must be removed because it pre- almost 100% sensitive for osteomyelitis, but
vents the wound from healing, hinders assess- unfortunately have low specificity. The purpose
ment of the wound bed, and serves as a substrate of a bone scan in this context is therefore mainly
for bacterial growth. Debridement may be sharp/ to rule out rather than to confirm the diagnosis.
surgical, mechanical (scrubbing or wound Treatment of infected pressure ulcers
irrigation), enzymatic, or autolytic. Autolytic includes local wound care and antibiotics.
debridement is facilitated by occlusive banda- Severe cases require more extensive surgical deb-
ging, which permits endogenous body enzymes ridement of necrotic tissue and sometimes mus-
to break down necrotic tissue. However, the culocutaneous flap surgery. In cases of chronic
latter method is inappropriate during active osteomyelitis, treatment with antibiotics often
wound infection. Once the ulcer is clean, a must be continued for several months.
several treatment options are available (please Unsatisfactory therapeutic response may be due
refer to the literature for more detailed descrip- to improper selection of antibiotics, deep-seated
tions). A number of more or less experimental infection, and/or fistula communicating with
methods are also available, including electrical the urinary or gastrointestinal tract.
stimulation, growth factors, hyperbaric oxygen, Typically, surgical treatment should be
electromagnetic field, therapeutic ultrasound, preceded by attempts at conservative treatment
and vacuum treatment. in accordance with the methods previously
It is commonplace for pressure ulcers to described. However, grade 4 ulcers rarely heal
become infected. Many pressure ulcers are without surgical treatment. This also applies to
located near the anus or urethral meatus, which ulcers complicated by fistulae, underlying osteo-
greatly increases the risk of bacterial contamina- myelitis, or pyarthrosis, and to ulcers with signifi-
tion. Local signs of infection include fever, cant undermining in the subcutaneous tissue
erythema, edema, induration, foul odor, and plane. Surgical treatment includes debridement
increased secretion, while laboratory tests show of all devitalized or necrotic tissue. Surgery for
elevated ESR, C-reactive protein, and white blood pressure ulcers is typically planned so that the
count. Common pathogens include gram-posi- skin flap will be sufficiently large to be used
tive cocci, especially Staphylococcus aureus and again, should the situation so require. If possible
streptococci, gram-negative bacteria such as the surgical scar should be positioned outside the
Pseudomonas aeruginosa, and anaerobes, mainly area that comes under direct pressure. Bony pro-
Bacteroides species. Ulcers that on superficial minences may be reduced through partial osteo-
inspection appear to be healed may harbor resi- tomies and through padding with soft tissue
dual infectious foci deep within the tissue. In (usually muscle). Musculocutaneous flaps are
such cases diagnosis may be verified with bone usually the procedure of choice since they have a
scan and/or computed tomography (CT). In richer blood supply than other types of flaps and
some cases, a deep focus of infection may man- provide sufficient bulk to reduce dead space and
ifest as a skin fistula. In such cases fistulography to pad bony prominences. Postoperative care
(contrast radiography) may be used to clarify the includes gradual mobilization, with careful mon-
anatomy of the fistula. In other cases, the infec- itoring of wound healing, as well as extensive
tion involves underlying bone tissue, causing patient education to involve the patient in actively
osteitis and/or osteomyelitis. Bone scans are preventing recurrence.
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28 Sleep Disturbances
Insomnia is common in the general population, resumes, the muscle tone of the pharynx again
and even more so among SCI patients. decreases and the process is repeated. Afflicted
Insomnia per se is, of course, not a diagnosis, patients often have dozens to hundreds of such
but a symptom. There are a number of treatable episodes of apnea each night. All this causes frag-
causes, and insomnia in persons with SCI mented sleep of poor quality. This condition often
should therefore always be carefully assessed results in daytime fatigue and poor performance,
before prescribing symptomatic treatment and may also lead to arterial hypertension and
with hypnotics. In this chapter we address the increase the risk of conditions such as stroke
most important underlying conditions that and myocardial infarction. The increased inci-
cause sleep disturbances. dence of obstructive sleep apnea syndrome asso-
ciated with SCI may be attributed to several risk
GENERAL CAUSES factors, including obesity, high consumption
of sedatives, and reduced lung capacity predis-
During the early stages following SCI, patients posing to collapse of the upper airways, as well
undergo a psychological crisis reaction, and the as to increased neck thickness regardless of
anxiety component may be prominent. Depressive body weight.
symptoms are equally common. Both anxiety The diagnosis should be suspected in the
and depression are highly likely to disrupt sleep. presence of loud snoring, frequent episodes
In addition, somatic factors may also have a nega- of apnea during sleep, morning headaches, and
tive impact. During the early phases following daytime fatigue. The diagnosis is confirmed by
trauma, patients must be turned every other polysomnography, which entails simultaneous
hour and the bladder must be catheterized every recording of air flow through nose and mouth,
46 hours. Pain and incontinence also frequently oxygen saturation, snoring, thoracic, abdominal,
disrupt sleep. and eye movements, electrocardiogram (EKG),
and electroencephalogram (EEG). Less complex
OBSTRUCTIVE SLEEP APNEA screening methods are also available.
Treatment of obstructive sleep apnea syndrome
Sleep apnea is overrepresented in SCI, especially includes weight loss and avoidance of alcohol
among persons with tetraplegia. It is also rela- and muscle relaxants. First-line treatment is with
tively common in the general population. continuous positive airway pressure (CPAP),
Pathogenetically, sleep is here associated with which is administered at night using a mask to
recurring obstruction of the airways in the cover the nose or the nose and mouth. Pharyngeal
pharynx, which results in snoring and inter- surgery may also come under consideration.
rupted breathing (apnea). Apnea is defined as
suspension of breathing lasting more than 10 seconds. INVOLUNTARY MOVEMENTS DURING SLEEP
Such periods result in hypoxia and carbon dioxide
retention, which lead to more superficial sleep or Spasticity is common following SCI and fre-
awakening and an associated increase in the quently leads to sleep disturbances. The patient
muscle tone of the pharynx, which then opens is chiefly awakened by frequent muscle spasms
the airways. Subsequently, when deeper sleep characterized by sudden flexion or extension of
249
250 SPINAL CORD INJURY
the extremities. In these cases, treatment with This structure controls functions such as mela-
baclofen at night may be advantageous, espe- tonin secretion via an efferent neural loop that
cially since its side effects may include drowsi- passes down through the cervical spinal cord,
ness. Clonazepam given at night is another where it reaches the superior cervical ganglion
treatment option. A relatively rare syndrome, from which it returns to the brain and innervates
periodic limb movements of sleep (PLMS), has the pineal body. Consequently, there exists an
also been reported following SCI. It has been anatomical basis for lesioning of this neural
linked to a dopamine deficiency in the central pathway in tetraplegia, and low basal melatonin
nervous system, and is characterized by stereo- levels and absence of normal physiological
typic repetitive movements during sleep. rhythm in melatonin secretion have in fact
been demonstrated in persons with high-level
DISRUPTION OF MELATONIN SECRETION SCI. Although the clinical significance has not
been established, the possibility of a SCI-spe-
The sleepwake cycle is mainly regulated by the cific underlying reason for sleep disturbance
suprachiasmatic nucleus in the hypothalamus. has thus been suggested.
29 Women with Spinal Cord Injury
Only about 20% of patients with traumatic SCI precaution with respect to decreased sensation
are women. This is one of the reasons that most in the genital area.
studies carried out to date have focused on men. Pregnancy in women with SCI should be
Gender distribution in nontraumatic spinal cord monitored by a gynecologist. Pregnancy may be
lesions varies based on etiology, but is typically associated with increased problems with urinary
more even. This section addresses only such incontinence, urinary tract infections, impaired
aspects that are either unique to women with pulmonary function, dependent edema, consti-
SCI, or in which differences compared to men pation, pressure ulcers, and impaired mobility.
are significant. The patients current medications should be
reviewed regarding potential teratogenicity, for
FERTILITY AND SEXUALITY example, benzodiazepines, carbamazepine, tet-
racyclines, and anti-inflammatories.
Following acute SCI, women often experience a Vaginal delivery is usually the method of
temporary loss of menstrual periods, amenorrhea. choice in women with SCI, except in cases in
Transient hyperprolactinemia with or without galac- which conventional obstetrical contraindications
torrhea (i.e., milk production in the mammary apply. However, possible musculoskeletal obsta-
glands) may often occur. Menstruation usually cles such as severe spasticity, heterotopic ossifi-
resumes within 36 months of injury, accompa- cation, and hip joint contractures must be ruled
nied by a return to normal fertility. This is in sharp out. Autonomic dysreflexia is the most common
contrast to the situation for men with SCI, where delivery-related complication among women
infertility remains a significant problem. with a lesion level above T6. Differential diag-
Dysmenorrhea may manifest through auto- nosis must take into account conditions such as
nomic dysreflexia, increased spasticity, and/or preeclampsia. Autonomic dysreflexia in con-
urinary urgency and frequency. The symptoms junction with labor can be avoided with epidural
may be alleviated with anti-inflammatory anesthesia.
medications.
Sexual function may be adversely affected by INCONTINENCE
impaired sensation, decreased vaginal lubrica-
tion, incontinence, autonomic dysreflexia, and Incontinence problems are for anatomical rea-
positioning problems due to spasticity, hetero- sons more common among women, while
topic ossification, and/or contractures. In all detrusorsphincter dyssynergia and high intra-
other aspects, sexual counseling for women vesical pressure are less common. Urinary diver-
with SCI entails the same holistic approach as sion surgery is considered more often in women,
for men. Because of the increased tendency for since a condom catheter of course cannot be
venous thromboembolism following SCI, cau- used to provide incontinence protection.
tion should be exercised in prescribing oral con-
traceptives, especially during the first year post MENOPAUSE
injury, among smokers, and in persons with a
history of thrombotic disease. Intrauterine Menopause in women with SCI is associated
devices and diaphragms also require special with symptoms similar to those experienced by
251
252 SPINAL CORD INJURY
women in general. However, it should be kept increased risk of pressure ulcers and urological
in mind that menopause-related osteoporosis problems. No studies are available to provide
will compound SCI-related osteoporosis, which definite guidance as to whether hormone repla-
results in a significant increase in the risk of cement therapy is more or less indicated in this
fracture. Changes in the skin and mucous mem- patient population compared with the popula-
branes related to menopause may lead to an tion at large.
30 Rehabilitative Neurosurgery
Neurological deterioration following SCI may Plate section). Persistent compression of the
result in minor additional disability or, in worst spinal cord due to displaced bony fragments is
cases, in dramatic loss of motor-, sensory-, and yet another cause of PPM (Fig. 30.2). Patients
autonomic function above, at and below the with PPM either suffer from a progressive post-
original level of lesion. The losses of function traumatic noncystic myelopathy (PPNCM) or a
following SCI are not static. Heterotrophic ossifi- progressive posttraumatic cystic myelopathy
cation, bladder and bowel disturbances, pressure (PPCM). The onset of symptoms related to
ulcers, and other common causes of functional PPM can range from months to decades post
impairment have been described in previous injury. However, other causes with symptoms
chapters. Additionally, consequences related to similar to PPM (see Chapter 19) also must be
the spinal cord proper have, during the latest excluded.
decades, received increased attention. Deteriora- The prevalence of developing PPM is
tion of motor- and/or sensory function, increased 3% and increases with severity of the initial
spasticity, and pain may further reduce quality of injury.
life. Improved diagnostic tools such as magnetic
resonance imaging (MRI) and surgical techni- Pathophysiology
ques have resulted in several new treatment
options. Here, we discuss troublesome pain, spas- The pathophysiological mechanisms behind
ticity, and posttraumatic myelopathy including PPM are not fully understood except in cases
the surgical viewpoint (Table 30.1). with bony compression. There is agreement
about the role of scar tissue tethering the
POSTTRAUMATIC MYELOPATHY spinal cord to the surrounding tissues, such as
the arachnoid (see Fig. 30.1D; also see same
Posttraumatic myelopathy (i.e., posttraumatic figure in Color Plate section). The extension
progressive neurological deficit related to the of scar tissue increases with injury severity.
spinal cord itself) is reflected in the occurrence The spinal cord is glued to the inside of the
of new symptoms added to the initial neurolo- dural sac via the scar tissue, and the flow of
gical deficits that arose in connection with the cerebrospinal fluid (CSF) in the subarachnoid
initial trauma. A characteristic feature is the pro- space is thus blocked. The presence of scar
gressive nature of these symptoms over time. tissue is the crucial mechanism behind forma-
Thus, the condition is usually referred to tion of both cranially and caudally located intra-
as progressive posttraumatic myelopathy (PPM). medullary cysts. A widening of the central
The spinal cord is typically subject to a persistent canal is probably the cause of syringomyelia
mechanical compression following trauma. below the level of lesion, whereas cyst forma-
Arachnoiditis (i.e., scar formation of the ara- tion cranial to the level of injury probably starts
chnoid caused by inflammation in the acute as a liquefaction of contused nervous tissue in
stage of injury) is the most frequent underlying the posterior part of the gray matter (see
cause of PPM. MRI may or may not visualize Chapter 3).
