Whole brain and regional rates of glucose metabolism were assessed by PET scanning in 25 adults with hyperactivity of childhood onset at the Section on Clinical Brain Imaging and Child Psychiatry Branch, National Institute of Mental Health, Bethesda, MD.
Whole brain and regional rates of glucose metabolism were assessed by PET scanning in 25 adults with hyperactivity of childhood onset at the Section on Clinical Brain Imaging and Child Psychiatry Branch, National Institute of Mental Health, Bethesda, MD. Global cerebral glucose metabolism was 8.1% lower in the adults with hyperactivity than in normal controls. The largest reductions in glucose metabolism were in the premotor cortex and the superior prefrontal cortex, areas of the brain shown to be involved in the control of attention and motor activity. No significant differences were found in global cerebral cortex metabolism between patients with hyperactivity who had current learning deficits and those who did not. [1]
COMMENT. The frontal lobes are important in maintaining attention, and disorders of the prefrontal regions may result in inattentiveness, distractibility, and an inability to inhibit inappropriate responses, such as motor restlessness, calling out in class, verbal interruptions, and acting before thinking.
Experimental neuroanatomical studies of hyperkinesia have been concerned with the effects of destruction of different cortical and subcortical structures on locomotor activity [2]. Bilateral removal of the prefrontal and frontal areas in the monkey causes the greatest total increase in activity [3]. Lesions in Walker’s area 13 of the orbital surface produce the most extreme degree of hypermobility. Hyperactivity induced by parietal lobe lesions is not as marked as in frontal lobe lesions. Destruction of subcortical structures including the striatum, interpeduncular nucleus, and parts of the hypothalamus may also induce hyperactivity. Diffuse brain lesions have been thought to be a major cause of a large percentage of clinical cases of hyperactive behavior. The correlation between functional and anatomical development and pathology is still unclear. Monaminergic transmitters such as norepinephrine are in high concentration in the frontal lobes and increase as the child grows older [4]. The hypometabolism in prefrontal areas noted in the above study might possibly extend to monaminergic metabolism and may explain the beneficial effects of methylphenidate which increases the neurotransmitters and activity of cortical inhibitory systems in hyperactive children. The efficacy of methylphenidate in hyperactive children has been related to the level of motor activity before treatment and the incidence of abnormal neurological signs and evidence of brain dysfunction. (Millichap 1975). It is apparent from these studies that ADHD must be distinguished diagnostically from behavioral disorders that may appear similar but are reactions to environmental crises or inappropriate school placement. [5]
ZametkinAJNordahlTEGrossMKingACSempleWERumseyJCerebral glucose metabolism in adults with hyperactivity of childhood onsetN Engl J Med1990Nov15323201361610.1056/NEJM1990111532320012233902MillichapJGThe paradoxical effects of CNS stimulants on hyperkinetic behaviorInt J Neurol1975101-4241511181313KennardMAJ Neurophysiol19414512NjiokiktjienCPediatric Behavioural Neurology: Clinical Principles Vol 1 Hardcover1988Suyi PublicationsAmsterdamWeissGHyperactivity in childhoodN Engl J Med1990Nov15323201413510.1056/NEJM1990111532320092233909