Spinal (Anatomy)
INTRODUCTION
1.
Because it is primary pathway of communication between brain and PNS, diseases that affect
spinal cord are clinically eloquent. Many of these disease processes have predilection for
targeting specific areas or tracts within spinal cord. As result, knowledge of spinal cord
anatomy and recognition of typical common spinal cord syndromes are useful in evaluation of
patient with myelopathy and can allow for more directed diagnostic evaluation.
2. The anatomy of spinal cord and its vascular supply and clinical features of common spinal
cord syndromes will be reviewed here. Diseases that affect spinal cord are discussed
separately.
ANATOMY
1.
There are 31 spinal cord segments, each with pair of ventral (anterior) and dorsal (posterior)
spinal nerve roots, which mediate motor and sensory function. The ventral and dorsal nerve
roots combine on each side to form spinal nerves as they exit from vertebral column through
neuroforamina.
2.
Longitudinal organization
A. The spinal cord is divided longitudinally into 4 regions: cervical, thoracic, lumbar, and
sacral cord. The spinal cord extends from base of skull and terminates near lower margin
B.
of L1. Below that level, spinal canal contains lumbar, sacral, and coccygeal spinal nerve
roots that comprise cauda equina.
Because spinal cord is shorter than vertebral column, vertebral and spinal cord
segmental levels are not necessarily the same. C1 through C8 spinal cord segments lie
between C1 through C7 vertebral levels. T1 through T12 cord segments lie between T1
through T8. The five lumbar cord segments are situated at T9 through T11 vertebral
levels, and S1 through S5 segments lie between T12 to L1. C1 through C7 nerve roots
emerge above their respective vertebrae; C8 nerve root emerges between C7 and T1
vertebral bodies. The remaining nerve roots emerge below their respective vertebrae.
C.
Cervical cord
i.
The first cervical vertebra (atlas) and second cervical vertebra (axis), upon which
atlas pivots, support head at atlanto-occiput junction. The interface between first
and second vertebra is called atlanto-axis junction.
ii.
Cervical spinal segments innervate skin and musculature of upper extremity and
diaphragm.
1. C3 through C5 innervate diaphragm, chief muscle of inspiration, via phrenic
nerve
2. C4 through C7 innervate shoulder and arm musculature
3. C6 through C8 innervate forearm extensors and flexors
4. C8 through T1 innervate hand musculature
D.
Thoracic cord
i.
The thoracic vertebral segments are defined by those that have attached rib. The
spinal roots form intercostal nerves that run along inferior rib margin and innervate
associated dermatomes, as well as intercostal abdominal wall musculature. These
muscles are main muscles of expiration. The thoracic cord also contains
sympathetic nerves that heart and abdominal organs.
E. Lumbosacral cord
i.
Lumbosacral spinal cord contains segment that innervate muscles and dermatomes
of lower extremity, as well as buttocks and anal regions. Sacral nerve roots S3
ii.
through S5 originate in narrow terminal part of cord, called conus medullaris.
1. L2 and L3 mediate hip flexion
2. L3 and L4 mediate knee extension
3. L4 and L5 mediate ankle dorsiflexion and hip extension
4. L5 and S1 mediate knee flexion
5. 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.
F.
3.
Cauda equina
i.
In adults, spinal cord ends at level of L1 and L2. The filum terminale, thin connective
tissue filament that descends from conus medullaris with spinal nerve roots, is
connected to third, fourth, and fifth sacral vertebrae; its terminal part is fused to
periosteum at base of coccygeal bone.
ii.
Pathology at T12 and L1 vertebral level affects lumbar cord. Injuries to L2 frequently
damage conus medullaris. Injuries below L2 usually involve cauda equina and
represent injuries to spinal roots rather than to spinal cord.
Cross-sectional anatomy
A.
The spinal cord contains gray matter, butterfly-shaped central region, and surrounding
white matter tracts. The spinal cord gray matter, which contains neuronal cell bodies, is
made up of dorsal and ventral horns, each divided into several laminae.
B. Dorsal horn
i.
The dorsal horn is entry point of sensory information into CNS. It is divided into 6
layers or laminae that process sensory information. More than relay station for
transmission of sensory information, dorsal horn also modulates pain transmission
through spinal and supraspinal regulatory circuits. Three major categories of
sensory input that are important to clinical examination of spinal cord pathology.
