The presence of a horizontally defined level below which sensory, motor, and autonomic function is impaired is a hallmark of spinal cord disease. This sensory level is sought by asking the patient to identify a pinprick or cold stimulus applied to the proximal legs and lower trunk and successively moved up toward the neck on each side. Sensory loss below this level is the result of damage to the spinothalamic tract on the opposite side one to two segments higher in the case of a unilateral spinal cord lesion, and at the level of a bilateral lesion. The discrepancy in the level of a unilateral lesion is the result of the course of the second-order sensory fibers, which originate in the dorsal horn, and ascend for one or two levels as they cross anterior to the central canal to join the opposite spinothalamic tract. Lesions that transect the descending corticospinal and other motor tracts cause paraplegia or quadriplegia with heightened deep tendon reflexes, Babinski signs, and eventual spasticity (the upper motor neuron syndrome). Transverse damage to the cord also produces autonomic disturbances consisting of absent sweating below the implicated cord level and bladder, bowel, and sexual dysfunction.
The uppermost level of a spinal cord lesion can also be localized by attention to the segmental signs corresponding to disturbed motor or sensory innervation by an individual cord segment. A band of altered sensation (hyperalgesia or hyperpathia) at the upper end of the sensory disturbance, fasciculations or atrophy in muscles innervated by one or several segments, or a muted or absent deep tendon reflex may be noted at this level. These signs also can occur with focal root or peripheral nerve disorders; thus, they are most useful when they occur together with signs of long tract damage. With severe and acute transverse lesions, the limbs initially may be flaccid rather than spastic. This state of "spinal shock" lasts for several days, rarely for weeks, and should not be mistaken for extensive damage to the anterior horn cells over many segments of the cord or for an acute polyneuropathy.
The main features of transverse damage at each level of the spinal cord are summarized below.
Cervical Cord
Upper cervical cord lesions produce quadriplegia and weakness of the diaphragm. Lesions at C4-C5 produce quadriplegia; at C5-C6, there is loss of power and reflexes in the biceps; at C7 weakness affects finger and wrist extensors and triceps; and at C8, finger and wrist flexion are impaired. Horner's syndrome (miosis, ptosis, and facial hypohidrosis) may accompany a cervical cord lesion at any level.
Thoracic Cord
Lesions here are localized by the sensory level on the trunk and by the site of midline back pain that may accompany the syndrome. Useful markers for localization are the nipples (T4) and umbilicus (T10). Leg weakness and disturbances of bladder and bowel function accompany the paralysis. Lesions at T9-T10 paralyze the lower—but not the upper—abdominal muscles, resulting in upward movement of the umbilicus when the abdominal wall contracts (Beevor's sign).
Lumbar Cord
Lesions at the L2-L4 spinal cord levels paralyze flexion and adduction of the thigh, weaken leg extension at the knee, and abolish the patellar reflex. Lesions at L5-S1 paralyze only movements of the foot and ankle, flexion at the knee, and extension of the thigh, and abolish the ankle jerks (S1).
Sacral Cord/Conus Medullaris
The conus medullaris is the tapered caudal termination of the spinal cord, comprising the lower sacral and single coccygeal segments. The distinctive conus syndrome consists of bilateral saddle anesthesia (S3-S5), prominent bladder and bowel dysfunction (urinary retention and incontinence with lax anal tone), and impotence. The bulbocavernosus (S2-S4) and anal (S4-S5) reflexes are absent. Muscle strength is largely preserved.
By contrast, lesions of the cauda equina, the nerve roots derived from the lower cord, are characterized by low back and radicular pain, asymmetric leg weakness and sensory loss, variable areflexia in the lower extremities, and relative sparing of bowel and bladder function. Mass lesions in the lower spinal canal often produce a mixed clinical picture with elements of both cauda equina and conus medullaris syndromes.
Special Patterns of Spinal Cord Disease
The location of the major ascending and descending pathways of the spinal cord are shown below:
Most fiber tracts—including the posterior columns and the spinocerebellar and pyramidal tracts—are situated on the side of the body they innervate. However, afferent fibers mediating pain and temperature sensation ascend in the spinothalamic tract contralateral to the side they supply. The anatomic configurations of these tracts produce characteristic syndromes that provide clues to the underlying disease process.
Brown-Sequard Hemicord Syndrome
This consists of ipsilateral weakness (corticospinal tract) and loss of joint position and vibratory sense (posterior column), with contralateral loss of pain and temperature sense (spinothalamic tract) one or two levels below the lesion. Segmental signs, such as radicular pain, muscle atrophy, or loss of a deep tendon reflex, are unilateral. Partial forms are more common than the fully developed syndrome.
Central Cord Syndrome
This syndrome results from selective damage to the gray matter nerve cells and crossing spinothalamic tracts surrounding the central canal. In the cervical cord, the central cord syndrome produces arm weakness out of proportion to leg weakness and a "dissociated" sensory loss, meaning loss of pain and temperature sensations over the shoulders, lower neck, and upper trunk (cape distribution), in contrast to preservation of light touch, joint position, and vibration sense in these regions. Spinal trauma, syringomyelia, and intrinsic cord tumors are the main causes.
Anterior Spinal Artery Syndrome
Infarction of the cord is generally the result of occlusion or diminished flow in this artery. The result is extensive bilateral tissue destruction that spares the posterior columns. All spinal cord functions—motor, sensory, and autonomic—are lost below the level of the lesion, with the striking exception of retained vibration and position sensation.
Foramen Magnum Syndrome
Lesions in this area interrupt decussating pyramidal tract fibers destined for the legs, which cross caudal to those of the arms, resulting in weakness of the legs (crural paresis). Compressive lesions near the foramen magnum may produce weakness of the ipsilateral shoulder and arm followed by weakness of the ipsilateral leg, then the contralateral leg, and finally the contralateral arm, an "around-the-clock" pattern that may begin in any of the four limbs. There is typically suboccipital pain spreading to the neck and shoulders.
Intramedullary and Extramedullary Syndromes
It is useful to differentiate intramedullary processes, arising within the substance of the cord, from extramedullary ones that compress the spinal cord or its vascular supply. The differentiating features are only relative and serve as clinical guides.
With extramedullary lesions, radicular pain is often prominent, and there is early sacral sensory loss (lateral spinothalamic tract) and spastic weakness in the legs (corticospinal tract) due to the superficial location of leg fibers in the corticospinal tract.
Intramedullary lesions tend to produce poorly localized burning pain rather than radicular pain and to spare sensation in the perineal and sacral areas ("sacral sparing"), reflecting the laminated configuration of the spinothalamic tract with sacral fibers outermost; corticospinal tract signs appear later.
Regarding extramedullary lesions, a further distinction is made between extradural and intradural masses, as the former are generally malignant and the latter benign (neurofibroma being a common cause). Consequently, a long duration of symptoms favors an intradural origin.
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