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Official websites use. Share sensitive information only on official, secure websites. Correspondence to: Matthias E Liechti; Email: matthias. The moral rights of the named author s have been asserted. Hyperthermia is a severe complication associated with the recreational use of 3,4-methylenedioxymethamphetamine MDMA, Ecstasy. In this review, the clinical laboratory studies that tested the effects of MDMA on body temperature are summarized. The mechanisms that underlie the hyperthermic effects of MDMA in humans and treatment of severe hyperthermia are presented. The data show that MDMA produces an acute and dose-dependent rise in core body temperature in healthy subjects. The increase in body temperature is in the range of 0. MDMA primarily releases serotonin and norepinephrine. Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation. The mediating role of serotonin is unclear. The management of sympathomimetic toxicity and associated hyperthermia mainly includes sedation with benzodiazepines and intravenous fluid replacement. Severe hyperthermia should primarily be treated with additional cooling and mechanical ventilation. Keywords: hyperthermia, hyperpyrexia, MDMA, norepinephrine, serotonin, treatment. MDMA-induced hyperpyrexia is relatively rare and not observed in placebo-controlled studies in humans. However, moderate effects of MDMA on body temperature have been documented in several placebo-controlled laboratory studies in human subjects. This review summarizes the clinical studies on MDMA-induced hyperthermic effects and the potential pharmacological mechanisms that are involved in humans. Many preclinical studies for review, see 1 but relatively few clinical studies have evaluated the effects of MDMA on body temperature. The present review focuses on the findings from placebo-controlled studies that assessed MDMA in humans and addresses treatment options for hyperpyrexia caused by recreational Ecstasy use. The thermal effects of Ecstasy in dance clubbers have previously been described and summarized. The association between Ecstasy use and hyperpyrexia is well-established, and reports were systematically compiled by Grunau and colleagues. Drug-induced hyperthermia resembles heat stroke. In heat stroke, heat dissipation is primarily impaired by a hot environment, and heat generation is often increased by exertion. In drug-induced hyperthermia, the drug exerts direct actions to increase metabolic heat generation and reduce heat dissipation as mostly studied in animals, 7, whereas a hot environment and exertion may act as additional permissive factors. Clinical laboratory studies that investigated the effects of MDMA using a placebo-controlled study design are summarized in Table 1. MDMA was administered orally in all these studies but different doses were used. Body temperature was not the primary outcome measure in these studies, with one exception. Pooled analyses of the effects of MDMA have been reported using aggregated data from smaller studies with 27 subjects by da la Torre and colleagues, 41 74 subjects by Liechti and colleagues, 34 and 80 subjects by Hysek and Liechti. Importantly, these body temperatures were measured with subjects at rest and at a mean room temperature of The time course of the increase in tympanic body temperature after MDMA administration at a dose of mg in 96 subjects is shown in Figure 2. The figure shows the pooled data from all our 6 published studies using the mg dose of MDMA. Effects of 3,4-methylenedioxymethamphetamine MDMA, mg orally and placebo on core body tympanic temperature in healthy subjects. MDMA was administered in a quiet hospital setting and the subjects were not physically active. Several other smaller studies have also evaluated the thermogenic effects of MDMA. Oral temperature slightly increased after doses of 75 and mg MDMA in 8 subjects, but no statistically significant differences were observed compared with placebo. Harris and colleagues measured both skin i. Unfortunately, no other studies have measured finger temperature to confirm this finding in a larger sample. Kirkpatrick and colleagues found that MDMA at an oral dose of mg had no effects on oral body temperature in 11 subjects. In all of the other studies, body temperature was a secondary measure. Core body temperature was measured in 10 subjects using an ingested radiotelemetry pill. Absolute core temperatures were higher after MDMA in the warm environment compared with the cold environment. However, core temperature was also higher in the warm environment compared with the cold environment after placebo. Thus, MDMA similarly increased core temperature at the low and high ambient temperatures compared with placebo. Skin temperature was markedly increased in the hot and decreased in the cold environment, and MDMA produced a near-significant increase in skin temperature under both temperature conditions and compared with placebo. Altogether, considering the pooled data analyses from our laboratory and those of the Freedman study, MDMA is well documented to produce an acute and dose-dependent elevation in core body temperature in healthy subjects. The increase in body temperature is also evidently rather small, in the range of 0. Importantly, no laboratory study observed MDMA-induced hyperpyrexia in a controlled