in the external environment. The brain is likely to attempt to achieve homeostasis in the presence of a mental, emotional, or behavioral disorder by engaging neural systems that help compensate for the functional impairment due to the disorder.

Indeed, findings from human brain imaging studies have increasingly suggested that many differences previously documented in disorders may not represent a primary dysfunction but compensatory responses to the presence of neural dysfunction elsewhere. For example, although longitudinal studies suggest that most cortical abnormalities in children with ADHD represent a maturational delay, some of the differences compared with healthy control children appear to represent a compensatory response. In one study, the right parietal cortex was initially thinner in children with ADHD, similar to most other cortical regions, but then normalized over time only in those with favorable clinical outcomes. These findings suggest that the relative thickening of the right parietal cortex represents a compensatory response (Shaw, Lerch, et al., 2006). In addition, in a different sample of youth with ADHD, the head of the hippocampus was found to be enlarged, with the degree of enlargement being inversely proportional to the severity of the ADHD symptoms, suggesting that the relative hypertrophy of this structure also represents a compensatory response (Plessen, Bansal, et al., 2006). This interpretation has added plausibility in light of the connections of the hippocampus with frontal and parietal cortices and the fact that neurons and synapses in the head of the hippocampus increase in number and size in response to experiential demand (Bruel-Jungerman, Davis, et al., 2006; Cameron and McKay, 2001; Christie and Cameron, 2006; Eriksson, Perfilieva, et al., 1998; Kempermann, Kuhn, and Gage, 1997; van Praag, Shubert, et al., 2005).

Evidence for brain-based compensatory responses is perhaps strongest in children with Tourette syndrome (TS) (Spessot, Plessen, and Peterson, 2004). The dorsal prefrontal and parietal cortices of children with TS have larger volume in inverse proportion to the severity of their tic symptoms, suggesting that the hypertrophy is a compensatory response to the presence of tics (Peterson, Staib, et al., 2001). This hypertrophy is likely to be a consequence of the need to suppress tic symptoms frequently in social settings, which has been shown to produce massive activation of the prefrontal, anterior temporal, and parietal cortices (Peterson, Skudlarski, et al., 1998). The hypertrophy increases inhibitory reserve for the self-regulatory functions that these regions subserve, so that children with TS perform normally and activate frontal tissues similarly to healthy controls. Adults with TS appear to fail to generate this compensatory frontal hypertrophy; as a result, they have more severe symptoms and require greater activation of frontal cortices to maintain adequate performance on tasks that require self-regulatory control (Marsh, Zhu, et al., 2007).



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