The traditional notion that cerebellar function is confined to the coordination of voluntary motor activity is in the midst of a paradigm shift. Converging lines of evidence from anatomical, clinical, experimental and functional neuroimaging studies indicate that the cerebellum is necessary for normal psychological and social behavior. At the core of this re-evaluation is the recognition that the cerebellum may contribute a unique modulating role to a wide array of functions, and that loss of cerebellar modulation degrades different behaviors in a unique manner (Schmahmann, 1991, 1996, 2000a).
The specific aims of this study are to address two issues central to the evolving understanding of the role of the cerebellum. First, what is the scope of the cerebellar role in non-motor performance, and is there topographic organization within cerebellum of sensorimotor, cognitive and emotional behaviors? Second, what are the mechanisms of the cerebellar contribution to cognition and emotion? This study attempts to answer these questions in adult patients with focal cerebellar injury from stroke. Lesion-deficit correlations will be performed using paradigms that identify defective strategies in cognitive performance, that evaluate language and mood states, and that determine the extent of motor incapacity. These approaches will address the scope and topographic organization of cerebellar function. Fluoro-2- deoxy-D-glucose positron emission tomography will examine whether there is decreased glucose utilization (diaschisis) in areas of the cerebral cortex that are anatomically linked with the cerebellum (prefrontal cortex, posterior parietal cortex, superior temporal region, cingulate gyrus), but not in areas devoid of cerebellar connections (inferotemporal cortex, ventral occipital cortex). This will address the functional relevance of the cerebrocerebellar circuits, and help assess whether a fundamental mechanism of cerebellar function can be discerned. The demonstration of a correlation between the scope of the functional impairment (which cognitive domains are involved), and the underlying mechanism (deprivation of the universal cerebellar transform from the cerebrocerebellar communication), would be a conceptual advance in understanding the cerebellar contribution to cognition, and the functional relevance of the cerebrocerebellar system. This study has implications for the recognition and treatment of disorders of higher order function in cerebellar patients. ? ?
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