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SCI Health Issues
Spinal Shock Following Spinal Cord Injury
Spinal Shock Sections
Spinal shock following a spinal cord injury is a specific term that relates to the loss of all neurological activity below the level of injury. This loss of neurological activity include loss of motor, sensory, reflex and autonomic function. Spinal shock is a short term temporary physiologic disorganisation of spinal cord function that can start between 30-60 minutes following a spinal cord injury. Spinal shock can last up to six weeks post injury.
The mechanism for spinal shock involves the sudden loss of conduction in the spinal cord as a result of the migration of potassium ions from the intracellular to extracellular spaces. This is associated with a transient loss of somatic and automatic reflex activity below the level of spinal cord segment damage. The spinal cord reflex arcs that are immediately above the injury may also be severely disrupted.
Spinal shock following a spinal cord injury results in flaccid paralysis, areflexia and anaesthesia below the level of injury. The return of the reflexes indicates the end of spinal shock. Assessment of the end of spinal shock is based on the return of reflexes, with the bulbocavernosus reflex typically being the first to return. However, some clinicians may classify the end of spinal shock as the return of deep tendon reflexes or the return of reflexive detrusor function, which may be months after injury.
Return of reflexes between 1-12 months post injury are characterised by hyper-reflexia, or abnormally strong reflexes usually produced with minimal stimulation. Inter neurons and lower motor neurons below the SCI begin sprouting, attempting to re-establish synapses. The first synapses to form are from shorter axons, usually from inter neurons - later changes are soma-mediated, and will take longer for the soma to transport various growth factors, including proteins, to the end of the axon.
In spinal cord injuries in the thoracic spinal segments of T6 and above, autonomic dysreflexia may occur, from the loss of autonomic innervation from the brain. Sacral parasympathetics (S2-S4) are lost, as are many sympathetic levels, depending on the level of the spinal cord injury. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrythmias – which resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs with the return of reflexes. Autonomic dysreflexia is characterised by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder/bowel control, sweating, headaches, and other sympathetic effects.
Spinal shock was first defined by Whytt in 1750 as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury – most often a complete transection.