Deep brain stimulation of the dentate nucleus improves cerebellar ataxia after cerebellar stroke

Abstract

The cerebrocerebellum receives input from the cerebral cortex and projects to the motor and premotor cortices and the ventrolateral nucleus of the thalamus via the dentate nucleus (DN). Dentothalamocortical projections modulate the activity of the contralateral primary motor (M1) cortex and are involved in movement planning. Acute ischemic injury of the cerebellar nuclei leads to ataxia and a loss of physiologic excitatory inputs from the DN to the contralateral M1 cortex.1 However, chronic cerebellar ischemic lesions have been associated with a reemerging decrease in intracortical inhibition (ICI) in the contralesional M1, leading to marked interhemispheric asymmetry in cortical excitability, which could account for the functional impairment observed after strokes.2