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Neuroimaging research in human MDMA users: a review

Buy Ecstasy (MDMA) Chang

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. It is debated whether ecstasy use has neurotoxic effects on the human brain and what the effects are of a low dose of ecstasy use. Outcomes of proton magnetic resonance spectroscopy 1 H-MRS , diffusion tensor imaging DTI , perfusion-weighted imaging PWI , and questionnaires on depression, impulsivity, and sensation seeking were compared in 30 subjects 12M, Interval between baseline and follow-up was on average 8. However, ecstasy use was followed by a sustained 0. After correction for multiple comparisons, only the rrCBV decrease in the dorsolateral frontal cortex remained significant. As no indications were found for structural neuronal damage with the currently used techniques, our data do not support the concern that incidental ecstasy use leads to extensive axonal damage. However, sustained decreases in rrCBV and ADC values may indicate that even low ecstasy doses can induce prolonged vasoconstriction in some brain areas, although it is not known whether this effect is permanent. Additional studies are needed to replicate these findings. There is increasing evidence that ecstasy 3,4-methylenedioxymethamphetamine, MDMA is toxic to the human brain, especially to the serotonergic system eg, McCann et al, ; Reneman et al, , although the validity of these findings is still highly debated Turner and Parrott, ; Grob, ; Kish, Many human studies are littered with methodological problems, including inadequate sampling of subjects and controls, lack of drug use analysis, and lack of baseline data eg, Morgan, ; De Win et al, The latter argument leads to interpretative difficulties concerning causality between ecstasy use and potential toxicity, because it leaves open the possibility that differences between ecstasy users and controls were pre-existent, as discussed previously by others Jansen and Forrest, ; Morgan, ; Dughiero et al, It may be possible that personality traits like impulsivity and sensation seeking, associated with substance misuse, are related to lower serotonergic function Khantzian, ; Zuckerman and Kuhlman, or that results are biased by confounding variables such as polydrug use, gender, and lifestyle. Most of these studies focused on acute and not on sustained or permanent effects of ecstasy. These studies have led to ongoing discussion on safety and ethics of administration of potentially neurotoxic drugs to healthy humans. Several authors objected to administering a potential neurotoxic drug to humans for the purpose of science Gijsman et al, ; McCann and Ricaurte, , while others supported these experiments Lieberman and Aghajanian, ; Vollenweider et al, , The discussion mainly persists, because it is assumed that heavy ecstasy use most probably causes adverse long-term effects eg, McCann et al, ; Reneman et al, a , while it is not known whether a low dose of ecstasy can cause lasting brain damage. In rats, neuronal damage was demonstrated in various brain areas following a single dose of MDMA Colado et al, ; Schmued, , including persistent effects on behavior Ho et al, The validity of animal data for the human situation has been questioned, however, because MDMA is usually administered to animals in higher dosages than generally used by humans. Some authors do not support the suggestion that a single oral dose at 1. On the other hand, it has been advocated that these dosages in animals are equivalent to typical recreational dosages in humans according to the principles of interspecies scaling Ricaurte et al, ; McCann and Ricaurte, It is important to know whether a low dose of ecstasy is neurotoxic for at least two reasons. Determining that the incidental use of ecstasy could cause persisting neuronal damage would have major clinical and social implications. Second, it is debated whether MDMA should become available for medical use, because MDMA may be useful as an adjunct in psychotherapy, or whether this would lead to neuronal damage Check, This discussion is of interest, since pilots have been approved that will study therapeutic effects of MDMA on anxiety in patients with post-traumatic stress disorder Check, and in terminally ill cancer patients Bender, When considering ecstasy as adjunct in psychotherapy, it is important that estimations of risk are available to decide whether potential risks outweigh potential benefits. With advanced magnetic resonance MR techniques, such as proton magnetic resonance spectroscopy 1 H-MRS , diffusion tensor imaging DTI , and perfusion weighted imaging PWI it is possible to study various aspects of neuronal damage in the brain. NAA is decreased in neuronal damage and