setting. Several mechanistic studies assessed the effects of pharmacological pretreatments on the response to MDMA in healthy subjects to evaluate the mediating role of different neurotransmitters and receptors. These human studies also provide important information on the mechanisms involved in MDMA-induced increases in body temperature and likely also in the more severe hyperpyrexia associated with uncontrolled use. MDMA mainly releases serotonin and norepinephrine and to a lesser extent dopamine through the corresponding presynaptic monoamine transporters. Serotonin transporter inhibitors block the interaction between MDMA with the transporter to release serotonin. Serotonin transporter inhibitors reduced the psychotropic and most physiological effects of MDMA in healthy humans, 43, suggesting a mediating role for serotonin in most effects of MDMA in humans. Regarding the thermogenic effects of MDMA, serotonin transporter inhibition reduced MDMA-induced increases in oral 55 but not axillary body temperature. Interestingly, in animals, serotonin transporter inhibition reduced MDMA-induced hyperthermia in mice 57 but not rats. The serotonin 5-HT 2A receptor antagonist ketanserin reduced the MDMA-induced elevation in body temperature in humans, 44 consistent with studies in rats. The serotonin 5-HT 1A receptor antagonist pindolol did not alter the MDMA-induced increase in body temperature in humans, 60 also consistent with preclinical data. Preclinical data suggest a role for the dopamine D 1 receptor in the mediation of hyperthermia associated with MDMA. The interaction between MDMA and the dopamine D 2 receptor antagonist haloperidol was examined in healthy subjects, but MDMA did not produce significant elevations in body temperature in that study to provide meaningful results. Further human studies examined the contributing role of different adrenergic receptors. Peripheral vasoconstriction and improper heat dissipation have also been identified as critical mechanisms that underlie MDMA-induced core brain hyperthermia in rats treated with MDMA under conditions that simulate drug use in humans. Dumont and colleagues studied the interactive effects of MDMA and tetrahydrocannabinol in healthy subjects. Tetrahydrocannabinol delayed the MDMA-induced increase in temperature, and the duration of the temperature elevation was prolonged, although the mean temperature increase was comparable to administration of MDMA alone. Several experimental human studies also tested the effects of other psychostimulants with a slightly different pharmacology than MDMA on body temperature. Various psychostimulants, including MDMA, enhance noradrenergic neurotransmission, but their relative dopaminergic vs. For example, Tancer and Johanson assessed the effects of MDMA, D-amphetamine mostly a dopamine and norepinephrine releaser , and metachlorophenylpiperazine a serotonin inhibitor and releaser on oral temperature in the same study. Similar to amphetamine, methylphenidate a selective dopamine and norepinephrine transporter inhibitor with no serotonergic properties also acutely increased body temperature in humans when given at a dose of 40 mg 47 or 60 mg. Therefore, norepinephrine likely contributes to the thermogenic effects of these substances, consistent with the reducing effects of carvedilol on the temperature response to MDMA. A series of novel psychoactive substances with structural similarity to MDMA have been implicated in hyperpyrexia. In particular, para-methoxyamphetamine and para-methoxymethamphetamine, which are occasionally sold as Ecstasy, 69 have been associated with an especially high risk of hyperthermia. Four-Methylthioamphetamine is another serotonergic compound 73 that has been linked to hyperthermia. Altogether, the mechanistic studies in humans provide support for the conclusion that MDMA mainly increases body temperature via the release of norepinephrine, which then increases metabolic heat generation and impairs heat dissipation via vasoconstriction. Additionally, the release of serotonin may also contribute to the thermogenic effects of MDMA in humans. The various treatments for hyperpyrexia induced by MDMA or other psychostimulants have not been systematically evaluated in the emergency room setting. Hyperthermic complications are relatively rare, and clinical trials are unlikely to be conducted. However, as described above, several placebo-controlled mechanistic experimental studies have been conducted with healthy subjects, which can inform us on the pharmacological mechanism of MDMA-induced hyperthermia in humans and potential effects of pharmacological treatments. As a limitation, the experimental studies used doses of pure MDMA in the range of mg while recreational users of ecstasy pills may ingest MDMA at lager doses or repeated doses. For example, in an naturalistic observational study among 49 partying people, 34 used doses of MDMA of mg while 15 took cumulative doses of mg. Paramedics and emergency department personnel must recognize hyperthermia in subjects with acute substance-induced disorders. It is not uncommon that agitated subjects die of hyperpyrexia because body temperature was not measured, and elevations in body temperature went unrecognized. Agitated subjects should not be restrained. Antipsychotics, such as haloperidol, should not be used as a routine