During July 2003, two studies of Ecstasy user demographics, one case report, one (brief) review, one report detailing drug use functions, five in-vitro or non-human animal studies and two forensic/chemistry studies (not summarized) were located. Several publications located in July had been published in 2002, but were missed either due to oversight (a study in rats) or to delayed appearance of the reference in PubMed, a database of medical pubolications (a brief review).

A post-mortem study of drivers killed in traffic accidents found that MDMA was detected in 6 of 3398 cases (Drummer et al. 2003), and approximately 10% of a random sample of undergraduates reported lifetime Ecstasy use (Boyd et al. 2003). By contrast, 25% of undergraduates spending 10 or more hours attending parties, and 25% of undergraduates who identified themselves as gay, lesbian or bisexual reported lifetime Ecstasy use.

Researchers surveyed polydrug users about their drug use patterns, and any factors related to extent of drug use, and problem drug use (Boys et al. 2003). Onset of Ecstasy use (age when it was first used) generally occurred later than onset of alcohol or cannabis use, and people reported that they used Ecstasy mostly to enhance social situations or to manage negative moods. Intensity of use was best predicted by perceived peer use, followed by the tendency to use Ecstasy for managing negative moods, use in best friend/partner, and age of first use, with younger onset of Ecstasy use associated with greater intensity of current use. Using Ecstasy to manage negative moods was more strongly associated with intensity (frequency x average dose per use) of use and drug-related problems than was the number of reported negative effects arising from drug use.

Case Report-Another Case of Parkinson’s Disease in an Ecstasy User.

A case of very early-onset Parkinson’s disease in a 19-year old man reporting previous Ecstasy use was described (Kuniyoshi and Jankovic 2003), with symptoms developing two months after his last use of Ecstasy. Prior to onset of Parkinson’s disease, the young man had used Ecstasy twice monthly for about six months. The man had a family history of early-onset Parkinson's disease, with the condition diagnosed in his father and his uncle prior to the appearance of his symptoms. Relying on findings from a study in non-human primates that has since been retracted (Ricaurte et al. 2003), the authors hypothesized that the effects of Ecstasy use on dopamine cells were sped up and more apparent in people predisposed to develop Parkinson’s disease. However, with findings supporting MDMA as dopamine cell neurotoxin retracted, this case cannot be considered evidence of MDMA-induced dopamine toxicity in humans.

A very brief review addressed the potential significance of the findings reported in Ricaurte et al. 2002 (Butcher 2002), with the review penned prior to the recent retraction of these findings.

Three studies employing models of Parkinsonian symptoms, and side effects of anti-Parkinson’s medications in rats, explored MDMA and related compounds as potential treatments for the conditoin and medication-related side effects. MDMA attenuated catalepsy (slow or reduced movement) after haloperidol (Banjaw et al. 2003; Schmidt et al. 2002). The related compound MDE was only somewhat effective at reducing catalepsy (Schmidt et al. 2002). One form of the active ingredient in the stimulant plant khat (S-(+)-cathinone), reduced catalepsy as well (Banjaw et al. 2003), while MDA and MBDB did little to reduce catalepsy (Schmidt et al. 2002). By contrast, MDA, followed by MDMA, was most effective in causing rats with damage to dopamine cells on one side of their brains to walk in the direction of the damage (Lebsanft et al. 2003). This model assumes that because dopaminergic drugs produce turning in the direction opposite the damage, potential treatments for Parkinson's disease medication side effects might make rats turn in the direction of the damage. Neither MDE nor MBDB were effective at causing circling in the direction of the damage. Inhibiting serotonin uptake reduced MDMA’s ability to induce circling, but inhibiting serotonin synthesis only slightly reduced circling. All three studies suggest that MDMA and related compounds might at least lead to means of controlling some symptoms of Parkinson's disease, as well as side effects from current anti-Parkinson's medication. Findings can be compared with those reported in a species of non-human primate (Iravani et al. 2003).

A study in mice found that early ("adolescent") exposure to MDMA and methylphenidate seemed to make cocaine more rewarding, as assessed by conditioned place preference (Achat-Mendes et al. 2003). 30 days after exposure, the appeal of cocaine was about the same in MDMA-treated and saline treated mice, but less appealing to methylphenidate-treated mice. When cocaine CPP was assessed again, both methylphenidate-treated and MDMA-treated mice showed greater CPP than saline-treated mice. A study in rats compared the long-term effects of repeated dose regimens of S-(+)-MDMA and d-methamphetamine on avoidance learning and locomotor activity (Timar et al. 2003). Both drugs acutely increased locomotor activity. S-(+)-MDMA and d-methamphetamine increased activity 3 days later, but not 1, 2 or 4 weeks later, and neither drug impaired passive or active avoidance learning. This was true both when avoidance learning was measured days or weeks later. Both studies suggest that MDMA and selected psychostimulants used as prescription drugs share similarities, both in the behavioral changes they produce and the changes they fail to produce after administration.