impaired cognition Ross et al, Cho is increased in brain diseases that involve increased membrane breakdown, myelination, or inflammation, and it is thought to reflect cellular density Miller et al, MI is a putative glial cell marker increased in diseases that involve gliosis Ross et al, Cr is often used as an internal reference Pouwels and Frahm, With DTI it is possible to measure diffusional motion of water molecules. In the brain, the motion is restricted in amplitude and direction by cellular structures such as axons. Sub acute processes that involve axonal injury and ischemia can lead to a decreased apparent diffusion coefficient ADC of water due to cytotoxic edema Haykin et al, However, in chronic stage of axonal damage, ADC can be increased and fractional anisotropy FA of water can be decreased due to increased extracellular water content. It is difficult to determine the time course of change in ADC. Only one article was published with ADC measurements in heavy ecstasy users, and showed increased ADC values in the globus pallidus Reneman et al, b. This is of interest because serotonin is involved in regulation of brain microcirculation Cohen et al, Previous publications described cerebrovascular accidents, such as cerebral infarction and hemorrhage, Hanyu et al, ; Lee et al, and cerebrovascular changes Chang et al, ; Reneman et al, , b in ecstasy users. It is expected that ecstasy use induces a sub acute increase of extracellular serotonin leading to vasoconstriction, whereas the long-term effect of ecstasy use may be a decrease in extracellular serotonin and thus vasodilatation. If a low dose of ecstasy is neurotoxic, it is important to know whether this has clinical consequences in terms of psychopathological parameters such as mood, impulsivity, and sensation seeking. The aim of the present study was to assess whether a low dose of ecstasy would be neurotoxic. Using a prospective naturalistic study design, parameters of neurotoxicity measured with 1 H-MRS, DTI, and PWI and outcomes of psychopathological self-report inventories on depression, impulsivity, and sensation seeking were compared between a baseline session before first ecstasy use and a follow-up session after ecstasy use. The current study is part of the NeXT Netherlands XTC Toxicity study, which investigates causality, course, and clinical relevance of ecstasy neurotoxicity. A detailed description of the NeXT study and recruitment strategies can be found in a special design paper De Win et al, Between April and April , young adults 77 M, F, age They had never used ecstasy, but were selected on a relatively high probability to start using ecstasy in the near future. Subjects were recruited using a combination of targeted site sampling, advertisement through a website on the project, and snowball sampling referrals. Exclusion criteria were: ecstasy use in the past at baseline , age below 18 or above 35 years, severe physical or mental illness, use of psychotropic medications such as serotonin reuptake inhibitors, pregnancy, use of intravenous drugs, and contraindications for MRI eg, claustrophobia, pacemaker. Subjects had to abstain from psychoactive substances for at least 2 weeks and from alcohol for at least 1 week before examinations. This was checked by urine drug screening enzyme-multiplied immunoassay for amphetamines, ecstasy, opiates, cocaine, benzodiazepine, cannabis, and alcohol. The study was approved by the local medical ethics committee. Subjects were informed about potential negative consequences of ecstasy use and all subjects signed informed consent. After baseline examination, subjects had to complete questionnaires four in total about their drug use at regular intervals over a period of approximately 18 months. For the present study, the first 31 incident ecstasy users were included in a first follow-up session, relatively soon after their first ecstasy use after we received their first drug use questionnaire indicating use of ecstasy and with a maximum cumulative ecstasy dose of 10 tablets. At both sessions, subjects had to complete questionnaires about potential confounders, such as demographic variables and education. Various aspects of lifetime ecstasy use frequency of use, cumulative dose, and duration of use , and last year use of alcohol units per week , tobacco cigarettes per week , cannabis number of joints last year , amphetamines number of times used last year , and cocaine number of times used last year were assessed using substance-use questionnaires Van de Wijngaart et al, MR imaging was performed on a 1. Throughout the study positioning of subjects in the scanner and positioning of the slices and voxels were performed by the same examiner and according to a protocol to keep positioning as reproducible