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Treatment of Parkinsonism With Levodopa
Melvin D. Yahr, MD;
Roger C. Duvoisin, MD;
Myrna J. Schear, MD;
Robert E. Barrett, MD;
Margaret M. Hoehn, MD
Arch Neurol. 1969;21(4):343-354.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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Some turn this sickness yet might take, Even yet. But he: "What drug can make A wither'd palsy cease to shake?"
"The Two Voices" —Tennyson 1833
FOR MORE than a century, the treatment of parkinsonism has relied on a variety of compounds whose limited therapeutic efficacy depend upon their central parasympatholytic effects. The shortcomings of these agents, notably their inability to completely reverse the signs and symptoms or materially alter the progressive disabling nature of the disorder and the high incidence of disturbing side effects, are well appreciated. Under the most optimal circumstances, the best that can be expected from their judicious administration is a 20% reduction in the severity of symptoms with a modest improvement of functional capacity. The demonstration within the past decade of the presence of dopamine in the brain localized chiefly in the striatum and substantia nigra1,2 and the subsequent discovery of its depletion
. . . [Full Text PDF of this Article]
Author Affiliations
New York
From the Parkinson's Disease Research Center and the Department of Neurology, College of Physicians and Surgeons, Columbia University, New York.
Footnotes
Submitted for publication May 7, 1969; accepted June 6.
Read in part before the 93rd annual meeting of the American Neurological Association, June 17-19, 1968.
Reprint requests to the New York Neurological Institute, 710 W 168th St, New York 10032 (Dr. Yahr).
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