Traumatic Spinal cord injury

Presented by:
Myra Leslie S . Viloria
SPT-IV

Causes of syndrome of acute paraplegia or
quadriplegia :
1.Trauma ( main cause )
2.) other factors :
a.) infarction or hemorrhage
b.) rapidly advancing compressive,
c.) necrotizing,
d.) demyelinative, or inflammatory lesions.
Mechanisms of Spinal Injury


1.) MVA,
2.) falls (sometimes during a state of alcoholic
intoxication),
3.) gunshot or stabwounds
4.) diving accidents,
5.) crushing industrial injuries,
6.) birth injury.
Although trauma may involve the spinal cord
alone, the vertebral column is almos invariably
injured at the same time

classification of vertebral column:
1.) fracture-dislocations,
2.) pure fractures,
3.) pure dislocations.
Specifically, all three types of spinal injury are
typically produced by a vertical compression of the
spinal column, to which either anteroflexion or
retroflexion (hyperextension) is added.

The most important variablesin the mechanics of
vertebral injury :
1.) structure of the bones and ligaments at the level
of the injury and the
2.) intensity,direction, point of impact of the force

Causes of cervical decompression
3.) whiplash or recoil injury:
most often the result of an automobile accident.
When a vehicle is struck sharply from behind,
the head of the occupant is flung back
uncontrollably, or if a fast moving vehicle stops
abruptly, there is sudden forward
flexion of the neck, followed by retroflexion.
4.
The presence of a congenitally narrow cervical
spinal canal or of acquired spinal diseases such
as cervical spondylosis, rheumatoid arthritis, or
ankylosing spondylitis adds greatly to the hazard
of damage to the cord or roots.
Neck trauma of almost any configuration may in particular
aggravate preexisting spondylotic symptoms.

There are in addition examples of spinal cord compression
that result from prolonged static hyperextension of the
cervical spine during a protracted period of stupor.

This accounts for some cases of quadriplegia following
a period of sustained unresponsiveness due to opiate or
sedative drug overdose Arterial hypotension
may be an added factor in some instance
Vertebral fracture and dislocation


What to do for suspected spinal
injury?
In cases of suspected spinal injury, the immediate
concern is that movement (especially flexion) of
the cervical spine be avoided. The patient should
ideally be placed supine on a firm, flat surface
(with one person assigned, if possible, to keeping
the head and neck immobile) and should be
transported by a vehicle that can accept the
litter. The board may be placed under the
patient, gently
rolling him to one side with the head, neck, and body
held in alignment. If moving the patient is not feasible,
the neck may be immobilized in place with a form collar
or an equivalent device that is contrived at the scene, or
even the examiner 's hands held firmly along the cervical
spine. The patient should ideally be transported by an
ambulance equipped with spine boards, to which the head
is fixed by straps. This provides a more effective means of
immobilization than sandbags or similar objects placed on
each side of the head and neck.
Pathology of Traumatic Spinal Cord
Injury
As a result of squeezing or shearing of the spinal
cord, there is destruction of gray and white
matter and a variable amount of hemorrhage,
chiefly in the more vascular central parts.
These changes, designated as traumatic
necrosis of the cord, are maximal at the level of
injury andat one or two segments above and
below
Separation of the components of traumatic necrosis,
such as hematomyelia, concussion, contusion, and
hema torrhachis (bleeding into the spinal canal) is not
of great value either clinically or pathologically.

