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Introduction —
Introduction —
The spinal cord is the main pathway connecting the brain and the peripheral nervous system, so diseases affecting the spinal cord are clinically significant. These lesions often occur in specific regions or nerve tracts within the spinal cord. Therefore, understanding the anatomy of the spinal cord and recognizing typical common spinal cord syndromes help clinicians evaluate patients with spinal cord lesions and conduct more targeted diagnostic assessments.
This article summarizes the anatomy of the spinal cord, its blood supply, and the clinical features of common spinal cord syndromes. Diseases involving the spinal cord will be discussed separately. (See “Disorders Affecting the Spinal Cord”)
Spinal Cord Anatomy —
The spinal cord has 31 segments, from which 31 pairs of spinal nerves arise. Each pair of spinal nerves is composed of a ventral root (anterior root) and a dorsal root (posterior root), responsible for motor and sensory functions, respectively. The ventral and dorsal roots converge bilaterally to form the spinal nerve, which then exits the vertebral column via the intervertebral foramen (Figure 1).
Longitudinal Structure — The spinal cord is longitudinally divided into four regions: cervical, thoracic, lumbar, and sacral. The spinal cord extends from the base of the skull and terminates near the inferior border of the first lumbar vertebral body (L1). Below L1 within the vertebral canal are the lumbar, sacral, and coccygeal nerve roots, collectively forming the cauda equina.
Because the spinal cord is shorter than the vertebral column, the segmental levels of vertebrae and spinal cord do not necessarily correspond. Cervical spinal cord segments C1-C8 lie at vertebral levels C1-C7; thoracic segments T1-T12 are located roughly at vertebral levels T1-T8; the five lumbar segments are found at T9-T11 vertebral levels; and sacral segments S1-S5 correspond to vertebral levels T12-L1. Cervical nerve roots C1-C7 emerge above the corresponding vertebrae, while the C8 nerve root emerges between vertebrae C7 and T1. All other nerve roots exit below their corresponding vertebrae (Figure 2).
Cervical Cord — The first cervical vertebra (atlas) and the second cervical vertebra (axis) support the head at the atlanto-occipital joint, with the atlas rotating around the axis as a pivot. The connection between the first and second cervical vertebrae is called the atlantoaxial joint.
Cervical spinal cord segments give rise to nerves that innervate the diaphragm, as well as the skin and muscles of the upper limbs (Figure 3 and Figure 4):
● C3-C5 innervate the diaphragm via the phrenic nerve, which is the primary muscle of inspiration.
● C4-C7 give rise to nerves that innervate the muscles of the shoulder and arm.
● C6-C8 send nerves controlling the extensor and flexor muscles of the forearm.
● C8-T1 innervate muscles of the hand.
Thoracic Cord — Thoracic cord segments correspond to vertebrae with attached ribs. Spinal nerve roots from the thoracic vertebrae form intercostal nerves that run along the inferior margin of the ribs, innervating the corresponding dermatomes and the intercostal and abdominal wall muscles, which act as major expiratory muscles. The thoracic cord also contains sympathetic nerves that innervate the heart and abdominal organs.
Lumbosacral Cord — The spinal cord segments in the lumbar and sacral regions give rise to nerves supplying the muscles and dermatomes of the lower limbs, buttocks, and perineal area (Figure 5 and Figure 6). Sacral nerve roots S3-S5 originate from the narrowed terminal portion of the spinal cord known as the conus medullaris.
● L2 and L3 control hip flexion.
● L3 and L4 control knee extension.
● L4 and L5 control ankle dorsiflexion and hip extension.
● L5 and S1 control knee flexion.
● S1 and S2 control ankle plantarflexion.
Sacral nerve roots also give off parasympathetic fibers that innervate pelvic and abdominal organs, while lumbar nerve roots L1 and L2 give off sympathetic fibers to some pelvic and abdominal organs.
Cauda Equina — In adults, the spinal cord terminates at vertebral levels L1 or L2. The filum terminale is a connective tissue strand extending downward from the conus medullaris, accompanying the spinal nerve roots as they travel downward and connected to the sacral vertebrae S3-S5; its terminal segment fuses with the periosteum at the base of the coccyx.
