Ecstasy (MDMA): a review of its possible persistent psychological effects

Morgan, M.

doi:10.1007/s002130000545

Cited by 342 publications

(305 citation statements)

References 122 publications

(226 reference statements)

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“…Similar findings have been observed by other authors (see Morgan, 2000, for a review of the literature). Apparent ecstasy-related deficits may be mediated by other drug use (Croft et al, 2001;Dafters et al 2004) although results from other studies suggest that ecstasy-related deficits remain following control for the use of other illicit drugs (Fisk et al, 2004;Reay et al 2006).…”

Section: Introductionsupporting

confidence: 92%

Self reported sleep quality and cognitive performance in ecstasy users

Montgomery

Fisk

Wareing

et al. 2007

Human Psychopharmacology

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Objectives: Research suggests that ecstasy users exhibit psychobiological changes relative to nonusers such as altered sleep patterns and cognitive deficits. In turn, it has been suggested that sleep quality may be a mediator of such cognitive deficits in ecstasy users. The present study sought to investigate this proposed relationship.Methods: Aspects of cognitive functioning in 104 ecstasy users and 103 nonusers obtained from our previous studies were reanalysed to explore the extent to which ecstasy-related group differences were attributable to differences in sleep quality.Cognitive function was assessed via the computation span test, consonant updating, paired associate learning, syllogistic reasoning and word fluency. Sleep quality was measured via the Epworth Sleepiness Scale (ESS), and the Karolinska Sleepiness Scale (KSS). Results: Ecstasy users performed worse than nonusers on all cognitive measures. While no differences were observed on the ESS, ecstasy users reported greater tiredness at the beginning of testing than nonusers. When the sleep variables were included as covariates, the effects of ecstasy on all cognitive measures remained significant. Conclusions: The results of the present study suggest little evidence for the mediating effects of sleep on cognitive function in ecstasy users.

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Section: Introductionsupporting

confidence: 92%

Self reported sleep quality and cognitive performance in ecstasy users

Montgomery

Fisk

Wareing

et al. 2007

Human Psychopharmacology

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“…Considering that the forced swim test is the most widely used tool for preclinical antidepressant activity (Cryan et al, 2002), these results strengthen the claim that a neurotoxic dose of MDMA leads to increased depressive-like symptoms in animals. This converges with increasing human research that links MDMA consumption with depression (MacInnes et al, 2001;Morgan, 2000;Parrott et al, 2002). The magnitude of the MDMA effect is marginal but reliable, consistent with a report showing that MDMA users manifest mild rather than severe symptoms of depression (MacInnes et al, 2001).…”

Section: Fluoxetine and Mdma Behavioral Effectssupporting

confidence: 85%

“…Recent studies have linked MDMA use in humans to longterm psychological problems including depressed mood (MacInnes et al, 2001;Morgan, 2000;Parrott et al, 2002) and increased anxiety (Gamma et al, 2000;McGuire, 2000;Parrott et al, 2002Parrott et al, , 2000Schifano et al, 1998;Verkes et al, 2001;Wareing et al, 2000). However, human studies rarely provide convincing proof of a causal role for MDMA in such effects.…”

Section: Introductionmentioning

confidence: 99%

Chronic Fluoxetine Treatment Partly Attenuates the Long-Term Anxiety and Depressive Symptoms Induced by MDMA (‘Ecstasy’) in Rats

Thompson

Clemens

et al. 2003

Neuropsychopharmacol

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Use of the drug 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy') can have long-term adverse effects on emotion in both humans and laboratory animals. The present study examined whether chronic treatment with the antidepressant drug fluoxetine could reverse such effects. Male Wistar rats were briefly exposed to MDMA (4 Â 5 mg/kg over 4 h) or vehicle on 2 consecutive days. Approximately 9-12 weeks later, half of the rats received a dose of approximately 6 mg/kg/day fluoxetine in their drinking water for a 5-week period. Fluoxetine administration reduced fluid intake and body weight in MDMA and vehicle pretreated rats. After several weeks of fluoxetine treatment, rats were assessed on the social interaction test, the emergence test of anxiety and the forced swim model of depression. MDMA pretreated rats showed reduced social interaction, increased anxiety on the emergence test, and increased immobility and decreased active responses in the forced swim test. Fluoxetine treatment reversed MDMA-induced anxiety in the emergence test and depressive-like effects in the forced swim test, yet exhibited no effects on the social interaction test. MDMA pretreated rats had decreased 5-HT and 5-HIAA levels in limbic and cortical regions, and decreased density of serotonin transporter sites in the cortex. Fluoxetine treatment did not greatly affect 5-HT levels in MDMA pretreated rats, but significantly decreased 5-HIAA levels in all brain sites examined. Postmortem blood serum levels of fluoxetine and norfluoxetine did not differ in MDMA and vehicle pretreated rats. These results indicate that fluoxetine may provide a treatment option for some of the deleterious long-term effects resulting from MDMA exposure.

