Neuropharmacology of methylphenidate and a neural substrate for childhood hyperactivity.
What began as a simple chemical question about the clinical utility of MPH SL measurement has led our group across a broad expanse of research endeavors, from the problem of nonintercorrelated stimulant effects to a theory of hyperactivity as a dysregulatory disorder based on frontal-striatal dysfunction or dysmaturation. The transition has been from a traditional and fairly circumscribed question in psychopharmacology to a new interest in the neuropsychological approach to hyperactivity and its treatment. Biologic psychiatry and neuropsychology have developed as distinct disciplines well insulated from one another, but a degree of cross-fertilization is beginning to occur. Rather than thinking of childhood hyperactivity in terms of vague metapsychological concepts such as "attention" or "arousal," it will be perhaps more constructive to base a model for the disorder on the foundation of known elements of brain function. Perhaps the most interesting research areas to pursue will be neuropsychological and neurodiagnostic (for example, PET). The specific locus of disorders, such as the HKS and the specific mechanisms of drug action, may not be so elusive after all.
Gualtieri
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Hicks
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D014150:Antipsychotic Agents / Q000627:therapeutic use; D001289:Attention Deficit Disorder with Hyperactivity / Q000188:drug therapy*; D001921:Brain / Q000187:drug effects*; D002648:Child; D006207:Half-Life; D006801:Humans; D008657:Metabolic Clearance Rate; D008774:Methylphenidate / Q000097:blood / Q000627:therapeutic use*; D009474:Neurons / Q000187:drug effects; D011379:Prognosis; D009435:Synaptic Transmission / Q000187:drug effects
D014150:Antipsychotic Agents; D008774:Methylphenidate