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Anatomy and localization of spinal cord disorders

Anatomy and localization of spinal cord disorders
Literature review current through: Jan 2024.
This topic last updated: Feb 11, 2022.

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 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: Epidemiology 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.

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.

A sensory level, with normal sensation above and reduced or absent below, can also often be defined and should be specifically sought.

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 (eg, dorsal versus ventral cord syndromes). Thus, careful testing of all spinal cord functions, including motor, reflex, and all sensory modalities, and sphincter function is important for clinical localization.

SPINAL CORD SYNDROMES — 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 — 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 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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References

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