Spinal shock The loss of motor function at the time of injury, tetraplegia with lesions of the fourth to fifth cervical segments or above, and paraplegia with lesions of the thoracic cord, are accompanied by immediate atonic paralysis of bladder and bowel, gastric atony, loss of sensation below a level corresponding to the spinal cord lesion, muscular flaccidity, and almost complete suppression of spinal segmental reflex activity below the lesion. As a result of their sudden separation from higher levels of control, the neural elements below the lesion essentially fail to perform their normal function. As dramatic as this state of reflex paralysis is, its physiologic basis is incompletely understood. Also impaired in the segments below the lesion is the control of autonomic function. Vasomotor tone, sweating, and piloerection in the lower parts of the body are temporarily abolished. As a result, there may be severe systemic hypotension that itself contributes to spinal cord damage. The lower extremities lose heat if left uncovered, and they swell if dependent. The skin over time becomes dry and pale, and ulcerations may develop over bony prominences. The sphincters of the bladder and the rectum remain contracted to some degree because of the loss of the normal inhibitory influence of higher centers, but the detrusor of the bladder and smooth muscle of the rectum become atonic. Urine accumulates until the intravesicular pressure is sufficient to overcome the sphincters, causing overflow incontinence. There is also passive distention of the bowel, retention of feces, and absence of peristalsis (paralytic ileus). Genital reflexes (penile erection, bulbocavernosus reflex, contraction of dartos muscle) are abolished or profoundly depressed.
The duration of the stage of spinal shock varies considerably. In a small number (e.g., 5 of Kuhn’s 29 patients) it is permanent, or only fragmentary reflex activity is regained, even many years after the injury. In such patients, the spinal segments below the level of transection may have themselves been injured, perhaps by a vascular mechanism, although this explanation is unproven. More likely there is a loss of the brainstem–spinal facilitatory mechanisms and an increase in inhibitory activity in the isolated segments. In other patients, minimal genital and flexor reflex activity can be detected within a few days of the injury and minimal reflex activity appears within a period of 1 to 6 weeks. Usually the bulbocavernosus reflex is the first to return. Contraction of the anal sphincter can be elicited by plantar or perianal stimulation, and other genital reflexes reappear at about the same time. The F-waves, electrophysiologic responses that reflect the functioning of the motor neurons of the isolated segment of the cord, are suppressed until spasticity supervenes, at which time they become overly easy to elicit. Noxious stimulation of the plantar surfaces evokes a tremulous twitching and brief flexion or extension movements of the great toes.
The explanation of spinal shock, which is brief in sub-mammalian animals and more lasting in higher mammals, especially in primates, is believed to be the sudden interruption of suprasegmental descending fiber systems that normally keep the spinal motor neurons in a continuous state of readiness. In the cat and monkey, Fulton found the facilitatory tracts in question to be the reticulospinal and vestibulospinal. Subsequent studies showed that in monkeys, some degree of spinal shock could result from interruption of the corticospinal tracts alone. This is probably not a significant factor, however, at least in humans, because spinal shock does not result from acute cerebral and brainstem lesions that interrupt the corticospinal tracts.