Spinal shock is a temporary neurological state that occurs immediately following an acute spinal cord injury (SCI). It involves a transient reduction or complete loss of motor, sensory, and reflex activity below the level of the injury. This condition represents a physiological disruption, not permanent anatomical damage to the spinal cord. It is distinct from circulatory or hypovolemic shock, which involves insufficient blood flow affecting the entire body. Spinal shock specifically describes the temporary loss of spinal cord function below the injury site.
Causes of Spinal Shock
Spinal shock primarily results from acute spinal cord injury, often caused by severe trauma. High-impact incidents such as motor vehicle collisions, falls, and sports injuries are common culprits, leading to fractures, dislocations, or compression of the spinal column. Less common causes include ischemia (a lack of blood flow to the spinal cord) or infection.
The physiological basis lies in the sudden disruption of nerve pathways within the spinal cord. This leads to a temporary cessation of descending input from the brain to the spinal cord segments below the injury. The sudden withdrawal of this facilitatory input causes spinal motor neurons to become hyperpolarized, meaning they are less responsive to stimuli. This temporary loss of nerve impulses below the injury level results in the characteristic symptoms of spinal shock.
Identifying the Manifestations
Individuals experiencing spinal shock exhibit a range of immediate and transient signs below the level of their spinal cord injury. A primary manifestation is flaccid paralysis, characterized by a complete loss of muscle tone and voluntary movement. Accompanying this is areflexia or hyporeflexia, which is the absence or significant reduction of deep tendon reflexes. Sensory function is also impaired, leading to a loss of touch, pain, and temperature sensation in affected areas.
Autonomic dysfunction is a common feature, particularly in injuries above the T6 spinal level. This can result in hypotension (low blood pressure) due to the loss of sympathetic nervous system control over blood vessel constriction. Bradycardia (a slow heart rate) may also occur due to unopposed parasympathetic activity. Impaired bowel and bladder control, including urinary retention and fecal incontinence, is also frequently observed, and patients may experience altered body temperature regulation.
The Phases of Resolution
Spinal shock is not a static condition; it resolves through a series of predictable, albeit variable, phases. The overall duration can range from days to several months, with an average duration of 4 to 6 weeks.
The first phase (0-24 hours) is characterized by areflexia or hyporeflexia and flaccid paralysis due to hyperpolarization of spinal neurons. During this initial period, some reflexes, such as the delayed plantar reflex, may be the first to show activity.
The second phase (1-3 days post-injury) marks the initial return of some reflexes. This is thought to be due to denervation supersensitivity, where nerve cells become more sensitive to neurotransmitters. Polysynaptic reflexes, such as the bulbocavernosus reflex, often reappear first.
Phase three (4 days-1 month) sees the return of deep tendon reflexes, and early hyperreflexia may develop. This stage is associated with the growth of new synapses. The final phase (1-12 months) is characterized by further hyperreflexia and the gradual development of spasticity, involving continued synapse growth.
Approach to Management
Management of spinal shock primarily centers on supportive care and stabilizing the patient, as the condition is temporary and resolves over time. There is no specific cure for spinal shock; instead, efforts focus on mitigating the spinal cord injury and preventing secondary complications. Maintaining stable blood pressure and ensuring adequate oxygenation are important to optimize blood flow to the injured spinal cord and prevent further damage. This often involves fluid resuscitation and, if necessary, medications to elevate blood pressure.
Preventing complications is a significant aspect of care. This includes vigilant monitoring and management to avoid pressure sores, which can develop from prolonged immobility. Measures to prevent deep vein thrombosis (DVT) and pulmonary embolism are also implemented. Bowel and bladder management, including the use of urinary catheters and laxative regimens, is important to prevent infections and maintain function. Careful attention to thermoregulation also helps manage body temperature fluctuations.