scar tissue and/or intramedullary cyst formation The scar tissue causes expansion of an
(Fig. 30.1AD; also see Fig. 30.1D in the Color initial microcyst at the level of injury to an
253
254 SPINAL CORD INJURY
expansile cyst ranging up to many decimeters In those cases, the character of symptoms resem-
caudally and cranially, potentially occupying bles those seen after spinal cord infarction. The
a major area of the spinal cord diameter seven cardinal symptoms of PPM are presented
(Fig. 30.1C). It is, as mentioned earlier, in Table 30.2. The frequency of symptoms listed
assumed that posttraumatic cysts above the in this table reflects those of a surgical clientele.
level of injury are not extensions of the central Two to four of the seven symptoms occurred
canal. Normal levels of proteins in cranially among 75% of the patients. Three symptoms
located cysts and lack of uptake of contrast were the most frequent number of manifesta-
agent following injection into the ventricular tions, at the time of the surgical procedure.
system further confirm this theory. Pain is usually presented in two forms (see
By contrast, it is speculated that tension in Chapter 21). The first type is described as
the vertebral column results in traction forces somatic pain (similar to sore muscles) localized
between the scar tissue and the spinal cord in at or above the level of injury and/or also below
patients with PPNCM (i.e., posttraumatic myelo- the injury site if the patient suffers from an
pathy without radiological signs of cyst forma- incomplete lesion. The second type is a neuro-
tion). Traction results in microtrauma to the pathic-type pain with a similar distribution.
spinal cord, and ischemia gradually spreads A progressive deterioration in motor function
caudally and cranially, resulting in symptoms occurs above the level of lesion in patients with
of posttraumatic myelopathy. complete lesions. A loss of hand function may be
the first motor sign in patients with thoracic level
Symptoms injuries. Patients with incomplete lesion may
display a similar pattern of motor loss above the
Clinical symptoms of PPM may begin several level of lesion but also additional loss of motor
decades following the injury. The symptoms function in the trunk muscles (manifested as
are typically slowly increasing, although a truncal instability when the person is sitting)
sudden onset of symptoms is sometimes seen. and lower extremities. An extreme case would
CHAPTER 30 REHABILITATIVE NEUROSURGERY 255
A) B)
C) D)
Figure 30.1 A collage showing spinal cord tethering and intramedullary cyst formation. A: Magnetic
resonance image (MRI)-obtained sagittal view. The upper arrow shows a minor cyst located intramedullary
(white structure compared to the gray color of the spinal cord). The lower arrow indicates posterior tethering
of the spinal cord to the surrounding arachnoid tissue at disk level of T23. The gray colored spinal cord is
retracted posteriorly in the spinal canal. B: MRI; corresponding axial view. The arrow marks the area of
tethering. The cerebrospinal fluid is absent precisely at 6 oclock indicating a adhesion of the spinal to the
surrounding tissue. C: An intramedullary cyst (arrow) occupying most of the spinal cord diameter.
D: Intraoperative illustration of scar formation surrounding the spinal cord. a, spinal cord; b, scar tissue;
c, dural sac. See also Color Plate Fig. 30.1D.
256 SPINAL CORD INJURY
TABLE 30.3 Preoperative investigations of PPM. TABLE 30.4. Indications for surgical treatment of
PPM.
Radiology
- MRI, CT, plain X-ray Significant progressive deterioration of motor and/
Neurophysiology or sensory function
- EMG, SEP, MEP Severe nociceptive-type (muscle soreness) pain
Functional tests starting months to years after injury
- Spasticity Severe neuropathic-type pain (onset >2 years after
- Neurological status injury)
ADL and quality of life The remaining four symptoms, if isolated
- FIM, COPM, SF-36 manifestations of PPM, constitutes no indication
for surgical treatment
MRI, magnetic resonance imaging;
CT, computed tomography;
EMG, electromyelography;
SEP, sensory evoked potential;
assisted dorsal root entry zone (CA-DREZ)
MEP, motor evoked potential;
FIM, Functional Independence Measure; lesion procedure is preferred (as discussed in a
COPM, Canadian Occupational Performance Measure; later section), if neuropathic pain starts in con-
SF-36, Short Form 36 Questions. nection with the primary spinal cord traumatic
event. The untethering procedure will be chosen
if symptoms of neuropathic pain starts 2 years or
neurological examination according to American later in relation to the trauma. This depends on
Spinal Injury Association (ASIA), an evaluation the type of underlying mechanism, see text
of the degree of spasticity, and finally an ADL ahead.
and a quality of life assessment. The final deci- There is usually no indication for surgical
sion is mainly based on the patients medical treatment if increased spasticity, autonomic dys-
history and on the results of the radiological reflexia, hyperhidrosis, or Horner syndrome pre-
investigation. The importance of the medical sent as isolated symptoms of PPM.
history cannot be overstated, because signs of The primary goal of surgical treatment is to
spinal cord tethering sometimes are absent on halt further progression of the pathophysiolo-
MRI. A false-negative MRI (i.e., one not showing gical process that is based on scar formation
scar formation) does not exclude the presence of and tethering of the spinal cord. The surgical
PPM. On the other hand, the presence of intra- goal is not to reverse symptoms, but rather to
medullary cysts does not, as such, indicate a need avoid further deterioration. A functional
for surgical intervention. improvement should be considered a bonus
result to the patient.
Surgical Treatment of PPM: Indications and
Goals Surgical Treatment of PPM: Technical
Considerations
Indications for the surgical treatment of PPM are
presented in Table 30.4. Clinical symptoms The aim of surgical treatment is to untether the
together with progressive signs of motor and spinal cord from surrounding tissues and to
sensory loss are the most common indication create an open space for the CSF to circulate in
for surgical treatment. Presence of a progressive the spinal subarachnoid space, thus also
muscular soreness-type pain, as well as neuro- allowing the spinal cord to move without restric-
pathic pain with a delayed onset in relation to the tions. The presence of intramedullary cysts, in
trauma, may likewise both indicate a need for addition to scar formation, will require a
surgical intervention. shunting procedure in order to reduce intrinsic
The choice of surgical method is based on the compression of the spinal cord. The patient is
onset of the neuropathic pain. The computer- initially placed in a prone position following the
258 SPINAL CORD INJURY
anesthetic procedure. The posterior approach As the cause of cyst formation (i.e., the scar tissue)
is suitable since most of the scar formation will has been removed, the insertion of a shunt catheter
be found in the posterior aspect of the intra- is not considered of the essence, and could actually
dural space. This is probably due to a posterior contribute to renewed scar formation.
accumulation of blood and inflammatory pro- Most of surgeons, however, choose to open the
ducts during the initial stage of injury, during midline of the spinal cord (i.e., myelotomy)
which the patient is typically lying in a supine (Fig. 30.5; also see same figure in Color Plate
position. section) and insert a cyst catheter, irrespective of
The surgical procedure starts with exposure the result of the previously performed ultrasono-
of the dura at the level of lesion and a few graphic investigation. The shunt catheter is then
segments above and below the level of lesion. inserted into the cyst and directed as cranially as
This exposure enables untethering of scar possible, after which the caudal part is implanted
tissue in both cranial and caudal directions. into the ventrolateral subarachnoid space at least
The presence of tethering/scar formation 68 cm below the level of tethering (Fig. 30.6; also
(see Fig. 30.1D, here and in Color Plate section see same figure in Color Plate section). The
and Fig. 30.3A,B), as well as intramedullary catheter is attached to the pia mater with unresorb-
cysts (Fig. 30.4) can be verified or excluded by able sutures to prevent shunt catheter migration. It
intraoperative ultrasonography. The dura is, is of extreme importance that the original dura is
after ultrasonographic investigation, opened in not closed. Instead, the original dura covering the
the midline and the spinal cord is now exposed. spinal cord is replaced by an artificial dural graft
The scar tissue is loosened from the surroun- (Fig. 30.7; also see same figure in Color Plate sec-
ding arachnoid/dura tissue, after which the tion). This prevents CSF leakage and reduces the
spinal cord should regain its physiological posi- risk for the spinal cord to reattach to the dura, a
tion in the spinal canal and no restrictions to condition known as retethering. The aim, once the
CSF flow remain at the level of lesion. Two dural graft is attached to the original dura, is to
options remain if an intramedullary cyst is pre- achieve a watertight seal between the two. A water-
sent: to perform a cyst shunting procedure or to tight attachment prevents leakage of CSF into the
leave the cyst untouched. An additional blood-containing (extra dural) space and prevents
intraoperative ultrasonography should be per- blood from sleeping into the intradural space. The
formed, according to Lee and coworkers, in risk of retethering increases if blood and CSF
order to visualize the cyst diameter after the once again mix inside of the dural graft. This
untethering procedure. According to these authors, may, after a period of good or excellent surgical
no cyst shunting is indicated if the cyst has collapsed outcome, result in a relapse of symptoms related to
by 50% or more compared to its preoperative size. new scar formation and PPM. A submuscular
b b a
A) B)
Figure 30.3 Scar formation. A: Intraoperative photo showing scar formation between the spinal cord and
dural sac (arrow). a, uninjured spinal cord; b, lesion level is characterized by its grayish color.
B: Intraoperative ultrasonography corresponding to the tethering (arrow) shown in Figure 30.3A. See also
Color Plate Fig. 30.3A.
CHAPTER 30 REHABILITATIVE NEUROSURGERY 259
Figure 30.4 Ultrasonography obtained previous to drainage tube, which remains in place until the
the opening of the dura. The single arrow points at second postoperative day, is inserted, after which
the intramedullary located cyst and the double the fascia, subcutaneous tissue, and skin are
arrow show the spinal cord diameter. The white closed. The patient is confined to bedrest until
structure at the tips of the double arrow marks the second postoperative day.
the outer border of the spinal cord. Mobilization starts cautiously on the second
postoperative day. During the entire postoperative
period, it is of greatest importance that patients be
turned regularly in order to avoid pressure ulcers.
The risk of retethering is also at least theoretically
reduced by this procedure, since regular turning
counteracts new formation of scar tissue at the
level of lesion. The time period of immobilization
in a given position during which any blood col-
lected between the dura and spinal cord may
organize into a scar is reduced by this turning
procedure. A postoperative MRI (Fig. 30.8) will
show a collabated cyst and that the spinal cord
has regained its normal diameter.
Figure 30.5 The spinal cord is exposed (midline
myelotomy). See also Color Plate Fig. 30.5. Surgical Treatment of PPM Caused by Persistent
Spinal Cord Compression
present for 6 months or more, and the success and postsynaptic neurons in the dorsal horns.
rate was further reduced to only a few percent if Focus has been directed to two opioid transmit-
symptoms had been present for 12 months or ters, namely the dynorphines and enkephalins.
more. Seventy-three percent of patients in a The opioid receptors are designated as m-, d-, or
study by Lee and coworkers exhibited good -receptors. Morphine exerts its analgesic effect
result, whereas 7% showed a further deteriora- mainly through the m-receptor, which is also the
tion. Improved motor function occurred in 56% target of endogenous opioids. The analgesic
of patients in the same study, and 46% of the effect of the opioids is achieved by the blocking
patients pre-operatively suffering from increased of the synaptic transmission between the pri-
spasticity improved as regards this symptom. An mary afferents and the postsynaptic neurons.
improved sensory function was seen in 45%, and The supraspinal inhibitory tracts are activated,
an improved walking ability was seen in 47% of and the transmission between the primary affer-
patients with incomplete lesions. The effect on ents and the postsynaptic neurons are reduced as
autonomic dysreflexia on the other hand, was a result of m-receptor activation.
poor. An implanted pump for intrathecal delivery
of morphine is an option for administrating
SURGICAL (INVASIVE) TREATMENT OF PAIN opioids in the treatment of neuropathic pain. A
catheter is initially placed intradurally in the CSF
Trauma to the spinal cord results in damage to space between the arachnoid and pia mater, after
the nociceptive neurons located in the posterior which the catheter is connected to an infusion
horns, and ectopic stimulation may be initiated pump placed in the abdominal layer of fat. The
from the dorsal root ganglia (for review, see amount of drug to be delivered is defined
Chapter 21). Impulses from C-fibers arise and through external presets, and drug refills are
wide-dynamic-range (WDR) neurons are performed using an insertion needle that pene-
further activated. A condition of hyperexcit- trates a central membrane in the infusion pump.
ability is initiated. A connection exists between Morphine is the drug most often used in the
hyperexcitability in the deafferentated nervous intrathecal treatment of neuropathic pain fol-
tissue located in the dorsal horns and the occur- lowing SCI. This treatment has previously
rence of spontaneous pain. Morphological been successful in the management of cancer-
changes, such as demyelinization and biochem- associated neuropathic pain. Its most prominent
ical alterations in the postsynaptic neurons advantage lies in the possibility of avoiding most
located in the dorsal horns, may also contribute side effects associated with systematically admi-
to the development of neuropathic pain. Physio- nistered morphine, since the intrathecally admi-
therapy and pharmacological treatment may nistered drug does not accumulate in brain
provide insufficient pain relief. In such cases, tissue. The therapeutic effect of 1 mg morphine
invasive therapies should be considered. delivered intrathecally corresponds to an oral
Surgical treatments of PPM have already been intake of 150 mg. An standard quantity of
discussed in this chapter; now, three additional intrathecally delivered morphine varies between
pain therapiesintrathecal administration of 1 and 20 mg during a 24-hour period, and the
morphine, spinal cord stimulation, and CA- effect is dose-dependent. The infusion pumps
DREZwill be presented. Unusual methods used are very safe and do not restrain patients
such as cordectomy, cordotomy, myelotomy, in their daily activities. The development of drug
and arachnoid grafting will not be presented in tolerance is the only real disadvantage and is
this chapter. reflected by the need for increasing doses of the
drug. Relatively high doses may be administered,
Intrathecal Morphine Administration (Spinal because it seems that tolerance develops more
Morphine Pump) rapidly if the drug is given as a continuos infu-
sion rather than on an as-needed basis. The
Various opioid transmitters and receptors have development of drug tolerance may be delayed
been localized among the presynaptic afferents by adding other drugs such as clonidine
262 SPINAL CORD INJURY
I
II
III
IV
V
VI
A) B)
Figure 30.11 Computer-assisted dorsal root entry zone (CA-DREZ) lesion. A: Preparation of the spinal cord
during the CA-DREZ lesioning procedure. a, dorsal root; b, dorsal root entry zone (DREZ); c, lesion
electrode. B: Placement of the lesion electrode during the CA-DREZ microcoagulation process.
electrical, burning, stabbing, or pins-and-nee- mapping, in which efforts are being made to
dles characterpreferably with segmental pro- localize body areas affected by neuropathic pain
jection at and below the level of injury. The onset and correlate these areas to a corresponding
of the pain should have been immediately fol- spinal cord segment(s). This is achieved by
lowing injury, and conservative treatment has simultaneous stimulation of the C-fibers (light
been proved not to offer any alleviation. CA- touch of the skin) and registration of the (hyper-)
DREZ is a method with great future potentials. activity in the DREZ during surgical procedures.