Lesions at vertebral levels T12 and L1 can affect the lumbar cord; injuries at the L2 level commonly involve the conus medullaris; and injuries below L2 usually involve the cauda equina, manifesting as spinal nerve root injury rather than spinal cord injury (Figure 2).
Cross-sectional Anatomy — The spinal cord contains gray matter and white matter tracts; the gray matter is butterfly-shaped and located centrally, while white matter surrounds the gray matter peripherally. The gray matter contains neuronal cell bodies organized into dorsal (posterior) and ventral (anterior) horns, each further subdivided into laminae [1,2].
Dorsal Horn — The dorsal horn is the entry point for sensory information into the central nervous system and is divided into six laminae that process sensory input. The dorsal horn is not only a relay station but also modulates pain transmission via spinal and supraspinal circuits. Three major types of sensory afferent inputs are critically important in clinical evaluation of spinal cord disorders, including:
● Afferents participating in spinal reflexes originating from muscle spindles.
● Axons mediating pain and temperature sensation, mostly thin and unmyelinated. These axons ascend or descend within several segments before synapsing with second-order neurons, then cross the spinal midline near the anterior commissure (close to the central canal) and enter the contralateral spinothalamic tract (anterior or lateral).
● Axons mediating proprioception, vibration, and discriminative touch. These larger myelinated fibers pass through the dorsal horn and enter the ipsilateral dorsal columns.
The sensory nervous system anatomy is discussed separately in detail. (See “Approach to the Patient with Sensory Loss”)
Ventral Horn — The ventral horn contains not only spinal motor nuclei but also interneurons that transmit information from the pyramidal and extrapyramidal descending motor pathways. These neurons eventually synapse on alpha and gamma motor neurons, which exit the ventral horn via the ventral root and terminate at the neuromuscular junction.
White Matter Tracts — The major white matter tracts relevant to clinical evaluation of spinal cord disease include:
● Dorsal columns / posterior columns: fasciculus gracilis and fasciculus cuneatus. These tracts carry sensory information regarding joint position and vibration, arranged anatomically with cervical segments lateral and sacral segments medial (Figure 7). These pathways decussate at the medulla; therefore, within the spinal cord, these tracts carry ipsilateral sensory representation.
● Anterior and lateral spinothalamic tracts carry sensory information related to pain, temperature, and touch. The axons cross at the anterior commissure and thus have contralateral sensory representation. The tracts are somatotopically organized, with cervical input most medial and sacral input lateral (Figure 7).
● Corticospinal tract (CST) contains motor neurons mediating cerebral cortex control over medullary and spinal cord activity. CST axons mainly arise from layer V of the primary motor and sensory cortices [3,4], with fewer arising from premotor, supplementary motor, and secondary somatosensory cortices. These axons synapse directly or indirectly on ventral horn cells and also form synapses with dorsal horn neurons (traditionally viewed as “sensory horn”). Different populations of corticospinal motor neurons are spatially segregated in neocortex, mediating different muscle functions [5]. Corticospinal motor neuron synapses may widely distribute over many ventral horn cells to coordinate skilled movements. The numerical relationship between corticospinal neurons, their axons, and ventral horn cells is not one-to-one. Each ventral horn cell receives impulses from multiple corticospinal neurons (convergence), and one corticospinal neuron controls many ventral horn cells in the same motor neuron pool (divergence), thereby regulating agonist and antagonist muscle functions [6,7].
Most (80%-85%) of these fibers are located in the lateral corticospinal tract and have crossed at the cervicomedullary junction, thus carrying impulses to ipsilateral muscles. Within the tract, fibers are arranged somatotopically; fibers controlling upper limb muscles lie most medially, while those controlling lower limbs lie laterally (Figure 7). The anterior corticospinal tract contains uncrossed fibers, some of which cross at the spinal level via the anterior commissure.
Other descending tracts include:
● Tectospinal tract, originating from the superior colliculus, mediating reflexive head movements in response to visual and/or auditory stimuli.
● Rubrospinal tract originates from the magnocellular portion of the red nucleus; it is well developed in reptiles, birds, and lower mammals but is less developed in primates, and is linked directly to motor neurons controlling wrist muscles.
