Anatomy and Localization of Spinal Cord Disorders

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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: Jul 2020. | This topic last updated: Jun 24, 2020.
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.
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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 tract (CST) contains the motor neurons that mediate cortical control of bulbar
and spinal cord activity. Most CST axons originate in cortical layer V of the primary motor and
sensory cortex [3,4]. A smaller proportion arise from the premotor cortex, supplementary motor
cortex, and secondary somatosensory cortices. These axons synapse either directly or indirectly
on the anterior horn cells, as well as the dorsal spinal cord, traditionally viewed as the "sensory
horn." Different muscle functions are generated by separate populations of cortical motoneurons,
which are widely separated within the neocortex [5]. Cortical motoneuronal synapses are likely
widely distributed onto many anterior horn cells, allowing for coordination of highly skilled
movements. The numeric relationship between cortical motoneurons, their axons, and anterior
horn cells is not one-to-one. Each anterior horn cell receives input from many
corticomotoneurons (convergence), and a single corticomotoneuron innervates many different
anterior horn cells of the same, agonist and antagonist, motor neuron pools (divergence) [6,7].
The lateral CST 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 CST 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; is
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 CST mediates fine movements,
particularly of the hand [8]. However, the reticulospinal system may form a parallel pathway to
distal muscles, alongside the CST. As a result, reticulospinal neurons may influence upper limb
muscle activity after damage to the corticospinal system, as may occur in stroke [9,10].
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 so-called neurogenic
bladder [11-14]. 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 [15-19]. 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 [20]. 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) [12,21-23]. 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 (CSTs), and descending central autonomic tracts to
bladder control centers in the sacral cord (figure 9). Dorsal column symptoms include gait ataxia and
paresthesias. CST 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 CSTs, the spinothalamic tracts,
and descending autonomic tracts to the sacral centers for bladder control (figure 10). CST
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 (hemicord) syndrome — A lateral hemisection syndrome, also known as the

Brown-Sequard syndrome, involves the dorsal column, CST, 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 — A symptomatic central cord lesion typically encroaches on the medial
aspect of the CSTs or on the anterior horn gray matter, producing weakness that is more prominent in
the arms than the legs. Fibers mediating the deep tendon reflexes are interrupted as they pass from
the dorsal to the ventral horn, thus causing tendon reflex loss at the level of the spinal cord lesion.
There are usually no bladder symptoms, but urinary retention may occur.
Loss of pain and temperature sensation in the distribution of one or several adjacent dermatomes at
the site of the spinal cord lesion is caused by disruption of crossing spinothalamic fibers in the ventral
commissure (figure 12). Dermatomes above and below the level of the lesion have relatively normal
pain and temperature sensation, creating the so-called "suspended sensory level." Vibration and
proprioception are often spared.
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
[24-26]. (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 human T-lymphotropic
virus type I (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 [11,27].
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 [28-30]:
● 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 [28].
● 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 reflects involvement of S3-S5 nerve roots [28,29].
● 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 [27,31-36]. 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".)
Lhermitte 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 [37], 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
[23,38]. 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 [39].
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
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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 10th 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 education: Central spinal cord syndrome (The Basics)" and "Patient
education: Cauda equina syndrome (The Basics)")
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".)
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34. Kebaish KM, Awad JN. Spinal epidural hematoma causing acute cauda equina syndrome.
Neurosurg Focus 2004; 16:e1.
35. Lenehan B, Sullivan P, Street J, Dudeney S. Epidural abscess causing cauda equina syndrome.
Ir J Med Sci 2005; 174:88.
36. Wright MH, Denney LC. A comprehensive review of spinal arachnoiditis. Orthop Nurs 2003;
22:215.
37. Baron EM, Young WF. Cervical spondylotic myelopathy: a brief review of its pathophysiology,
clinical course, and diagnosis. Neurosurgery 2007; 60:S35.
38. 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.
39. 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 10.0
GRAPHICS
Cross-sectional anatomy of the spinal cord
Graphic 65024 Version 3.0
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.
In: Introduction to Clinical Neurology. Woburn, MA, Butterworth-Heinemann 2000.
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.
Figure redrawn with permission from Gelb DJ. The Neurologic Examination. In:
Introduction to Clinical Neurology. Woburn, MA, Butterworth-Heinemann 2000.
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
Reproduced with permission from: Craven, J. Spinal Cord. Anaesthesia and intensive
care medicine 2004; 5:144. Copyright ©2004 Elsevier.
Spinal cord syndromes
Syndrome Clinical manifestations Causes
Segmental Loss of all sensory modalities, Trauma, hemorrhage, epidural abscess, transverse
(transection) weakness below affected level; myelitis, epidural metastasis
syndrome bladder dysfunction
Dorsal cord Loss of proprioception, vibratory Tabes dorsalis, Friedreich ataxia, subacute combined
syndrome sensation; variable weakness and degeneration, AIDS myelopathy, epidural metastases,
bladder dysfunction cervical spondylotic myelopathy, multiple sclerosis
Ventral cord Loss of pain and temperature Spinal cord infarction, disc herniation, radiation
syndrome (anterior sensation, weakness, bladder myelopathy, HTLV-1
spinal artery dysfunction
syndrome)
Brown Sequard Ipsilateral weakness and loss of Knife or bullet injury, multiple sclerosis
syndrome proprioception; contralateral loss of
pain and temperature sensation
Central cord Segmental loss of pain and Syringomyelia, intramedullary tumor, acute injury in
syndrome temperature, weakness often cervical spondylotic myelopathy
greater in the arms than legs
Pure motor Weakness without sensory Poliomyelitis, amyotrophic lateral sclerosis, HTLV-1,
syndrome disturbance hereditary spastic paraplegia, lathyrism
Conus medullaris Bladder and rectal dysfunction, Disc herniation, trauma, tumors
syndrome saddle anesthesia
Cauda equina Asymmetric multiradicular pain, leg Disc herniation, arachnoiditis, tumor, lumbar spine
syndrome weakness, and sensory loss; bladder stenosis
dysfunction
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*
Age Course Clinical features Diagnosis
Cervical spondylotic Usually >60 Progressive or Moderate-severe cases MRI cervical

