You are on page 1of 23

Anatomy and localization of spinal cord disorders

Author
Andrew Eisen, MD, FRCPC
Section Editor
Michael J Aminoff, MD, DSc
Deputy Editor
Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Nov 2015. | This topic last updated: Nov 18, 2015.
INTRODUCTION Because it is the primary pathway of communication between the brain and
peripheral nervous system, diseases that affect the spinal cord are clinically eloquent. Many of
these disease processes have a predilection for targeting specific areas or tracts within the spinal
cord. As a result, knowledge of spinal cord anatomy and recognition of typical common spinal
cord syndromes are useful in the evaluation of a patient with a myelopathy and can allow for a
more directed diagnostic evaluation.
The anatomy of the spinal cord and its vascular supply and clinical features of common spinal
cord syndromes will be reviewed here. Diseases that affect the spinal cord are discussed
separately. (See "Disorders affecting the spinal cord".)
SPINAL CORD ANATOMY There are 31 spinal cord segments, each with a pair of ventral
(anterior) and dorsal (posterior) spinal nerve roots, which mediate motor and sensory function,
respectively. The ventral and dorsal nerve roots combine on each side to form the spinal nerves
as they exit from the vertebral column through the neuroforamina (figure 1).
Longitudinal organization The spinal cord is divided longitudinally into four regions: the
cervical, thoracic, lumbar, and sacral cord. The spinal cord extends from the base of the skull and
terminates near the lower margin of the first lumbar vertebral body (L1). Below that level, the
spinal canal contains the lumbar, sacral, and coccygeal spinal nerve roots that comprise the
cauda equina.
Because the spinal cord is shorter than the vertebral column, vertebral and spinal cord segmental
levels are not necessarily the same. The C1 through C8 spinal cord segments lie between the C1
through C7 vertebral levels. The T1 through T12 cord segments lie between T1 through T8. The
five lumbar cord segments are situated at the T9 through T11 vertebral levels, and the S1 through
S5 segments lie between T12 to L1. The C1 through C7 nerve roots emerge above their
respective vertebrae; the C8 nerve root emerges between the C7 and T1 vertebral bodies. The
remaining nerve roots emerge below their respective vertebrae (figure 2).
Cervical cord The first cervical vertebra (the atlas) and the second cervical vertebra (the axis),
upon which the atlas pivots, support the head at the atlanto-occiput junction. The interface
between the first and second vertebra is called the atlanto-axis junction.
Cervical spinal segments innervate the skin and musculature of the upper extremity and
diaphragm (figure 3 and figure 4):
C3 through C5 innervate the diaphragm, the chief muscle of inspiration, via the phrenic
nerve
C4 through C7 innervate the shoulder and arm musculature
C6 through C8 innervate the forearm extensors and flexors
C8 through T1 innervate the hand musculature