1.
2.
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 few segments before
synapsing with 2nd order neurons, which then cross midline of cord in anterior
commissure, just anterior to central canal, and then enter contralateral
anterior or lateral spinothalamic tract.
3. Axons mediating sensory modalities of proprioception, vibration, and touch
discrimination. These large myelinated fibers pass through dorsal horn to enter
ipsilateral dorsal column.
ii.
The anatomy of sensory system is discussed in more detail separately.
C. Ventral horn
i.
The motor nuclei of spinal cord are contained within ventral horn, which also
contains interneurons mediating information from other descending tracts of
pyramidal and extrapyramidal motor systems. These ultimately synapse on α and γ
motor neurons, which subsequently leave ventral horn via ventral nerve root to
terminate at NMJ.
D. White matter tract
i.
The major WM tracts of clinical importance in assessment of spinal cord disease.
1. The dorsal or posterior columns, fasciculus gracilis, and 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. These pathways will cross in medulla;
hence, in spinal cord, these tracts contain ipsilateral sensory representation.
2.
3.
ii.
iii.
commissure and therefore contain contralateral sensory representation. This
tract is somatotopically organized with cervical inputs located most medially
and sacral inputs most laterally.
The corticospinal tracts contain UMN that originate in M1 of primary motor
cortex. These axons synapse either directly or indirectly on anterior horn cells,
and as such have distinct sites of anatomic origin within M1. 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 majority (80 to 85%) of these fibers, which
have previously decussated (crossed) at cervicomedullary junction and therefore
provide input to ipsilateral musculature. Fibers are somatotopically organized
within tract such that fibers destined for upper extremity motor control lie most
medially, while fibers controlling lower extremity lie more laterally. The anterior
corticospinal tract contains undecussated fibers, some of which will subsequently
cross at spinal level through anterior commissure.
Other descending tracts.
1. The tectospinal tract originates in superior colliculus and mediates reflex
postural movements of head in response to visual and/or acoustic input.
2.
3.
4.
iv.
The anterior and lateral spinothalamic tracts contain sensory information
regarding pain, temperature, and touch. These axons have crossed in ventral
The rubrospinal tract originates from magnocellular subdivision of 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 tract arises from vestibular nuclei and facilitates spinal
cord reflexes and muscle tone to maintain posture.
Reticulospinal tract are widely assumed to be responsible for coordinated
gross movements primarily of proximal muscles, whereas corticospinal tract
mediates fine movements, particularly of hand. However, reticulospinal
system may form parallel pathway to distal muscles, alongside corticospinal
tract. As result, reticulospinal neurons may influence upper limb muscle
activity after damage to corticospinal system as may occur in stroke.
Other ascending tracts.
1. The dorsal and ventral spinocerebellar tracts carry inputs mediating
unconscious proprioception directly to cerebellum
2. The spinoreticular tract carries deep pain input to reticular formation of
brainstem
4.
Autonomic fiber
A. Autonomic fibers of hypothalamic and brainstem origin descend in lateral aspect of
B.
C.
D.
E.
F.
5.
spinal cord but not in well-defined tract. These synapse with cell bodies in
intermediolateral columns of central gray matter of spinal cord. Sympathetic fibers exit
between T1 and L2, and parasympathetic fibers exit between S2 and S4.
The sympathetic neurons lie in lateral horn of central gray matter at spinal levels T1-L3.
The preganglionic fibers exit via ventral root, spinal nerve, and ventral ramus to reach
paravertebral ganglion. Many will synapse at paravertebral ganglion, others pass
through it to terminate on postganglionic neurons more proximate to their end organ.
Parasympathetic neurons originate in sacral spinal cord and exit spinal cord with other
efferents to ventral ramus. After leaving ventral ramus, they may subsequently join with
sympathetic nerves to reach viscera. These preganglionic fibers then synapse with
diffuse network of terminal ganglion cells that affect organs in pelvis.
Autonomic dysfunction is 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 anterior horn cells at levels S2-S4. A
spinal cord lesion that interrupts descending motor and autonomic tracts above S2 level
produces "automatic bladder" that cannot be emptied voluntarily, but empties reflexly
when expanded to certain degree, so-called neurogenic bladder. Loss of descending
inhibition of segmental reflex control leads to urinary urgency and incontinence. Injury
to S2-S4 spinal levels interrupts bladder reflex circuit; 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 colon and rectum are similar to those on bladder. Spinal cord transections
interrupt voluntary control of external sphincter and produce constipation. Sacral lesions
cause loss of anal reflex and rectal incontinence. Impotence can result from spinal cord
lesions at any level. Spinal cord injuries can also affect CV function, most dramatically
with lesions above T6 which can produce phenomenon of autonomic dysreflexia.