● Vestibulospinal tract arises from vestibular nuclei, assisting spinal reflexes and muscle tone for postural maintenance.
● The reticulospinal tract is generally believed to coordinate gross motor activity (mainly proximal muscles), whereas the CST mediates fine motor control, especially of the hands [8]. However, the reticulospinal system may form parallel pathways to distal muscles in parallel with the CST. Thus, after corticospinal system injury (e.g., stroke), neurons in the reticulospinal tract may influence upper limb muscle activity [9,10].
Other ascending tracts include:
● Posterior and anterior spinocerebellar tracts that directly transmit unconscious proprioceptive input to the cerebellum.
● Spinoreticular tract that transmits deep pain input impulses to the brainstem reticular formation.
Autonomic Nerve Fibers — Autonomic fibers originating from the hypothalamus and brainstem descend laterally in the spinal cord, but the exact descending tracts are unclear. These fibers synapse with cell bodies in the intermediolateral column of the spinal cord gray matter. Sympathetic fibers exit from spinal segments T1-L2; parasympathetic fibers exit from S2-S4 segments.
Sympathetic neurons reside in the lateral horn of the spinal cord gray matter at T1-L3. Preganglionic fibers exit through the ventral root, spinal nerve, and ventral ramus, reaching the paravertebral ganglia. Many fibers synapse at these paravertebral ganglia; others pass through to synapse on postganglionic neurons closer to their target organs, such as the celiac ganglia, superior mesenteric ganglia, and inferior mesenteric ganglia.
Parasympathetic neurons arise from the sacral spinal cord and exit the spinal cord with other efferent nerves, reaching the ventral ramus. After leaving the ventral ramus, these parasympathetic nerves may run parallel to sympathetic nerves en route to the viscera. Preganglionic fibers then synapse with a dense network of terminal parasympathetic ganglion cells that innervate pelvic organs.
Autonomic dysfunction is an important determinant of the location, extent, and severity of spinal cord lesionsLike longitudinal localization within the spinal cord, clinical localization also helps distinguish specific functional loss regions at a given spinal cord level (in cases of non-segmental injury, it aids in differentiating functional loss regions across spinal cord levels). Certain diseases affecting the spinal cord tend to involve different structures (for example, dorsal and ventral spinal cord syndromes). Therefore, a thorough examination of all spinal cord functions (including motor, reflexes, and all sensory functions) and sphincter functions is crucial for clinical localization.
Spinal Cord Syndromes —
Several different spinal cord syndromes should be distinguished. These syndromes often correspond to lesions at specific locations, making them very useful in clinical assessment. Specific summaries are provided in the table and will be discussed below (Table 1).
Segmental Syndromes — Lesions affecting all functions of the spinal cord at one or more levels cause segmental syndromes. Functional loss can be complete or partial. When the functions of all ascending and descending spinal cord pathways are lost, a complete transverse spinal cord syndrome occurs, leading to the loss of all sensory and motor functions below the lesion level. Less severe injuries can also produce similar deficits but with milder impairment, i.e., patients show weakness rather than paralysis and sensory attenuation rather than loss.
Acute transverse lesions may cause spinal shock with flaccid paralysis, urinary retention, and reduced tendon reflexes. This presentation is generally short-lived, with evolution within days or weeks after injury to increased muscle tone, spasticity, and hyperactive reflexes.
Transverse injuries above C3 can cause respiratory arrest, which can be fatal if acute. If cervical cord lesions affect intercostal nerve function but spare the phrenic nerve, respiratory insufficiency can result. Lesions above the L2 spinal cord level cause impotence and spastic bladder paralysis. Patients lose voluntary bladder control and empty the bladder automatically via reflexes.
Causes of spinal cord segmental syndromes include acute myelopathy such as traumatic injury and spinal cord hemorrhage. Epidural or intramedullary abscesses, tumors, and transverse myelitis often have a subacute presentation. (See “Disorders Affecting the Spinal Cord”)
Dorsal (Posterior) Spinal Cord Syndrome — Lesions involving bilateral posterior columns, the corticospinal tract (CST), and descending autonomic fibers to the sacral bladder control center cause dorsal spinal cord syndrome (Figure 9). Symptoms of posterior column damage include gait ataxia and sensory abnormalities. CST dysfunction results in muscle weakness; if acute, accompanied by flaccidity and decreased reflexes; if chronic, accompanied by increased muscle tone and hyperreflexia. Patients may also have an extensor plantar reflex and urinary incontinence.
