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G. Cohen, M. Spina (1989)
Deprenyl suppresses the oxidant stress associated with increased dopamine turnoverAnnals of Neurology, 26
G. Cohen (1987)
Monoamine oxidase, hydrogen peroxide, and Parkinson's disease.Advances in neurology, 45
U. Rinne (1987)
Early combination of bromocriptine and levodopa in the treatment of Parkinson's diseaseNeurology, 37
U. Rinne (1985)
Combined bromocriptine‐levodopa therapy early in Parkinson's diseaseNeurology, 35
JW Tetrud, J. Langston (1989)
The effect of deprenyl (selegiline) on the natural history of Parkinson's disease.Science, 245 4917
Magyar K Knoll J (1972)
Some puzzling effects of monoamine oxidase inhibitorsAdv Biochem Psychopharmacol, 5
R. Heikkila, J. Hwang, Senyo Ofori, Herbert Geller, W. Nicklas (1990)
Potentiation by the Tetraphenylboron Anion of the Effects of 1‐Methyl‐4‐Phenyl‐1,2,3,6‐Tetrahydropyridine and Its Pyridinium MetaboliteJournal of Neurochemistry, 54
T. Elizan, M. Yahr, D. Moros, M. Mendoza, S. Pang, C. Bodian (1989)
Selegiline use to prevent progression of Parkinson's disease. Experience in 22 de novo patients.Archives of neurology, 46 12
R. Heikkila, L. Manzino, F. Cabbat, R. Duvoisin (1984)
Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase inhibitorsNature, 311
J. Langston, I. Irwin, E. Langston, L. Forno (1984)
Pargyline prevents MPTP-induced parkinsonism in primates.Science, 225 4669
A. Schapira, J. Cooper, D. Dexter, J. Clark, P. Jenner, C. Marsden (1990)
Mitochondrial Complex I Deficiency in Parkinson's DiseaseJournal of Neurochemistry, 54
J. Knoll (1988)
Extension of life span of rats by long-term (-)deprenyl treatment.The Mount Sinai journal of medicine, New York, 55 1
Yahr, Duvoisin Rc, Mendoza Mr, Schear Mj, Barrett Re (1971)
Modification of L-dopa therapy of Parkinsonism by alpha-methyldopa hydrazine (MK-486).Transactions of the American Neurological Association, 96
I. Shoulson, S. Fahn, D. Oakes, C. Odoroff, A. Lang, J. Langston, P. LeWitt, W. Olanow, J. Penney, C. Tanner, W. Koller, R. Rodnitzky, J. Fink, J. Growdon, G. Paulson, R. Kurlan, J. Friedman, S. Gancher, J. Nutt (1989)
Effect of deprenyl on the progression of disability in early Parkinson's disease.The New England journal of medicine, 321 20
Riederer P Birkmayer W (1975)
The potentiation of the antiakinetic effect after L-dopa treatment by an inhibitor of MAO-B, deprenylJ Neural Transm, 36
Przuntek H Riederer P (1987)
MAO-B inhibitor selegiline (R-(-)-deprenyl: a new therapeutic concept in the treatment of Parkinson's diseaseJ Neural Transm, 25
I. Libman, M. Gawel, R. Riopelle, S. Bouchard (1987)
A Comparison of Bromocriptine (Parlodel®) and Levodopa-Carbidopa (Sinemet®) For Treatment of “De Novo” Parkinson's Disease PatientsCanadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, 14
G. Cohen, P. Pasik, B. Cohen, A. Leist, C. Mytilineou, M. Yahr (1984)
Pargyline and deprenyl prevent the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in monkeys.European journal of pharmacology, 106 1
T. Elizan, M. Yahr, D. Moros, M. Mendoza, S. Pang, C. Bodian (1989)
Selegiline as an adjunct to conventional levodopa therapy in Parkinson's disease. Experience with this type B monoamine oxidase inhibitor in 200 patients.Archives of neurology, 46 12
Irwin I Langston JW (1984)
Pargyline prevents MPTP-induced parkinsonismScience, 225
Rinne UK (1987)
Early combination of bromocriptine and levodopa in the treatment of Parkinson's disease: a 5-year follow-upNeurology, 37
Abstract • Thirty-eight patients newly diagnosed as having Parkinson's disease (mean age, 57.3 years; mean Parkinson's disease duration, 2.7 years) in the earlier phase of the disease (mean Hoehn/Yahr stage, 2; mean motor scores, 11.4) were given selegiline (Deprenyl), 10mg daily, and maintained on this drug alone until significant clinical worsening warranted the addition of low-dose levodopa (Sinemet, 25/100 three to four doses per day). Five of these patients were not yet receiving additional levodopa despite some worsening of motor scores. Of the 33 patients now taking combined therapy, seven have been followed up for 6 months or less. Twenty-four (92%) of the 26 patients taking combined therapy for a mean of 26 months (8.5 to 99 months) who have had Parkinson's disease for 6 years showed a dramatic improvement in their parkinsonism shortly after the addition of levodopa, with significant decreases in their rated motor scores, such improvement being maintained at their latest neurologic evaluation. Eighteen (75%) of these 24 patients responded to the combined selegiline/levodopa therapy with degrees of improvement equal to or greater than 50%, compared with their motor status at the start of combined therapy just before the addition of levodopa. This degree of "reversal" of parkinsonism on addition of levodopa (mean carbidopa/levodopa dose, 