Evidence from animal and human research suggests that the cerebellum may play a role in cognition. This includes domains of executive function that are normally attributed to the prefrontal cortex and are typically deficient in individuals with attention-deficit hyperactivity disorder (ADHD). To investigate cerebellar structure in ADHD, magnetic resonance imaging morphometry was used to measure the area of the cerebellar vermis in 12 males with ADHD and 23 male controls matched for age and Wechsler Full-Scale IQ. Analyses were conducted to evaluate group differences, as well as differences between matched pairs of subjects with ADHD and those without ADHD. All measurements were corrected for overall brain size. Both analyses revealed that the size of the posterior vermis was significantly decreased in males with ADHD (P < .05 in both analyses), and that within the posterior vermis, the inferior posterior lobe (lobules VIII-X) was involved in this reduction (P < .05 for group analysis, P < .005 for matched pair analysis), while the superior posterior lobe (lobules VI/VII) was not involved in the reduction. The finding of abnormal inferior posterior vermal size suggests that dysfunction within this region of the cerebellum may underlie clinical deficits seen in individuals with ADHD.

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Having an appreciation for neurobiologic complexity in developmentally disabled children and adolescents with behavior disorders improves our ability to treat them with drugs that have become increasingly specific in their effects. Reductionist analysis of phenotypic and genotypic disorders improves our understanding of the pathogenesis of unique patterns of adverse behaviors. Although drugs can be effective for treating specific behaviors, the cerebral mechanisms underlying these behaviors are not simple or linear in their pathways from genotype to phenotype. Our emerging knowledge about Lesch‐Nyhan disease demonstrates unexpected complexity from a single abnormal gene of purine metabolism and its diverse effects on cells, receptors, and neurotransmitters that produce characteristic self‐injurious behaviors. Several hypotheses for pathogenesis suggest ways that a defective gene might affect the developing brain and strategies for treatment. For disorders that have several abnormal genes, such as autism and bipolar disorder, biologic effects are likely to be even more complex due to gene interactions and compounded with added environmental effects, learning, and experience. There is a high incidence of comorbidity in conditions that affect behavior in children with mental retardation and developmental disabilities. Accurate diagnoses and follow‐up are essential for advanced neuropharmacology to be effective. Guidelines for the evaluation and treatment of patients who have comorbid neuropsychiatric disorders are suggested. MRDD Research Reviews 1998;4:26–35. © 1998 Wiley‐Liss, Inc.

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