An extremely powerful approach to understanding the neurobiology of psychiatric syndromes is to study the nature and frequency of these conditions in brain diseases in which the neuropathology is well-defined. For instance, studies of Alzheimer's disease, Parkinson's disease, and Huntington's disease have helped to implicate regions of the cerebral cortex and basal ganglia as potentially important to the pathophysiology of mood disorders. Preliminary evidence suggests that the cerebellum and related structures may also be relevant to such disorders. We now propose to test the hypothesis that the cerebellum and related structures have a role in affective and other psychiatric syndromes by examining the nature and frequency of these syndromes in patients with degenerative diseases of the cerebellum. Three lines of evidence support this hypothesis. First, it has long been emphasized that the cerebellum is an important modulator of movement, a functional role reflected in the connections the cerebellum makes to cortical and spinal regions that regulate movement. However, recent work has demonstrated that the cerebellum is anatomically connected to regions of the cerebral cortex (prefrontal, superior temporal, and posterior parietal) that regulate emotion and cognition rather than motor function. Second, the cerebellum and related structures appear to have a role in cognition, including learning, decision making, language, orientation in space and time, and attention. Third, preliminary studies have found evidence for prominent but short-live depression after cerebellar strokes, a higher overall rate of psychiatric illness among patients with ataxia (loosely defined) than in a control population, and a 12-14% rate of depression, euphoria, and impulsivity (all loosely defined) in patients with progressive ataxia. This evidence strongly suggests a link between the cerebellum and psychiatric phenomenology. However, to date no study has systematically used reliable and validated methods to examine psychiatric phenomenology in patients with cerebellar degeneration. We propose to remedy this oversight.
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