Thoracic cord The thoracic vertebral segments are defined by those that have an attached
rib. The spinal roots form the intercostal nerves that run along the inferior rib margin and innervate
the associated dermatomes, as well as the intercostal abdominal wall musculature. These
muscles are the main muscles of expiration. The thoracic cord also contains the sympathetic
nerves that innervate the heart and abdominal organs.
Lumbosacral cord The lumbosacral spinal cord contains the segments that innervate the
muscles and dermatomes of the lower extremity, as well as the buttocks and anal regions (figure
5 and figure 6). Sacral nerve roots S3 through S5 originate in the narrow terminal part of the cord,
called the conus medullaris.
L2 and L3 mediate hip flexion
L3 and L4 mediate knee extension
L4 and L5 mediate ankle dorsiflexion and hip extension
L5 and S1 mediate knee flexion
S1 and S2 mediate ankle plantar flexion
Sacral nerve roots also provide parasympathetic innervation of pelvic and abdominal organs,
while lumbar nerve roots L1 and L2 contain sympathetic innervation of some pelvic and abdominal
organs.
Cauda equina In adults, the spinal cord ends at the level of the first or second lumbar vertebral
bodies. The filum terminale, a thin connective tissue filament that descends from the conus
medullaris with the spinal nerve roots, is connected to the third, fourth, and fifth sacral vertebrae;
its terminal part is fused to the periosteum at the base of the coccygeal bone.
Pathology at the T12 and L1 vertebral level affects the lumbar cord. Injuries to L2 frequently
damage the conus medullaris. Injuries below L2 usually involve the cauda equina and represent
injuries to spinal roots rather than to the spinal cord (figure 2).
Cross-sectional anatomy The spinal cord contains the gray matter, the butterfly-shaped
central region, and the surrounding white matter tracts. The spinal cord gray matter, which
contains the neuronal cell bodies, is made up of the dorsal and ventral horns, each divided into
several laminae [1,2].
Dorsal horn The dorsal horn is the entry point of sensory information into the central nervous
system. It is divided into six layers or laminae that process sensory information. More than a relay
station for the transmission of sensory information, the dorsal horn also modulates pain
transmission through spinal and supraspinal regulatory circuits. Three major categories of
sensory input that are important to the clinical examination of spinal cord pathology include:
Afferents from muscle spindles that participate in spinal cord reflexes.
Axons, mostly small and unmyelinated, mediating sensory modalities of pain and
temperature. These can travel up and down a few segments before synapsing with the
second order neurons, which then cross the midline of the cord in the anterior commissure,
just anterior to the central canal, and then enter the contralateral anterior or lateral
spinothalamic tract.
Axons mediating the sensory modalities of proprioception, vibration, and touch
discrimination. These large myelinated fibers pass through the dorsal horn to enter the
ipsilateral dorsal column.
The anatomy of the sensory system is discussed in more detail separately. (See "Approach to the
patient with sensory loss".)

Ventral horn The motor nuclei of the spinal cord are contained within the ventral horn, which
also contains interneurons mediating information from other descending tracts of the pyramidal
and extrapyramidal motor systems. These ultimately synapse on the alpha and gamma motor
neurons, which subsequently leave the ventral horn via the ventral nerve root to terminate at the
neuromuscular junction.
White matter tracts The major white matter tracts of clinical importance in the assessment of
spinal cord disease include:
The dorsal or posterior columns, the fasciculus gracilis, and the fasciculus cuneatus. These
contain sensory information regarding joint position and vibration. They are organized
anatomically such that cervical sections lie most laterally and sacral segments most medially
(figure 7). These pathways will cross in the medulla; hence, in the spinal cord, these tracts
contain ipsilateral sensory representation.
The anterior and lateral spinothalamic tracts contain sensory information regarding pain,
temperature, and touch. These axons have crossed in the ventral commissure and therefore
contain contralateral sensory representation. This tract is somatotopically organized with
cervical inputs located most medially and sacral inputs most laterally (figure 7).
The corticospinal tracts contain the upper motor neurons that originate in M1 of the primary
motor cortex. These axons synapse either directly or indirectly on the anterior horn cells,
and as such have distinct sites of anatomic origin within M1 [3]. A single corticomotoneuronal
axon synapses with many anterior horn cells of its own motor neuron pool and also with
those of agonists and antagonists, allowing for coordination of highly skilled movements.
The lateral corticospinal tract contains the majority (80 to 85 percent) of these fibers, which have
previously decussated (crossed) at the cervicomedullary junction and therefore provide input to
the ipsilateral musculature. Fibers are somatotopically organized within the tract such that fibers
destined for upper extremity motor control lie most medially, while fibers controlling the lower
extremity lie more laterally (figure 7). The anterior corticospinal tract contains undecussated
fibers, some of which will subsequently cross at the spinal level through the anterior commissure.
Other descending tracts include:
The tectospinal tract originates in the superior colliculus and mediates reflex postural
movements of the head in response to visual and/or acoustic input.
The rubrospinal pathway originates from the magnocellular subdivision of the red nucleus,
markedly developed in reptiles, birds, and other lower mammals, but is much less evident
in primates, in which there are direct connections with motoneurons innervating wrist
muscles.
The vestibulospinal tracts arise from the vestibular nuclei and facilitate spinal cord reflexes
and muscle tone to maintain posture.
Reticulospinal connections are widely assumed to be responsible for coordinated gross
movements primarily of proximal muscles, whereas the corticospinal tract mediates fine
movements, particularly of the hand [4]. However, the reticulospinal system may form a
parallel pathway to distal muscles, alongside the corticospinal tract. As a result,
reticulospinal neurons may influence upper limb muscle activity after damage to the
corticospinal system as may occur in stroke [5,6].
Other ascending tracts include:
The dorsal and ventral spinocerebellar tracts carry inputs mediating unconscious
proprioception directly to the cerebellum