As the lesion heals, it leaves a gliotic focus or
cavitation with variable amounts of hemosiderin and
iron pigment. Progressive cavitation (traumatic
syringomyelia) may develop after an interval of
months or years and, as the cavity enlarges beyond
the main lesion, lead to a delayed central or
incomplete transverse cord syndrome.
Experimental Spinal Cord Injury

Investigation of the pathophysiology of acute
spinal cord injury dates from the experimental
studies of Allen in the early 1900s.
His method consisted of dropping graded
weights onto the dura-covered thoracic cord of surgically
prepared animals. The technique was refined over the
years by precise measurements of the velocity, force, and
direction of the dropped weights. This type of impact
on the cord, of sufficient severity to render the ani
mal immediately paraplegic and abolish sensory-evoked
responses from structures below the lesion, indicates
that action potentials can no longer be conducted across
the injured spinal cord segment
Clinical Effects of Spinal Cord Injury
1) all voluntary movement in parts of the body below
the lesion is immediately lost
(2) sensation from the lower parts of the body is
abolished;
(3) reflex functions in segments of the isolated spinal
cord are suspended.

The last effect, termed spinal shock, involves tendon
as well as autonomic reflexes
Spinal Shock.

The loss of motor function at the time of injury,
tetraplegia with lesions of the fourth to fifth cervical
segments or above, and paraplegia with lesions of the
thoracic cord, are accompanied by immediate atonic
paralysis of bladder and bowel, gastric atony, loss of
sensation below a level corresponding to the spinal
cord lesion, muscular flaccidity, and almost complete
suppres sion of spinal segmental reflex activity below
the lesion
Stage of Heightened Reflex Activity

dorsiflexion of the big toe (Babinski sign);
fanning of the other toes; and later,
flexion or slow withdrawal movements of the
foot, leg,and thigh with contraction of the
tensor fascialata muscle
the "triple flexion
Tactile stimulation of the foot may suffice as a stimulus,
but a painful stimulus is more effective.

The Achilles reflexes and then the patellar reflexes return.
Retention of urine becomes less complete, and at
irregular intervals urine is expelled by spontaneous
contractions of the detrusor muscle.
Reflex defecation also begins.

After several months the withdrawal reflexes become
greatly exaggerated, to thepoint of flexor spasms, and
they may be accompanied by profuse sweating,
piloerection, and automatic emptying of the bladder
(occasionally of the rectum). This is the "mass reflex,"
which can be evoked by stimulation of the skin of the legs
or by some interoceptive stimulus, such as a full bladder.
Transient Cord Injury (Spinal Cord
Concussion)

These terms refer to a transient loss of motor sensory function of the spinal
cord that recovers within minute or hours but may persist in mild form for
days or more.
In most instances, the symptoms are rapidly diminish ing and few neurologic
abnormalities are found at the time of the first examination.

There are a number of such transient syndromes:
bibrachial weakness;
quadriparesis (occasionally hemiparesis);
paresthesias and dysesthesias in a similar distribution to the weakness;
sensory
symptoms alone ("burning hands syndrome")
Spinal cord concussion from direct impact is
observed
most frequently in athletes engaged in contact
sports (football, rugby, and hockey). An
incomplete and reversible myelopathy is
referable to the site and level of the injury.
Central Cord ("Schneider") Syndrome and Cruciate
Paralysis

A special from of acute cervical cord inj ury implicates
mainly central cord damage, resulting in the
loss of motor function solely or more severely in the upper
limbs than in the lower ones, and it particularly affects
the hands.
Bladder dysfunction with urinary retention occurs in some
cases
sensory loss is often slight (hyperpathia over the
shoulders and arms may be the only sensory abnormality).

Many of these instances are reversible but damage to the
centrally situated graymatter may leave an atrophic,
interruption of crossing pain and thermal fibers:
areflexic paralysis of the arms and hands
segmental loss of pain and thermal sensation from
most often associated with central cord :
Retroflexion injuries of the head and
necksyndrome,
other causes :
hematomyelia, fibro cartilaginous embolism, and
infarction from dissection of the vertebral artery

TREATMENT
1.) methylprednisolone in high dosage (bolus of 30
mg/kg followed by
5.4 mg/kg every hour), beginning within 8 h of the
injury and continued for 23 h for improvement of
motor and sensory function


2.) Hypotension is treated with infusions of nor mal
saline and may require the transient use of pressor
agents.

imaging examinations
to deter mine:
the alignment of vertebrae and pedicles,
fracture of the pedicle or vertebral body,
compression of the spinal cord or cauda equina as a
consequence of malalignment, or bone debris in the
spinal canal,
and the presence of tissue damage within the cord.

