Neuropharmacology of Hyperkinetic Behavior: Response to Methylphenidate Correlated with Degree of Activity and Brain Damage
Neurological mechanisms of hyperkinesia are not completely understood. Diffuse brain lesions are thought to be a major cause of a large percentage of clinical cases of hyperactive behavior (Strauss and Lehtinen, 1947). In a recent study (Millichap et al., 1968) on hyperkinesia in children, fifty-seven per cent of the patients had a history of brain injury or other cerebral damage, and all but one patient had neurological signs of minimal brain dysfunction. In certain cases where the diagnosis of brain damage may be uncertain, other etiological factors such as delayed maturation of the brain and psychogenic disorders have been invoked (Eisenberg, 1964). In many patients the hyperactivity may be controlled and learning disabilities benefited by various drugs (Millichap and Fowler, 1967), and central nervous system stimulants such as methylphenidate (Ritalin) and dextroamphetamine (Dexedrine) are most effective. In contrast, phenobarbital has an excitant effect (Millichap and Millichap, 1966) and is contraindicated in the treatment of hyperactive behavior. The paradoxical calming effect of stimulants on hyperactive children has not been fully explained and the present clinical and laboratory studies were designed to investigate the relation of the degree of activity and brain damage to the drug response and to develop an experimental model for the development of new pharmacological therapies for hyperactivity.
KeywordsLocomotor Activity Brain Damage Auditory Perception Orbital Surface Hyperactive Behavior
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