Of significant interest is the result of so-called The future goal is to create a map portraying each
CHAPTER 30 REHABILITATIVE NEUROSURGERY 265
spinal cord segment responsible for the neuro- method to alleviate severe spasticity. Baclofen,
pathic pain in different body areas, thus mini- a derivative of GABA, acts as an inhibitor of
mizing the lesion area to only those involved presynaptic spinal reflexes, and monosy-
segment(s). This is of great importance, since naptic, as well as polysynaptic, reflexes are
one of the side effects, added motor loss, may influenced by this drug. Baclofen has a lim-
occur following this type of surgery. The risk for ited penetration of the bloodbrain barrier,
added motor loss usually prevents lesions above and it is postulated to exert its inhibitory
the injury level of T5 since lesions five segments effect by binding to a brain and spinal cord
above T5 will potentially damage that part of the (central nervous system) GABA-B receptor.
spinal cord which supplies motor impulses for The effect of this is to slow down the signals
hand and arm movement. sent to the muscles, thus helping to reduce
stiffness and restore mobility. The possibility
Lesioning Using Laser Technique to achieve a high concentration of baclofen in
the CSF is the main advantage of intrathecal
The laser lesioning technique is still not fully devel- delivery. This is of great advantage, from the
oped. In this method, heat from a laser is directed anatomical point of view, since the distance to
to a specific area. Laser types such as carbon the GABA-B receptors located in Rexed
dioxide (CO2), argon, and neodymium: yttrium lamina II is short. The baclofen concentration
aluminum-garnet (Nd:YAG) have been used. Side at the thoracic spinal cord level is reduced to
effects, such as added motor loss on the lesioned approximately 50% if the drug is delivered at
side, have been reported in a high frequency of the lumbar level. The concentration is further
cases, probably depending on the imprecision of reduced to 25% of original lumbar concentra-
the heat-generating beam. The method is therefore tion at the cervical and intracranial levels. The
not used often in clinical practice. cerebral side effects associated with the oral
intake of the drug are thus practically elimi-
SURGICAL (INVASIVE) TREATMENTS FOR nated as a result of this reduced concentra-
SPASTICITY tion, gradients, which, of course, is a great
advantage.
Spasticity is, as previously mentioned, one A spastic increase in muscular tone causes
symptom of PPM, but spasticity as an isolated restriction of movement, pain, and/or impaired
symptom is not an indication for an untethering bladder function. These symptoms constitute
procedure. Two invasive treatments will be pre- the main indications for this type
sented in the following text that can be used in of intervention if oral intake of baclofen results
the management of spasticity if oval baclofen in therapeutic failure and/or unacceptable
and other conservative treatments fail to relieve side effects. The intrathecal administration of
the problem: intrathecal baclofen administration baclofen is also used to reduce spasticity among
(spinal baclofen pump) and percutaneous patients with multiple sclerosis.
thermal rhizotomy (PTR). (We refer readers to
literature of special interest for selective sensory Surgical Procedure
microrootlet section [SSMS].)
The placement of pumps for intrathecal admin-
Intrathecal Administration of Baclofen (Spinal istration of baclofen is a two-step procedure;
Baclofen Pump) In step 1, test doses of baclofen are admini-
strated intrathecally either through a spinal
Background and Indications catheter or lumbar puncture; 25 mg followed
by 50 mg are delivered as test doses, after
Implantation of the subcutaneously located which changes in spasticity, flexor automatisms,
infusion pump for intrathecal delivery of rigidity, and bladder function are evaluated.
baclofen is the most frequently used invasive The peak effect of the drug is reached 24 hours
266 SPINAL CORD INJURY
after administration, and the effect is practically symptoms occur, this can be achieved by cutting
gone after 6 hours. The patients are offered the catheter located between the pump and
Step 2 if a significant beneficial response is its entry into the spinal canal. It is, however,
demonstrated. more convenient to reduce or stop the infusion
In step 2, subcutaneously located pumps are using the external pump-regulating device.
implanted for continuous intrathecal delivery of Administration of 12 mg of physostigmine
baclofen. A spinal catheter is initially inserted and 1 mg of atropine, as well as lumbar puncture
into the subarachnoid space at the levels of to directly drain the drug from the intrathecal
L3L4 or L4L5, after which it is threaded cra- space, are additional measures to reverse an
nially up to the level of T10T12. The caudal part inadvertent intrathecal baclofen overdose. The
of the catheter is then directed subcutaneously to concentration of baclofen in the CSF is reduced
the abdominal region, usually below the left or significantly if 3040 mL of CSF are drained. In
right costal arc. The catheter is then connected to the long run, complications such as catheter dis-
the infusion pump, after which baclofen is continuity, orthostatic hypotension, erectile dys-
instilled into the pump reservoir. The placement function, and tolerance adaptation is seen. A
of the pump is usually in a suprafascial pocket, major disadvantage is the dependence on expen-
not more than 3 cm from the surface of the skin, sive equipment that requires monitoring, main-
as this will simplify the refilling procedure. The tenance, and refilling three to six times per year,
infusion pump is then started. as the maximal shelf life of the drug is 4 months.
The start dose during the first 24 hours is twice
as high as the lowest effective 24-hour test dose. Percutaneous Radiofrequency Thermal
The dose are gradually increased until spasticity Rhizotomy
and other symptoms reach an acceptable level. A
24-hour total dose of baclofen of about 200 mg is Percutaneous radiofrequency thermal rhi-
quite common. A concentration of 250 mg/L in the zotomy (PTR) is performed under local anaes-
CSF fluid is reached after administration of 200 mg thesia and could be summarized as a thermal
per 24 hours, compared to 24 mg/L after oral intake lesion to peripheral nerves. The indication for
of 60 mg. The purpose of the intrathecal adminis- this treatment is typically a severe increase of
tration is to limit rather than to eliminate spasticity.
A certain amount of muscular tone exerts a bene-
ficial effect on, for instance, the ability of the trunk
muscles to maintain a certain stability of the trunk.
Patients are observed in an intensive care unit
following the implantation of the pump. Side
effects of overdose may present with symptoms
such as tiredness, indolence, confusion, brady- L4
cardia, reduced blood pressure, unconsciousness
and, ultimately, respiratory arrest as the most
feared condition. The complications usually L5
occur in connection with administration of the
test doses, implantation and/or starting proce-
dure of the pump, or following changes of the
delivered doses of baclofen. Patients are there-
fore kept under observation for 24 hours fol-
lowing administration of the test doses and for
5 days following the implantation procedure.
Patients are also observed for 24 hours if the
test dose is corrected by 5% or more.
The pump must be turned off if signs of over-
dose (i.e., side effects) appear. If alarming Figure 30.12 Percutaneous rhizotomy.
CHAPTER 30 REHABILITATIVE NEUROSURGERY 267
269
270 SPINAL CORD INJURY
disease, hypertension, insulin resistance, muscu- consuming in part due to placement of elec-
loskeletal complications and obesity. trodes on the lower extremities. Furthermore,
As mentioned elsewhere, high-level SCI, in FES bicycles are expensive, and the exercise
particular, leads to pathophysiological cardiovas- method has not gained a significant foothold
cular changes that further limit aerobic capacity. outside the U.S.
Moreover, paralyzed muscles atrophy to a greater The father of modern SCI care, Ludwig
or lesser extent, which contributes to an unfavor- Guttmann, emphasized early on the importance
able body composition, insulin resistance, and of sports in the rehabilitation process because
associated adverse conditions. For many rea- of its therapeutic value for physical, psycholo-
sons, patients with SCI should become more gical, and social reasons. Many national and
physically active. international centers for SCI rehabilitation have
Arm cycling is a good exercise option for many designated recreational therapists (RTs) and/or
patients, especially to achieve cardiovascular fit- rehabilitation instructors. There is significant
ness. Since arm strength is also important for overlap and a blurred distinction between their
most patients with paraplegia and low tetra- work on the one hand and that of physical thera-
plegia, regular strength training should be added pists, occupational therapists, and social
to the program. A modified version of circuit workers. A variety of hobbies, leisure activities,
training, in which the patient goes from one sports, and athletic pursuits are available with
strength training station to the next without or without major or minor adaptations. Some
pausing, has proven to be particularly effective of the activities shown to be particularly
since it combines strength and cardiovascular appealing to persons with SCI include horseback
training. To prevent muscular imbalance, the riding, archery, wheelchair basketball, quad-
focus is mainly on strengthening the upper rugby (wheelchair rugby for people with tetra-
back and shoulder muscles, as well as on plegia), wheelchair tennis, kayaking, wheelchair
stretching the pectorals. The strength training marathons, and sailing. In the context of sports
and cardiovascular exercise programs for SCI for people with disabilities, athletes are classified
patients should be designed in cooperation with according to their neurological and functional
qualified healthcare personnel and be combined status. The purpose is to achieve the fairest
with other health-promoting initiatives, including grounds for competition possible by defining
diet modification, smoking cessation, and moder- persons with comparable degrees of disability.
ating alcohol consumption to achieve optimal
results. WHEELCHAIRS
Functional electrical stimulation (FES) has
been used mainly in the United States as a The most basic type of manual wheelchair is that
mode of exercise. Through electrical impulses, often seen in settings such as hospitals and air-
FES stimulates paralyzed muscles to contract, ports. These wheelchairs are solely intended for
which exercises them. Electrically induced short distances and must be pushed by an assis-
muscle activity leads to increased muscle mass tant. Such wheelchairs are not adapted uniquely
as long as the stimulation program continues. If to the individual, and because they are heavy and
electrical stimulation is used for leg cycling, cumbersome they are only useful for very short
especially combined with regular arm cycling, periods of assisted use.
cardiovascular benefit can also be achieved. This
approach has demonstrated regression of left Modern Manual Wheelchairs
ventricular atrophy and, thus, improved aerobic
capacity improved lower extremity circulation, The modern wheelchair, which is intended to be
improved body composition with more muscle an individually customized means of transport,
and less fat, decreased insulin resistance and, is lightweight, with a frame constructed of mate-
according to some studies, some degree of anti rials such as aluminum or titanium (Fig. 31.1).
osteoporosis effect. Naturally, such benefits pre- These wheelchairs are available in a variety of
sume continued, regular exercise, which is time- designs. Many are equipped with folding
CHAPTER 31 PARAMEDICAL REHABILITATION 271
(PAPAW). These wheelchairs are equipped with although vehicle adaptations are often necessary.
an electrical power assist which is activated when Such adaptations may involve measures to facil-
the patient applies torque to the wheels grip itate access to the vehicle and drivers seat,
rings. adjustments of controls to maneuver the vehicle,
Another recent mobility concept, similar to and modifications to ensure driver safety.
the wheelchair, is the IBOT Transporter. The Choice of vehicle is important. Especially in
IBOT is operated via a hand-controlled joystick. tetraplegia, a van or minivan is preferable because
It has two pairs of rear drive wheels and, thanks it offers more space for ramps, wheelchair lifts,
to built-in electronic stabilizers, the IBOT can and special adjustable drivers seats. Vehicle doors
perform tasks such as climbing stairs and balan- may be electronically equipped to open and close
cing on a single pair of wheels. Because of this if necessary. In regard to actual operation of the
latter feature, the wheelchair is able to rise up vehicle, hand controls for the accelerator, brake
on its rear wheels, thereby increasing the users and automatic transmission are often necessary to
reach in the vertical plane, making it possible to compensate for absent or impaired lower extre-
reach a book in a bookcase or dishes in a kitchen mity function. Thanks to devices such as steering
cabinet. However, the IBOT is heavy and expen- knobs, power steering, and/or joysticks or other
sive, and the stair-climbing feature requires controls for single-handed operation, even persons
either that the user has sufficient arm strength with significant physical disabilities can become
and function to support-pull on a railing or adequate drivers. With decreased truncal stability,
have an assistant. a conventional safety belt may need to be adapted
and/or expanded. A detailed description of the
Wheelchair Cushions often sophisticated and complex vehicle adapta-
tions is outside the scope of this book. The reader
Yet another crucial part of the wheelchair is the is referred to vehicle manufacturer and custo-
seat cushion. The most common fillings for mizing websites for more information.
cushions include foam, air, or viscoelastic fluids
(gel). Since users typically spend many hours a ORTHOSES
day sitting in the chair, the weight distribution
and pressure-relieving properties of its cushion Spinal Orthoses
are of great significance in preventing pressure
ulcers. However, no matter how state-of-the-art In the acute phase following traumatic injury to
the seat cushion, it can never replace the need the spine, various methods can be used to fix the
for meticulously fitting the wheelchair to the spinal column for purposes of transport and
users body measurements, nor can it replace initial management (see Chapters 6 and 15).
the need for repeated skin inspections, pressure After the acute phase, orthoses can be used to
relief, and other prophylactic measures to pre- provide additional stability and support.
vent pressure ulcers (see Chapter 27).