The spinoreticular tract carries deep pain input to the reticular formation of the brainstem
Autonomic fibers Autonomic fibers of hypothalamic and brainstem origin descend in the
lateral aspect of the spinal cord but not in a well-defined tract. These synapse with cell bodies in
the intermediolateral columns of the central gray matter of the spinal cord. Sympathetic fibers exit
between T1 and L2, and parasympathetic fibers exit between S2 and S4.
The sympathetic neurons lie in the lateral horn of the central gray matter at spinal levels T1-L3.
The preganglionic fibers exit via the ventral root, spinal nerve, and ventral ramus to reach the
paravertebral ganglion. Many will synapse at the paravertebral ganglion, others pass through it
to terminate on postganglionic neurons (eg, coeliac, superior mesenteric, and inferior mesenteric
ganglia) more proximate to their end organ.
Parasympathetic neurons originate in the sacral spinal cord and exit the spinal cord with other
efferents to the ventral ramus. After leaving the ventral ramus, they may subsequently join with
sympathetic nerves to reach the viscera. These preganglionic fibers then synapse with a diffuse
network of terminal ganglion cells that affect organs in the pelvis.
Autonomic dysfunction is an important determinant of site, extent, and severity of spinal cord
pathology. Many autonomic functions can be affected by spinal cord pathology, but for clinical
evaluation, the most useful symptoms relate to bladder control.
Autonomic bladder control is primarily parasympathetic, and is unaffected by isolated injury to the
sympathetic fibers. Voluntary bladder control is under somatomotor control, mediated by motor
fibers originating from the anterior horn cells at levels S2-S4. A spinal cord lesion that interrupts
descending motor and autonomic tracts above the S2 level produces an "automatic bladder" that
cannot be emptied voluntarily, but empties reflexly when expanded to a certain degree, the socalled neurogenic bladder [7-10]. Loss of descending inhibition of segmental reflex control leads
to urinary urgency and incontinence. Injury to S2-S4 spinal levels interrupts the bladder reflex
circuit; the bladder becomes flaccid, and fills beyond capacity with overflow incontinence.
Other autonomic functions are disturbed by spinal cord pathology. The effects of spinal cord injury
on the colon and rectum are similar to those on the bladder. Spinal cord transections interrupt
voluntary control of the external sphincter and produce constipation. Sacral lesions cause a loss
of the anal reflex and rectal incontinence. Impotence can result from spinal cord lesions at any
level. Spinal cord injuries can also affect cardiovascular function, most dramatically with lesions
above T6 which can produce a phenomenon of autonomic dysreflexia. (See "Chronic
complications of spinal cord injury and disease", section on 'Autonomic dysreflexia'.)
Blood supply A single anterior and two posterior spinal arteries supply the spinal cord (figure
8). The anterior spinal artery supplies the anterior two-thirds of the cord [11-15]. The posterior
spinal arteries primarily supply the dorsal columns. The anterior and posterior spinal arteries arise
from the vertebral arteries in the neck and descend from the base of the skull. Various radicular
arteries branch off the thoracic and abdominal aorta to provide additional blood supply to the
spinal arteries. The largest and most consistently present of these radicular branches is the great
ventral radicular artery or the artery of Adamkiewicz, which supplies the anterior spinal artery [16].
This artery enters the spinal cord anywhere between T5 and L1 (usually between T9 and T12).
In most people, the anterior spinal artery passes uninterrupted along the entire length of the spinal
cord; in others, it is discontinuous, usually in its midthoracic segment, making these individuals
more susceptible to vascular injury. The primary watershed area of the spinal cord in most people
is in the midthoracic region.

