Abstract
Spinal shock occurs as a consequence of an abrupt interruption of descending supraspinal pathways. The term spinal shock describes a phenomenon when a trauma, ischemia, hemorrhage or inflammation results in sudden loss of neurological functions below the level of the injury.
Clinically, transient loss or decrease of reflex activity below the level of the injury, hypotonia and disturbance of motor, sensory and autonomic functions predominate. In order to clarify the mechanism behind the spinal shock and subsequent return of reflex activity or even hyperreflexia, we need to understand the changes taking place in motor neurons below the level of the injury.
These changes consist of three main phases. Reduction of reflex activity results from decreased excitability of spinal motor neurons.
Resumption of reflex activity or voluntary movement is attributed to denervation hypersensitivity and hyperreflexia occurs due to new synaptic growth. Consequently, the motor neuron below the level of injury is predominantly under either voluntary or reflex control.
As a result, various levels of spasticity develop or, in case of an incomplete lesion, voluntary movement might be recovered, depending on the extent of spinal cord injury.