Orthoses for the Upper Extremities
DRIVING
Orthoses for the upper extremities are mainly
Automotive vehicles comprise the most impor- intended for use in tetraplegia. The purpose of
tant assistive devices in daily life, especially fol- orthotic support may be to prevent hyperexten-
lowing SCI. Even if public transport is a realistic sion of certain muscles, correct deformities, pre-
option for some, and even though transportation vent joint contractures, support the wrist and
services are often available, the possibility of hand in a functional position, support a weak
driving a car should always be considered. Most wrist or hand, support weak muscles, and/or
SCI patients with preserved sensorimotor inner- facilitate general function. Orthoses may be clas-
vation of the rotator cuff, and even more so those sified as static (i.e., those intended to maintain a
with partial or completely preserved upper extre- certain position) or dynamic (i.e., those intended
mity function, may be able to drive a car, to facilitate and/or stabilize certain joint
CHAPTER 31 PARAMEDICAL REHABILITATION 273
275
276 SPINAL CORD INJURY
Although successfully rehabilitated people who the general population, fasting lipids, resting
are left with para- or tetraplegia following SCI blood pressure, and fasting blood sugar should
are not actually ill, they do face a lifelong be obtained, and preferably an electrocardiogram
vulnerability to complications involving most (EKG).
organ systems. According to international Two-thirds of all SCI patients have some form
norms, persons with SCI should be offered of significant, chronic pain problem. The app-
follow-up at least annually at a specialized roach to these problems should not be tinted by
center. Whether such an annual recheck nihilism, especially not so as such problems do
focuses only on problems specific to SCI or have a strong detrimental effect on quality of life,
also includes age- and gender-related screening and many therapeutic strategies are available, as
measures may vary from one clinic to the next. discussed elsewhere this book.
Therefore it is of the essence that patients The same applies to significant spasticity.
clearly understand what their annual rechecks Increased spasticity during the chronic phase
actually cover, so that they are not lulled into a should always motivate a workup for underlying
false sense of security that everything is fine factors, such as posttraumatic myelopathy, infec-
in case the check-up is limited solely to those tion, or pressure ulcers.
problems specific to SCI. Regarding problems from muscles, joints, and
The primary purpose of regular follow-up bones, special mention should be given to the risk
for patients with SCI in the chronic phase is of overuse injuries in the shoulders and elsewhere
to prevent ill-health through proactive and in the upper extremities, as well as to osteoporosis
health-promoting measures and to enable related to paralysis and immobilization, which
early diagnosis and treatment of complications. predisposes for fractures.
Annual recheck should include a structured Heterotopic ossification, should it occur, typi-
checklist for review of common problems, as cally manifests itself early during the course of
well as a general physical and neurological rehabilitation. Diagnosis and treatment of het-
examination. erotopic ossification is discussed elsewhere in
this book.
MEDICAL ASPECTS Persons with tetraplegia seem to have some
degree of protection against arterial hypertension
Persons with tetraplegia or high paraplegia owing to the lower level of activity within the
should be offered immunization against the sympathetic nervous system caused by their
influenza virus and pneumococci. lesion. However, other risk factors for developing
Skin examination should look for signs of hypertension, such as physical inactivity and
pressure ulcers, with special attention to the obesity, are present to a greater extent, which
sacrum, ischial tuberosities, trochanter regions, especially increases the incidence of hypertension
and heels. Ulcers, if present, should be analyzed in persons with paraplegia. When the diagnosis
in the conventional manner. of hypertension is made, additional workup of
Since diabetes mellitus and low high-density underlying etiology (autonomic dysreflexia, renal
lipoprotein (HDL) cholesterol levels are more artery stenosis, renal failure, hyperaldosteronism,
common among individuals with SCI than in etc.) should be carried out. Important and
277
278 SPINAL CORD INJURY
frequently neglected interventions include assis- overweight and obesity are more common than
tance with smoking cessation and moderation underweight.
of alcohol consumption. Consequently, many No increased risk of colorectal cancer has been
clinicians routinely include questions on these demonstrated in relation to SCI, and the decision
issues in their annual rechecks. Pulmonary to include screening tests such as fecal hemo-
function may gradually decline in smokers and globin and colonoscopy should be dictated by
with increasing neurologic deficit and/or progres- local recommendations for the population at large.
sive spinal deformity. Arterial blood gases and Many centers recommend that the urogenital
pulmonary function tests (spirometry, polysom- system be checked annually, with creatinine
nography) should be carried out as needed. clearance and/or renal scintigraphy and/or
With respect to overweight, it is well to ultrasound of the urinary tract. Annual prostate
remember that the ideal weight for a person palpation for men over the age of 40 is also often
with paraplegia is roughly 80% of the corre- recommended.
sponding weight of a mobile person of the There are no indications that diseases
same height, and for tetraplegia only 60% of specific to women, such as gynecological and
that weight. breast cancers, are more common in those with
Recommended laboratory tests include com- SCI. However, these patients are definitely at risk
plete blood count, electrolytes, blood urea of not being included in the general screening
nitrogen, creatinine, lipid panel, liver function system. Again, we would like to underscore that
tests, and fasting blood sugar. In patients with either the doctor responsible for providing spinal
diabetes, tests should also include Hgb A1c, injury care must include these studies in their
fundus examination, and a foot check. annual rechecks or else make it clear to the patient
A screening questionnaire should be used to that these screening measures should be done at
assess nutritional status. In the chronic phase, another healthcare facility.
34 Research and Development
The recorded history of SCI starts with the the experimental weight-drop technique that
Edwin Smith Surgical Papyrus (37,71). In the initiated the modern era of SCI research.
well-known case 33, Instructions concerning a Both these researchers were aware of the con-
crushed vertebra in his neck, the authors con- tribution of secondary injury mechanisms to
clusion is that this is an ailment not to be the final neurological deficit after an injury to
treated. Imhotep describes in that case symp- the spinal cord. During that period, which
toms associated with SCI such as loss of included World War I, mortality was as high
motion in arms and legs (tetraplegia), loss of as 80% within the first 2 weeks following SCI
sensation below level of injury, and loss at the cervical level. A fatalistic attitude
of bladder control. accompanied the treatment of SCI during
Hippocrates (circa 460377 BC) first corre- the period between the two world wars.
lated vertebral injuries with paralysis. He intro- However, in 1943, the modern era of rehabi-
duced the Hippocratic board to reduce spinal litation began when Sir Ludwig Guttmann
deformities, and advocated, in the treatment of opened his Stoke-Mandeville National Spinal
SCI patients, a diet consisting of four to nine Centre. The creation of rehabilitation clinics
pints of donkey milk combined with honey and that focused on the special challenges asso-
a special mild white wine from Mendez in ciated with SCI, together with the introduc-
Egypt. Hippocrates also described the difficul- tion of antibiotics, revolutionized care for this
ties facing patients with paralysis, such as con- group of patients. In the decades following,
stipation, dysuria, skin problems, and edema. improved healthcare resulted in a substantial
The Greek Galen (130201 AD) was the first to improvement in quality of life and life expec-
perform animal experiments. He described tancy. Today, for a person with SCI, life
that a longitudinal incision to the spinal cord expectancy is approaching that of the general
did not produce loss of function, whereas a population.
transverse incision at the cervical level resulted Our knowledge about the pathophysiological
in loss of both motor and sensory function process of SCI has increased in parallel with
below level of injury. Five hundred years later, improved medical management. The concept of
the surgeon Paulus (625690) from the Greek primary and secondary mechanisms of injury
island of Eagina introduced laminectomy, the has been accepted both experimentally and in
removal of the vertebral arch in order to decom- the acute care of these patients. All this knowl-
press the dural sac and spinal cord. In 1543, edge, however, has led only to improved medical
Andreas Vesalius published one of the greatest management, not to a cure. There exists no ther-
medical books ever written, De Humani apeutic method to restore, even partially, lost
Corporis Fabrica, in which the human nervous neurological function.
system was, for the first time, illustrated in The prevention of secondary damage or the
detail. self-destruction of neurons following an injury
The Father of Neuroscience Santiago and the desirable effort to rescue viable tissue
Ramon y Cajal was awarded the Nobel Prize is summarized as neuroprotection. A variety
in medicine 1906 for his description of CNS of therapeutic agents have been used, targeting
structure. In 1911, Reginald Allen introduced one or more mechanisms of secondary
279
280 SPINAL CORD INJURY
injury in order to confer neuroprotection and TABLE 34.1 Reported positive effects of MPSS in
prevent unnecessary tissue damage. The insuf- animal experimental studies.
ficient neuroprotective effects, however, have
Improves energy Reduces edema
switched the focus of research to the more
metabolism formation by
long-range consequences of injury to the
maintaining the
spinal cord. Present (and future) research
bloodbrain barrier
encompasses the field of neural regeneration.
Reduces posttraumatic Reduces degeneration
In 1981, breakthrough work in this field was
ischemia of nervous structures
presented by David and Aguayo (18), who con-
Stabilizes phospholipid Counteracts formation
cluded that, in order for axonal regeneration to
membrane structures of free radicals
occur, both intrinsic cellular and CNS environ-
Reduces inflammatory Reduces neurological
mental factors must be addressed.
response deterioration
The purpose of this chapter is to highlight
those selected experimental and clinical studies
that we believe form the basis for undertaking
future challenges in the research field of SCI. various substances in animal experiments, been
We focus our discussion on methods for either focused on a number of clinical studies aimed at
preventing the consequences of secondary injury minimizing neurological deficits post trauma
in the acute period (neuroprotection) and/or (4). Baptiste and Fehlings published a survey of
various techniques of neural regeneration in ten randomized, prospective, and controlled
the subacute and chronic phase. Finally, we neuroprotective studies, considered by the
discuss possible future avenues within this authors to be most scientifically reliable
research field. (Table 34.2). Although numerous other attempts
have been made to support the neuroprotective
NEUROPROTECTION potential of the spinal cord these studies are the
most quoted.
Neuroprotection is defined as measures to Although we concentrate our attention in
counteract secondary injury mechanisms and/ this chapter on experimental studies, it should
or limit the extent of damage caused by self- be emphasized that all types of immediate
destructive cellular and tissue processes. The therapeutic interventions also have as their
hypothesis of secondary events was, during the underlying objective to support the organisms
1970s, focused on vascular damage leading to intrinsic neuroprotective potential. A common
edema, free radical formation, and norepi- and enduring problem for all treatments
nephrine release, whereas calcium processes, administered during the acute stage is knowing
opiate receptor mechanisms, cytokine involve- the length of the so-called therapeutic window,
ment, nitrous oxide formation, and lipid per- that period of time after injury within which
oxidation were highlighted during the 1980s. treatment must start to be effective. Extensive
Knowledge about apoptosis, energy metabo- efforts have been made to translate experimental
lism, inflammation, and excitoxicity increased data on secondary injury mechanisms to
markedly during the 1990s. The coexistence of help define therapeutic windows in clinical
several distinct injury mechanisms post situations.
trauma has provided opportunities to explore In a series of clinical studies (see Table 34.2)
a large number of potentially neuroprotective by the National Acute SCI Studies (NASCIS I-
agents in animal experiments. III), MPSS was given alone or in combination
Methylprednisolone sodium succinate (MPSS) with either the opioid antagonist naloxone or the
is the most extensively studied agent, Table 34.1 lipid peroxidation inhibitor, tirilazad mesylate
summarizes its reported positive effects in animal (9,10). In addition, based on beneficial effects
experiments. in animal experiments, clinical studies have
Neuroprotection research has, in addition been carried out with GM-1 ganglioside (25),
to characterizing injury mechanisms and testing thyrotropin-releasing hormone (TRH), the
CHAPTER 34 RESEARCH AND DEVELOPMENT 281
TABLE 34.2 Summary of ten randomized, prospective and controlled neuroprotective studies (from
Baptiste and Fehlings, 2006).
