Schreckenberger M, Gouzoulis-Mayfrank E, Sabri O, Arning C, Zimny M, Zeggel T, Wagenknecht G, Kaiser HJ, Sass H, Buell U (1999) "Ecstasy"-induced changes of cerebral glucose metabolism and their correlation to acute psychopathology. An 18-FDG PET study. Eur J Nucl Med 26: 1572-1579.

15 healthy volunteers (11 men, 5 women, age range = 27-45) were given either placebo or 2 mg/kg MDE, and brain glucose metabolism was measured using PET with [F18]-fluorodeoxyglucose (FDG) and co-registered with MRI. Data appears to be drawn from the same sample described in two papers examining the effects of psilocybin, MDE and methamphetamine (Gouzoulis-Mayfrank, Franke et al. 1999; Gouzoulis-Mayfrank, Thelen et al. 1999). Participants were all physicians and psychologists, and all volunteers were healthy as established through medical and psychiatric examination, and none reported any occurrence of major mental illness in themselves or in first-degree relatives. Subjective effects, vital signs and neuroendocrine effects were also measured, but only one measure of psychological effects is reported in this study; the observer-scored Positive and Negative Syndrome Scale (PANSS), and scores on this scale are correlated with changes in brain glucose metabolism, as was the case in other publications by the same authors. The PET scan occurred while participants performed a word repetition task for 32 minutes, wherein recordings of common words were repeated; this task was used in lieu of a "resting state" scan. Brain glucose metabolism was examined across subjects using ROIs normalized via using global glucose metabolism. In this paper, 108 regions of interest were summarized into 17 ROI groups. Participants in the MDE condition had decreased glucose metabolism in bilateral frontal regions, including left frontal posterior and right prefrontal superior regions. Increased glucose metabolism was found bilaterally in cerebellum and in right putamen. There was a positive correlation between increased metabolism in the right cingulate and grandiosity, between increased glucose metabolism in right amygdala and difficulties in abstract thinking, between both right prefrontal interior, and right and left cingulate and attentional difficulties. Decreased metabolism in left frontal operculum was associated with attentional deficits. The authors note that decreased glutamate metabolism in frontal areas have occurred after administering markedly different drugs, including amphetamine (stimulant), morphine (opiate) and scopolamine (anticholinergic). This suggests that hypofrontal metabolism alone cannot serve as an indicator of a particular drug or any specific psychological or subjective effects it produces.

Participants in previous clinical trials with MDMA reported difficulty concentrating and some impaired thought processes (Vollenweider et al. 1998), so it is possible that these effects, when seen, arise from alterations in cingulate or amygdala. Findings reported in this paper are somewhat different from those reported in another publication comparing the effects of MDE with psilocybin and methamphetamine as well as placebo. While that study also reported decreased brain glucose metabolism in frontal regions and increased cerebellar metabolism, some of the significantly decreased areas differ, and relationships between changes in glucose metabolism and PANSS scores are not identical. Beyond findings potentially relating to the brain mechanisms producing some effects of MDE, this paper indicates that MDE, like MDMA, can be safely administered to humans.

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