Parkinson's disease is characterized by the progressive loss of dopamine neurons in the substantia nigra of the midbrain. These neurons project widely throughout the cerebral hemispheres, but the motor symptoms of Parkinson's disease — bradykinesia, muscle rigidity, and resting tremor — are almost certainly due to the loss of dopamine nerve terminals in the caudate and putamen nuclei (the striatum) of the basal ganglia and the unbalancing of circuits required for coordinated movement. One of the therapeutic successes of clinical neurology has been the use of levodopa, the precursor of dopamine, in patients with Parkinson's disease. In nearly all patients, . . .
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Fischbach et al. (2001) studied this question.
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