Abstract
Over the last decade two important developments have taken place in the treatment of Parkinsonism. The first and most important was the widespread assimilation of levodopa into routine therapy, which derived from evidence that dopamine is a striatal neurotransmitter that becomes depleted in idiopathic and postencephalitic Parkinsonism. Since dopamine does not readily cross the blood–brain barrier, its precursor was administered, and yielded an unequivocal and often dramatic therapeutic response.The second major advance was the introduction of peripheral decarboxylase inhibitors (carbidopa in Sinemet, and benserazide in Madopar), which block conversion of levodopa to dopamine outside the blood–brain barrier and thereby . . .