Parkinson's disease (PD), the most common neurodegenerative movement disorder, has traditionally been considered a "classic" basal ganglia disease, as the most obvious pathology is seen in the dopaminergic cells in the substantia nigra pars compacta. Nevertheless recent discoveries in anatomical connections linking the basal ganglia and the cerebellum have led to a re-examination of the role of the cerebellum in the pathophysiology of PD. This review summarizes the role of the cerebellum in explaining many curious features of PD: the significant variation in disease progression between individuals; why severity of dopaminergic deficit correlates with many features of PD such as bradykinesia, but not tremor; and why PD subjects with a tremor-predominant presentation tend to have a more benign prognosis. It is clear that the cerebellum participates in compensatory mechanisms associated with the disease and must be considered an essential contributor to the overall pathophysiology of PD.
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