Ascertaining which changes in brain activation in Parkinson's disease are, in fact, compensatory represents a serious challenge. Compensatory mechanisms have been demonstrated from the microscopic, synaptic level to the macroscopic, system level. Augmentation of compensatory mechanisms, in addition to ameliorating the loss of dopaminergic neurons, may represent a joint strategy for overall minimization of disability.

The key motor symptoms in Parkinson's disease (PD) include tremor at rest, bradykinesia (slowness of movement), rigidity and, later in the disease, gait disorder/postural instability. These clinical features of PD have assumed to be the direct and indirect result of unexplained degeneration of dopaminergic substantia nigra pars compacta (SNpc) cells of the basal ganglia. Given that many of the motor symptoms in PD can be attributed to dopamine cell loss in the SNpc, the classic model of PD has emphasized the role of basal ganglia dysfunction in PD pathology. However, several key features of the disease cannot be explained adequately by basal ganglia dysfunction alone, including the apparent heterogeneity of the disease (i.e., the existence of PD subtypes) 1 , why patients with akinetic-rigiditydominant PD subtype have a worse prognosis than those with a tremor-dominant PD presentation 2-7 , why PD tremor is less reliably responsive to dopaminergic medications compared to the symptoms of bradykinesia and rigidity 8,9 , or why there is no correlation between rest tremor and striatal 18 F-fluorodopa uptake in PD patients 10 . it is likely that other brain structures outside the basal ganglia play a role in the pathophysiology of the disease. The purpose of this review is to summarize the evidence that cerebellar structures and their connections also may contribute significantly to the signs and symptoms of PD. ABSTRACT: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.RÉSUMÉ: Rôle du cervelet dans la physiopathologie de la Maladie de Parkinson. La Maladie de Parkinson (MP), le trouble du mouvement de nature neurodégénérative le plus fréquent, a traditionnellement été considérée comme une maladie « classique » des noyaux gris centraux, étant donné que la pathologie la plus évidente se retrouve dans les cellules dopaminergiques de la substance noire de la pars compacta. Néanmoins, des découvertes récentes concernant les connections anatomiques liant les noyaux gris centraux et le cervelet ont mené à un nouvel examen du rôle du cervelet dans la physiopathologie de la MP. Cette revue expl...

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