MRI is ideally suited to display these processes, but if it
is not available, myelog raphy with CT scanning is an
alternative
If a cervical spinal cord injury is associated
with vertebral dislocation, traction on the
neck may be necessary to secure proper
alignment and maintain immobilization
Early y surgical management of spinal cord injury:

1.) immobilization and traction
2.) surgical decompression, correction of
bony displacements, and removal of herniated disc tis
sue and intra- and extramedullary hemorrhage; often
the
spine is fixed at the same time by a bone graft or other
form of stabilization.
The greatest risks to the patient with spinal
cord injury occur in the first 10 days:
gastric dilatation, ileus, shock, and infection
are threats to life.
The aftercare of patients with paraplegia, in
addition
to substantial psychological support to allow
accommo dation to new limitations while
encouraging a productive life, is concerned
with management of bladder and bowel
disturbances, care of the skin, prevention of
pulmo nary embolism, and maintenance of
nutrition.
Decubitus ulcers can be reduced by frequent
turning to avoid pres sure necrosis, use of
special mattresses, and meticulous skin care.
Deep decubitus lesions require debridement
and full-thickness grafting.
Close surveillance is needed for bladder infection, which
is treated promptly .

Morning suppositories and periodically spaced enemas are
effective means of controlling fecal incontinence.

Chronic pain (present in 30 to 50 percent of cases)
requires the use of nonsteroidal antiinflammatory
medication, injections of local anesthetics, and
transcutaneous nerve stimulation.

A combination of carbamazepine or gabapentin and either
clonazepam or tricyclic antidepressants may be helpful in
cases of burning leg and trunk pain.

Effects of Radiation therapy
Transient Radiation Myelopathy:
An "early" type of radiation myelopathy
(appearing 3 to 6 months after radiotherapy)
is characterized mainly by spontaneous
uncomfortable sensations in the extremi ties.
The paresthesias may be evoked by neck
flexion (Lhermitte symptom).
Delayed Progressive Radiation Myelopath:
This is one of the most dreaded complications of
radiation therapy. sensory symptoms

The neurologic disorder first appears 6 months or more
after the course of radiation therapy, usually between
12 and 15 months (latent peri ods as long as 60 months
or longer have been reported).

paresthesia& and d ysesthesias of the feet or a
Lhermitte phenomenon, and similar symptoms in the
hands in cases of cervical cord damage.

Weakness of one or both legs usually follows the
sensory loss. Initially, local pain is absent, in distinction
to the effects of spinal metastases.

the sensory abnormalities are transitory as in the
syndrome described above; more often, additional
signs make their appearance and progress, at first
rapidly and then more slowly and irregularly, over a
period of
several weeks or months, with involvement of the cor
ticospinal and spinothalamic pathways.

Spinal Cord Injury caused by electrical
injuries
Any part of the peripheral or central nervous system
may be injured by electric currents and lightning. The
effects may be immediate, which is understandable, but
of greater interest are the instances of neurologic damage
that occur after a delay of 1 day to 6 weeks (1 week on
average) and a rarer syndrome of anterior hom cell dam
age that arises after many years. The immediate effects
are the result of direct heating of the nervous tissue, but
the pathogenesis of the delayed effects is not well under
stood.

