Central Cord Syndrome

Central cord syndrome, first described by Schneider and colleagues in 1954, is the most prevalent of the partial cord syndromes.7,8 Because of the anatomic organization of the spinal cord, a central cord injury is characterized by bilateral motor paresis; upper extremities are affected to a greater degree than lower extremities, and distal muscle groups are affected to a greater degree than proximal muscle groups. Sensory impairment and bladder dysfunction are variable features. At times, burning dysesthesias in the upper extremities may be the dominant feature.⁹ Central cord injury affects the central gray matter and the central portions of the corticospinal and spinothalamic tracts. It is caused most often by a hyperextension injury; the postulated mechanism is squeezing or pinching of the spinal cord anteriorly and posteriorly by inward bulging of the ligamentum flavum. The most common cause of such injuries is a fall, followed in frequency by a motor vehicle crash.^7,8 The result is contusion to the spinal cord, with the central portion being most affected. This injury often occurs in elders with degenerative arthritis and spinal stenosis in the cervical area but may affect any patient with cervical canal narrowing of any etiology (e.g., congenital narrow canal as seen in achondroplasia or canal narrowing from disk protrusion or tumor). The prognosis with central cord syndrome depends on the degree of injury at presentation and the patient’s age.^10,11 In patients younger than 50 years, more than 80% regain bladder continence, and approximately 90% return to ambulatory status. In patients older than 50 years, only 30% regain bladder function, and approximately 50% regain the ability to ambulate.¹¹

Brown-Séquard Syndrome

Brown-Séquard syndrome, first described in 1846 by the one physician for whom it is named,¹² is the result of an anatomic or functional hemisection of the spinal cord. Usually associated with penetrating injuries,¹³ Brown-Séquard syndrome also may be seen with compressive or intrinsic lesions. The syndrome has been reported in association with spinal cord tumors, spinal epidural hematoma, vascular malformations, cervical spondylosis, degenerative disk disease, herpes zoster myelitis, and radiation injury and as a complication of spinal instrumentation.^13,14 The syndrome in its pure form is characterized by ipsilateral loss of motor function and proprioception or vibration, with contralateral loss of pain and temperature sensation below the spinal cord level of injury. Because fibers associated with the lateral spinothalamic tract ascend or descend one or two spinal cord segments before crossing to the contralateral side, ipsilateral anesthesia (pain and temperature modalities) may be noted one or two segments above the lesion, although this observation is variable. Most patients with Brown-Séquard syndrome incur only partial sensory and motor impairment, and the classic pattern is not seen.^11,13,15 Brown-Séquard syndrome carries the best prognosis of any of the incomplete spinal cord syndromes. Fully 80 to 90% of patients with Brown-Séquard syndrome regain bowel and bladder function, 75% regain ambulatory status, and 70% become independent in their activities of daily living.¹¹

Anterior Cord Syndrome

Anterior cord syndrome is characterized by loss of motor function, pinprick, and light touch below the level of the lesion with preservation of posterior column modalities, including some touch, position, or vibratory sensation. Although most reported cases of anterior spinal syndrome follow aortic surgery,¹⁶ the syndrome also may occur after severe hypotension, infection, myocardial infarction, vasospasm from drug reaction, and aortic angiography.¹⁷ The anatomic lesion may be caused by a cervical hyperflexion injury resulting in a cord contusion or by protrusion of bone fragments or herniated cervical disk material into the spinal canal. Rarely, it is produced by laceration or thrombosis of the anterior spinal artery or a major radicular feeding vessel.¹¹ Patients present with characteristic mixed motor and sensory neurologic findings as noted before. Functional recovery varies; most improvement occurs during the first 24 hours, but little improvement is expected thereafter.⁴ Although anterior cord lesions from ischemia usually are incomplete, patients without motor function at 30 days have little or no likelihood of regaining any motor function by 1 year.^16,18 Overall, only 10 to 20% of patients with this entity regain some muscle function, and even in this group, there is little power or coordination.¹¹

Motor Function

Testing of motor function encompasses examination of muscle bulk, tone, and strength. Muscle bulk is easily examined in large motor groups, such as the thigh or calf muscles, the biceps, and the triceps. Inspection of the intrinsic hand muscles also may be helpful for determination of muscle bulk; wasting may be evident as hollowed or recessed regions of the hand. Decreased mass, asymmetry, or fasciculations should be noted. Tone is tested with repeated passive knee, elbow, or wrist flexion, with the examiner feeling for abnormally increased or decreased resistance. Rapid pronation-supination of the forearm is another useful method to assess tone. Increased tone may indicate spasticity or an upper motor neuron lesion, whereas decreased tone corresponds with lower motor neuron, motor endplate, or muscle problems. Finally, motor strength is graded in the upper and the lower extremities. Motor grading for the neurologic examination is relatively straightforward. Note that a tremendous gradient of strength is within the fourth grade of the scale. Scored on a scale of 0 to 5, neuromuscular functioning is graded as follows:

A rectal examination is performed to assess voluntary sphincter contraction, resting tone, and, as described previously, the bulbocavernosus reflex. Although it is not commonly thought of as a physical examination maneuver, a post-void residual urine volume may be important for assessment of bladder function. A post-void residual volume of more than 100 to 200 mL in a patient without prior voiding difficulty might suggest bladder dysfunction of neurologic cause.

Sensory Function

Sensory testing requires a cooperative patient and an attentive examiner. The spinal cord–related modalities that may be clinically useful include testing for pinprick and light touch (contralateral lateral spinothalamic tract) and proprioception (ipsilateral posterior column). Assessment of the patient’s response to pinprick, light touch, and proprioception in all four extremities is necessary if a neurologic injury is suspected. Testing of sacral dermatomes is an important part of the examination in some patients. As previously noted, sacral sparing is an important finding indicating that spinal cord dysfunction may be incomplete. The sensory fibers from sacral dermatomes are more peripherally located in the ascending fiber bundles; central or partial cord lesions may ablate sensation in the extremities yet allow some perception of sensation in the sacral area.

Reflexes

Muscle stretch (deep tendon) reflexes may be tested rapidly at the bedside. Responses are graded on a scale of 0 to 4+, with 2 being normal. Hyperactive reflexes suggest upper motor neuron disease (affecting the neurons or their outflow from the brain or spinal cord), as do sustained clonus and Babinski’s sign. The absence of these reflex changes does not constitute evidence that a myelopathy is not present. In fact, one small series noted a low incidence of extensor plantar responses as well as a lack of hyperreflexia in patients presenting to the ED with acute or progressive cord compression or myelopathies.²¹ Reflexes also may be diminished or absent when sensation is lost or when spinal shock is present. Diseases of muscles or neuromuscular junctions also may decrease reflexes. In acute cord injury, reflexes may be diminished in the acute phase. The bulbocavernosus reflex may be helpful in this assessment.