Two studies of ecstasy users, one brief review and one non-human animal study were located during this time period.

Polydrug users/memory
Polydrug users reporting ecstasy use were compared with polydrug users reporting no ecstasy use on a battery of tests of working memory and executive function (Fox et al. 2002), with a large percentage of these tests relying on visual rather than verbal skills. When compared with participants reporting no ecstasy use, ecstasy users obtained lower scores on one measure of executive function that used verbal skills, and on several measures of working memory, and ecstasy users also performed less well on another, more visual measure of executive function. However, most of the differences between ecstasy users and controls were subtle and selective, appearing in the most difficult trials of any given task. Furthermore, there was no single assessment that consistently distinguished ecstasy users from non-users.

PET Imaging A PET imaging study measuring regional and global glucose metabolism in ecstasy users and age-matched oncology patients via the radioligand 2-[18F]-fluoro-2-deoxy-glucose (FDG) found that FDG uptake in ecstasy users was lower in left and right putamen and caudate, and in the left amygdala (Obrocki et al. 2002). However, the authors were unable to identify a single area that differentiated ecstasy users from oncology patients. People who first used ecstasy before they were 18 years old had lower global FDG uptake than people who first used ecstasy when they were 18 or older, and greater global FDG uptake was associated with a longer interval from the last use of ecstasy to the study day. Surprisingly, cumulative ecstasy use was not associated with changes in global FDG uptake or regional FDG uptake in ecstasy users. While providing some interesting information about differences in glucose metabolism, imaging with FDG cannot serve as a direct measure of serotonergic function or neurotoxicity.

MDMA Neurotoxicity in Rats
An examination of the effects of MAO-B inhibition via anti-MAO-B antisense oligonucleotide (AS ODN) on MDMA-induced neurotoxicity in rats found that MAO-B inhibition attenuated serotonergic neurotoxicity without preventing hyperthermia (Falk et al. 2002). Findings from a microdialysis study of MDMA-mediated DA release in anti-MAO-B AS ODN treated animals that was presented in the same report found that MAO-B inhibition did not reduce DA release, and that only DA turnover was lower after the AS ODN-MDMA combination. These findings support a role for a dopamine metabolite in producing MDMA-induced neurotoxicity. However, the authors never tested for possible antioxidant properties of the AS ODN or of chronic MAO-B inhibition, leaving open the possibility that the reduction in MDMA-induced neurotoxicity resulted from reduction of oxidative stress, and not from reduced presence of DA metabolites.