treatment of drug-induced agitation or only with great care and after treatment with benzodiazepines. Antipsychotics are associated with hyperthermia in the context of neuroleptic malignant syndrome and some e. Additionally, haloperidol has been shown to enhance acute anxiety and the negative mood effects of MDMA 46 and psilocybin. The atypical antipychotic clozapine has been shown to reverse hyperthermia and cutaneous vasoconstriction induced by MDMA in rats or rabbits 82 but human data to support its clinical use are lacking. Hyperthermia is often associated with other signs of sympathomimetic stimulation, including agitation, tachycardia, and hypertension. Benzodiazepines are also beneficial in the treatment of these symptoms. However, additional hypertensive treatment with vasodilators, such as nitrates, may be needed. Adrenergic receptor antagonists can be useful. Phentolamine was successfully used to treat a hypertensive emergency caused by amphetamine overdose. Besides from hyperthermia, brain edema is another severe complication of MDMA use. MDMA induces a syndrome of inappropriate secretion of antidiuretic hormone which may lead to symptomatic hyponatremia including brain edema in particular in women. Additionally, animal studies indicate that the blood-brain barrier is disrupted during MDMA-induced hyperthermia also leading to brain edema. MDMA increases body temperature in humans. The MDMA-induced elevations in body temperature in humans appear to depend on the MDMA-induced release of norepinephrine and involve cutaneous vasoconstriction and likely also enhanced metabolic heat generation. The role of serotonin needs further clarification. The management of overdose cases includes sedation treatment with benzodiazepines, intravenous fluid replacement, and additional cooling and mechanical ventilation in severe cases. As a library, NLM provides access to scientific literature. Temperature Austin. Find articles by Matthias E Liechti. Open in a new tab. Placebo-controlled studies that investigated effects of MDMA on body temperature. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel.

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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. The use of 3,4-methylenedioxymethamphetamine MDMA has frequently been associated with increased levels of impulsivity during abstinence. The effects of MDMA on measures of impulsivity, however, have not yet been studied during intoxication. The present study was designed to assess the acute effects of MDMA and alcohol, alone and in combination, on behavioral measures of impulsivity and risk-taking behavior. A total of 18 recreational users of MDMA entered a double-blind placebo-controlled six-way crossover study. Alcohol dosing was designed to achieve a peak blood alcohol concentration BAC of about 0. Laboratory tests of impulsivity were conducted between 1. MDMA decreased stop reaction time in the stop-signal task indicating increased impulse control. Signal detection analyses of alcohol-induced commission errors indicated that this effect may reflect impairment of perceptual or attentive processing rather than an increase of motor impulsivity per se. Performance in the Iowa gambling task was not affected by MDMA and alcohol, but there was a nonsignificant tendency towards improvement following alcohol intake. The lack of interaction indicated that the CNS stimulant effects of MDMA were never sufficient to overcome alcohol-induced impairment of impulse control or risk-taking behavior. Theories of drug use have proposed links with risk-taking behavior and impulsivity particularly among polydrug users de Wit et al, McCann et al reported a decrement in impulsivity ratings of MDMA users as measured by the Multidimensional Personality Questionnaire, whereas others reported elevated scores of impulsivity in heavy MDMA users, using different subjective measures of impulsivity Butler and Montgomery, ; Morgan, , ; Parrott, MDMA-induced impulsivity could be accounted for by both mechanisms. Research on MDMA-related impulsivity has generally relied on subjective questionnaires and self-report, which have provided valuable information about impulsivity as a trait in abstinent MDMA users. It has been argued, however, that these measures may not be very well suited for pharmacological studies of impulsivity because they are subjective, measure a relatively stable characteristic, and cannot be directly related to biological models of impulsivity Swann et al, These problems have been overcome by using behavioral measures of impulsivity as defined by the inability to anticipate and reflect on the consequences of decision making or by the failure to inhibit a response in a rapid response task Bechara et al, ; Logan et al, Studies in MDMA research employing behavioral tests have been relatively sparse but those that were conducted seem to support subjective reports of enhanced impulsivity. In addition, current and former MDMA users produced faster responses and more incorrect choices in a matching familiar figures test designed to measure reflection-impulsiveness Morgan, Yet, despite mounting evidence that inhibitory control may be impaired in abstinent MDMA users, the discussion as to its underlying cause remains controversial. A number of confounding factors have been suggested that may account for