Cerebellar outflow lesions: A comparison of movement deficits resulting from lesions at the levels of the cerebellum and thalamus

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Abstract
Previous work has shown that lesions in the lateral cerebellum involving the dentate nucleus impair both reaching and pinching movements in humans and monkeys. This study addressed the question of whether disruption of the cerebellar‐thalamo‐cortical pathway at the level of the thalamus would produce behavioral deficits similar to those seen after dentate damage. We compared the performance of both reaching and pinching movements in patients with lateral cerebellar lesions and in patients with discrete lesions of the ventrolateral thalamus. The patients with thalamic lesions had minimal or no sensory loss and no corticospinal signs, suggesting that the abnormal movements were due to disruption of the cerebellar projection to the thalamus. We found that lesions of the ventrolateral thalamus resulted in impaired pinching movements, but remarkably normal reaching movements with the exception of a slight tremor. This is in contrast to the profound pinching and reaching impairments of patients with lateral cerebellar lesions involving the dentate nucleus. Implications about the functional organization of cerebellar output are discussed.