myelopathy years stepwise course demonstrate gait and leg spine
spasticity and amyotrophy of
hand or arms
Transverse myelitis Children, Subacute Segmental cord syndrome MRI and CSF
(including multiple young adults
sclerosis and other
causes)
Viral myelitis Any age Acute-subacute Pure motor syndrome or MRI and CSF
segmental cord syndrome
Epidural abscess Any age Subacute; may Segmental cord syndrome MRI
worsen abruptly
Infarction Usually >60 Abrupt onset Anterior cord syndrome MRI with
years diffusion-
weighted
sequences
Vascular malformation >40 years Acute and/or stepwise Radiculomyelopathy MRI, spinal
(dural fistula) angiography
20s
(intramedullary
AVM)
Subacute combined Any age Slowly progressive Dorsal cord syndrome Vitamin B12
degeneration levels
Radiation Any age Slowly progressive; Segmental cord syndrome or MRI, clinical
beginning 6 to 12 ventral cord syndrome history
months after radiation
therapy
Syringomyelia Children, Slowly progressive Central cord syndrome MRI

young adults
Epidural metastasis Usually >50 Subacute; may Segmental cord syndrome MRI
years worsen abruptly
Intramedullary tumor Young adults Slowly progressive Central cord syndrome MRI with
gadolinium
enhancement
ALS Usually >60 Progressive Pure motor syndrome Electromyography

years
MRI: magnetic resonance imaging; CSF: cerebrospinal fluid; AVM: arteriovenous malformation; ALS: amyotrophic lateral
sclerosis.
* This is a partial list of causes. Refer to UpToDate topics on disorders affecting the spinal cord for a more complete
differential diagnosis.
Contributor Disclosures
Andrew Eisen, MD, FRCPC Nothing to disclose Michael J Aminoff, MD, DSc Equity Ownership/Stock
Options: Trust [The portfolio may include medical or drug companies]. Equity Ownership/Stock Options
(Spouse): Trust [The portfolio may include medical or drug companies]. Janet L Wilterdink, MD Nothing to
disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
Conflict of interest policy

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8/3/2020 Anatomy and localization of spinal cord disorders - UpToDate

Official reprint from UpToDate®

SPINAL CORD ANATOMY

● L2 and L3 mediate hip flexion

● Afferents from muscle spindles that participate in spinal cord reflexes.

Other descending tracts include:

● Reticulospinal connections are widely assumed to be responsible for coordinated gross

Other ascending tracts include:

Brown-Sequard (hemicord) syndrome — A lateral hemisection syndrome, also known as the

Causes include disc herniation, spinal fracture, and tumors [11,27].

INFORMATION FOR PATIENTS

Use of UpToDate is subject to the Subscription and License Agreement.

1. REXED B. SOME ASPECTS OF THE CYTOARCHITECTONICS AND SYNAPTOLOGY OF

5. Fornia L, Ferpozzi V, Montagna M, et al. Functional Characterization of the Left Ventrolateral

12. BAKER AB. SPINAL CORD LOCALIZATION. J Lancet 1965; 85:269.

17. Kawaharada N, Morishita K, Hyodoh H, et al. Magnetic resonance angiographic localization of

Topic 5110 Version 10.0

Cross-sectional anatomy of the spinal cord

Graphic 65024 Version 3.0

Longitudinal organization of spinal cord, spinal nerves,

Graphic 50257 Version 2.0

Nerve roots and peripheral nerves corresponding to the

In: Introduction to Clinical Neurology. Woburn, MA, Butterworth-Heinemann 2000.

Graphic 58656 Version 1.0

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

Graphic 53006 Version 3.0

Nerve roots and peripheral nerves corresponding to the

Graphic 64884 Version 2.0

Graphic 50419 Version 2.0

Major white matter tracts of the spinal cord

Graphic 74602 Version 3.0

Cross section of the spinal cord demonstrating arterial

Graphic 72176 Version 2.0

Spinal cord syndromes

Syndrome Clinical manifestations Causes

Graphic 62066 Version 1.0

Location of lesion in dorsal cord syndrome

Graphic 63862 Version 2.0

Location of lesion in ventral cord syndrome

Graphic 63739 Version 2.0

Location of lesion in Brown-Sequard syndrome

Graphic 58103 Version 2.0

Location of lesion in central cord syndrome

Graphic 60859 Version 3.0

Important causes of spinal cord dysfunction*

Age Course Clinical features Diagnosis

Cervical spondylotic Usually >60 Progressive or Moderate-severe cases MRI cervical

Syringomyelia Children, Slowly progressive Central cord syndrome MRI

ALS Usually >60 Progressive Pure motor syndrome Electromyography

Graphic 50336 Version 4.0

Conflict of interest policy

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