Study Animal Experimental Background Effect on Neurological Outcome
1 NASCIS-I, 1984 MPSS No difference in recovery
MPSS in high and low Antioxidative/antiinflammatory: following administration of
doses see table 1 high and low doses of MPSS
2 NASCIS-II, 1990 Naloxone improved impulse MPSS improved neurological
MPSS, naloxone or propagation and reduced edema recovery
placebo formation
3 NASCIS-III, 1997 Tirilazad mesylate prevents lipid MPSS improved neurological
MPSS and tirilazad peroxidation, stabilizes phospholipid recovery
mesylate membranes, and restores the level of
vitamin E in the spinal cord
4 Japanese MPSS study, MPSS improved neurological
1994 recovery
MP or placebo
5 Maryland ganglioside GM-1 stimulates axonal growth GM-1 improved neurological
study (GM-1), 1991 through the site of injury recovery
6 Sygen ganglioside study Minimal neurological
(GM-1), 1998 recovery was seen among
patients with incomplete
lesions
7 Thyrotropin-releasing TRH counteracts the effect of excitatory TRH improved neurological
hormone (TRH), 1995 amino acids and endogenous opioids recovery among patients
TRH or placebo and has antioxidant and membrane with incomplete lesions
stabilizing properties
8 Nimodipine, 1998 Calcium-channel blocker No neurological improvement
Nimodipine, MPSS, in was observed
combination or
placebo
9 Gacyclidine study, 1999 NMDA receptor antagonist No neurological improvement
Gacyclidine or placebo was observed
10 Decompression, 1997 Decompression performed less than No difference in neurological
72 h, or more than 5 d, respectively, recovery between the
after trauma groups
REGENERATION
Transmitting Dendrites
cell
Myelin damage
Axon
Nerve signal
Myelin sheath
Neuro-
transmitters
Synapse
impairment. Interruption of descending and
ascending white matter pathways (i.e., severing
Receptors on receiving cell of axons from their nerve cell bodies) results in
Wallerian degeneration of axons and myelin.
Axonal injury may also cause death of the parent
Figure 34.1 Intact nerve cell making synaptic nerve cell body, particularly if the lesion is close to
connections with a postsynaptic neuron. The it. To restore lost functions, injured neurons must
enlarged figure to the right shows the synaptic survive, and their axons must regenerate across or
complex with the presynaptic terminal, release of around the lesion site and also make functionally
its neurotransmitter and the postsynaptic site useful connections caudal (descending tracts) or
where the neurotransmitter is bound to specific rostral (ascending tracts) to it. As a result of
postsynaptic receptors. mechanical compression, myelinated axons may
CHAPTER 34 RESEARCH AND DEVELOPMENT 283
lose their myelin (demyelination), and hence their Nerve Cell Disability
ability to propagate nerve impulses. These axons
must become remyelinated to resume impulse Following axonal injury, signals to the affected
propagation. nerve cell body induce a shift in neuronal gene
The failure of injured spinal cord axons to expression (62,78). In contrast to the situation in
regenerate was originally demonstrated by the peripheral nervous system, central neurons
Ramon y Cajal in the end of the 19th century. are able to maintain the expression of regenera-
The dogma that spinal cord neurons were unable tion-associated genes only for a limited period,
to regenerate axons dramatically changed with the presumably due to the absence of sufficient
results of the experiments by David and Aguayo growth-stimulating factors in their environment.
in the early 1980s (18). Their experiments clearly As a result, the injured neurons gradually enter
demonstrated that central nervous axons are able an atrophic state, and may eventually degenerate
to regenerate, provided they are exposed to a sup- and die.
portive environment (peripheral nerve tissue), but
that they cease to elongate when confronted with Environmental Factors
CNS tissue. During the subsequent two decades,
several regeneration obstacles have been identi- The injured axons are surrounded by factors
fied. Based on these findings, various regenera- that inhibit axon growth. These include
tion strategies have been developed with the aim NOGO-A (63) and myelin-associated glycopro-
of modifying the growth inhibitory properties of tein (MAG; 76), which are both produced by
the spinal cord environment (35,57). Here, we oligodendroglial cells. Astrocytes, microglial
present some regeneration obstacles followed by cells, oligodendrocytes, and meningeal cells
a selection of interesting regeneration strategies. contribute to the formation of a scar at the
injury site. The scar presents a mechanical
REGENERATION OBSTACLES barrier, but the main obstacle for axon growth
is the presence of a chemical barrier composed
The adult CNS environment contains a variety of of proteoglycans and collagens (21). The addi-
mechanisms that actively inhibit axonal growth. tion of extensive necrotic and apoptotic cell
Various processes, in the acute as well as in the death in the injury region promotes the devel-
chronic stage following SCI, counteract the opment of cavities and cysts in the spinal cord
potential of injured axons to cross the level of itself. A is fully formed, scar undoubtedly pro-
injury and finally to reconnect with nerve cells vides a mechanical obstacle to axon growth.
below the injury site. These obstacles include an However, this process requires many weeks
insufficient growth response by the injured to complete. The question therefore remains:
nerve cells (nerve cell disability) and environ- Why are axons unable to grow across the injury
mental factors surrounding the nerve cell site before the scar has formed? The most
(Table 34.3). plausible explanation is that a growth-inhibitory
environment is created early post injury,
including the expression of myelin-associated
TABLE 34.3 Regeneration obstacles. inhibiting components, as a result of the com-
bined activity of local glial cells and invading
Nerve Cell Environmental Factors
hematogenous cells. Finally, the emergence of
Disability
mature scar tissue adds yet another obstacle to
Nerve cell body Presence of growth inhibiting regeneration.
response factors
Scar tissue formation
Formation of cavities and cysts REGENERATION STRATEGIES
at, below, and above the level
of injury
In the light of these considerations, successful
regeneration in the spinal cord requires the
284 SPINAL CORD INJURY
combination of several approaches, which will be Subsequent studies showed that NGF is a
discussed in the following sections: member of the neurotrophin family of growth
factors, which also include brain-derived neuro-
Promoting intrinsic neuronal capacity for
trophic factor (BDNF) and neurotrophins (NT)-3
regeneration
and -4 (NT-4). Neurotrophic growth factors are
Counteracting early inhibitory mechanisms
small molecules with a wide range of properties,
to axonal growth in the environment of the
including the promotion of neuron survival and
injured neurons
axonal outgrowth, as well as the regulation of
Overcoming late inhibitory mechanisms to
neuron-target interactions (Table 34.5; 26,32).
axonal growth in the environment of the
The most interesting properties of these factors
injured neurons
in the context of SCI seem to be their ability to
stimulate the survival of injured neurons, as well
Promoting Intrinsic Neuronal Capacity for as to regulate the expression of RAGs in a way
Regeneration that increases the regeneration capacity of
injured axons (29,38,55,66).
Neurons are endowed with a normally inactive
Although several growth factors have well-
regeneration program, which becomes acti-
documented effects on axonal growth, there are
vated following injury. To restore neuronal capa-
problems with their application in SCI. The spe-
city following damage, injured axons need to
cificities of the growth factors are incompletely
activate their regeneration-associated genes
known in terms of their effect on neuronal popu-
(RAG). This activation program is markedly
lations and peripheral tissues, such as muscle.
stimulated by appropriate growth factors
Several growth factors stimulate axons that
(Table 34.4).
convey nociceptive information, which can lead
The first of these factors, named nerve growth
to increased pain prevalence (53). Different
factor (NGF), was identified in the 1960s. Nerve
growth factors also appear to stimulate neuronal
growth factors that influence the development
growth at different stages in the repair process,
and maintenance of neurons are often referred
and sometimes in an antagonistic manner
to as neurotrophic factors (nourishing neurons).
(Table 34.5; 50). It is therefore a challenging task
for the future to determine which growth factors
are optimal for promoting survival and regenera-
TABLE 34.4 Examples of growth factors
tion of different types of neuron populations, and
(neurotrophic factors).
at what time point they should be administered.
Neurotrophic Factors Abbreviation Moreover, growth factors do not pass the blood
brain barrier, which raises the issue of how to
Nerve growth factor NGF
deliver them in an efficient and controlled way.
Neurotrophin 3 or 4 NT-3/NT-4
Intrathecal delivery via osmotic pumps con-
Brain-derived neurotrophic factor BDNF
taining genetically modified neurotrophin-
Fibroblast growth factor FGF
releasing cells (e.g., fibroblasts), the implantation
Glia cell line-derived neurotrophic GDNF
of slow-release cell-free systems, or gene therapy
factor
(8) are possible options. Taken together, there are
a number of well-defined growth factors with The interaction between NOGO-A and the
established positive effects on axonal growth that NOGO-A receptor results in a receptor-
might be used in future treatment of SCI. mediated inhibition of axonal growth. This
mechanism is prevented by the administration
Counteracting Early Inhibitory Mechanisms to of antibodies (IN-1) that binds to NOGO-A
Axonal Growth itself (neutralizing antibodies; 17) or that act
as antagonists to the NOGO-A receptor (36).
Axonal regeneration is counteracted in the early Thus, intrathecal infusion of these neutralizing
period after an injury by the emergence of antibodies blocks the effect of NOGO-A, and
myelin-associated inhibitors and by factors that thereby indirectly stimulates axon regeneration
accelerate the formation of scar tissue in the (Fig. 34.4).
environment surrounding the nerve cell. Here, In addition to NOGO-A, other axonal growth
we discuss some of the main strategies that have inhibitory proteins, such as myelin associated
been adopted to counteract the effects of early glycoprotein (MAG) and oligodendrocyte
inhibitory mechanisms in the nerve cell environ- myelin glycoprotein (OMP) also exert their
ment (Table 34.6). effects at the receptor level. Thus, the presence
of myelin-associated inhibitors to regeneration is
Blocking Axonal Growth Inhibitory Molecules fully recognized. In addition to studies with IN-1
antibodies against NOGO-A, experimental
The spinal cord of healthy uninjured adults con- studies has been performed using a passive or
tains powerful inhibitory substances that prevent active immunization approach toward myelin-
axonal growth. These factors are vital since they inhibitory molecules (Fig. 34.5, 73). Substantial
stop axonal growth after the axons achieve con- anatomical regeneration and functional recovery
tact to other nerve and muscle cells. Following have been reported using this approach (28).
trauma, these same factors create a major However, this approach is controversial, since
obstacle at the molecular level by delaying and/ other studies have reported that passive or
or preventing the onset of the regeneration pro- active immunization increases structural
cess. Pioneering work by Schwab and collabora- damage and functional impairment following
tors led to the identification of a myelin growth- SCI (3,21). Recent studies have shown that the
inhibiting factor, NOGO-A, a myelin protein pro- growth inhibitory influence of myelin-associated
duced by oligodendrocytes (see Table 34.6; 63). proteins can be overcome by increasing the levels
NOGO-A exerts its inhibitory effect by blocking of cyclic adenosine monophosphate (cAMP) in
specific NOGO-A-receptors on the surface of the the injured axons to promote axonal elongation
axons (Fig. 34.3AC; 24,75). in the injured spinal cord (52,56).
TABLE 34.6 Strategies to counteract the early inhibitory mechanisms of the CNS environment.
Factor Target Delivery Effect
Antibodies (IN-1) NOGO-A receptors on Pumps Blocked inhibition of axonal
regenerating axons Pills? outgrowth immunization
4-amino pyridine Demyelinated axons Intravenous Restored signal
Intrathecal transmission
Monoclonal ICAM Immunization Reduced edema
antibody Increased SCBF
Interleukins Unknown Systemically; Switches of the
IP inflammatory response
Chondroitinase Proteoglycans Local infusion Digestion of scar
ABC Functional improvement
286 SPINAL CORD INJURY
Before vaccination
Myelin
Axons Myelin inhibitors
NOGO-A Oligodendrocyte
Axon
A)
Scar tissue
NOGO-A
Receptor damaged
oligodendrocyte
Axon after damage
B) Myelin
A)
Antibodies
After vaccination
Antibodies
Regenerated
axons
C)
B)
trauma. Transection of the spinal cord rarely Modulating the Immune System
occurs, and the majority of spinal cord injured
patients probably have some axons that sur- Modulation of the immune system is a potentially
vived the acute mechanical damage as well as useful strategy to reduce the inflammatory
the effects of the secondary injury mechan- response after trauma and in this way improve
isms. In both situations, degeneration of oli- the environment for neuron survival and regen-
godendrocytes, largely by apoptosis, occurs, eration. The inflammatory response after SCI
resulting in demyelination and thereby inse- encompasses degenerative as well as reparative
cure impulse propagation or complete con- processes (1,23,59). Cellular debris and break-
duction failure. The myelin that covers the down products from degenerating neurons, glial
axons is partially or totally lost, resulting in cells, and hematogenous cells are eliminated
impaired or completely lost impulse propaga- through of variety of processes, thereby promoting
tion. In addition, the propagated electrical the restoration of a beneficial environment for
impulses could be spread between demyeli- surviving cells. Inflammatory cells and their med-
nated axons like a short-circuit in an electrical iators also help to build novel structural compo-
cable when the outer insulation is damaged. nents, including the scar, which isolates the
When an axon is demyelinated post injury, a trauma area from surrounding healthy tissues.
large number of potassium channels are The inflammatory response can be divided
exposed and potassium (K) leaks into the into three overlapping phases: the phase of
extracellular space, resulting in conduction initiation (the phase of disintegration), the
failure (Fig. 34.6). phase of maintenance (the scar-forming phase),
Infusion of the fast voltage-sensitive potas- and the phase of shutting off. All tissues harbor
sium channel blocker fampridine-SR (4-amino- mononuclear cells, which together form the
pyridine, 4-AP) blocks the potassium channels at mononuclear phagocyte system, and have the
those gaps and makes it possible for the demye- ability to rapidly transform into macrophages in
linated axon to propagate action potentials trauma and disease. Macrophages have long
(Table 34.6; 27). This agent has been tested in been known to play a key role in inflammation,
phase 2 studies, and trials are ongoing to study including the repair of injured peripheral nerves
the effects of its administration in the early stage (16). Recent studies indicate that an inadequate
of the injury (15). macrophage response in the injured CNS is an
important factor behind the failure of axon
regeneration in the spinal cord. In the injured
spinal cord, most of the macrophages originate
from microglia, the intrinsic members of the
mononuclear phagocyte system. Local factors in
the CNS (from, for example, astrocytes) exert a
Nerve impulse much tighter control of the activation of micro-
K+ glia to fully competent macrophages compared
4-AP to the situation in other tissues. While this con-
Potassium trol may serve to minimize the extent of sec-
channel
ondary damage from a fully developed
Axon after inflammation, it also appears to hamper the
damage
neuroregenerative response.