SPINAL CORD TUMORS
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Neoplasms and other space-occupying lesions within
the
spinal canal can be divided into two groups
1) those that arise within the substance of the
spinal cord, either as a primary neural
neoplasm or as a metastasis, and invade and
destroy tracts and central gray structures
(intramedullary)
(2) those arising outside the spinal cord
(extramedullary), either from vertebral bodies
and epidural tissues (extradural) or in the
leptomeninges or roots (intradural
Intraspinal Tumors
The most common primary extramedullary
tumors are the neurofibromas and
meningiomas, which together constitute
approximately half of all intraspinal
neoplasms.
Primary intramedullary tumors of the spinal
cord have the same cellular origins as those
arising in the brain although the proportions
of particular cell types differ.
astrocytoma is the most common intra
medullary tumor if one excludes tumors
arising in the filum terminate
Oligodendrogliomas
are much less common. The remainder
(approximately 15 percent) consists of a
diverse group of nonglioma
tous tumors: lipomas, epidermoids, dermoids,
teratomas, hemangiomas,
hemangioblastomas, chordomas, schwan
nomas, and intraspinal metastatic carcinomas.
Spinal ependymomas arise from ependymal lining
of the central canal of the spinal cord.
The myxopapillary type originates from clusters of
ependymal cells in the
filum terminate.
The myxopapillary ependymoma that originates in the
filum terminate causes a special syndrome referable to
both lumbar roots (cauda equina) and
conus.
Intramedullary growths invade as well as compress
and distort fasciculi in the spinal cord white matter. As the
cord enlarges from the tumor growing within it or is com
pressed by a tumor from without, the free space around
the cord is eventually consumed, and the CSF below the
lesion becomes isolated or loculated from the remainder
of the circulating fluid above the lesion. This is marked by
Froin syndrome (xanthochromia and clotting of CSF from
greatly elevated protein content) and an interruption of
flow of contrast medium in the subarachnoid space.
secondary spinal cord tumors can also be subdivided
into intramedullary and extramedullary types.

Extradural metastases (carcinoma, lymphoma, myeloma) are the
most common of all spinal tumors . They account for the largest
group of patients who develop symptoms of myelopathy
while being cared for in hospital and are therefore likely
to be encountered in the course of neurologic consultations.

Extradural metastases arise from hematogenous deposits or extend
from tumors of the vertebral bodies or from a paraspinal tumor
extending via the intervertebral
foramina
Symptomato logy
Patients with spinal cord tumors are likely to
present with one of three clinical syndromes:
(1) a sensorimotor spinal tract syndrome, (2) a
painful radicular-spinal cord syndrome, or (3)
least often, an intramedullary
syringomyelic syndrome.
Pain and stiffness of the back may antedate signs of
spinal
cord disease or dominate the clinical picture in some
cases
of extramedullary tumor.
The back pain is usually worse when the patient lies
down or may become worse after several hours in the
recumbent position and be improved by sitting up.
In children, severe back pain associated with
spasm of paravertebral muscles is often prominent ini-
tially; scoliosis and spastic weakness of the legs come
later.
sensorimotor Spinal Tra ct Syndrome

The clinical picture is related predominantly to compression
and less often to invasion and destruction of spinal cord
tracts.
The signs of compression consist of a combination of (1)
an asymmetrical spastic weakness of the legs with thora
columbar lesions and of the arms and legs with cervical
lesions, (2) a sensory level on the trunk below which
perception of pain and temperature is reduced or lost, (3)
posterior column signs, and (4) a spastic bladder under
weak voluntary control.
Radicular- Spinal Cord Syndrome

Here the syn drome of spinal cord compression is combined with
radic ular pain, i.e., pain in the distribution of a sensory nerve
root.
The discomfort is described as knife-like or as a dull ache with
superimposed sharp stabs of pain, which radi ate in a distal
direction, i.e., away from the spine, and are intensified by
coughing, sneezing, or straining.

Segmental sensory changes (paresthesias, impaired perception of
pinprick and touch) or motor disturbances (cramp, atro
phy, fascicular twitching, and loss of tendon reflexes) and
an ache in the spine, in addition to the radicular pain,
are the usual manifestations.
Intramedullary Syringo myelic Syndrome No
single symptom is unique to the
intramedullary tumors . Some degree of pain,
sometimes minor, is common and isalmost
invariably present with tumors of the filum
ter minale.