increments in risk taking or impulsivity observed in MDMA users, besides or instead of MDMA use per se. For example, MDMA users are generally polydrug users of a range of recreational drugs, which makes attribution of impulsivity to either one drug virtually impossible. In addition, it cannot be excluded that impulse and risk-taking behaviors are related to pre-existing low levels of serotonin in MDMA users or that a predisposition to elevated impulsivity underlies the use of MDMA or self-reports and laboratory results from studies in abstinent MDMA users Butler and Montgomery, ; Cole and Sumnall, Consequently, a better approach for determining a causal relation between MDMA use and change in impulse control may be to conduct placebo-controlled studies on the acute effects of MDMA on laboratory measures of impulse control. Acute studies will be crucial for showing a direct pharmacological link between MDMA use and impulse control during intoxication and may even provide a mechanistic blueprint for MDMA-induced long-term changes in impulse control. The aim of the present study is to assess the acute effect of MDMA alone and in combination with alcohol on impulsivity in a double-blind placebo-controlled within-subject design. Alcohol has been previously shown to decrease impulse control in rapid response tasks de Wit et al, ; Fillmore and Vogel-Sprott, , and was included in the present study design as an active control and to assess potential MDMA by alcohol interaction effects. A total of 18 recreational MDMA users nine males and nine females aged 20—37 years were recruited through advertisements in local newspapers. All subjects were light-to-moderate users of MDMA who reported to have taken the drug on 2—25 occasions mean: 9 occasions in the previous year. Overall, subjects reported to have taken between 2 and MDMA tablets mean: 18 tablets in the previous year. Initial screening was accomplished on the basis of a questionnaire on medical history. Subjects who were accepted were examined by the medical supervisor, who also checked vitals signs and took blood and urine samples. Standard blood chemistry, hematological and drug screen tests were conducted on these samples. This study was conducted according to the code of ethics on human experimentation established by the declaration of Helsinki and amended in Edinburgh All subjects gave their informed consent, in writing. Approval for the study was obtained from the University's Medical Ethics committee. A permit for obtaining, storing, and administering MDMA was obtained from the Dutch drug enforcement administration. The study followed a double-blind placebo-controlled six-way crossover design. Complete balancing of the treatment orders yielded six treatment orders randomly assigned to 18 subjects. Alcohol dosing was designed to achieve a peak BAC of about 0. The minimum wash-out period between successive treatments was 1 week. Laboratory tests were conducted between 1. Subjects were asked to refrain from any drugs starting 1 week before the medical screening and physical examination until 2 weeks after the last experimental session. The subjects were not allowed to use alcohol on the day prior to an experimental session and were requested to arrive at experimental sessions well rested. Drug and alcohol screens in breath and urine were performed prior to experimental sessions upon arrival of the subject. Drugs and placebo were only administered in case a subject had passed the urine drug screen on a given test day. Three subjects tested positive for cannabis in urine prior to drug or placebo administration. These subjects were all sent home to return to our laboratory at a later time. Subjects were transported from their homes to the laboratory or vice versa by one of the experimenters in order to prevent subjects from driving under the influence on the day of testing. Additional clinical blood chemistry, with particular reference to liver and renal function was conducted at day 7 after each treatment. All subjects received a training session prior to onset of the experimental sessions in order to familiarize them with the tests and procedures. This task requires subjects to make quick key responses to visually presented go signals and to inhibit any response when a visual stop signal is suddenly presented. The current test is adapted from an earlier version of Fillmore et al The go signals are four 1. Subjects are required to respond to each letter as quickly as possible by pressing one of two response buttons. A single test consists of trials in which each of the four-letter stimuli is presented equally, often. A stop signal occurred in 48 trials during a test. Subjects are required to withhold any response in case a stop signal is presented. Dependent variables are the proportion of commission errors on stop trials and the reaction times RT on go and stop-signal trials ie stop reaction time. Stop reaction time to stop-signal trials represents the estimated mean time required to inhibit a response. The method for calculating stop reaction time was taken from the race model of inhibitory control Logan, This model proposes that the response to stop-signal trials is defined by two parallel processes: execution of a motor action in response to a signal and inhibition of a motor action in response to stop signal. Crucial to the outcome