To the
Editor: Mintzer et al. hypothesized that their patient had parkinsonism
as a result of a delayed neurotoxic effect of 3,4-methylenedioxymethamphetamine (MDMA) on his basal ganglia
and noted that his condition most closely resembled nigrostriatal
damage induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We question this conclusion. The patient’s positron-emission tomographic scan was normal, and his condition did not
respond to antiparkinsonian agents, unlike
MPTP-induced parkinsonism. There is currently no evidence to suggest
that MDMA damages dopaminergic neurons, and none of
the thousands of animals or humans exposed to MDMA have shown evidence of parkinsonism.
MDMA is a phenethylamine,
MPTP a phenylpiperidine. Aside from a coincidental similarity in their
acronyms, they are chemically unrelated and have in common neither precursors
nor intermediates. The purity of street
drugs is far from perfect, and since no chemical analysis was performed, we
have no evidence that this patient ingested either MDMA or MPTP. Samples of putative MDMA obtained and
analyzed in January 1998 found that 29 of 35 pills (83 percent) contained no
MDMA whatsoever,1 and more detailed
analyses of street MDMA by high-performance liquid chromatography show a wide
variety of non-MDMA contaminants.2
The patient probably ingested a wide variety of chemicals, any one of
which might have been responsible for his parkinsonian
symptoms. Whether MPTP is the culprit is
doubtful, because the metabolite MPP+ (1-methyl-4-phenylpyridinium),
thought to be responsible for the parkinsonism induced
by MPTP, does not appear to be present in the brain after oral administration.3
References
1. Saunders N.
Trends in quality in January 1998.
(See: http://www.ecstasy.org/testing/analysis.html)
2. Rothe M, Pragst F, Spiegel K, Harrach T, Fischer K, Kunkel J. Hair concentrations and self-reported abuse
history of 20 amphetamine and ecstsy users. Forensic Sci Int 1997; 89
(1-2):111-128.
3. Fuller RW,
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