This review specifically addresses issues relating to research intended to detect or measure serotonergic neurotoxicity in humans, with a critique of many studies employing brain imaging techniques to compare ecstasy users and non-users. Commonly recognized difficulties with the research design and methods used in these studies are described and addressed. Kish remarks on the use of log transformed data in an imaging study comparing serotonin transporter density in ecstasy users and non-users (McCann et al. 1998), a step that others examining the study had not taken into account before. This data transformation actually makes the degree of reduced serotonin transporter binding smaller in ecstasy users, suggesting that log transformation was undertaken as a means to reduce within-group variance. Kish expresses disbelief at the degree of reduced serotonergic function indicated via untransformed data, particularly since ecstasy users did not exhibit any behavioral or physiological indicators of greatly reduced serotonin. The author also describes difficulties with a number of brain imaging studies, with attention to alternate sources of variation in serotonin transporter density, including gender and the impact of other drug use. The author argues for the use of more post-mortem examinations whenever possible (similar to his own investigation of a single ecstasy userŐs brain (Kish 2000). The paper fails to examine or critique studies assessing 5HT2A receptor site density, or their relevance in assessing serotonergic function. References are not always provided for some of the authorŐs assertions, as when discussing the specific effects of gender on serotonin transporter site density, or when stating that differences in a serotonin transporter promoter gene can effect SERT expression. Nevertheless, this is a thorough exploration of current research into the potential neurotoxicity of ecstasy/MDMA, and Kish includes recommendations for future research in the area.