Abstract

Cerebral palsy (CP) is a disorder of movement and posture resulting from a nonprogressive injury to the immature brain that is marked by changes in muscle tone at rest and with activity [1]. The diagnosis is usually made during childhood. Affected children have delayed motor development that usually is substantiated by magnetic resonance imaging findings [1]. Hypotonia may be present in the early stages of CP, but upper motor neuron findings ultimately predominate, with increased tone and hyperreflexia and impaired motor control, balance, and coordination. These changes often lead to secondary contractures and deformities. Various movement disorders are found in patients with CP, including spasticity, dystonia, choreoathetosis, and ataxia. Dystonia is usually treated medically with agents that stimulate dopaminergic activity. The combination drug consisting of levodopa and carbidopa uses levodopa as a precursor to dopamine that is able to cross the blood-brain barrier for conversion to dopamine in the central nervous system [2]. Trihexyphenidyl and benztropine are anticholinergic medications used to treat dystonia by antagonizing remaining cholinergic receptors. All these medications are used to re-establish a balance between injured dopamine and acetylcholine pathways, which are hypothesized to coexist in the substantia nigra of the basal ganglia [3]. Neuroleptic malignant syndrome (NMS), a disorder thought to be caused by dopamine receptor blockade, causes fever, rigidity, and altered mental status [4,5]. Normally this disorder is caused by antipsychotic medications or abrupt withdrawal of dopamine agonists [6].

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