**1.1 Overview**

In a majority of the cases, spinal shock result secondary to trauma (motor vehicle accidents, falls, sporting accidents, and self-harm) [5] causing either transection, hemorrhage, or ischemic injury to the spinal cord [6], other less-common causes

include mechanical cord compression, hypotension, and hypoxia [7]. In spinal shock, descending facilitation of upper motor neurons in spinal cord injury patients is impaired, leading to difficulties differentiating upper motor neuron lesions from lower motor neuron lesions [8]. The somatic component of spinal shock and autonomic reflexes are variably affected depending on the level of injury and phase of recovery [8]. Clinically, the spinal shock is characterized by reversible and temporary loss of all neurological function (that includes motor and sensory dysfunction, variably depressed reflexes, detrusor and rectal tone) below a particular spinal level [6, 9–12]. During the recovery phase, acute loss of functions is followed by the development of spasticity with increased muscle tone, exaggerated deep tendon reflexes, and muscle spasms [13]. Usually, reflex detrusor contractility returns if the distal portions of the spinal cord are not damaged but rather isolated from higher centers. Initially, such reflex activity is not maintained correctly and the return of reflex bladder activity typically occurs with the recovery of deep tendon reflexes in the lower extremities [8].