Causes include multiple sclerosis (more typical in 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) Spinal Cord Syndrome — The ventral spinal cord or anterior spinal artery syndrome often involves the anterior two-thirds of the spinal cord, including the CST, spinothalamic tract, and descending autonomic fibers to the sacral bladder center (Figure 10). CST involvement results in muscle weakness and altered reflexes. Spinothalamic tract defects cause bilateral loss of pain and temperature sensation. Touch, proprioception, and vibration sensation remain normal. Urinary incontinence is common.
Causes include spinal cord infarction, herniated disc, and radiation myelopathy. (See “Disorders Affecting the Spinal Cord”)
Brown-Sequard Syndrome (Hemisection Syndrome) — Brown-Sequard syndrome involves unilateral posterior column, CST, and spinothalamic tract (Figure 11). It presents with ipsilateral weakness, loss of vibration and proprioception, and contralateral loss of pain and temperature sensation. Unilateral involvement of descending autonomic fibers does not cause bladder symptoms. Though this syndrome has various causes, stab or gunshot wounds causing demyelination are most common. Less common causes include spinal tumors, herniated discs, infarction, and infection. (See “Disorders Affecting the Spinal Cord”)
Central Cord Syndrome — Symptomatic central spinal cord lesions typically affect the medial portion of the CST or anterior horn gray matter, resulting in weakness more pronounced in the upper limbs than lower limbs. Fibers mediating deep tendon reflexes interrupted as they pass from the posterior horn to the anterior horn cause loss of tendon reflexes at the spinal injury level. Patients usually have no bladder symptoms but may have urinary retention.
There is loss of pain and temperature sensation in one or more dermatomes adjacent to the lesion site, due to interruption of spinothalamic fibers crossing in the anterior commissure (Figure 12). Pain and temperature sensation above and below the lesion levels remain relatively normal, forming the so-called “suspended sensory level.” Vibration and proprioception are usually spared.
Classical causes of central cord syndrome are slowly progressive lesions such as syringomyelia or intramedullary tumors. However, in patients with chronic cervical spondylosis, central cord syndrome is most commonly caused by hyperextension injury. Hallmarks include disproportionately severe upper limb motor impairment (greater than lower limbs), bladder dysfunction, and variable sensory loss below the lesion level [24-26]. (See “Cervical Spondylotic Myelopathy”)
Pure Motor Syndromes — Pure motor syndromes cause weakness without sensory loss or bladder involvement. This may involve only upper motor neurons causing hyperreflexia and extensor plantar responses, or only bilateral lower motor neurons causing muscle atrophy and fasciculations. Other diseases may affect both upper and lower motor neurons, producing mixed signs.
Causes of pure motor syndromes include chronic myelopathies such as human T-lymphotropic virus 1 (HTLV-1) myelopathy, hereditary spastic paraplegia, primary lateral sclerosis, amyotrophic lateral sclerosis, progressive muscular atrophy, post-polio syndrome, and myelopathies due to electric shock. (See “Disorders Affecting the Spinal Cord”)
Conus Medullaris Syndrome — Lesions at the L2 vertebral level frequently affect the conus medullaris. Early prominent sphincter dysfunction occurs with flaccid paralysis of the bladder and rectum, impotence, and saddle anesthesia (S3-S5 dermatomes). If lesions are very localized sparing the lumbar cord and adjacent sacral and lumbar nerve roots, leg weakness may be mild.
Causes include herniated disc, spinal fractures, and tumors [11,27].
Cauda Equina Syndrome — Although cauda equina syndrome is not a spinal cord syndrome per se, because the cauda equina is located within the spinal canal many lesions causing spinal cord disease also involve the cauda equina, so it is described here. Cauda equina syndrome occurs when 2 or more of the 18 spinal nerve roots constituting the cauda equina lose function. Deficits usually affect both lower limbs but often asymmetrically. Symptoms include [28-30]:
● Low back pain with radiation to one or both legs. Radicular pain indicates dorsal root involvement and may have localization value [28].