as possible. The voxel size for 1 H-MRS was 6. Shimming and water suppression were automatically performed by the scanner. Diffusion was measured in six non-collinear directions and in the six opposite directions. The gadobutrol injection was followed by a ml saline flush 0. This is a user-independent analysis method that estimates absolute metabolite concentrations by fitting the in vivo spectra to a set of previously acquired in vitro spectra the basis set. This procedure allows the absolute quantification of metabolite concentrations. From the resulting diffusion weighted images, ADC, and FA maps were calculated as described elsewhere Hunsche et al, All images were skull-stripped program bet, FSL, Smith, The scans were segmented into three classes of tissue CSF, white, and gray matter , and the tissues of interest were isolated into separated binary maps only white matter, only gray matter, and combined white and gray matter. Regions of interest ROIs were drawn on the MNI brain template in the thalamus, putamen, globus pallidus, head of the caudate nucleus, centrum semiovale frontoparietal white matter , and dorsolateral frontal, mid-frontal, occipital, superior parietal, and temporal cortex see Figure 2. For the cortical ROIs, only voxels within the gray matter mask were included and for the ROIs of the basal ganglia only voxels within the combined white and gray matter mask were included CSF voxels were excluded. Selection of ROIs was based on findings of previous studies, which indicated that ecstasy-induced abnormalities are most prominent in basal ganglia and cortical areas; ecstasy-induced abnormalities in white matter were rarely reported and thus not expected. As cortical gray matter has very low anisotropy, it is very difficult to get reliable FA and ADC measurements in cortical areas. Region of interests used for analyses of DTI measuring FA and ADC and PWI measuring rrCBV drawn on the MRI brain template at three levels: 1 thalamus, 2 globus pallidus, 3 putamen, 4 caudate nucleus, 5 dorsolateral frontal cortex, 6 mid-frontal cortex, 7 occipital cortex, 8 superior parietal cortex, 9 temporal cortex, and 10 white matter of the centrum semiovale. For each individual scan, all steps in the post-processing and analysis were visually inspected to check the quality of image registration and segmentation. Current depressive symptoms were assessed using the Beck Depression Inventory BDI Beck et al, , a item self-report inventory that measures characteristic attitudes and symptoms of depression in the week before assessment. The Dutch BIS contains 31 self-reported items. The Spannings Behoefte Lijst SBL , a Dutch adaptation of the Sensation Seeking Scale Zuckerman and Link, with 51 items, was used to measure sensation seeking as it has proven to be a reliable measure for research populations Feij et al, ; Feij and van Zuilen, All substance-use variables were log-transformed because they were not normally distributed. First, paired t -tests, uncorrected for multiple comparisons, were used to assess whether parameters of substance use, imaging, and self-report questionnaires had changed between baseline session before ecstasy use and follow-up session after ecstasy use. Third, previous studies showed that effects of ecstasy might be dose-dependent McCann et al, ; Reneman et al, a and that females are more vulnerable for the effects of ecstasy than males Reneman et al, a ; Buchert et al, Other studies suggested a relationship between brain perfusion and time since last ecstasy use and between ADC and time since onset of neuronal damage Chang et al, ; Reneman et al, Therefore, we performed separate multiple linear regression analyses with follow-up measures of imaging and self-reported psychopathology as dependent variable and gender, cumulative dose of ecstasy, period of abstinence weeks since last ecstasy tablet and change in cocaine use because this was the only significantly increased drug-use parameter as independent variable and baseline measures of imaging and self-reported psychopathology as covariates. Finally, Pearson correlations were calculated between statistically significant changes in MR outcomes and significant changes in outcomes of the psychopathology questionnaires. All statistical analyses were performed using SPSS version Of the ecstasy-naive subjects at baseline, 31 subjects were included in the first follow-up session relatively soon after their first ecstasy use 12 M, 19 F, age One female was excluded because of a positive urine test on cocaine, leaving 30 volunteers for analysis with a mean age of Characteristics of the sample and their substance use are described in Table 1. The interval between the baseline and follow-up sessions was on average 8. At this first follow-up