The vascular anatomy of the spinal cord is discussed in detail separately. (See "Spinal cord
infarction: Vascular anatomy and etiologies", section on 'Vascular anatomy'.)
CLINICAL LOCALIZATION A spinal cord lesion may be suspected when there are bilateral
motor and sensory signs or symptoms that do not involve the head or face. Motor deficits are
manifest by weakness and long tract signs (spasticity, increased reflexes, Babinski sign) [8,1719]. When the pathology is localized or segmental, these findings will be present in muscle groups
innervated below that level and will be normal above. A sensory level, with normal sensation
above and reduced or absent below, can also often be defined and should be specifically sought.
Other so-called segmental signs include lower motor neuron findings (atrophy, flaccid weakness,
loss of reflexes) in a myotomal distribution at the specific level of involvement; however, these
are usually not elicitable in thoracic lesions. (See "The detailed neurologic examination in adults",
section on 'Motor examination' and "The detailed neurologic examination in adults", section on
'Reflex examination' and "The detailed neurologic examination in adults", section on 'Sensory
examination'.)
As well as longitudinal localization within the spinal cord, it can also be helpful to distinguish
specific areas of functional loss with a spinal cord level (or across spinal cord levels for
nonsegmental pathologies). Some disorders affecting the spinal cord preferentially affect different
structures, and therefore careful testing of all spinal cord functions, including motor, reflex, and
all sensory modalities, and sphincter function is important for clinical localization.
Several distinct spinal cord syndromes are recognized. These are useful in the clinical evaluation,
as they often correspond to distinct pathologies. These are summarized in the table and are
discussed below (table 1).
Segmental syndrome Pathologies that affect all functions of the spinal cord at one or more
levels produce a segmental syndrome. Loss of function may be total or incomplete. A total cord
transection syndrome results from the cessation of function in all ascending and descending
spinal cord pathways and results in the loss of all types of sensation and loss of movement below
the level of the lesion. Less profound injuries produce a similar pattern of deficits, which are less
severe: ie, weakness rather than paralysis and decreased sensation rather than anesthesia.
Acute transection can cause spinal shock, with a flaccid paralysis, urinary retention, and
diminished tendon reflexes. This is usually temporary, and increased tone, spasticity, and
hyperreflexia will usually supervene in days or weeks after the event.
Transverse injuries above C3 involve cessation of respiration and are often fatal if acute. Cervical
cord lesions that spare the phrenic nerve but impair intercostal nerve function can produce
respiratory insufficiency. Lesions above the L2 cord level will cause impotence and spastic
paralysis of bladder. There is loss of voluntary control of the bladder, which will empty
automatically by reflex action.
Causes of a cord segmental syndrome include acute myelopathies, such as traumatic injury and
spinal cord hemorrhage. Epidural or intramedullary abscess, tumors, and transverse myelitis may
have a more subacute presentation. (See "Disorders affecting the spinal cord".)
Dorsal (posterior) cord syndrome Dorsal cord syndrome results from the bilateral
involvement of the dorsal columns, the corticospinal tracts, and descending central autonomic
tracts to bladder control centers in the sacral cord (figure 9). Dorsal column symptoms include
gait ataxia and paresthesias. Corticospinal tract dysfunction produces weakness that, if acute, is
accompanied by muscle flaccidity and hyporeflexia and, if chronic, by muscle hypertonia and
hyperreflexia. Extensor plantar responses and urinary incontinence may be present.

