Department of Radiology, Academic Medical Center, University of Amsterdam, and The Netherlands and Graduate School of Neurosciences, Amsterdam
Rudolf Magnus Institute of Neuroscience, Department of Psychiatry, University Medical Center, Utrecht
Department of Nuclear Medicine, Academic Medical Center, University of Amsterdam
Department of Radiology, Academic Medical Center, University of Amsterdam
Amsterdam Institute for Addiction Research and Department of Psychiatry, Academic Medical Center, University of Amsterdam
Department of Radiology, Academic Medical Center, University of Amsterdam
Informatics Institute, University of Amsterdam
Rudolf Magnus Institute of Neuroscience, Department of Neurosurgery, University Medical Center, Utrecht
Department of Radiology, Academic Medical Center, University of Amsterdam
Amsterdam Institute for Addiction Research and Department of Psychiatry, Academic Medical Center, University of Amsterdam, The Netherlands
Correspondence: Maartje M.L. de Win, Department of Radiology, G1-229, University of Amsterdam, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Email: m.m.dewin{at}amc.uva.nl
None. Funding detailed in Acknowledgements.
Background
Neurotoxic effects of ecstasy have been reported, although it remains unclear whether effects can be attributed to ecstasy, other recreational drugs or a combination of these.
Aims
To assess specific/independent neurotoxic effects of heavy ecstasy use and contributions of amphetamine, cocaine and cannabis as part of The Netherlands XTC Toxicity (NeXT) study.
Method
Effects of ecstasy and other substances were assessed with 1H-magnetic resonance spectroscopy, diffusion tensor imaging, perfusion weighted imaging and [123I]2β-carbomethoxy-3β-(4-iodophenyl)-tropane ([123I]β-CIT) single photon emission computed tomography (serotonin transporters) in a sample (n=71) with broad variation in drug use, using multiple regression analyses.
Results
Ecstasy showed specific effects in the thalamus with decreased [123I]β-CIT binding, suggesting serotonergic axonal damage; decreased fractional anisotropy, suggesting axonal loss; and increased cerebral blood volume probably caused by serotonin depletion. Ecstasy had no effect on brain metabolites and apparent diffusion coefficients.
Conclusions
Converging evidence was found for a specific toxic effect of ecstasy on serotonergic axons in the thalamus.
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