session incident ecstasy users had used a mean of 1. The interval between the last ecstasy use and follow-up measurements was 7. However, due to technical problems with the scanner it was not possible to perform 1 H-MRS in two subjects at the follow-up session. Anatomical images T1 3D scans and T2-weighted scans were read by a neuroradiologist for atrophy or white matter lesions, and no significant abnormalities were detected. However, one subject had enlarged lateral ventricles and visual inspection showed this hampered matching to the standard brain, and therefore the measurements of FA, ADC, and rrCBV of this subject were not included. Table 2 shows results of all measurements and Figure 3 illustrates the statistically significant findings. With DTI, we observed a small but significant increase of 0. When adjusted for multiple comparisons using the Bonferroni correction, only the decreased rrCBV value in the dorsolateral frontal gray matter remained statistically significant. On the left, FA, ADC, and rCBV maps with brain regions, that significantly differed between baseline and follow-up uncorrected for multiple comparisons , marked in white. On the right, columns reflect corresponding FA values in the centrum semiovale, ADC values in the thalamus, and rrCBV values in thalamus, dorsolateral frontal gray matter. Only significant results are shown, for complete results of all analyses see Table 2. Note that the vertical axis does not start at zero. Similar to the first set of analyses, the second set of analyses, excluding subjects with increased cocaine use between both sessions, showed no significant changes in metabolite concentrations and ratios. After correction for multiple comparisons, only the rrCBV value in the dorsolateral frontal gray matter remained statistically significant. Of these regression analyses only the positive effect of the total amount of ecstasy tablets on FA in white matter remained significant after correction for multiple comparisons. Results of the self-report questionnaires on depression, impulsivity, and sensation seeking at baseline and follow-up sessions are shown in Table 1. No changes were observed in sensation seeking. There were no significant correlations between increased depression and impulsivity scores and significant changes in MR outcomes. To our knowledge, this is the first imaging study that prospectively examined sustained effects of a low dose of ecstasy on the human brain. Given the existing data on potential neurotoxicity, it is highly controversial to give ecstasy to ecstasy-naive individuals in a controlled experiment Gijsman et al, ; Lieberman and Aghajanian, ; Vollenweider et al, ; McCann and Ricaurte, Therefore, we used a naturalistic design in which young adults with a relatively high probability for first time ecstasy use were included in a follow-up study. Only a few subjects incidentally used amphetamines and cocaine, and the use of alcohol, tobacco, and cannabis before the two sessions was very similar. This is not unexpected, because previous observations showed that neurotoxic effects of ecstasy are probably dose-related McCann et al, ; Reneman et al, a ; Buchert et al, Therefore, these effects probably only appear after cumulative heavy use. On the other hand, we observed a small but significant decrease of 3. We can speculate that this might be related to ecstasy-induced cytotoxic edema, as observed in other neurotoxic substances Heaney et al, ; Haykin et al, , although it also could be related to protracted vasoconstriction, since we also observed a decreased rrCBV in the thalamus Pearson correlation between these findings is 0. With DTI we also encountered the unexpected finding of increased FA in the centrum semiovale related to the total amount of ecstasy tablets, although this 0. Functional parameters were measured with PWI and self-report questionnaires. Decreases in cerebral blood flow CBF , mainly in the caudate nucleus, and superior parietal and right dorsolateral frontal cortices, were previously observed after only two doses of MDMA Chang et al, As this happened within 3 weeks after MDMA administering and because microcirculation in these areas has a strong relationship with serotonergic terminals Cohen et al, , the authors hypothesized that the decreased CBF was caused by sub-acute vasoconstriction due to MDMA-mediated serotonergic effects. The same study reported an increased CBF 2—3 months after MDMA intake although only studied in two subjects and no differences were found in CBF between controls and abstinent ecstasy users with a mean abstinence period of 6. They speculated that these findings might reflect depletion of serotonin after a longer period of abstinence and normalization of brain perfusion, respectively. Based