Spinal Shock

Spinal shock (from Latin spinalis — spinal and French choc — shock, impact) is a transient state of total suppression of all reflex and conductive functions of the spinal cord below the level of injury, developing in response to acute mechanical spinal damage.

Etiology and pathophysiology

The phenomenon is based on the sudden structural or functional cessation of tonic (ongoing excitatory) influence from the higher brain centers on the spinal cord motor neurons. As a result, there is a sharp hyperpolarization of the neuronal cell membranes below the site of injury, rendering them unresponsive to any signals.

The condition is clinically characterized by flaccid paralysis of skeletal muscles, complete loss of all types of sensitivity (anesthesia), total areflexia, and atony of the smooth muscles of the pelvic organs (acute urinary retention and paralytic ileus).

Clinical significance

Spinal shock masks the true extent of anatomical nerve tissue damage. In the acute phase (in the first few days after injury), it is neurologically impossible to distinguish complete anatomical transection of the spinal cord from severe contusion, as the clinical picture appears equally hopeless.

The duration of the shock phase in humans varies from a few days to several weeks. The return of the bulbocavernosus reflex is considered an objective criterion for emerging from the state of spinal shock. Only after its appearance does the nervous system transition to a stage of spasticity, allowing the physician to reliably assess the rehabilitation prognosis.