An open-randomized clinical trial of selegiline in amyotrophic lateral sclerosis
- 27 Downloads
Based on the hypothesis that free radicals play a general role in the neurodegenerative process in motor neuron disease, we tested selegiline in a group of patients affected by amyotrophic lateral sclerosis (ALS) to examine whether it might modify the progression of the disease. Patients were admitted if they were 25–80 years old and had a confirmed diagnosis of ALS with symptoms lasting no longer than 24 months. Patients with familial ALS, pure progressive bulbar palsy, primary lateral sclerosis or progressive muscle atrophy were excluded; a total of 111 patients were recruited. Fifty-three patients were randomly assigned to receive the drug (selegiline 10 mg/day orally for 6 months) and the remaining 58 were considered ALS controls. Mortality was similar in the two groups (4 and 5 patients respectively), though the difference was not statistically significant. Among the survivors, mean MRC and Norris disability scores and forced vital capacity were fairly similar in the two groups at all times and no statistically significant difference between treated and untreated patients was found. The results did not change when the data were related to age, duration and characteristics of onset of the disease. The rate of progression was significantly more rapid in patients with bulbar symptoms in both groups. Our data do not show any significant effect of selegiline in modifying the progression of ALS.
Key wordsAmyotrophic lateral sclerosis Free radicals Selegiline
Unable to display preview. Download preview PDF.
- 2.Gajdusek DC (1990) Cycad toxicity is not the cause of high incidence of amyotrophic lateral sclerosis/parkinsonism-dementia on Guam, Kii peninsula of Japan or in West New Guinea. In: Hudson AJ (ed) Amyotrophic lateral sclerosis: concepts in pathogenesis and etiology. University of Toronto Press, Toronto, pp 317–325Google Scholar
- 4.Halliwell B, Guttzridge JMC (1985) Oxygen radicals and the nervous system. Trends Neurosci 8:22–26Google Scholar
- 5.Hudson AJ (1991) Dementia and parkinsonism in amyotrophic lateral sclerosis. In: Vinken PJ, Bruyn GW, Klawans HL (eds) Handbook of clinical neurology, vol 59. Elsevier, New York, pp 231–240Google Scholar
- 8.Mitchell DJ, Houghton E, Rostron G, Phillips TM, Bailey C, Gatt JA (1992) Serial studies of parameters of antioxidant activity in ALS-towards biochemical correlates of disease progression; Research updates, controversial issues in amyotrophic lateral sclerosis. Abstract Book 1992, AISLA symposium, September 14–17, Veruno, p 17Google Scholar
- 10.Plaitakis A, Smith J, Mandeli J, Melvin DY (1988) Piliot trial of branched chain aminoacids in amyotrophic lateral sclerosis. Lancet I:1015–1018Google Scholar
- 12.Spencer PS (1987) Guam ALS/Parkinsonism-dementia: a long-latency neurotoxic disorder caused by “slow toxins” in food. Can J Neurol Sci 14:347–357Google Scholar
- 14.The Italian ALS Study Group (1993) Branched-chain amino acids and amyotrophic lateral sclerosis. Neurology (in press)Google Scholar
- 15.The Parkinson Study Group (1993) Effects of tocopherol and deprenyl on the progression of disability in early Parkinson's disease. N Engl J Med 21:176–183Google Scholar
- 16.World Federation of Neurology Subcommittee on Motor Neuron Disease (1990) Criteria for diagnosis of amyotrophic lateral sclerosis. World Neurol 15:12Google Scholar
- 17.Yase Y (1972) The pathogenesis of amyotrophic lateral sclerosis. Lancet II:292–296Google Scholar