To facilitate the entry of monocytes into the
K+ degenerating spinal cord white matter and their
subsequent differentiation into competent
Myelin
macrophages may therefore promote tissue
Figure 34.6 Fampridine-SR (4-AP) blocks open repair and axon growth.
potassium channels and helps to maintain a resting Circulating monocytes first have to attach to
potential. endothelial cells in the capillaries to be able to
288 SPINAL CORD INJURY
TABLE 34.7 Strategies to overcome the late inhibitory mechanisms of the CNS environment
supportive structures.
Factor Target Delivery Effect
Peripheral nerve Axotomized axons Locally with glue Structural and functional
aFGF recovery
Schwann cells (SC) Axotomized axons Placement of SC Reduced secondary
Growth factors transplants in guidance degeneration
channels Functional improvement
Olfactory ensheathing Axotomized axons Local deposition Reduced secondary
glial cells (OEC) degeneration
Functional improvement
Noncellular elements Cut axons Placement of stem cells in Improved tissue sparing
stem cells Scar forming glia transplanted polymers Reduced scar formation
Functional improvement
Erythropoietin (EPO) Systemically Retain neuroprotective
properties
Rho Actin cytoskeleton Improves SCBF and
locomotion
Activated macrophages Injury epicenter Improved motor function
Reduces cyst formation
Schwann cells
supporting this growth, and are fully integrated
Nerve cell Axon Axon Nerve cell in the adult CNS, properties that make them
interesting with regard to SCI repair (58). OECs
release growth factors, as well as other
growth promoting molecules, and are able to
produce myelin around regenerated CNS axons
(Table 34.7). Locally implanted OECs stimulate
Supporting structure
regrowth of damaged axons in the spinal cord, as
Spinal cord
well as growth of axons through areas with scar
Figure 34.9 Bridge created by Schwann cells and tissue formation. Furthermore, functional
extracellular matrix components provides a growth recovery of sensory and postural functions was
supportive substrate for injured axons. observed. The mechanisms underlying func-
tional improvement associated with transplanta-
when using Schwann cells is the hostile astro- tion of OECs are incompletely understood, but
cytic reaction toward the Schwann cells in the appear not only to be the result of their suppor-
damaged area, which decreases their ability to tive and guiding properties, but also of their
produce myelin. ability to promote synaptic plasticity (6).
Furthermore, stem cells from the olfactory
Olfactory Ensheathing Cells. Olfactory ensheathing mucosa may be present in OEC transplants,
cells (OECs) have emerged as an attractive source and contribute to structural and functional
for supportive structures (5). OECs envelop olfac- repair (48). The capacity of OECs to fully inte-
tory sensory axons along their way to the target grate in the CNS environment and migrate
neurons in the olfactory bulb. There is a contin- through connective tissue makes them more
uous growth of axons into the olfactory bulb favorable candidates than Schwann cells for sup-
from newly formed olfactory sensory neurons porting axonal regeneration within the injured
in the olfactory mucosa. OECs are continuously spinal cord.
CHAPTER 34 RESEARCH AND DEVELOPMENT 291
OECs can easily be harvested under local anaes- been found to exert potent neuroprotective effects
thesia from the human olfactory mucosa, grown by diminishing lipid peroxidation and inflamma-
in vitro, and thereafter used for transplantation. tion, as well as by counteracting apoptosis. The
Clinical trials with autologous transplantation of agent carbamyl erythropoietin (CEPO) retains
OECs into the spinal cord have been initiated in neuroprotective properties without having hema-
patients with chronic, complete spinal cord lesions topoietic potential. Administration of CEPO
in Brisbane, Australia. The technique and ima- within the first 24 hours after experimental SCI
ging results using magnetic resonance imaging reduces the neurological deficits compared to
(MRI) 1 year after transplantation have been control (Table 34.7; 67).
reported (22).
Rho Pathway Antagonists
Artificial Supportive Structures. Various artificial
structures have been presented (49). As an Rho is a GTPase-associated signalling protein
example Schneider and colleagues (61) grafted that transduces extracellular signals to altera-
a multicomponent polymer into the gap of the tions in the actin cytoskeleton, thereby influen-
hemisected spinal cord (Fig. 34.10). The inner cing cell motility (45). Injury to CNS axons
part of the polymer was filled with stem cells and induces increased Rho activity, which correlates
the outer part contained a suitable substrate for with growth cone collapse and neurite retraction.
axons to grow beyond the level of injury. Grafted The administration of Rho-associated kinase
animals showed better hindlimb functional inhibitors such as C3 in the early period after
recovery than did controls (Table 34.7). SCI in rats promotes neurite extension,
improves spinal cord blood flow, and results in
Erythropoietin improved locomotion (Table 34.7; 19). Currently,
phase 1 and 2 multicenter studies are under way,
Erythropoietin (EPO), the prime stimulator of using extradural administration of the Rho-asso-
erythroid progenitor cell proliferation, has ciated kinase inhibitor cethrin during the first 2
weeks after injury.
Transplantation of Embryonic/Fetal Neural Tissue for axons from transplanted cells to neurons
Spinal Cord Repair caudal/rostral to the lesion
Embryonic/fetal neural tissue contains undiffer- Embryonic/fetal tissue has a number of proper-
entiated neurons with a potential to survive trans- ties that make it attractive in SCI treatment
plantation to the mature CNS, develop into (Table 34.8). However, ethical aspects complicate
mature neurons, and make functional synaptic the use of such tissue for experimental and clin-
connections in the host spinal cord. In addition, ical purposes. Different strategies have been
embryonic/fetal tissue contains stem cells and used when transplanting embryonic/fetal tissue
non-neuronal cells, which may provide trophic in experimental SCI studies (Table 34.9; 47).
and substrate support for transplanted immature
neurons, as well as for the injured neurons in Animal Tissue to Animal Recipients. Solid embryonic
the host spinal cord. Thus, transplantation of tissue transplanted to a liquid-filled cavity in the
embryonic/fetal tissue has four prime objectives: rubrospinal tract was found to counteract retro-
grade cell death of neurons within the red
To replace specific cells in order to restore nucleus, probably due to a release of growth
lost functions factors (Table 34.9). An increase in local reinner-
To minimize neuronal degeneration and vation, as well as a functional recovery was seen
scar formation after transplantation of embryonic brainstem
To promote regeneration and plasticity by tissue to a spinal cord segment below the level
providing a scaffold and trophic influence of injury.
for axonal growth
To serve as a relay station in which des- Human Tissue to Animal Recipients. Human embr-
cending or ascending impulses can termi- yonic spinal cord tissue can survive, grow, differ-
nate and subsequently be transferred via entiate, and become morphologically integrated
TABLE 34.9 Strategies to overcome the late inhibitory mechanisms of the CNS environment
transplantation of embryonic/foetal tissue.
Factor Target Delivery Effect
Solid embryonic/fetal Red nucleus axons Transplantation to cavity Rescue axotomized
tissue neurons
Brainstem fragments Denervated terminal Injection Local reinnervation
field Functional restitution
Solid embryonic/fetal Axotomized axons Transplantation to cavity Axonal elongation into
tissue and out of transplant
Human embryonic/ fetal Axotomized axons Transplantation Feasibility
tissue Cyst obliteration
CHAPTER 34 RESEARCH AND DEVELOPMENT 293
following transplantation into the animal spinal individuals whole life. The first publication on
cord. Human fetal tissue, including spinal cord isolation of neural stem cells was published in
tissue, harvested from early abortions (58 1994 (46), and the first report on the use of stem
weeks) has been used to fill experimentally cells in SCI was published in 1999 (43). In this
induced posttraumatic cavities, and these trans- study, embryonic stem cells from mice were
plants were found to promote survival of injured injected into the damaged rat spinal cord, and
neurons and axons, as well as to provide a bridge the results indicated some functional recovery.
for axonal growth (Table 34.9; 79,80). The injected cells differentiated into neurons,
oligodendrocytes, and astrocytes. The results
Human Tissue to Patients with SCI. Embryonic/ proved that transplanted embryonic stem cells
fetal tissue has been used in humans in the are able to survive and differentiate in the adult
treatment of Parkinson disease, diabetes, and spinal cord. Stem cell research is the only field in
leukemia, and in blindness due to macular which clear evidence has been demonstrated that
degeneration. Given the observations that cell therapy might repair damage within the CNS
human embryonic/fetal tissue was able to coun- (40,54,69).
teract cyst expansion in experimental SCI, the
question arose whether implanting such tissue Embryonic Stem Cells. Embryonic stem cells are
into the posttraumatic cyst cavity in humans derived from in vitro fertilized eggs and there-
could counteract further cyst expansion in after donated to research with permission from
patients with posttraumatic syringomyelia. The the donor. Consequently, embryonic stem cells
transplant may consist of solid tissue or a sus- are not derived from eggs fertilized within the
pension of cells (20,68,72). Injection of cell sus- female body (Fig. 34.11AC). Embryonic stem
pensions is associated with less injury to the cells are obtained from the inner cells of a blas-
surrounding tissue but solid transplants have tocyst, corresponding to a 4- or 5-day old ferti-
the advantage of being harvested from older lized egg, and thereafter transferred to a solution
fetuses. with special substrate. Embryonic stem cells kept
Experience of transplanting human in this solution without differentiation for 6
embryonic/fetal tissue to patients with SCI has months are called pluripotent (Fig. 34.11A).
provided information on transplant survival, how The term pluripotent is used to describe stem
the transplant fills the cavity, and whether rejec- cells that are able to differentiate to cells repre-
tion is provoked (Table 34.9). The final objective is senting all three embryonic layers: ecto-, meso-
that the embryonic/fetal tissue will integrate with and endoderm. The neural stem cell is an
the host spinal cord and provide structural and example of a multipotent stem cell (Fig. 34.11B).
molecular support for cyst retraction. It is impor- When the cells in a culture are genetically iden-
tant to stress in this context that embryonic tissue tical and contain a normal set of chromosomes,
transplant research today is not focused on func- they are called embryonic stem cells (Fig.
tional recovery, but merely to study its feasibility 34.11A). When a cell line is established it can
in transplantation. This research has provoked be stored frozen. New embryonic stem cell
heated ethical discussions, since the tissue is har- lines have continuously been produced. In
vested from aborted foetuses. 2001, it was reported that it was possible to
control the differentiation of embryonic stem
Transplantation of Stem Cells for Spinal Cord Repair cell lines in vitro toward a certain type of cells.
Thus, it is possible to isolate human embryonic
Stem cell research has opened a new arena for stem cells from blastocysts, maintain these
regenerative science. Stem cells are the source of cells as pluripotent cells in vitro for extended
all cells in the organism and have the potential to periods of time, and possibly, control their
differentiate to functionally competent cells of differentiation to desired cell type(s). However,
different types. They provide a repair system, the risk of tumor formation by transplanted
and are theoretically able to divide without lim- embryonic stem cells must be seriously consid-
itations and substitute other cells throughout an ered (7,60).