of the race is the speed of both processes. Response inhibition will fail if the time required to inhibit exceeds the time to complete a motor response at the time of the stop signal. The speed of the inhibition response cannot be observed directly but can be derived mathematically on the basis of three factors: stop-signal delay, reaction time distribution on go trials, and the probability of successful response inhibitions in stop-signal trials. First, RT to go trials were rank ordered from shortest to longest. The finishing time of the inhibition response was then determined from the probability of successful response inhibition and the distribution of RT. Stop reaction time was then determined by subtracting the appropriate stop-signal delay from reaction time at the n th percentile of the RT distribution. The resulting values for each stop-signal delay were then averaged to yield a single measure of stop reaction time for the test. During the test, a series of letters A, E, H, L, K, and X appear one at a time in the center of the computer screen, and participants are instructed to press the spacebar at the appearance of each letter go condition. Dependent variables include average RT on go trials and errors of commission; that is, pushing the spacebar during no-go trials. Hit and false alarm rates were referred to standardized normal distributions in order to yield z H and z FA. Two respondents may differ considerably in their criterion, even when they are equally sensitive. A subject's response criterion may be liberal or risky, thereby detecting most of the no-go signals at the cost of many false alarms, or it may be conservative, leading to few false alarms while reducing the probability of detecting no-go signals. The subject sees four decks of cards on a computer screen labeled A, B, C, and D at the top end of each deck. With a mouse, the subject can click on a card on any of the four decks. Each deck of cards is programmed to have 40 cards. The majority of normal people choose advantageously on this task ie select more cards from the advantageous relative to the disadvantageous decks. Patients with frontal lobe lesions do the opposite, that is, select more disadvantageous cards. The sensitivity, reliability, and validity of this task in detecting decision-making impairments has been tested in neurological as well as psychiatric populations. Thus there is one dependent measure that we collect from this task: net score total no. Parallel versions of the gambling task are used over six treatment sessions Bechara et al, , In case of the stop-signal task, incomplete data sets were recorded from one subject due to technical problems. Only complete data sets entered the statistical analyses. In general, MDMA decreased stop reaction time as compared to placebo treatments. Mean SE stop reaction times in every treatment condition are shown in Figure 1. During alcohol treatments the proportion of commission errors was significantly higher as compared to treatments without alcohol in both tests. Mean SE sensitivity in each treatment condition is shown in Figure 3. On average, the number of advantageous cards selected during alcohol treatments were higher as compared to treatments without alcohol. MDMA did not affect performance in the gambling task. Mean BAC did not significantly differ between treatments. At onset of the laboratory test, that is, 1. The present study has been the first to assess the acute effects of MDMA on behavioral measures of impulsivity. In the third task, ie the Iowa gambling task, impulsivity was defined as the inability to anticipate and reflect on the consequences of decision making. In both response inhibition tasks, MDMA did not affect the proportion of commission errors but significantly improved stop reaction time in the stop-signal task. These data indicate that a single dose of MDMA has the potential to stimulate inhibitory motor control in a stop-signal task during intoxication. The pharmacological mechanism underlying improvement in impulse control may be related to acute serotonergic or dopaminergic suppletion following a single dose of MDMA. Improved impulse control during serotonergic suppletion seems in line with reports on impaired impulse control in heavy users of MDMA during periods of abstinence. Studies on serotonergic function in recreational MDMA users have repeatedly shown low levels of 5HIAA in CSF Bolla et al, ; McCann et al, ; Peroutka et al, ; Ricaurte et al, , reduced density of 5-HT transporters Reneman et al, and blunted neuro—endocrine responses in serotonergic challenge tests Gerra et al, ; McCann et al, ; Verkes et al, when compared to nondrug using controls. In addition, serotonergic depletion has been linked to behaviors characterized by impaired impulse control Linnoila et al, , Thus, acute improvement of inhibitory control in the stop-signal task following MDMA administration can be interpreted as supportive evidence for current notions on the link between serotonin and impulsivity. Impulsivity levels may drop following serotonin suppletion during acute MDMA intoxication but rise during periods of abstinence when serotonin levels are low. Alternatively, the reduction in stop reaction time during MDMA intoxication may have also resulted from increased dopaminergic neurotransmission. MDMA is known to also stimulate the release