Abstract
T HE PATHOGENESIS OF levodopa-related motor complications (motor fluctuations and dyskinesias) is still far from clear, but there is converging evidence to suggest that presynaptic mechanisms play a major role. In fact, we have recently developed a mathematical probability model that can accommodate the whole spectrum of motor complications often seen in Parkinson disease (PD). The model is based on dynamic studies using positron emission tomography and other sources of research evidence. It is pertinent to emphasize that dopamine cell loss seems to be a requirement for levodopa-related motor fluctuations but not for dyskinesias. In fact, recent animal experiments have shown that dyskinesia can occur in normal subjects treated with higher doses of levodopa. Although it may seem trivial, one should also bear in mind that the objective of dopaminergic treatment in PD is not simply to reach normal levels of dopamine in the striatum but rather to restore normal stimulation of postsynaptic dopamine receptors. Our probabilistic model of motor complications in PD can be summarized as follows:
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