● Mid-caudal cauda equina lesions involving S1 and S2 nerve roots present with bilateral loss of plantar flexion power and absent ankle jerks. Lesion levels ascending produce weakness in other corresponding muscle groups (Figure 5).
● Bladder and rectal sphincter paralysis usually reflect S3-S5 nerve root involvement [28,29].
● All types of sensory loss can occur in dermatomes supplied by the involved nerve roots (Figure 6).
Cauda equina syndrome has diverse causes including herniated disc, epidural abscess, epidural tumors, extramedullary intradural tumors, lumbar degenerative disease, and various inflammatory diseases such as arachnoiditis, chronic inflammatory demyelinating polyneuropathy, and sarcoidosis [27,31-36]. The cauda equina can also be a primary site of neoplastic meningitis and various infections, including cytomegalovirus, herpes simplex virus, varicella-zoster virus, EBV, Lyme disease, mycoplasma infection, and tuberculosis. (See “Pathophysiology, Clinical Features, and Diagnosis of Lumbar Spinal Stenosis” and “Clinical Features and Diagnosis of Neoplastic Epidural Spinal Cord Compression”)
Lhermitte Sign — This sign has been extensively described as an electric shock-like sensation radiating down the back and/or limbs upon neck flexion. It generally occurs with lesions involving the cervical cord but is nonspecific and can be seen in cervical spondylotic myelopathy [37], multiple sclerosis, radiation myelopathy, vitamin B12 deficiency, and cervical radiculopathy.
Assessment —
The differential diagnosis of myelopathy is broad but can be significantly narrowed by the clinical syndrome (Table 1). Other examination and history features can further limit the differential and assist clinicians in selecting appropriate diagnostic tests. Clinical features of some common causes of myelopathy are summarized in the appendix (Table 2) and discussed elsewhere. (See “Disorders Affecting the Spinal Cord”)
When the clinical presentation suggests a focal lesion within the spinal cord (e.g., transverse spinal cord syndrome, central cord syndrome, ventral cord syndrome), imaging of the corresponding spinal cord segments is usually indicated, typically with MRI [23,38]. Gadolinium enhancement often aids diagnosis. Cerebrospinal fluid examination may be helpful if infection or inflammatory disease is suspected [39]. The role of PET-CT in evaluating patients with myelopathy is still under study; it appears particularly sensitive for neoplastic conditions [40].
In general, the speed of onset of spinal cord deficits determines the urgency of the neurological evaluation. Even if deficits are mild, acute myelopathy requires prompt assessment because sudden neurological deterioration is possible, and existing clinical deficits often determine prognosis for recovery. This is especially true for compressive causes such as spinal metastases and epidural abscesses.
Patient Education —
UpToDate offers two types of patient education materials, “Basics” and “Essentials.” Basics are written at about a fifth- to sixth-grade reading level (U.S.) and address four or five key questions patients may have about a disease. These are suitable for patients seeking an overview and who prefer brief, easy-to-read material. Essentials are longer and more detailed, written at about a tenth- to twelfth-grade reading level (U.S.), suitable for patients seeking in-depth information and comfortable with some medical terminology.
The following patient education materials are related to this topic. We recommend providing these to patients via print or email. (More related topics can be found by searching “patient education” plus relevant keywords.)●Basics (see “Patient Education: Central Spinal Cord Syndrome (Basics)” and “Patient Education: Cauda Equina Syndrome (Basics)”)
Summary
●Spinal Cord Syndromes – Diseases affecting the spinal cord typically involve specific structural and functional anatomical regions, leading to different clinical syndromes that can be identified through thorough neurological examination. A summary of spinal cord syndromes is provided in the table (Table 1) and discussed above. (See above ‘Spinal Cord Syndromes’)
●Etiologies of Myelopathy – Various lesions may affect the spinal cord. Common causes of myelopathy include autoimmune, infectious, neoplastic, vascular, and hereditary degenerative diseases. (See “Disorders Affecting the Spinal Cord”)
●Diagnostic Approach – Based on the spinal cord syndrome, clinical context, disease course, and neuroimaging studies (usually MRI), the underlying pathogenesis can be identified in most cases (Table 2). (See)