Causes of a dorsal cord syndrome include multiple sclerosis (more typically the primary
progressive form), tabes dorsalis, Friedreich ataxia, subacute combined degeneration, vascular
malformations, epidural and intradural extramedullary tumors, cervical spondylotic myelopathy,
and atlantoaxial subluxation. (See "Disorders affecting the spinal cord" and "Cervical spondylotic
myelopathy".)
Ventral (anterior) cord syndrome Ventral cord or anterior spinal artery syndrome usually
includes tracts in the anterior two-thirds of the spinal cord, which include the corticospinal tracts,
the spinothalamic tracts, and descending autonomic tracts to the sacral centers for bladder control
(figure 10). Corticospinal tract involvements produce weakness and reflex changes. A
spinothalamic tract deficit produces the bilateral loss of pain and temperature sensation. Tactile,
position, and vibratory sensation are normal. Urinary incontinence is usually present.
The causes of a ventral cord syndrome include spinal cord infarction, intervertebral disc
herniation, and radiation myelopathy. (See "Disorders affecting the spinal cord".)
Brown-Sequard (hemi-cord) syndrome A lateral hemisection syndrome, also known as the
BrownSequard syndrome, involves the dorsal column, corticospinal tract, and spinothalamic
tract unilaterally (figure 11). This produces weakness, loss of vibration, and proprioception
ipsilateral to the lesion and loss of pain and temperature on the opposite side. The unilateral
involvement of descending autonomic fibers does not produce bladder symptoms. While there
are many causes of this syndrome, knife or bullet injuries and demyelination are the most
common. Rarer causes include spinal cord tumors, disc herniation, infarction, and infections.
(See "Disorders affecting the spinal cord".)
Central cord syndromes The central cord syndrome is characterized by loss of pain and
temperature sensation in the distribution of one or several adjacent dermatomes at the site of the
spinal cord lesion caused by the disruption of crossing spinothalamic fibers in the ventral
commissure (figure 12). Dermatomes above and below the level of the lesion have normal pain
and temperature sensation, creating the so-called "suspended sensory level." Vibration and
proprioception are often spared.
As a central lesion enlarges, it may encroach on the medial aspect or the corticospinal tracts or
on the anterior horn gray matter, producing weakness in the analgesic areas. Fibers mediating
the deep tendon reflexes are interrupted as they pass from the dorsal to the ventral horn, thus
causing tendon reflex loss in the analgesic areas. There are usually no bladder symptoms.
The classic causes of a central cord syndrome are slow-growing lesions such as syringomyelia
or intramedullary tumor. However, central cord syndrome is most frequently the result of a
hyperextension injury in individuals with long-standing cervical spondylosis. This form of central
cord syndrome is characterized by disproportionately greater motor impairment in upper
compared with lower extremities, bladder dysfunction, and a variable degree of sensory loss
below the level of injury [20-22]. (See "Cervical spondylotic myelopathy".)
Pure motor syndrome A pure motor syndrome produces weakness without sensory loss or
bladder involvement. This may involve only the upper motor neurons, producing hyperreflexia and
extensor plantar responses, or only the lower motor neuron bilaterally, producing muscle atrophy
and fasciculations. Other disorders involve both the upper and lower motor neurons and produce
mixed signs.
The causes of a pure motor syndrome include chronic myelopathies such as HTLV-I myelopathy,
hereditary spastic paraplegia, primary lateral sclerosis, amyotrophic lateral sclerosis, progressive

