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Brain Advance Access published online on November 25, 2003
Brain, doi:10.1093/brain/awh046
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© 2003 Published by Oxford University Press

Article

Why is parkinsonism not a feature of human methamphetamine users?

Anna Moszczynska 1, Paul Fitzmaurice 1, Lee Ang 2, Kathryn S. Kalasinsky 3, Gregory A. Schmunk 4, Frank J. Peretti 5, Sally S. Aiken 6, Dennis J. Wickham 7, and Stephen J. Kish 1*

1 Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health, Toronto, Ontario M5T 1R8, Canada
2 Division of Neuropathology, London Health Science Centre, University of Western Ontario, London, Ontario, Canada
3 Division of Forensic Toxicology, Office of the Armed Forces Medical Examiner, Division of Forensic Toxicology, Armed Forces Institute of Pathology, Rockville, MD
4 Santa Clara County Medical Examiner-Coroner, San Jose, CA
5 Arkansas State Crime Laboratory, 3 Natural Resources Drive, Little Rock, AR
6 Spokane County Medical Examiner’s Office, Spokane, USA
7 Clark County Office of the Medical Examiner, Vancouver, WA, USA

* Corresponding author. E-mail: stephen_kish{at}camh.net.

Received 8 July 2003 ; revised 23 September 2003 ; accepted 26 September 2003

Abstract

For more than 50 years, methamphetamine has been a widely used stimulant drug taken to maintain wakefulness and performance and, in high doses, to cause intense euphoria. Animal studies show that methamphetamine can cause short-term and even persistent depletion of brain levels of the neurotransmitter dopamine. However, the clinical features of Parkinson’s disease, a dopamine deficiency disorder of the brain, do not appear to be characteristic of human methamphetamine users. We compared dopamine levels in autopsied brain tissue of chronic methamphetamine users with those in patients with Parkinson’s disease and in a control group. Mean dopamine levels in the methamphetamine users were reduced more in the caudate (-61%) than in the putamen (-50%), a pattern opposite to that of Parkinson’s disease. Some methamphetamine users had severely decreased dopamine levels, within the parkinsonian range, in the caudate (up to 97% dopamine loss) but not in the putamen. As the putamen and caudate subserve aspects of motor and cognitive function, respectively, our data suggest that methamphetamine users are not parkinsonian because dopamine levels are not sufficiently decreased in the motor component of the striatum. However, the near-total reduction in the caudate could explain reports of cognitive disturbances, sometimes disabling, in some drug users, and suggests that treatment with dopamine substitution medication (e.g. levodopa) during drug rehabilitation might be helpful.

Keywords: Parkinson’s disease; caudate; putamen; methamphetamine; cognition
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