Spasticity is an involuntary increase in muscle tone (tension) that occurs following injury to the brain or spinal cord, causing the muscles to resist being moved, in other words, the muscles are continuously contracted, almost like having a permanent cramp in the muscle. Characteristics may include increase in deep tendon reflexes, resistance to passive stretch, clasp knife phenomenon, and clonus.
Spasticity, depending on its severity, causes tightness in the muscles, and can cause problems with walking, movement and speech.
Spasticity can be one of the most disabling and intransigent aspects following a severe brain injury. It can cause severe pain and disfigurment. It is terribly important to have a brain injury survivor with spasticity problems evaluated by a specialist, as numerous drug interventions exist, with potentially dramatic results. The problem in pharmacological managment of spasticity is that each case involves a different interplay of the spasticity symptoms, with the overall symptoms and disabilities of the client. It is inappropriate to evaluate the treatment of the spasticity disorder, without an evaluation of the full emotional and cognitive function of an individual. Even an evaluation of the motor problems can be complex, as some degree of spasticity may help certain individuals.
Treating spasticity in brain injured individuals, involves different approaches that in spinal cord injury and in MS. Current thinking is that oral medications are not effective. The emphasis instead is to local administered medications and treatments (meaning directly into the affected area) both from a therapy and a pharmacolocal standpoint. General drug Treatment for spasticity includes Dantrolene, Baclofen, Diazepam and Botox (botulimum toxin.)
Baclofen, while widely used with MS and spinal cord patients, causes significant fatigue, drowsiness and confusion, so it is contraindicated for those with brain injury. Likewise with Benzodiazepines, such as diazepaman and clonidine. While dantotrolene is better with brain injured persons, as it effects cognition and arousal less, questions remain about a scientific basis for efficacy in such individuals.
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