294 SPINAL CORD INJURY
In summary, embryonic stem cells: appropriate types of cells for that region. In rea-
lity, stem cellmediated positive outcomes are
likely to depend on complex mechanisms, as
discussed earlier with regard to implantation of
Are derived from the inner cells of the
blastocyst embryonic/fetal neurons. Thus, much of the
Have possibilities to undergo an unlimited morphological and functional improvements
number of symmetrical divisions without reported in experimental neural stem cell
differentiation over a long period of time research on the injured or diseased nervous
Exhibit and keep a stable and full set of system may be the result of neuroprotective
chromosomes and/or neurotrophic mechanisms, rather than
Are undifferentiated and might generate specific cell replacement (12).
differentiated types of cells to any of the
three primary layers within the embryo Stem Cells for Reparation of Injured Spinal Cord. In
Have the capacity to integrate in all kinds of
conditions such as Parkinson disease, only one
fetal tissue that is under development
type of cell may need to be replaced, the
Have clonogenic properties and can produce
a colony of genetically identical cells dopamine producing cells, in order to achieve
long-term alleviation of the symptoms. In a trau-
matically injured spinal cord, the repair proce-
dure will be much more complex, as many
Adult Stem Cells. Adult stem cells are able to pro- different kinds of cells are affected and, hence,
liferate during long periods of time and generate in need of being replaced. The primary aim of
identical copies without undergoing differentia- stem cell research is to restore/repair diseased
tion (Fig. 34.11C). In response to specific white matter, often referred to as partial repair of
extrinsic factors, adult stem cells differentiate SCI (Table 34.10).
into functional cells that are appropriate for the The gray matter damage in SCI is of less
surrounding tissue. Some adult stem cells even interest since it only produces peripheral loss
have the ability to differentiate into cells typical of function within the injured segments. The
for other than the surrounding tissue although predominating functional defects following
there is still no evidence that adult stem cells are SCI are caused by interruption of axonal con-
pluripotent. This phenomenonthe ability to, tinuity and/or by focal demyelination as a
within limits, transform into various cell result of oligodendrocyte degeneration (41).
typesis denoted plasticity. In both pathologies, the affected axons are
Two fundamental strategies for the use of unable to propagate impulses to their axon
stem cells in the repair of nervous system dis- terminals. Experimentally, it has not yet been
eases and trauma are used. First is the use of possible to achieve more than limited long-
cells prepared in vitro with the ultimate aim of distance axonal regeneration of injured axons
making them suitable for implantation in in the spinal cord. However, to repair a site of
patients. Second is the use of growth factors demyelination appears to be a more realistic
and other molecules to stimulate a patients goal. Therefore, the primary goal in the use of
own stem cells to repair the injury, by migrating stem cells in SCI is to learn how to replace lost
to the injury and differentiating to the oligodendrocytes with cells that are able to
TABLE 34.10 Strategies to overcome the late inhibitory mechanisms of the CNS environment
transplantation of stem cells.
Factor Target Delivery Effect
Neural stem cells Axotomized axons Transplantation to cavity Reconstitute cellular matrix
NT 3 Supporting axonal growth
CHAPTER 34 RESEARCH AND DEVELOPMENT 295
make sufficient myelin for impulse propaga- in immunosuppressed rats. A large number of
tion to resume. the cells died but some survived, and these cells
McDonald and coworkers (41,42,44) used were able to disperse in both directions within
embryonic stem cells aimed at transplantation, the spinal canal. Ten percent of the cells stayed
and they initiated the cells to generate progenitor in the injured area and differentiated to neurons.
cells that differentiated to astrocytes, oligoden- After transplantation, the animals showed
drocytes, and neurons. The neurons had inhibi- improved motor function.
tory and excitatory properties, including the
ability to form synapses. One million embryonic An important goal
Aims of Stem Cell Research.
stem cells were injected into injured spinal cords for stem cell research is to learn how to
ESC ASC
Embryonic somatic Adult somatic
stemcell stemcell
Figure 34.11 A: Principal types of stem cells and their developmental potential. With ongoing maturation of
the embryo, stem cells become restricted in their developmental potential. B: Stem cells from the embryonic
nervous system give rise to all intrinsic neural cells, except microglia. C: Stem cells from the adult nervous
system.
296 SPINAL CORD INJURY
Continued from
Fig. 34.11A
NSC
NSC NSC
NSC NP
Neural precursor
Np
Neural progenitor
Gp
Glial progenitor
Nerve cell
Astrocyte Oligodendrocyte
Continued from
Fig. 34.11A
Precursor
Progenitor
Specialized cell
(nerve cell)
control the differentiation of human pluripo- introduce new genes into the stem cell, so
tent embryonic stem cells to a certain kind of that they might differentiate into the cell
cells, for example neurons. It is also impor- type of interest.
tant to learn how to identify these differen- Laboratory studies have shown that human
tiated cells. By using growth factors or by embryonic stem cells are able to differentiate
changing the chemical composition of the into different kinds of cells, such as cells that
surface that the cells are growing on, it is build vascular structures, as well as into neurons
possible to stimulate stem cells to differ- producing dopamine. However, it is still not
entiate to neurons. Another method is to known how stem cells are able to divide without
298 SPINAL CORD INJURY
differentiating to more specialized cell types and measures, such as MRI, that will further improve
whether this is influenced by genetic changes. the therapeutic possibilities for patients.
Nor is it known at which level of differentiation There is a great need for combined treatment
the human embryonic stem cells are optimal for approaches to achieve additional functional
transplantation. improvement. In this chapter, strategies such as
Much research today is focused on the pro- closing the gap within the injured spinal cord are
duction of stem cells for use in transplantation of discussed, but at the same time the necessity of
dopamine-producing cells in patients with closing the gap between researchers within var-
Parkinson disease, b-cells in patients with dia- ious fields cannot be emphasized enough. To
betes mellitus, and heart muscle cells in patients build bridges between scientists in the field of
with heart failure. However, in the near future basic science and clinicians interested in research
embryonic stem cells will be used in SCI is a challenge in itself. The interpretation of new
research, rather than in human therapy. information of common interest demands good
relations between these groups. The most impor-
FUTURE CHALLENGES tant future challenge is to create a multidisci-
plinary approach to basic science and clinical
In this chapter, selected examples of research on management that enables all those who are inter-
neuroprotection and neural regeneration perti- ested in helping patients with SCI work together
nent for the search for new treatment strategies to test various hypothesis from a broad view.
for SCI have been presented. The amount of Early treatment in the acute stage after SCI is
knowledge regarding posttraumatic events fol- advocated in most countries in the Western
lowing SCI has increased tremendously, particu- world today. Patients sustaining SCI are treated
larly during the past three decades, but the in intensive care units and submitted to early
challenge to cure paralysis still remains. The surgery in order to avoid unnecessary neurolo-
achievement of functional recovery in experi- gical deterioration and to establish early mobili-
mental models, although limited, raises hope for zation. This is, according to our opinion, an
the future. The examples of research and devel- accepted and established treatment for the
opment described here show very clearly that majority of these patients. But, additional ques-
knowledge about the pathological processes is a tions arise, questions that must be answered
prerequisite for future research and development, through a multidisciplinary approach.
and hopefully, in a later stage, treatment options What actually is the importance of all sec-
for SCI patients. No single therapy will encom- ondary mechanisms in relation to future neuro-
pass all the secondary injury mechanisms or logical deterioration, and could our knowledge
increase the capability for regeneration of injured about the secondary pathophysiological pro-
or transected axons. To achieve the goal of mini- cesses indicate the exact time for any eventual
mizing neurological deficits following SCI, sev- regeneration strategy?
eral combined strategies must be used within the Do the results of regeneration research impli-
fields of neuroprotection and neural regeneration. cate changes of the treatment protocol in the
The golden drug or treatment has not yet been acute stage?
developed, and new questions arise as soon as a What is optimal tissue treatment in the acute
new piece of knowledge is acquired. stage, in order to facilitate regeneration? How do
Every additional increase in knowledge of SCI we optimize the chemical environment sur-
processes will be an important piece in the rounding the nerve cells in order to maintain
puzzle that frames the future development of surviving nerve tissue in the acute stage in as
new treatment strategies. Future challenges are good a condition as possible?
based on further increased knowledge within Is decompression of the dural sac and fixation
every major field of SCI research, ranging from of the spinal column in the acute stage sufficient
experimental basic science to pharmacological to optimize the possibility for the spinal cord to
treatment and medical management. Our expec- recover? Should, if such is not the case, the dural
tations also include improved diagnostic sac be opened and the subarachnoid space be
CHAPTER 34 RESEARCH AND DEVELOPMENT 299
exposed and flushed to eliminate blood accumu- estimated scar formation period, usually 26
lated subarachnoidally? Could such a therapeutic weeks, ends. The inflammatory response is
measure decrease or eliminate the inflammatory stopped by adding ILs, once we estimate that
response and minimize the accumulation of pro- the injured area is cleared of damaged spinal
teoglycans and reduce the scar formation at the cord tissue and debris.
level of injury? Various scaffold structures are prepared
Is it meaningful to decompress and stabilize all during the infusion period, depending on the
patients, or will we, in the future, use fetal tissue, level and severity of injury. A second posterior
stem cells, OECs, or scaffold structures with or approach is performed, and the artificial dural
without neural growth factors in the acute stage sac is opened. Scaffold structures are attached,
as complementary treatments in some cases? along with Schwann cells, neurotrophic factors,
Should we delay surgical procedures until we stem cells, and possibly rolipram to act as a
artificially induce regeneration in a later stage cAMP preserver. By using a special scaffold-like
and if so, when is the most appropriate time for gel, these factors are gradually released. OECs
this combined treatment? could, in addition, be administered either
Should a two-step surgical procedure be per- through infusion or as a cell suspension (the
formed in the acute stage addressing both the infusion of a concentration of macrophages
compression of the spinal cord and the damage from the injured patient himself to counteract
to the spinal cord itself. the inflammatory response is an exciting alter-
Let us consider a hypothetical case of SCI at native now being tested clinically).
the cervical level due to a burst fracture com-
As our knowledge continues to increase in con-
pressing the spinal cord anteriorly. In the
troversial fields such as stem cell and foetal
future, it may theoretically be possible to
tissue research, ethical and jurisdictional ques-
begin treatment with an anterior decompres-
tions will have to be answered in parallel to
sion of the dural sac followed by a stabilizing
medical questions. In the future, will it be pos-
procedure. The patient is then rotated and
sible to create stem cell or fetal tissue banks, or
placed in a prone position. The dural sac is
will purified adult stem cells harvested from the
exposed posteriorly following a laminectomy,
injured patient be used as replacement tissue for
after which it is opened through a midline
the spinal cord? Will it be possible to use such
incision to visualize the spinal cord. The
cells in the acute phase?
spinal cord is probably covered with various
These speculations verge on medical science
blood products and inflammatory debris, and
fiction; our current knowledge is not sufficient
these products are eliminated through careful
enough to give SCI patients the ultimate treatment
rinsing, since they are the prerequisites for scar
of restoring neurological function, and the route to
formation (an obstacle to regeneration). Next,
that goal is paved with controversy and disagree-
in our hypothetical future treated SCI patient,
ment. Our knowledge has, however, increased tre-
an artificial dura is applied in such a fashion
mendously during the past three decades, and the
that it counteracts the compression from pos-
hope is that continued work will eventually solve
terior extradural blood. This is followed by the
one of the most pressing of medical challenges in
intradural infusion of factors that counteract
the treatment of SCI: the regeneration of damaged
scar formation and increase the speed of regen-
axons and the restoration of neurological function.
eration. This infusion cocktail includes neuro-
trophic growth factors, antibodies against
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302 SPINAL CORD INJURY
Note: Page numbers followed by f and t denote figures and tables, respectively.
