Here water is entering into the cell.it occurs when the solution is hypotonic

Hypertonicity due to upper motor neuron dysfunction may be caused by lesions at many levels within the brain and spinal cord. Among patients with traumatic brain injury (TBI), the most severe hypertonicity is found in those with diffuse axonal injury(DAI) or hypoxic-ischemic injury (HII) following cardiopulmonary arrest. Rigidity, spasticity, and dystonia all contribute to joint abnormalities and restricted function. Hypertonicity is usually greatest within the first 6 months of injury. Because this is the period of spontaneous neurologic recovery, one should avoid any permanent surgical procedure intended to control hypertonicity. Without any treatment, disabling musculotendinous contracture and abnormal, dyssynergic patterns of movement occur, further complicating the patient’s recovery and outcome. Peripheral nerve blockade may be useful during this interval to aid in the treatment of spasticity.

A large number of patients with TBI and spinal cord injury require localized nerve blocks designed to depress the final common pathway during reorganization and recovery of the central nervous system. Noninvasive treatment of spasticity should be maximized before proceeding with neurolytic blocks. This includes medications, stretching, serial casting, icing, electrical stimulation, and positioning. Any cerebral or spinal cord anomalies, such as hydrocephalus and syringomyelia, should be corrected surgically. Any noxious stimuli, such as urinary tract infection and skin lesion, should be eliminated when possible. Drug-induced movement disorders should be evaluated and, when possible, the offending drug should be discontinued.

The prognosis for motor return and stage of recovery should be established. The physician must determine if the hypertonicity is generalized or focal. Generalized hypertonicity is usually not responsive to nerve blocks unless it is for the purposes of hygiene. Consistent patterns of hypertonicity need to be established and treatment should initially be directed toward proximal tone. Any block should affect the most proximal nerve capable of denervating the maximum number of spastic myotomes. All residual voluntary motor function of the affected limb is to be preserved. Phenol, a common neurolytic agent, generally results in alleviation of spasticity with little decrease of voluntary contraction.35