Blood supply
A. A single anterior and two posterior spinal arteries supply spinal cord. The anterior spinal
artery supplies anterior two-thirds of cord. The posterior spinal arteries primarily supply
dorsal columns. The anterior and posterior spinal arteries arise from VA in neck and
descend from base of skull. Various radicular arteries branch off thoracic and abdominal
aorta to provide additional blood supply to spinal arteries. The largest and most
consistently present of these radicular branches is the great ventral radicular artery or
artery of Adamkiewicz, which supplies anterior spinal artery. This artery enters the
spinal cord anywhere between T5 and L1 (usually between T9 and T12).
B.
C.
In most people, anterior spinal artery passes uninterrupted along entire length of 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 spinal
cord in most people is in midthoracic region.
The vascular anatomy of spinal cord is discussed in detail separately.
LOCALIZATION
1. A spinal cord lesion may be suspected when there are bilateral motor and sensory signs or
symptoms that do not involve head or face. Motor deficits are manifest by weakness and
long tract signs (spasticity, increased reflexes, Babinski sign). When 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
myotomal distribution at specific level of involvement; however, these are usually not
elicitable in thoracic lesions.
2.
3.
As well as longitudinal localization within spinal cord, it can also be helpful to distinguish
specific areas of functional loss with spinal cord level (or across spinal cord levels for
non-segmental pathologies). Some disorders affecting 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 clinical evaluation,
as they often correspond to distinct pathologies. These are summarized in table and are
discussed below (table 1).
4.
Segmental syndrome
A. Pathologies that affect all functions of spinal cord at one or more levels produce
B.
segmental syndrome. Loss of function may be total or incomplete. A total cord
transection syndrome results from cessation of function in all ascending and descending
spinal cord pathways and results in loss of all types of sensation and loss of movement
below level of lesion. Less profound injuries produce 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 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.
C.
5.
Transverse injuries above C3 involve cessation of respiration and are often fatal if acute.
Cervical cord lesions that spare phrenic nerve but impair intercostal nerve function can
produce respiratory insufficiency. Lesions above L2 cord level will cause impotence and
spastic paralysis of bladder. There is loss of voluntary control of bladder, which will
empty automatically by reflex action.
D. Causes of cord segmental syndrome include acute myelopathies, such as traumatic
injury and spinal cord hemorrhage. Epidural or intramedullary abscess, tumors, and
transverse myelitis may have more subacute presentation.
Dorsal (posterior) cord syndrome
A. Dorsal cord syndrome results from bilateral involvement of dorsal columns,
B.
corticospinal tracts, and descending central autonomic tracts to bladder control centers
in sacral cord. 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 dorsal cord syndrome include multiple sclerosis (more typically primary
progressive form), tabes dorsalis, Friedreich ataxia, subacute combined degeneration,
vascular malformations, epidural and intradural extramedullary tumors, cervical
spondylotic myelopathy, and atlantoaxial subluxation.
6.
Ventral (anterior) cord syndrome
A. Ventral cord or anterior spinal artery syndrome usually includes tracts in anterior 66% of
spinal cord, which include corticospinal tracts, spinothalamic tracts, and descending
autonomic tracts to sacral centers for bladder control. Corticospinal tract involvements
produce weakness and reflex changes. A spinothalamic tract deficit produces bilateral
loss of pain and temperature sensation. Tactile, position, and vibratory sensation are
normal. Urinary incontinence is usually present.
B.
The causes of ventral cord syndrome include infarction, HIVD, and radiation
myelopathy.
7.
Brown-Sequard (hemi-cord) syndrome
A. A lateral hemisection syndrome, also known as Brown–Sequard syndrome, involves
dorsal column, corticospinal tract, and spinothalamic tract unilaterally. This produces
weakness, loss of vibration, and proprioception ipsilateral to lesion and loss of pain and
temperature on 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 infection.
8.
