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Obrocki J, Thomasius R. 
“Ecstasy use and neuropathology: Reply”. 
Br J Psychiatry. 1999 Dec;175:589.
Abstract
We agree that there is a theoretical possibility that the alterations in glucose metabolic rates detected by positron emission tomography within the ecstasy user group might be caused by preexisting aberrant neuronal activity. Yet, to our knowledge, conclusive neuropathological findings that are characteristic for secondary drug misuse do not exist. Putative psychopathological phenomena mediating the secondary use of ecstasy are most likely heterogeneous and too diffuse with regard to the 2-(18F)-fluoro-2-deoxy-D-glucose PET method. It therefore seems more reasonable that the detection of altered glucose metabolic rates in ecstasy users is a consequence of experimentally well-documented neurotoxic serotonergic lesions caused by MDMA. In this sense, we disagree that it is equally plausible that MDMA abuse results from measurable pre-existing 5-HT function abnormalities. We have examined the relations between psychiatric disorders and PET findings mentioned by Dr Morgan in a completed study with 107 ecstasy users (Thomasius, 1998). The publication of the results is in preparation.
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