The present findings suggest that self-reported psychopathology in ecstasy users is predominantly attributable to concomitant use of cannabis. Abstinence from cannabis and not ecstasy seems to be a reliable predictor for remission of psychological complaints in ecstasy users.

Numerous animal studies have been able to demonstrate neurotoxic damage to central serotonergic systems after exposure to 3,4-methylenedioxymethamphetamine (MDMA, ecstasy). It has been suggested that a high loudness dependence of auditory evoked potentials (LDAEP) and, particularly, of the tangential N1/P2 source activity is associated with a low functioning of serotonergic activity. Therefore, the LDAEP may be used as a non-invasive indicator for a possible neurotoxic damage caused by the long-term use of ecstasy in recreational users. We recorded auditory evoked potentials (AEP) with a passive listening paradigm in 18 polydrug ecstasy users at baseline (t1) and after 18 months (t2). Several aspects of ecstasy use, such as frequency of use, cumulative lifetime dose or period of abstinence were associated with the LDAEP for several tangential dipoles at both measuring times. However, we failed to demonstrate any significant relationship between drug use reported at follow-up and AEP changes from baseline to follow-up. Despite some incertitude these data suggest, yet do not unambiguously con.rm, the hypothesis that abstinent ecstasy users present with diminished central serotonergic activity. This feature of information processing is potentially related to the neurotoxic potential of ecstasy. However, alternative interpretations of these data refer to possible preexisting traits and the potential impact of other illicit drugs, particularly amphetamine, since ecstasy users typically exhibit polydrug use patterns. Thus, further research with larger sample sizes and prospective study designs are needed to definitively establish a causative link between ecstasy use and neurotoxicity-related dysfunctions in sensory processing.