98/389 mg) was not observed in any of these same patients receiving selegiline alone for an average of 13.8 months. Four patients taking combined therapy developed mild, transient, abnormal involuntary movements, and end-of-dose pattern of response after more than 2 years of combined therapy (24.75 and 33.5 months, respectively). Our results on combined selegiline/levodopa therapy reemphasize the continuing dominant role of levodopa as the primary drug for the symptomatic treatment of Parkinson's disease. A possible synergistic role of selegiline with levodopa in the early cases is suggested by the sustained therapeutic effectiveness of even low doses of the latter for a period of 26 months, with a delay in the appearance of relatively minor side effects developing only after more than 2 years of combined therapy. At an average disease duration of 6 years, no patient has had a major functional disability. A concurrently studied control group of patients treated with low-dose levodopa alone, or one treated with a combination of low-dose levodopa and a dopamine agonist like bromocriptine or pergolide, may have clarified further the role of selegiline, but such control subjects were not available to us at this time. We suggest the early combination of a selective monoamine oxidase type B inhibitor like selegiline, and the original dopamine replacement drug, levodopa (as low-dose Sinemet), as initial symptomatic therapy in newly diagnosed cases of Parkinson's disease. References 1. Birkmayer W, Riederer P, Youdim MBH, Linauer W. The potentiation of the antiakinetic effect after L-dopa treatment by an inhibitor of MAO-B, deprenyl . J Neural Transm . 1975;36:303-326.Crossref 2. Knoll J, Magyar K. Some puzzling effects of monoamine oxidase inhibitors . Adv Biochem Psychopharmacol . 1972;5:393-408. 3. Knoll J. Extension of life span of rats by long-term (-)deprenyl treatment . Mt Sinai J Med . 1988;55:67-74. 4. Riederer P, Przuntek H. MAO-B inhibitor selegiline (R-(-)-deprenyl: a new therapeutic concept in the treatment of Parkinson's disease . J Neural Transm 1987;25:( (suppl) )1-197. 5. Elizan TS, Yahr MD, Moros DA, Mendoza MR, Pang S, Bodian CA. Selegiline as an adjunct to conventional levodopa therapy in Parkinson's disease: experience with this type of monoamine oxidase inhibitor in 200 patients . Arch Neurol . 1989;46:1280-1283.Crossref 6. Langston JW, Irwin I, Langston EB, Forno LS. Pargyline prevents MPTP-induced parkinsonism . Science . 1984;225:1480-1482.Crossref 7. Heikkila RE, Manzino L, Duvoisin RC, Cabbat FS. Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by monoamine oxidase inhibitors . Nature . 1984;311:467-469.Crossref 8. Cohen G, Pasik P, Cohen B, Leist A, Mytilineou C, Yahr MD. Pargyline and deprenyl prevent the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in monkeys . Eur J Pharmacol . 1984;106:209-210.Crossref 9. Cohen G. Monoamine oxidase, hydrogen peroxide, and Parkinson's disease . Adv Neurol . 1986;45:119-125. 10. Cohen G, Spina MB. Deprenyl suppresses the oxidant stress associated with increased dopamine turnover . Ann Neurol . 1989;26:689-690.Crossref 11. Elizan TS, Yahr MD, Moros DA, Mendoza MR, Pang S, Bodian CA. Selegiline use to prevent progression of Parkinson's disease: experience in 22 de novo patients . Arch Neurol . 1989;46:1275-1279.Crossref 12. Tetrud JW, Langston JW. The effect of deprenyl (selegiline) on the natural history of Parkinson's disease . Science . 1989;245:519-522.Crossref 13. The Parkinson Study Group. Effect of deprenyl on the progression of disability in early Parkinson's disease . N Engl J Med . 1989;321:1364-1371.Crossref 14. Yahr MD, Duvoisin RC, Mendoza MR, Schear MJ, Barrett RE. Modification of L-dopa therapy of parkinsonism by alpha-methyl-dopa-hydrazine (MK-486) . Trans Am Neurol Assoc . 1971;96:55-58. 15. Libman I, Gawd MJ, Riopelle RJ, Bouchard S. A comparison of bromocriptine (Parlodel) and levodopa-carbidopa (Sinemet) for treatment of 'de novo' Parkinson's disease patients . Can J Neurol Sci . 1987;14:576-580. 16. Rinne UK. Combined bromocriptinelevodopa therapy early in Parkinson's disease . Neurology . 1985;35:1196-1198.Crossref 17. Rinne UK. Early combination of bromocriptine and levodopa in the treatment of Parkinson's disease: a 5-year follow-up . Neurology . 1987;37:826-828.Crossref 18. Heikkila RE, Huang J, Ofori S, Geller HM, Nicklas WJ. Potentiation by the tetraphenyl boron anion of the effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and its pyridium metabolite . J Neurochem . 1990;54:743-750.Crossref 19. Schapira AVH, Cooper JM, Dexter D, Clarke JB, Jenner P, Marsden CD. Mitochondrial complex I deficiency in Parkinson's disease . J Neurochem . 1990;54:823-827.Crossref
Archives of Neurology – American Medical Association
Published: Jan 1, 1991
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