muscular atrophy, post-polio syndrome, and electric shock-induced myelopathy. (See "Disorders
affecting the spinal cord".)
Conus medullaris syndrome Lesions at vertebral level L2 often affect the conus medullaris.
There is early and prominent sphincter dysfunction with flaccid paralysis of the bladder and
rectum, impotence, and saddle (S3-S5) anesthesia. Leg muscle weakness may be mild if the
lesion is very restricted and spares both the lumbar cord and the adjacent sacral and lumbar
nerve roots.
Causes include disc herniation, spinal fracture, and tumors [7,23].
Cauda equina syndrome Though not a spinal cord syndrome, cauda equina syndrome is
considered here because its location within the spinal canal subjects it to many of the same
disease processes that cause myelopathy. The syndrome is caused by the loss of functions of
two or more of the 18 nerve roots constituting the cauda equina. Deficits usually affect both legs
but are often asymmetric. Symptoms include [24-26]:
Low back pain accompanied by pain radiating into one or both legs. Radicular pain reflects
involvement of dorsal nerve roots and may have localizing value [24].
Weakness of plantar flexion of the feet with loss of ankle jerks occurs with mid cauda
equina lesions, involving S1, S2 roots. Involvement of progressively higher levels leads to
corresponding weakness in other muscles (figure 5).
Bladder and rectal sphincter paralysis usually reflect involvement of S3-S5 nerve roots
[24,25].
Sensory loss of all sensory modalities occurs in the dermatomal distribution of the affected
nerve roots (figure 6).
Many etiologies can cause a cauda equina syndrome, including intervertebral disc herniation,
epidural abscess, epidural tumor, intradural extramedullary tumor, lumbar spine spondylosis, and
a number of inflammatory conditions including spinal arachnoiditis, chronic inflammatory
demyelinating polyneuropathy, and sarcoidosis [23,27-32]. The cauda equina can also be the
primary site of involvement in carcinomatous meningitis and a number of infections (eg,
cytomegalovirus, herpes simplex virus, herpes zoster virus, Epstein Barr virus, Lyme disease,
mycoplasma, and tuberculosis). (See "Lumbar spinal stenosis: Pathophysiology, clinical features,
and diagnosis" and "Clinical features and diagnosis of neoplastic epidural spinal cord
compression, including cauda equina syndrome".)
Lhermitte's sign This well-described sign describes a sensation of electric shock-like
sensations that run down the back and/or limbs during flexion of the neck. This generally occurs
with pathologies involving the cervical spinal cord, but is not specific to etiology, occurring in
patients with cervical spondylotic myelopathy [33], multiple sclerosis, radiation myelopathy, and
vitamin B12 deficiency, among others. It can also occur with cervical nerve root pathology.
DIAGNOSIS The differential diagnosis of myelopathy is wide, but can be significantly narrowed
by the clinical syndrome (table 1). Other features in the examination and history also limit the
differential diagnosis and tailor the diagnostic work-up. Clinical features of some of the more
common causes of myelopathy are outlined in the Table (table 2). These are discussed in detail
separately (see "Disorders affecting the spinal cord").
For patients with a clinical syndrome that suggests a localized process within the spinal cord (eg,
transection syndrome, central cord syndrome, ventral cord syndrome, etc), an imaging study,
usually magnetic resonance imaging (MRI), of the relevant section of the spinal cord is usually
required [19,34]. Administration of gadolinium contrast is often helpful. When an infectious or

inflammatory disorder is suspected, cerebrospinal fluid examination may be helpful. The role of
positron emission tomography in evaluating patients with myelopathy is under investigation; it
appears to be particularly sensitive for neoplastic disease [35].
In general, the pace at which spinal cord deficits appear dictate the urgency of the neurologic
evaluation. Even when the deficits are not severe, acute myelopathic signs need to be evaluated
urgently because neurologic deterioration can occur abruptly, and the clinical deficit at the time
of intervention often dictates the chances of recovery. This is true particularly for compressive
etiologies such as spinal cord metastases and epidural spinal abscess.
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials,
The Basics and Beyond the Basics. The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or five key questions a
patient might have about a given condition. These articles are best for patients who want a general
overview and who prefer short, easy-to-read materials. Beyond the Basics patient education
pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to
12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a variety
of subjects by searching on patient info and the keyword(s) of interest.)
Basics topics (see "Patient information: Central spinal cord syndrome
Basics)" and "Patient information: Cauda equina syndrome (The Basics)")

(The

SUMMARY Disorders that affect the spinal cord often target specific structural and functional
anatomic regions, producing distinct clinical syndromes. The spinal cord syndromes are
summarized in the table (table 1). The clinical syndrome along with other features in the
examination and history usually significantly limits the differential diagnosis and tailors the
diagnostic work-up (table 2). (See "Disorders affecting the spinal cord".)
Use of UpToDate is subject to the Subscription and License Agreement.