of dopamine and to bind to the presynaptic dopamine reuptake transporters, albeit with less affinity then for the 5HT transporter Green et al, Studies on the effects of dopamine agonists on behavioral measures of impulsivity have shown patterns of improvement in impulse control that are similar to the one presented here, following MDMA. D-amphetamine for example, was shown to decrease stop reaction time of healthy volunteers in a stop-signal paradigm without affecting reaction time to go trials de Wit et al, , However, opposite effects of amphetamine on behavioral tests of impulsivity have also been found when tested in long-term stimulant abusers. Similarly, single doses of cocaine reduced the ability to inhibit responses of cocaine abusers in a stop-signal task Fillmore et al, It has been suggested that repeated dopaminergic stimulation of prefrontal pathways leads to impairment of inhibitory functions Volkow et al, a , b and that neural changes following chronic stimulant use may alter the behavioral response to acute dopaminergic stimulation Fillmore et al, In the present study, the subjects can be best qualified as light-to-moderate MDMA users. Therefore, subject characteristics in the present study would seem more comparable to those in healthy volunteer studies than to those in studies employing long-term drug abusers. MDMA did not affect measures of impulsivity in every behavioral task employed in the present study. Decision-making processes in the Iowa gambling task were not affected by MDMA, which seems to indicate that its effect on stop reaction time in the stop-signal task is rather selective. It has been argued before that impulsivity is a broad conceptual construct that encompasses multiple mechanisms of behavioral control that may be linked to different regions of the brain Bechara Two types of impulsivity that can be distinguished are cognitive impulsivity and motor impulsivity. Cognitive impulsivity as measured by the Iowa gambling task is believed to reflect complex processes involved in the control of several cognitive, behavioral and effective processes. More in particular, it assesses the ability to think and reflect on the consequences of a choice prior to making a decision. The ventromedial section in the prefrontal cortex has been indicated as the most critical neural structure underlying these processes Bechara, ; Ridderinkhof et al, Thus, it is entirely possible that a pharmacological manipulation can affect these control systems independently and selectively. The present study thus suggests that MDMA selectively improves control over motor impulsivity, while leaving cognitive impulsivity intact. It is interesting to note that selectivity of MDMA effects have been reported in other psychological domains as well. Lamers et al demonstrated that a single dose of MDMA produced dissociable effects on psychomotor skills and attention. The effects of alcohol on measures of behavioral impulsivity were intriguing. Similar findings have been reported in the scientific literature. Previous studies employing stop-signal paradigms have reported that alcohol increased stop reaction time de Wit et al, or increased the number of commission errors Fillmore and Vogel-Sprott, , ; Mulvihill et al, , suggesting increased impulsivity. Sensitivity is a measure of sensory capabilities of the observer or of the effective signal strength, whereas response criterion is a measure of cautiousness and reflects such things as motives and attitudes. The present data thus suggest that the increase in commission errors may reflect impairment of perceptual or attentive processing rather than an increase of motor impulsivity. It would be preferable to increase task difficulty in future studies to further assess the contribution of alcohol-induced changes in sensitivity and response criterion to performance under more compelling laboratory circumstances. Performance on the Iowa gambling task tended to improve following alcohol treatment but this effect only approached statistical significance. It is still noteworthy, however, since similar effects have been reported in models, where cognitive impulsivity is defined as the inability to wait for a larger reward. Ortner et al employed a delay-discounting task, where healthy volunteers made a series of hypothetical choices between a small, immediate reward and a large, delayed reward. In the alcohol condition, subjects tended to discount delayed reward at lower rates than during the sober condition. This difference was not statistically significant, but suggested that alcohol led to more cautious decision making. Performance stimulating effects were not found by Richards et al but they did show that alcohol did not detrimentally affect discounting of delayed monetary reward. Although conceptual differences between tasks measuring cognitive impulsivity do exist, it has been shown that performance on delay-discounting tasks is significantly correlated to performance on the Iowa gambling task Monterosso et al, Together these results indicate that alcohol does not increase cognitive impulsivity in this type of decision-making tasks. The absence of an alcohol effect on decision-making tasks vs the presence of a detrimental effect of alcohol on motor inhibition tasks demonstrates once more that impulsivity is not a unitary concept or brain structure