Neuropsychological evidence of a relatively selective profile of temporal dysfunction in drug-free MDMA ("ecstasy") polydrug users

Fox, Helen; McLean, Andrew N.; Turner, John; Parrott, Andrew C.; Rogers, Robert D.; Sahakian, Barbara J.

doi:10.1007/s00213-002-1071-9

Cited by 160 publications

(182 citation statements)

References 62 publications

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“…However, by way of mitigation, it is noteworthy that most of the published studies that have probed cognitive deficits among ecstasy users have not resorted to urine, hair, or saliva testing (e.g., Fox et al, 2002;Morgan, 1998;Morgan, 1999;Parrott & Lasky, 1998;Rodgers, 2000). The importance of not over generalising from the present findings must also be stressed.…”

Section: Resultsmentioning

confidence: 81%

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

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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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Section: Resultsmentioning

confidence: 81%

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

Fisk

Montgomery

Wareing

et al. 2006

Human Psychopharmacology

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“…Once a token or object is found in a certain place during one trial, the subject has to keep in mind not to return to that place. Fox et al (2002) demonstrated that Ecstasy users performed worse on this task, on the most difficult level, as compared to normal controls, but this finding conflicted with results from an earlier study (Semple et al 1999). In other words, categorization of spatial memory tasks has not yet provided additional insight into the conflicting pattern of spatial memory deficits that has emerged in studies employing current and/or abstinent drug users.…”

mentioning

confidence: 72%

“…Some studies have found Ecstasy polydrug users to be impaired on this kind of tasks, as compared to a polydrug control group (Verkes et al 2001;Fox et al 2001), whereas others did not (McCann et al 1999;Semple et al 1999). Fox et al (2002) also reported conflicting results on delayed matching to sample tasks. The third category comprises studies using "search tokens tasks".…”

mentioning

confidence: 97%

Acute dose of MDMA (75 mg) impairs spatial memory for location but leaves contextual processing of visuospatial information unaffected

Kuypers

Ramaekers

2006

Psychopharmacology

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Rationale: Research concerning spatial memory in 3,4-methylenedioxymethamphetamine (MDMA) users has presented conflicting results showing either the presence or absence of spatial memory deficits. Two factors may have confounded results in abstinent users: memory task characteristics and polydrug use. Objectives: The present study aims to assess whether a single dose of MDMA affects spatial memory performance during intoxication and withdrawal phase and whether spatial memory performance after MDMA is task dependent. Materials and methods: Eighteen recreational MDMA users participated in a doubleblind, placebo-controlled, three-way crossover design. They were treated with placebo, MDMA 75 mg, and methylphenidate 20 mg. Memory tests were conducted between 1.5 and 2 h (intoxication phase) and between 25.5 and 26 h (withdrawal phase) post-dosing. Two spatial memory tasks of varying complexity were used that required either storage of stimulus location alone (spatial memory task) or memory for location as well as processing of content or contextual information (change blindness task). Results: After a single dose of MDMA, the subjects made larger localization errors and responded faster compared to placebo in the simple spatial memory task during intoxication phase. Inaccuracy was not due to increased response speed, as determined by regression analysis. Performance in the change blindness task was not affected by MDMA. Methylphenidate did not affect performance on any of the tasks. Conclusion: It is concluded that a single dose of MDMA impairs spatial memory for location but leaves processing of contextual information intact.

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“…Introduction 3,4-Methylenedioxymethamphetamine (MDMA, 'ecstasy') is widely used as a recreational drug by young people despite having been shown to be a neurotoxin in the brains of rodents and non-human primates (Green et al 2003) and to produce lasting specific memory deficits in humans (Bolla et al 1998;Verkes et al 2001;Fox et al 2002;Verbaten 2003;Soar et al 2004;Wareing et al 2000;2004a,b;Montgomery et al 2005;Gouzoulis-Mayfrank et al 2003. These psychopathological disturbances are probably a consequence of the long-term neurochemical changes induced by the drug (Reneman et al 2000;Cowan et al 2003;Daumann et al 2005).…”

mentioning

confidence: 99%

Binge ethanol administration enhances the MDMA-induced long-term 5-HT neurotoxicity in rat brain

et al. 2006

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Rationale Ecstasy abuse commonly occurs in hot, overcrowded environments in combination with alcohol. Around 90% of ecstasy users take ethanol; over 70% of these users also often drink alcohol at hazardous levels. Objectives We wished to examine whether binge ethanol administration enhanced the long-lasting 5-HT neurotoxicity induced by 3,4-methylenedioxymethamphetamine (MDMA) in rats maintained at high ambient temperature and the role of acetaldehyde. Materials and methods Rats were treated with a 4-day ethanol regimen leading to plasma ethanol levels of around 450 mg/dl. On day 5, rats were placed at 30°C and administered MDMA (5 mg/kg). Rectal temperature and hydroxyl radical formation were measured immediately before and up to 6 h after MDMA. 5-HT concentration and 5-HT transporter density were determined 7 days later. A group of rats received cyanamide (50 mg/kg) on days 1 and 3 of the 4-day-ethanol inhalation. Results In ethanol treated rats, MDMA produced a hyperthermic response similar to that observed in controls but enhanced the loss of 5-HT concentration and 5-HT transporter density in the hippocampus. Cyanamide elevated the plasma acetaldehyde concentration fivefold to sevenfold, reduced the MDMA-induced hyperthermia and increased the neuronal damage with neurotoxicity also appearing in the cortex. MDMA increased hydroxyl radical production in the hippocampus, the effect being more marked in rats pre-exposed to ethanol.Conclusions Binge ethanol administration enhances the MDMA-induced long-term 5-HT neurotoxicity by a mechanism not related to changes in acute hyperthermia but probably involving hydroxyl radical formation. The magnitude of this effect is more pronounced after increasing plasma acetaldehyde levels by aldehyde dehydrogenase inhibition.

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Neuropsychological evidence of a relatively selective profile of temporal dysfunction in drug-free MDMA ("ecstasy") polydrug users

Abstract: Initial cognitive deficits in ecstasy polydrug users may be more apparent in tasks known to be sensitive to temporal functioning.

Cited by 160 publications

References 62 publications

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

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

Acute dose of MDMA (75 mg) impairs spatial memory for location but leaves contextual processing of visuospatial information unaffected

Binge ethanol administration enhances the MDMA-induced long-term 5-HT neurotoxicity in rat brain

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