GRAPHICS

Cross-sectional anatomy of the spinal cord

Longitudinal organization of spinal cord, spinal nerves, and


vertebrae

Nerve roots and peripheral nerves corresponding to the


principal movements of the upper extremity

The letters labeling the movements form a spiral down the extremity. The nerve
roots and peripheral nerves corresponding to each movement are listed below. Figure
redrawn with permission from Gelb, DJ. The Neurologic Examination.

Cervical dermatomes

Schematic representation of the cervical and T1 dermatomes. There is no C1


dermatome. Patients with nerve root syndromes may have pain, paresthesias, and
diminished sensation in the dermatome of the nerve that is involved.

Nerve roots and peripheral nerves corresponding to the


principal movements of the lower extremity

The letters labeling the movements proceed in order from proximal to distal down the
front of the limb, and then repeat from proximal to distal down the back of the limb.
The nerve roots and peripheral nerves corresponding to each movement are listed
below.

Lumbosacral dermatomes

Schematic representation of the lumbosacral dermatomes. Patients with sciatica may


have pain, paresthesias, and diminished sensation in the dermatome of the nerve root
that is involved.

Major white matter tracts of the spinal cord

Cross section of the spinal cord demonstrating arterial blood


supply

Spinal cord syndromes

Location of lesion in dorsal cord syndrome

Location of lesion in ventral cord syndrome

Location of lesion in Brown-Sequard syndrome

Location of lesion in central cord syndrome

Important causes of spinal cord dysfunction*

REFERENCES
1. REXED B. SOME ASPECTS OF THE CYTOARCHITECTONICS AND SYNAPTOLOGY OF
THE SPINAL CORD. Prog Brain Res 1964; 11:58.
2. REXED B. A cytoarchitectonic atlas of the spinal cord in the cat. J Comp Neurol 1954; 100:297.
3. Rathelot JA, Strick PL. Subdivisions of primary motor cortex based on cortico-motoneuronal
cells. Proc Natl Acad Sci U S A 2009; 106:918.
4. Kuypers H. Anatomy of the descending pathways. In: Handbook of Physiology: The Nervous
System II, Brookhart J, Mountcastle VB. (Eds), American Physiological Society, Bethesda, MD
1981.
5. Baker SN. The primate reticulospinal tract, hand function and functional recovery. J Physiol
2011; 589:5603.
6. Riddle CN, Edgley SA, Baker SN. Direct and indirect connections with upper limb motoneurons
from the primate reticulospinal tract. J Neurosci 2009; 29:4993.
7. Wagner R, Jagoda A. Spinal cord syndromes. Emerg Med Clin North Am 1997; 15:699.
8. BAKER AB. SPINAL CORD LOCALIZATION. J Lancet 1965; 85:269.
9. Abdel-Azim M, Sullivan M, Yalla SV. Disorders of bladder function in spinal cord disease. Neurol
Clin 1991; 9:727.
10. Seftel AD, Oates RD, Krane RJ. Disturbed sexual function in patients with spinal cord disease.
Neurol Clin 1991; 9:757.
11. Biglioli P, Roberto M, Cannata A, et al. Upper and lower spinal cord blood supply: the continuity
of the anterior spinal artery and the relevance of the lumbar arteries. J Thorac Cardiovasc Surg
2004; 127:1188.
12. GILLILAN LA. The arterial blood supply of the human spinal cord. J Comp Neurol 1958; 110:75.
13. Kawaharada N, Morishita K, Hyodoh H, et al. Magnetic resonance angiographic localization of
the artery of Adamkiewicz for spinal cord blood supply. Ann Thorac Surg 2004; 78:846.
14. Lasjaunias P, Vallee B, Person H, et al. The lateral spinal artery of the upper cervical spinal
cord. Anatomy, normal variations, and angiographic aspects. J Neurosurg 1985; 63:235.
15. McCormick PC, Stein BM. Functional anatomy of the spinal cord and related structures.
Neurosurg Clin N Am 1990; 1:469.
16. Skalski JH, Zembala M. Albert Wojciech Adamkiewicz: the discoverer of the variable vascularity
of the spinal cord. Ann Thorac Surg 2005; 80:1971.