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“…Given that most ecstasy users are also cannabis users (Morgan, 2000) the question arises as to whether concurrent use of cannabis by ecstasy users might make them less susceptible to MDMA related neurotoxicity. The present paper is intended to investigate this issue.…”

Section: Edge Hill College Of Higher Educationmentioning

confidence: 99%

The effects of concurrent cannabis use among ecstasy users: neuroprotective or neurotoxic?

Fisk

Montgomery

Wareing

et al. 2006

Human Psychopharmacology

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Edge Hill College of Higher EducationRunning head: concurrent cannabis use among ecstasy users. The research evidence regarding the potential effects of ecstasy suggests that it may be neurotoxic and that its use is associated with cognitive impairment. In recent years evidence has emerged suggesting that cannabinoids, the active ingredients in cannabis, can be neuroprotective under certain conditions. Given that many ecstasy users also consume cannabis at the same time, the possibility emerges that these individuals might be less susceptible to ecstasy-related impairment. The present paper reanalyses the data from a number of previous studies, contrasting the performance of those individuals who generally consume cannabis and ecstasy at the same time with those who generally consume ecstasy on its own. The two ecstasy-using groups are compared with non-ecstasy users on a range of measures including processing speed, random letter generation, verbal and visuo-spatial working memory span, reasoning and associative learning. The two ecstasy user groups did not differ significantly from each other on any of the measures. Both user groups were significantly worse than non-ecstasy users on measures of associative learning, verbal and visuo-spatial working memory, and reasoning. The results suggest that consuming cannabis at the same time as ecstasy does not reduce the likelihood of cognitive impairment.There is abundant evidence that ecstasy (MDMA) is neurotoxic, disrupting serotonergic systems in diverse brain regions. There is also a considerable body of evidence that cannabis can have neuroprotective as well as neurotoxic properties.Given that most ecstasy users are also cannabis users (Morgan, 2000) the question arises as to whether concurrent use of cannabis by ecstasy users might make them less susceptible to MDMA related neurotoxicity. The present paper is intended to investigate this issue.Although there is abundant evidence that MDMA is neurotoxic in a range of animal species, evidence of neurotoxicity in humans is less extensive and sometimes controversial (Curran, 2000). A review of the neuroimaging evidence can be found in Reneman et al (2006). A number of studies have found evidence of neurotoxicity among ecstasy users. For example, using PET neuroimaging, McCann, et al (1998), investigated 5-HT neural damage in the brains of ecstasy users. Regions of interest included the frontal cortex, pariental cortex, temporal cortex, occipital cortex and cingulate cortex, as well as the caudate, putamen, thalamus, mid-brain, pons, hypothalamus and cerebellum. The results showed that, compared to a control group, ecstasy users had significantly lower densities of 5HT transporter sites in all brain regions. Further, the reductions observed were correlated with the extent of ecstasy use. Reneman, et al (2002a) also assessed neural injury in ecstasy users using single-voxel (1H) MR spectroscopy imagining. N-Acetylasportate (NAA)/Creatine (CR), NAA Choline (CHO), and Myoinositol (MI) CR ratios in ecstasy users were meas...

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Ecstasy (MDMA): a review of its possible persistent psychological effects

Cited by 342 publications

References 122 publications

Self reported sleep quality and cognitive performance in ecstasy users

Self reported sleep quality and cognitive performance in ecstasy users

Chronic Fluoxetine Treatment Partly Attenuates the Long-Term Anxiety and Depressive Symptoms Induced by MDMA (‘Ecstasy’) in Rats

The effects of concurrent cannabis use among ecstasy users: neuroprotective or neurotoxic?

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