303
304 INDEX
Burning hands syndrome, 176, 177, 178. Central venous catheter (CVC), 63, 69, 70
See also Central cord syndrome CEPO. See Carbamyl erythropoietin (CEPO)
Burst fractures, 112, 125, 141, 141t, 142f, 14647, 149, Cerebrospinal fluid (CSF), 15, 187, 253
171, 299 fistulae, 184, 185
compression and, 14344 Cervical collars, 5458, 56f, 63, 67, 100t, 106,
108, 109, 110, 113, 119, 125, 128, 159,
C 165, 169
CA-DREZ lesion. See Computer-assisted dorsal root Cervical enlargement, 13, 14f
entry zone (CA-DREZ) lesion Cervical orthoses (COs), 15860
Ca+ ion influx, following damage to cellular Cervical spine, 9, 10t, 56. See also Upper cervical
membranes, 35f spine
Calcium stones, 238 diagnostic checklist of clinical instability in middle
Camber angle, 271 and lower, 117t
cAMP. See Cyclic adenosine monophosphate (cAMP) immobilization, 57f
CAMs. See Cell adhesion molecules (CAMs) lower cervical spine fractures and ligament
The Canon of Medicine, 5 injuries, 170
Carbamyl erythropoietin (CEPO), 291 anatomical overview, 11516
Cardiovascular dysfunction concept of instability, 11618
arterial hypotension, 21920 fracture classifications, 11828
autonomic dysreflexia, 219 treatment guidelines following, 120t
coronary heart disease, 221 open mouth view of, 79, 79f
deep vein thrombosis and pulmonary embolism, 222 surgical management of injuries to
impaired thermoregulation, 222 fusion and internal fixation techniques, 129
orthostatic hypotension, 22021 internal instrumentation techniques, 13337
peripheral vascular disease, 222 upper cervical spine, 12933
reduction in cardiovascular fitness, 221 swimmers view of, 78
vagotonia, 219 upper cervical spine fractures and ligament injuries
Cardiovascular management, 64t, 65 anatomical overview, 9798
Car driving, 272 atlantooccipital dislocation, 103
Carotid artery, 133, 184 atlas fractures, 105
Carpal tunnel syndrome, 208, 217 axis fractures, 10613
Cauda equina, 13, 14f, 17f, 191 classification and treatment options for, 100t
injuries, 184 occipital condyle fractures, 101
syndrome, 50, 50f surgical management of injuries to, 12937
Causalgia, 207, 209 x-ray of, 78, 79f
CBC. See Complete blood count (CBC) Cervical spine fracture, classifications of
CDC. See Disease Control, U.S. Centers for (CDC) Bechterew disease, 12728
Cell adhesion molecules (CAMs), 288 compression-burst injuries, 12426
Cell necrosis, 36 extension injuries
Central canal, 18 compression-extension, 127
Central cord syndrome, 48, 48f, 66, 68, 177, 194. distraction-extension, 126
See also Burning hands syndrome flexion-compression injuries, 12324
Central nervous system (CNS), 34, 36, 187, flexion-dislocation injuries, 11819
213, 289 bilateral facet dislocation, 12123
regeneration obstacles for facet subluxation, 11920
environmental factors, 283 floating vertebra, 123
nerve cell disability, 283 unilateral facet dislocation, 12021, 120t, 121f
regeneration strategies for Cervical spondylotic myelopathy, 187, 198
counteracting early inhibitory mechanisms to Cervicothoracicolumbar orthosis (CTLO), 161
axonal growth, 28589 Cervicothoracic orthosis (CTO), 100t, 106, 160, 160f
overcoming late inhibitory mechanisms to axonal C-fibers, 206f
growth, 28998 ChABC. See Chondroitinase ABC (ChABC)
promotion of intrinsic neuronal capacity for Chance fracture, 142, 143f, 145t, 147
regeneration, 28485 Chiari II malformations, 197
306 INDEX
Crush injury, 29, 31t DTRs. See Deep tendon reflexes (DTRs)
CSF. See Cerebrospinal fluid (CSF) Dual energy X-ray absorptiometry (DXA), 214
CSPG. See Chondroitin sulfate proteoglycans (CSPG) Duchenne-Aran disease, 198
CT. See Computed tomography (CT) Dura mater, 14f, 15, 16f, 99f
CTLO. See Cervicothoracicolumbar orthosis (CTLO) Duroferon, 88t
CTO. See Cervicothoracic orthosis (CTO) DVT. See Deep vein thrombosis (DVT)
CVC. See Central venous catheter (CVC) DXA. See Dual energy X-ray absorptiometry (DXA)
Cyclic adenosine monophosphate (cAMP), 285 Dysesthesia, 172, 177, 207
Cyst formation, 38, 253, 254, 258, 259, 289, 290, 290t Dyspepsia
Cystic myelopathy/syringomyelia, 19899 gastroesophageal reflux, 225
Cystometrogram (cystometry), 233 gastroparesis, 225
Cytomegalo virus, 189 peptic ulcer, 22526
superior mesenteric artery syndrome, 226
D Dysphagia, 225
Da Vinci, Leonardo, 5
Deafferentation pain, 263 E
Decompression illness, 199200 Edema, 32, 33, 34t, 37, 38, 63, 68f, 68t, 82, 168, 247, 251,
Decortication procedure, for exposing spongiotic 279, 280, 288
bone, 153 Edwin Smith Papyrus, 3, 279
Deep tendon reflexes (DTRs), 39, 40, 41, 44, 45, EEG. See Electroencephalogram (EEG)
48, 168, 199, 200 Ejaculation, 239
Deep vein thrombosis (DVT), 69, 171, 213, 222 EKG. See Electrocardiogram (EKG)
De Humani Corporis Fabrica, 5, 6f, 279 Electric wheelchairs, 27172
Denis classification, 141t Electrocardiogram (EKG), 249, 277
Depression, 45, 202, 221, 241, 245, 249, 269 Electroejaculation, 242
Dermatome, 15, 16, 41, 42, 48, 73, 74, 75f, 193, 208 Electroencephalogram (EEG), 249
Detrusorsphincter dyssynergia, 233, 234, 23637, 251 Electromyography (EMG), 198
Devic disease (neuromyelitis optica), 188 Embryonic stem cells, 293
Devices, for reducing malformations, 4 Embryonic tissue, properties of, 292t
Diagnostic methods for treatment of EMG. See Electromyography (EMG)
clinical assessment and classification according to Emission, 239
ASIA, 7378 Endotracheal intubation, 54, 61, 223
radiologic workup for spinal column trauma, 7883 Enteric nervous system, 226
Diarrhea, 228 Ependymoma, 19596
Diffuse or solid injury, 30 Ephapses, 207
Digestive system, 22f Ephedrine, 88t
nerve supply of, 227f Epidemic poliomyelitis, 192
Diprivan, 88t Epidemiological data relating to traumatic, 10t
Disk herniation, of cervical and thoracic spine, 19293 Epidural abscesses, 40, 41, 19091
Discriminative touch, 19, 42 Epidural hematoma, 29, 190f
Disease Control, U.S. Centers for (CDC), 10 Epidural space, 15, 16f, 262
Dissociated sensory loss, 20, 23, 198, 256 Epidural tumors, 19495
Distraction-extension, 126 Epiphysiolysis, of odontoid process, 169
Distraction fractures, 154 EPO. See Erythropoietin (EPO)
Disturbed temperature regulation, 17172 Epstein-Barr virus, 189
Disturbed thermoregulation, 222 Erectile dysfunction, 40, 77, 241, 266
Dormicum, 88t Erection, types of, 239
Dorsal column, 19, 19f Erysipelas, 213
Dorsal nerve root, 14f Erythropoietin (EPO), 239, 29091, 290t
Dorsal root entry zone (DREZ), 205, 206f, 257, 263, 264f Escherichia coli (E. coli), 238
Dorsal root ganglion, 16f, 18, 19f, 20f Esmeron (Zemuron), 88t
Down syndrome, 163 Esophagitis, 225
DREZ. See Dorsal root entry zone (DREZ) ESWL. See Extra-corporeal shock wave lithotripsy
Drug therapy in treatment of, 65 (ESWL)
308 INDEX
Guanine monophospthate synthetase (GMP), 241 Hypotension, 21, 32, 33, 52t, 54, 55, 55t, 61, 63, 64, 189,
Guidance channel, 289 220, 226, 266
Gunshot wounds. See Bullet wounds Hypovolemic shock, 63, 64, 184
Guttmann, Sir Ludwig, 7 Hypoxia, 61, 62, 166t, 190, 249
Gymnastics, 177
I
H IASP. See International Association for the Study of
Haber-Weiss reaction, catalysed by iron Pain (IASP)
ions, 35f IBOT transporter, 272
Halo vest, 67, 121, 126, 157, 158f, 167 ICAM. See Intercellular cell adhesion molecule (ICAM)
Hand surgery, for patients with SCI, 215 Ice hockey, 177
Hangmans fracture, 107, 107f, 11011 ICSI. See Intracytoplasmic sperm injection (ICSI)
diagnosis and classification, 110 Immobilization, 5558
treatment, 11 Immune system, 287
Harrington fixation device, 150, 150f Impaction fractures, 14546, 148
HDL. See High-density lipoprotein (HDL) Incidence, 9
Head injuries, relationship to SCI, 10 Incomplete injury, 77
Hemopneumothorax, 183 Incontinence, 226. See also Constipation in women
Hemorrhages, 81, 82, 166, 168, 190 with SCI
Hemorrhagic shock, 54 Indwelling catheter, 70, 219, 234, 235f
vs. neurogenic shock, 55t Infertility, 239, 24243, 251
Hereditary spastic paraplegia, 199 Inflammation, 32, 34t, 36, 38, 189, 192, 198, 212, 253,
Hernia, 197 280, 287, 288, 291
Herniated disk, 40, 193f Inflammatory bowel disease, 128
cervical, 19293 Insomnia, 249
lumbar, 193 Intensive care of injured spinal cord
Herpes simplex virus, 189 additional measures for
Heterotopic ossification (HO), 171, 17273, 21314, bladder care, 70
213f, 277 contracture prevention, 70
High-density lipoprotein (HDL), 221, 277 deep venous thrombosis, 69
High-voltage electric shock, 199 gastrointestinal and nutritional measures, 70
Hip deformities, 172 pressure ulcer prevention, 70
Hippocrates, 4, 279 pulmonary embolism, 69
traction device, 4f cardiovascular considerations, 6364
HO. See Heterotopic ossification (HO) neurological examination, 6465
Hodgkin disease, 198 pharmacological treatment, 65
Holding reflex, 226, 228 radiological evaluation, 65
Homunculus, 19f, 20f respiratory management, 6263
Horner syndrome, 23, 40, 69t, 196, 256t, 257 surgical decision making, 6566
H-shaped gray matter, 17, 18 conservative vs. surgical treatment, 6667
HTLV-1. See Human T-lymphotropic virus type 1 guidelines for surgical intervention, 6769
(HTLV-1) Intercellular cell adhesion molecule (ICAM), 285t, 288,
HTLV-1-associated myelopathy, 192 288f, 299
Human T-lymphotropic virus type 1 (HTLV-1), 192 Intercostal artery, 23, 23f, 24, 25f
Hydrocephalus, 197 Interleukin (IL), 288
Hydrosyringomyelia, 197 Intermittent catheterization, 233
Hydroxyl radicals, formation of, 35f Internal fixation techniques, 129
Hyperalgesia, 207 Internal instrumentation techniques, for cervical spine
Hypercalcemia, 171 injury treatment, 12930, 133
Hyperesthesia, 42, 185, 207 International Association for the Study of Pain
Hyperpathia, 207 (IASP), 205
Hyperprolactinemia, 251 International Standards for Neurological and
Hypertension, 32, 220, 221, 239, 249, 276, 277 Functional Classification of Spinal Cord Injury
Hypoperfusion, 32, 220 (ASIA), 73
310 INDEX
Paradoxical diarrhea, 228 Pia mater, 13, 15, 16f, 258, 261
Paralysis, 3, 5, 6, 21, 39, 40, 41, 43, 44, 47, 49, 54, 62, 62t, PIEE. See Pulsed irrigation enhanced evacuation
172, 189, 192, 193, 197, 211, 213, 222, 238, 269, (PIEE)
277, 279, 298 Pincer fractures, 145t, 146, 147f
Paralytic ileus, 70, 226 Plaques, 187, 188, 225
Paramedical rehabilitation, 26973 Plaster-cast model, of three-point corset, 161
Paraplegia, 10, 11, 24, 43, 181, 192, 199, 200, 206, 208, Plegia, 10
211, 214, 219, 222, 223, 270, 277, 278 Plexus neurapraxia. See Burning hands syndrome
Paraplegia-in-extension, 45 PLMS. See Periodic limb movements of sleep (PLMS)
Paraplegia-in-flexion, 45 Pneumonia, 11, 63, 69, 70, 86, 223
Parenchymal hemorrhage, 183 Poikilothermia, 171, 222
Paresis, 10 Polio, 192
Paresthesias, 39, 42, 43, 177, 178, 187, 188, 199, 217 Polysomnography, 249, 278
Parkinson disease, 44, 293, 294, 298 Posterior commissure, 18
Pathophysiology, 29, 34t Posterior cord syndrome, 4849, 48f
PDE5. See Phosphodiesterase type 5 (PDE5) Posterior funiculus, 18, 19, 23, 263
Pediatric, medical treatment of, 168 Posterior horn, 18
Pedicle screw fixation technique, for treating cervical Posterior instrumentation, 134f, 13537
spine injury, 136f Posterior spinal artery, 24
Penetrating injuries Posterior spinocerebellar tract, 1920
bullet wounds Posterior stabilization, for surgical management
ballistic aspects, 18182 of cervical spine injury
local and systemic pathophysiology, 18285 combination techniques, 131
epidemiology, 181 facet screw fixation, 131
knife wounds, 185 intralaminar clamps (hooks), 132
surgical treatment for, 18485 occipitocervical fixation, 132
Penile prostheses, 241 wire techniques, 13031
Penis prosthesis, 241 Posterolateral sulcus, 17
Penn Spasm Frequency Score, 45 Post-polio syndrome, 192
Peptic ulcer, 22526 Post stimulus voiding, 236
Percutaneous epididymal sperm aspiration Posttraumatic myelopathy
(PESA), 242 investigation, 25657
Percutaneous radiofrequency thermal rhizotomy pathophysiology, 25354
(PTR), 26667 results, 26061
Percutaneous rhizotomy, 266f surgical treatment of PPM
Percutaneous thermal rhizotomy (PTR), 265 caused by persistent spinal cord compression,
Periodic limb movements of sleep (PLMS), 250 25960
Peripheral nerves, 20, 25, 40, 42, 61, 65, 183, 199, 209, indications and goals, 257
242, 266, 267, 275, 283, 287, 288, 28990, 290t technical considerations, 25759
Peripheral vascular disease, 222 symptoms, 25456
Permanent spinal cord injury, 177 Posttraumatic stress disorder (PTSD), 202
PESA. See Percutaneous epididymal sperm Potts disease. See Tuberculosis
aspiration (PESA) Powers index, 103, 105f
PGE1, 241 PPCM. See Progressive posttraumatic cystic
Pharmacological treatment of myelopathy (PPCM)
GM-1-ganglioside, 88 PPM. See Progressive posttraumatic myelopathy
methylprednisolone, 8586 (PPM)
other pharmacological treatment, 88 PPNCM. See Progressive posttraumatic noncystic
Phasic reflex activity, 45 myelopathy (PPNCM)
Phlegmon, 191 Pregnancy, 251
Phosphodiesterase type 5 (PDE5), 241 Pre-hospital management, 52
Phospholipids, 35f, 88, 263 Pressure ulcers, 171, 246f
Physical activity, 221, 26970 incidence and pathogenesis, 245
Physical training, 178 management of, 24647
314 INDEX