17. HADDEN SB. Diagnosis of spinal cord disease. Med Clin North Am 1951; 35:1765.
18. Miller DH, McDonald WI, Blumhardt LD, et al. Magnetic resonance imaging in isolated
noncompressive spinal cord syndromes. Ann Neurol 1987; 22:714.
19. Offenbacher H. The diagnostic impact of magnetic resonance imaging on the evaluation of
suspected spinal cord disease. Wien Klin Wochenschr 1992; 104:589.
20. Morse SD. Acute central cervical spinal cord syndrome. Ann Emerg Med 1982; 11:436.
21. Dickman CA, Hadley MN, Pappas CT, et al. Cruciate paralysis: a clinical and radiographic
analysis of injuries to the cervicomedullary junction. J Neurosurg 1990; 73:850.
22. Harrop JS, Sharan A, Ratliff J. Central cord injury: pathophysiology, management, and
outcomes. Spine J 2006; 6:198S.
23. Podnar S. Epidemiology of cauda equina and conus medullaris lesions. Muscle Nerve 2007;
35:529.
24. Orendcov J, Czkov D, Kafka J, et al. Cauda equina syndrome. Prog Neurobiol 2001;
64:613.
25. Valen B, Rolfsen LC. [The cauda equina syndrome]. Tidsskr Nor Laegeforen 2003; 123:643.
26. Fraser S, Roberts L, Murphy E. Cauda equina syndrome: a literature review of its definition and
clinical presentation. Arch Phys Med Rehabil 2009; 90:1964.
27. Belinchn JM, Campos J, Merino J, et al. [Chronic spontaneous lumbar epidural hematoma].
Neurocirugia (Astur) 2005; 16:533.
28. Cohen DB. Infectious origins of cauda equina syndrome. Neurosurg Focus 2004; 16:e2.
29. Johnsson KE, Sass M. Cauda equina syndrome in lumbar spinal stenosis: case report and
incidence in Jutland, Denmark. J Spinal Disord Tech 2004; 17:334.
30. Kebaish KM, Awad JN. Spinal epidural hematoma causing acute cauda equina syndrome.
Neurosurg Focus 2004; 16:e1.
31. Lenehan B, Sullivan P, Street J, Dudeney S. Epidural abscess causing cauda equina syndrome.
Ir J Med Sci 2005; 174:88.
32. Wright MH, Denney LC. A comprehensive review of spinal arachnoiditis. Orthop Nurs 2003;
22:215.
33. Baron EM, Young WF. Cervical spondylotic myelopathy: a brief review of its pathophysiology,
clinical course, and diagnosis. Neurosurgery 2007; 60:S35.
34. Do-Dai DD, Brooks MK, Goldkamp A, et al. Magnetic resonance imaging of intramedullary
spinal cord lesions: a pictorial review. Curr Probl Diagn Radiol 2010; 39:160.
35. Flanagan EP, Hunt CH, Lowe V, et al. [(18)F]-fluorodeoxyglucose-positron emission
tomography in patients with active myelopathy. Mayo Clin Proc 2013; 88:1204.
Topic 5110 Version 8.0

You might also like