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Should Levodopa Therapy Be Started Early or Late?

Published online by Cambridge University Press:  18 September 2015

Manfred D. Muenter*
Affiliation:
Department of Neurology. Mayo Clinic and Mayo Foundation, Rochester, Minnesota
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Abstract

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Clinical and experimental evidence suggests that, in Parkinson’s disease, the late-occurring fluctuations in response to levodopa therapy are due to progression of the disease rather than to the therapy. Therefore, treatment with carbidopa/levodopa should be started early, because postponement does not provide patients with added benefits but deprives them of the most satisfying period of the therapeutic response.

Type
7. Treatment of Parkinson’s Disease
Copyright
Copyright © Canadian Neurological Sciences Federation 1984

References

Fahn, S (1982) Fluctuations of disability in Parkinson’s disease: pathophysiology. In Movement Disorders. Edited by Marsden, CD and Fahn, S.London, Butterworth Scientific Publications, pp. 123145.Google Scholar
Goldstein, M, Battista, AF, Ohmoto, T, Anagnoste, B, Fuxe, K (1973) Tremor and involuntary movements in monkeys: effect of L-dopa and ofa dopamine receptor stimulating agent. Science, 179:816817.CrossRefGoogle Scholar
Hoehn, MM (1983) Comparison of the progression of Parkinson’s disease before and since the levodopa era (abstract). Ann. Neurol., 14: 135.Google Scholar
Lang, AE, Meadows, JC, Parkes, JD, Marsden, CD (1982) Early onset of the “on-off” phenomenon in children with symptomatic parkinsonism. J. Neurol. Neurosurg. Psychiatry, 45: 823825.CrossRefGoogle ScholarPubMed
Lesser, RP, Fahn, S, Snider, SR, Cote, LJ, Isgreen, WP, Barrett, RE (1979) Analysis of the clinical problems in Parkinsonism and the complications of long-term levodopa therapy. Neurology (N.Y.), 29: 12531260.CrossRefGoogle ScholarPubMed
Markham, CH, Diamond, SG (1981) Evidence to support early levodopa therapy in Parkinson disease. Neurology (N.Y.), 31: 125131.CrossRefGoogle ScholarPubMed
Meunter, MD, Sharpless, NS, Tyce, GM (1972) Plasma 3–0-methyldopa in L-dopa therapy of Parkinson’s disease. Mayo Clinic Proc, 47: 389395.Google Scholar
Muenter, MD, Sharpless, NS, Tyce, GM, Darley, FL (1977) Patterns of dystonia (“1-D-I” and “D-I-D”) in response to L-dopa therapy for Parkinson’s disease. Mayo Clin. Proc, 52: 163174.Google Scholar
Muenter, MD, Tyce, GM (1971) L-dopa therapy of Parkinson’s disease: plasma L-dopa concentration, therapeutic response, and side effects. Mayo Clin. Proc, 46: 231239.Google ScholarPubMed
Nutt, JG, Woodward, WR, Hammerstad, JP, Carter, JH, Anderson, J (1983) Do the pharmacokinetics of L-dopa explain the on-off phenomenon (abstract). Neurology (N.Y.), 33: 91.Google Scholar
Quinn, NP, Parkes, JD, Marsden, CD (1983) The control of clinical fluctuations in Parkinson’s disease by continuous intravenous administration of levodopa (abstract). Neurology (N.Y.), 33:9091.Google Scholar
Shoulson, I, Glaubiger, GA, Chase, TN (1975). On-off response: clinical and biochemical correlation during oral and intravenous levodopa administration in parkinsonian patients. Neurology (N.Y.), 25: 11441148.CrossRefGoogle ScholarPubMed
Spencer, SE, Wooten, GF (1983) Altered pharmacokinetics of L-dopa metabolism in rat striatum deprived of dopaminergic innervation (abstract). Neurology (N.Y.), 33: 62.Google Scholar
Yahr, MD (1976) Evaluation of long-term therapy in Parkinson’s disease; mortality and therapeutic efficacy. In Advances in Parkinsonism: Biochemistry, Physiology, Treatment. Edited by Birkmayer, W and Hornykiewicz, O.Basle, Editiones Roche, pp. 435443.Google Scholar