Central cord syndrome
A. The central cord syndrome is characterized by loss of pain and temperature sensation in
distribution of one or several adjacent dermatomes at site of spinal cord lesion caused
by disruption of crossing spinothalamic fibers in ventral commissure. Dermatomes above
and below level of lesion have normal pain and temperature sensation, creating the
so-called "suspended sensory level." Vibration and proprioception are often spared.
B. As central lesion enlarges, it may encroach on medial aspect or corticospinal tracts or on
anterior horn gray matter, producing weakness in analgesic areas. Fibers mediating DTR
are interrupted as they pass from dorsal to ventral horn, thus causing tendon reflex loss
C.
in analgesic areas. There are usually no bladder symptoms.
The classic causes of central cord syndrome are slow-growing lesions such as
syringomyelia or intramedullary tumor. However, central cord syndrome is most
frequently result of 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 variable degree of sensory loss below level of injury.
9.
Pure motor syndrome
A. A pure motor syndrome produces weakness without sensory loss or bladder
involvement. This may involve only upper motor neurons, producing hyperreflexia and
extensor plantar responses, or only lower motor neuron bilaterally, producing muscle
atrophy and fasciculations. Other disorders involve both upper and lower motor neurons
and produce mixed signs.
B.
The causes of 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.
10. Conus medullaris syndrome
A. Lesions at vertebral level L2 often affect conus medullaris. There is early and prominent
sphincter dysfunction with flaccid paralysis of bladder and rectum, impotence, and
saddle (S3-S5) anesthesia. Leg weakness may be mild if lesion is very restricted and
spares both lumbar cord and adjacent sacral and lumbar nerve roots.
B. Causes include HIVD, spinal fracture, and tumors.
11. Cauda equina syndrome
A. Though not spinal cord syndrome, cauda equina syndrome is considered here because
its location within spinal canal subjects it to many of same disease processes that cause
myelopathy. The syndrome is caused by loss of functions of two or more of 18 nerve
roots constituting cauda equina. Deficits usually affect both legs but are often
asymmetric.
i.
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.
ii.
Weakness of plantar flexion 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.
iii.
Bladder and rectal sphincter paralysis usually reflect involvement of S3-S5 nerve
roots.
iv.
Sensory loss of all sensory modalities occurs in dermatomal distribution of affected
nerve roots.
B. Many etiologies can cause cauda equina syndrome, including HIVD, epidural abscess,
epidural tumor, intradural extramedullary tumor, lumbar spine spondylosis, and
number of inflammatory conditions including spinal arachnoiditis, CIDP, and sarcoidosis.
The cauda equina can also be primary site of involvement in carcinomatous meningitis
and number of infections (CMV, HSV, VZV, EBV, Lyme disease, mycoplasma, and TB).
12. Lhermitte's sign
A. This well-described sign describes sensation of electric shock-like sensations that run
down back and/or limbs during flexion of neck. This generally occurs with pathologies
involving cervical spinal cord, but is not specific to etiology, occurring in patients with
cervical spondylotic myelopathy, multiple sclerosis, radiation myelopathy, and vitamin
B12 deficiency, among others. It can also occur with cervical nerve root pathology.
DIAGNOSIS
1. The differential diagnosis of myelopathy is wide, but can be significantly narrowed by clinical
syndrome. Other features in examination and history also limit differential diagnosis and
2.
3.
tailor diagnostic work-up. Clinical features of some of more common causes of myelopathy
are outlined in the Table (table 2). These are discussed in detail separately.
For patients with clinical syndrome that suggests localized process within spinal cord
(transection syndrome, central cord syndrome, ventral cord syndrome), imaging study,
usually MRI, of relevant section of spinal cord is usually required. Administration of
gadolinium contrast is often helpful. When infectious or inflammatory disorder is suspected,
CSF examination may be helpful. The role of PET in evaluating patients with myelopathy is
under investigation; it appears to be particularly sensitive for neoplastic disease.
In general, pace at which spinal cord deficits appear dictate urgency of neurologic evaluation.
Even when deficits are not severe, acute myelopathic signs need to be evaluated urgently
because neurologic deterioration can occur abruptly, and clinical deficit at time of
intervention often dictates chances of recovery. This is true particularly for compressive
etiologies such as spinal cord metastases and epidural spinal abscess.
SUMMARY
1. 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. The clinical syndrome along with other features in examination and history usually
significantly limits the differential diagnosis and tailors the diagnostic work-up.