Addiction
February 27, 2006
Euphrosyne Gouzoulis‐mayfrank, Jörg Daumann
189 citations
The popular dance drug ecstasy (MDMA) causes selective and persistent damage to serotonin-producing neurons in laboratory animals. Serotonin regulates many brain functions, so damage could lead to psychiatric, cognitive, and other disorders. This review of studies on ecstasy users finds that, despite major methodological problems, the evidence suggests lasting changes in serotonin transmission, though partial recovery may occur after long-term abstinence. The most consistent finding links heavy ecstasy use with subtle cognitive impairments, especially in memory. However, the evidence is not definitive, and questions about pre-existing traits or polydrug use remain unresolved.
Journal of Psychopharmacology
March 1, 2006
Euphrosyne Gouzoulis‐mayfrank, Jörg Daumann
179 citations
The popular dance drug ecstasy (MDMA) is neurotoxic to central serotonergic neurons in laboratory animals and possibly in humans. Studies have reported alterations in serotonergic transmission and neuropsychiatric abnormalities in ecstasy users that may relate to MDMA-induced neurotoxic brain damage. The most consistent findings associate subtle cognitive, particularly memory, deficits with heavy ecstasy use. However, most studies have important methodological problems, especially the widespread pattern of polydrug use—commonly alcohol, cannabis, and stimulants (amphetamines and cocaine)—which makes it difficult to link findings to MDMA alone. Stimulants are also neurotoxic and may act synergistically with MDMA, while cannabis has complex interactions, including neuroprotective actions that can partially block MDMA-induced neurotoxicity in animals. Future longitudinal research should clarify these relationships.
Dialogues in Clinical Neuroscience
September 30, 2009
Euphrosyne Gouzoulis‐mayfrank, Jörg Daumann
115 citations
High doses of MDMA (ecstasy) and stimulant amphetamines like methamphetamine (speed) are clearly neurotoxic in laboratory animals. MDMA selectively damages central serotonergic nerve terminals, while amphetamines harm both serotonergic and dopaminergic systems. In human drug users, evidence suggests residual alterations of serotonergic transmission from MDMA, with possible partial recovery after long-term abstinence, though functional impairments may persist. Subtle cognitive impairments, especially memory deficits, are the most consistent findings. For methamphetamine, preliminary evidence indicates dopaminergic system alterations may persist after years of abstinence, linked to motor and cognitive performance deficits.
Human Psychopharmacology Clinical and Experimental
December 1, 2001
Jörg Daumann, Susanna Pelz, Stefanie Becker et al.
77 citations
Recreational Ecstasy (MDMA) is known to damage serotonin neurons in animals, and human studies link it to memory problems. This investigation examined psychological profiles of 28 abstinent Ecstasy users who also used cannabis, compared with equal-sized groups of cannabis-only users and non-users. Ecstasy users reported higher impulsiveness, anxiety, sensation seeking, somatic complaints, obsessive-compulsive behavior, and psychoticism. However, after accounting for cannabis use, most group differences were no longer statistically significant. The findings suggest that psychological problems in Ecstasy users are closely tied to concomitant cannabis use, making them less reliable indicators of Ecstasy-related neurotoxic damage than cognitive deficits.
Addiction
July 26, 2012
Daniel Wagner, Benjamin Becker, Philip Koester et al.
54 citations
A prospective cohort study followed 109 nearly MDMA-naive subjects for 12 months to determine whether cognitive deficits appear after beginning MDMA use. Twenty-three subjects who used more than 10 MDMA pills (mean 33.6 pills) were compared with 43 subjects who used no illicit drugs besides cannabis. Groups did not differ in age, intelligence, cannabis, alcohol, or other lifestyle confounders. MDMA users showed significant impairments in immediate and delayed recall of a visual paired associates learning task compared with controls, but no differences emerged on other tests of memory, learning, or executive function. The findings suggest MDMA specifically impairs visual paired associates learning, possibly due to serotonergic dysfunction in the hippocampus.
Journal of Psychopharmacology
May 1, 2007
Karsten Heekeren, Anna Neukirch, Jörg Daumann et al.
49 citations
Schizophrenia patients show reduced prepulse inhibition (PPI) of the startle reflex, but hallucinogen models of psychosis in healthy volunteers do not replicate this effect. In a double-blind crossover study with 15 healthy volunteers, the serotonergic hallucinogen DMT had no significant effect on PPI, while the NMDA antagonist S-ketamine increased PPI and decreased startle magnitude. Neither drug affected the attentional modulation of PPI. These results highlight differences between human hallucinogen models and both animal models and schizophrenia itself.
Neuroreport
October 1, 2003
Jörg Daumann, Ralph Schnitker, Jürgen Weidemann et al.
46 citations
Working memory performance and brain activation were examined in eight abstinent people who used only MDMA (ecstasy), a group who used MDMA plus other drugs, and non-users. Pure MDMA users showed lower brain activation than controls and polyvalent users, particularly in the inferior temporal regions, angular gyrus, and striate cortex. Polyvalent users did not differ from controls. The findings suggest that altered brain activation during cognitive tasks may be primarily linked to prior MDMA use, and that concomitant use of other drugs may modify this effect.