but is comprised of several independent psychological domains or brain regions that can respond very selectively to a pharmacological manipulation. None of the behavioral parameters showed any significant MDMA by alcohol interaction effect. This suggests that MDMA does not alter the effects of alcohol on behavioral measures of impulsivity. This notion seems in line with conclusions from a previous study that assessed combined effects of alcohol and MDMA on psychomotor function during intoxication in humans Hernandez-Lopez et al, These investigators reported that MDMA reversed the subjective sedation induced by alcohol but did not change the impairing effect of alcohol on measures of psychomotor function such as simple reaction time and digit symbol substitution. The lack of mitigating effects of MDMA on alcohol-induced impairment on measures of impulsivity or risk tasking may be of particular importance in terms of road safety issues. The present data indicates that the CNS-stimulating effects of MDMA do not suffice to overcome alcohol-induced impairment of motor control, which is one of the most common causal factors in vehicle crashes. Bechara A Separate neural substrates underlie different mechanisms of performance monitoring and behavioral control. In: Ullsperger M, Falkenstein M eds. Errors, Conflicts and the Brain. Google Scholar. Emotion, decision making and the orbitofrontal cortex. Cereb Cortex 10 : — Decision-making deficits, linked to a dysfunctional ventromedial prefrontal cortex, revealed in alcohol and stimulant abusers. Neuropsychologia 39 : — Neurology 51 : — Drug Alcohol Depend 76 : 55— Altered states: the clinical effects of Ecstasy. 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Altered neuroendocrine and behavioral responses to m-chlorophenylpiperazine in 3,4-methylenedioxymethamphetamine MDMA users. Psychopharmacology Berlin : 56— Neuropsychopharmacology 10 : — Addict Disord Treatment 1 : 47— Three decision-making tasks in cocaine-dependent patients: do they measure the same construct? Addiction 96 : — Morgan MJ Neuropsychopharmacology 19 : — Ecstasy MDMA : a review of its possible persistent psychological effects. Alcohol and the ability to inhibit behavior in men and women. J Stud Alcohol 58 : — Nash JF Ketanserin pretreatment attenuates MDMA-induced dopamine release in the striatum as measured by in vivo microdialysis. Life Sci 47 : — Alcohol intoxication reduces impulsivity in the delay-discounting paradigm. Alcohol Alcohol 38 : — Parrott AC Human research on MDMA 3,4-methylene-dioxymethamphetamine neurotoxicity: cognitive and behavioural indices of change. 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Drug Alcohol Depend 55 : — Cognitive performance and serotonergic function in users of ecstasy. Imaging studies of cocaine in the human brain and studies of the cocaine addict. Ann NY Acad Sci : 41—54; discussion 54— Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature : — Download references. You can also search for this author in PubMed Google Scholar. Correspondence to Johannes G Ramaekers. Reprints and permissions. Ramaekers, J. Neuropsychopharmacol 31 , — Download citation. Received : 05 April Revised : 02 August Accepted : 05 August Published : 14 September Issue Date : 01 May Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content Thank you for visiting nature. Download PDF. Abstract The use of 3,4-methylenedioxymethamphetamine MDMA has frequently been associated with increased levels of impulsivity during abstinence. Design, Doses, and Administration The study followed a double-blind placebo-controlled six-way crossover design. Procedures Subjects were asked to refrain from any drugs starting 1 week before the medical screening and physical examination until 2 weeks after the last experimental session. Behavioral Tests of Impulsivity Stop-signal task This task requires subjects to make quick key responses to visually presented go signals and to inhibit any response when a visual stop signal is suddenly presented. The Iowa gambling task The subject sees four decks of cards on a computer screen labeled A, B, C, and D at the top end of each deck. Figure 1. Mean SE stop reaction times in each treatment condition in the stop-signal task. Full size image. Figure 2. Figure 3. References Bechara A View author publications. Rights and permissions Reprints and permissions. About this article Cite this article Ramaekers, J. Copy to clipboard. This article is cited by MDMA alone affects sensorimotor and prepulse inhibition responses in mice and rats: tips in the debate on potential MDMA unsafety in human activity Matteo Marti Margherita Neri Emanuela Turillazzi Forensic Toxicology Individual differences in voluntary alcohol intake in rats: relationship with impulsivity, decision making and Pavlovian conditioned approach Marcia Spoelder Jacques P. Flores Dourojeanni Louk J. Vanderschuren Psychopharmacology Geweld door alcohol en drugs II Jan van Amsterdam Raymond Niesink Verslaving Cannabis and cocaine decrease cognitive impulse control and functional corticostriatal connectivity in drug users with low activity DBH genotypes J. Ramaekers J. Fillmore Current Addiction Reports Search Search articles by subject, keyword or author. Show results from All journals This journal. Advanced search.

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