Spinal shock is a temporary physiological response occurring immediately after an acute spinal cord injury. It involves a sudden loss or impairment of spinal cord function below the injury level, characterized by a loss of reflexes, sensation, and motor control. This condition is distinct from permanent paralysis, representing a transient state of neurological depression.
Understanding Spinal Shock
Spinal shock occurs due to the immediate cessation of electrical activity and neural communication below the injury site. This leads to flaccid paralysis, where muscles become limp and reflexes are absent or significantly reduced. The “shock” refers to the suppression of spinal reflexes, not circulatory collapse.
Common causes of spinal cord injury that trigger spinal shock include high-impact trauma, such as car accidents or falls. Ischemia, or insufficient blood supply to the spinal cord, can also lead to this condition. Swelling following spinal cord damage is suggested to contribute, though exact mechanisms are not fully understood.
The body’s immediate healing attempt after a spinal cord injury involves an inflammatory response. While protective, these processes can cause secondary damage, including cell deaths, inflammation, swelling, and reduced blood flow. These events contribute to the temporary dysfunction observed during spinal shock.
Phases and Duration of Spinal Shock
The duration of spinal shock is variable, typically ranging from days to weeks, often cited as 4 to 12 weeks, and rarely extending beyond a month. Its resolution progresses through recognized phases, as proposed by Ditunno et al. in 2004.
Phase 1 (0-1 day) is characterized by a complete loss or weakening of all reflexes below the injury (areflexia or hyporeflexia), along with flaccid paralysis. Spinal neurons become hyperpolarized and less responsive to stimuli due to lost excitatory input from the brain.
Phase 2 (1-3 days) involves the initial return of some reflexes. This phase is marked by denervation supersensitivity, making reflex muscles more responsive to neurotransmitters. Polysynaptic reflexes, such as the bulbocavernosus reflex, are often the first to reappear.
Phase 3 (4 days to 1 month) sees the development of early hyperreflexia, or abnormally strong reflexes, associated with axon-supported synapse growth. Phase 4 (1-12 months) is characterized by persistent hyperreflexia and the gradual development of spasticity, linked to soma-supported synapse growth.
Recovery and Resolution of Spinal Shock
The primary indicator of spinal shock resolution is the return of reflexes below the injury level. The reappearance of the bulbocavernosus reflex (contraction of the anal sphincter in response to stimulation) often signals resolution. Other reflexes, such as deep tendon reflexes, may return later, sometimes taking weeks.
The resolution of spinal shock signifies the end of this temporary physiological phase, but not a full recovery from the underlying spinal cord injury. It indicates that the spinal cord’s reflex pathways below the injury are beginning to regain function. Once resolved, the true extent of neurological damage and potential for long-term recovery can be more accurately assessed.
The return of sensation, motor control, or reflexes below the injury level after spinal shock is an encouraging sign. It suggests the spinal cord injury may be incomplete, meaning some neural connections between the brain and areas below the injury still exist. While spinal shock resolves on its own, management focuses on supportive care and preventing further damage.