Deprenyl monotherapy improves visuo-motor control in early parkinsonism

  • S. Hocherman
  • G. Levin
  • N. Giladi
  • M. B. H. Youdim
Part of the Journal of Neural Transmission. Supplement book series (NEURAL SUPPL, volume 52)


Deprenyl is a potent MAO-B inhibitor which is commonly prescribed for treatment of parkinsonism. Despite prevalent use its effects on the symptoms and course of Parkinson’s disease (PD) are still debated. The present study was therefore undertaken in order to measure quantitatively changes in visuo-motor control (VMC), consequent to deprenyl monotherapy in early PD. Previous work from our laboratory has shown typical VMC deterioration in PD patients, that correlates with disease severity. Thus, measurements of such changes provides a sensitive tool with which the symptomatic effects of drug treatment can be assessed quantitatively. Fourteen newly diagnosed, PD patients with light symptoms were studied. The VMC of all patients was tested after the first neurological examination, before drug treatment commenced. A second test was done after 30 days of treatment with deprenyl at a dose of 2.5mg/day. Following this test, dosage was increased to 10mg/day and a third VMC test was given after 30 more days of treatment. Our results show significant improvement in VMC functions following 30 days of 2.5mg/day treatment and a continuing improvement after the next 30 days of 10mg/day treatment. This improvement pertains mainly to directional control of self initiated movements and is smaller for movements that are guided externally. We conclude that deprenyl monotherapy has a clear symptomatic beneficial effect for patients with early PD.


Symptomatic Effect Tyrosine Hydroxylase Activity Parkinson Study Group Increase Superoxide Dismutase Activity Striatal Tyrosine Hydroxylase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Carrillo MC, Kitani K, Kanai S, Sato Y, Ivy GO (1992) The ability of (-)deprenyl to increase superoxide dismutase activities in the rat is tissue and brain region selective. Life Sci 50: 1985–1992PubMedCrossRefGoogle Scholar
  2. Chia LG, Liu SP, Lee EH (1992) Differential effects of deprenyl and MPTP on catecholamines and activity in BALB/c mice. Neuroreport 3: 777–780PubMedCrossRefGoogle Scholar
  3. Hocherman S, Aharon-Peretz J (1994) Two dimensional tracing and tracking in patients with Parkinson’s disease. Neurol 44: 111–116CrossRefGoogle Scholar
  4. Hocherman S, Giladi N (1995) Early diagnosis of Parkinson’s disease in new neurological patients by testing of Visuo — Manual coordination. In: Ohye C, Kimura M, McKenzie SJ (eds) The basal ganglia V. Plenum, New York, pp 427–431Google Scholar
  5. Hubble JP, Koller WC, Waters C (1993) Effects of selegiline dosing on motor fluctuations in Parkinson’s disease. Clin Neuropharmacol 16: 83–87PubMedCrossRefGoogle Scholar
  6. Jenkins IH, Fernandez W, Playford ED, Lees AJ, Frackowiak RSJ, Passingham RE, Phil D, Brooks DJ (1992) Impaired activation of the supplementary motor area in Parkinson’s disease is reversed when akinesia is treated with apomorphine. Ann Neurol 32: 749–757PubMedCrossRefGoogle Scholar
  7. Knoll J (1992) (-)Deprenyl-medication: a strategy to modulate the age-related decline of the striatal dopaminergic system. J Am Geriatr Soc 40: 839–847PubMedGoogle Scholar
  8. Knoll J, Toth V, Kummert M, Sugar J (1992) (-)Deprenyl and (-)parafluorodeprenyl-treatment prevents age-related pigment changes in the substantia nigra. A TV-image analysis of neuromelanin. Mech Ageing Dev 63: 157–163PubMedCrossRefGoogle Scholar
  9. Okuda C, Segal DS, Kuczenski R (1992) Deprenyl alters behavior and caudate dopamine through an amphetamine-like action. Pharmacol Biochem Behav 43: 1075–1080PubMedCrossRefGoogle Scholar
  10. Parkinson Study Group (1993) Effects of tocopherol and deprenyl on the progression of disability in early Parkinson’s disease. N Engl J Med 3: 176–183Google Scholar
  11. Parkinson Study Group (1996) Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP patients requiring levodopa. Ann Neurol 39: 37–45CrossRefGoogle Scholar
  12. Shoulson I (1992) An interim report of the effect of selegiline (L-deprenyl) on the progression of disability in early Parkinson’s disease. The Parkinson Study Group. Eur Neurol 32: 46–53PubMedCrossRefGoogle Scholar
  13. Shults CW (1993) Effect of selegiline (deprenyl) on the progression of disability in early Parkinson’s disease. Parkinson Study Group. Acta Neurol Scand [Suppl] 146: 36–42Google Scholar
  14. Schulzer M, Mak E, Calne DB (1992) The antiparkinson efficacy of Deprenyl derives from transient improvement that is likely to be symptomatic. Ann Neurol 32:795–798PubMedCrossRefGoogle Scholar
  15. Tardos L, Janvarine Kanyo E (1992) Pharmacology of selegiline (recent considerations). Acta Pharm Hung 62: 237–241PubMedGoogle Scholar
  16. Tatton WG, Greenwood CE (1991) Rescue of dying neurons: a new action of deprenyl in MPTP parkinsonism. J Neurosci Res 30: 666–672PubMedCrossRefGoogle Scholar
  17. Vezina P, Mohr E, Grimes D (1992) Deprenyl in Parkinson’s disease: mechanisms, neuroprotective effect, indications and adverse effects. Can J Neurol Sci 19: 142–146PubMedGoogle Scholar
  18. Vrana SL, Azzaro AJ, Vrana KE (1992) Chronic selegiline administration transiently decreases tyrosine hydroxylase activity and mRNA in the rat nigrostriatal pathway. Mol Pharmacol 41: 839–844PubMedGoogle Scholar
  19. Yasar S, Schindler CW, Thorndike EB, Szelenyi I, Goldberg SR (1993) Evaluation of the stereoisomers of deprenyl for amphetamine-like discriminative stimulus effects in rats. J Pharmacol Exp Ther 265: 1–6PubMedGoogle Scholar
  20. Ziv I, Achiron A, Djaldetti R, Dressier R, Melamed E (1993) Short-term beneficial effect of deprenyl monotherapy in early Parkinson’s disease: a quantitative assessment. Clin Neuropharmacol 16: 54–60PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Wien 1998

Authors and Affiliations

  • S. Hocherman
    • 1
    • 4
  • G. Levin
    • 1
  • N. Giladi
    • 2
  • M. B. H. Youdim
    • 3
  1. 1.Department of PhysiologyCarmel HospitalHaifaIsrael
  2. 2.Department of Pharmacology, Faculty of Medicine, TechnionCarmel HospitalHaifaIsrael
  3. 3.Department of NeurologyCarmel HospitalHaifaIsrael
  4. 4.Department of Physiology, Faculty of Medicine, TechnionHaifaIsrael

Personalised recommendations