on these results, they suggested a relationship between brain perfusion and abstinence period. Previous findings of higher rrCBVs in ecstasy users with an average period of abstinence of The latter study also showed low rrCBV values in combination with lower cortical 5-HT 2 receptor densities, suggesting downregulation of 5-HT 2 receptors, in ecstasy users with a mean abstinence period of 7 weeks, and they hypothesized this was caused by excessive ecstasy-induced serotonin release. The currently observed decreased rrCBV values in subjects with a mean period of abstinence of 7. On the other hand, we did not find significant correlations between rrCBV and the time since last ecstasy tablet abstinence interval. Another speculation is that decreased rrCBV values might reflect decreased brain function, because a single ecstasy dose was shown to cause degenerating neurons in parietal cortex and thalamus of rats Schmued, In line with this, deficits in brain perfusion were reported in polydrug Levin et al, and methamphetamine abusers Iyo et al, ; Chang et al, Outcomes of the self-report questionnaires after first ecstasy use showed increased impulsivity, as previously observed in other studies Morgan, However, the magnitude of the effect is limited 3. Subjects also reported lower levels of depression after ecstasy use than before, an unexpected finding that might be related to a euphoric feeling about the first ecstasy experience Korf et al, Also here, the clinical relevance of the reduction from 4. Moreover, it should be noted that the findings were not reproduced after a longer follow-up period in a larger sample of the same baseline population De Win et al, Although this study and some other studies showed that adverse effects of a low ecstasy dose are limited Downing, ; Vollenweider et al, , there are various factors eg, poor metabolism, hypertension, young age, simultaneous use of other substances, environmental conditions that might contribute to individual or situational vulnerability for acute adverse effects and long-term neurotoxicity of ecstasy Buchert et al, ; Obrocki et al, ; Green et al, ; Segura et al, Therefore, it is not possible to state that incidental use of ecstasy is completely safe. For example, neurocognitive data from a larger sample of the current study population suggest that even low-dose ecstasy use is associated with small but significant decreases in verbal memory relative to non-users Schilt et al, As we used multiple techniques as indicators for ecstasy-induced brain damage and multiple regions of interests, there is an increased probability of type I errors false positive results. Therefore, additional post hoc Bonferroni corrections on all imaging analyses were performed. The results showed that most of the significant findings did not remain significant after Bonferroni correction. On the other hand, the Bonferroni correction may be too conservative especially because a priori we expected small effects as we studied early indicators of potential brain damage in subjects with only low cumulative doses of ecstasy use. Moreover, all imaging techniques and ROIs were chosen based on a priori hypothesis. Therefore, it is likely that the Bonferroni-correction induces type II errors false negative findings. The risk of such corrections was previously discussed by Rothman who showed that they can obscure possibly important findings Rothman, As a result of its social impact, additional research is needed to establish whether the current uncorrected significant findings can be replicated. Also the environmental circumstances under which ecstasy was taken and the simultaneous use of other substances was heterogeneous. As a result of these changing circumstances, it is possible that the observed changes in FA, ADC, rrCBV, depression, and impulsivity are not related to ecstasy use, but to other time- or ecstasy-related variables. Confounding by the use of other substances, such as alcohol, nicotine, cannabis, amphetamines, and cocaine, cannot be totally excluded, although alcohol, nicotine, cannabis, and amphetamine use did not change between sessions and most effects remained significant after exclusion of subjects with increased use of cocaine between sessions. Another limitation is that we did not include a control group. Therefore, we cannot be completely sure about the reproducibility of our measurements. ROIs were drawn in the spatially normalized MNI brain template, which may have introduced additional variance due to inherent variations in mapping of individual brains to the MNI brain. On the other hand, compared to drawing ROIs for each individual subject, the current procedure is user-independent and reproducible, because the same procedure is performed for all subjects exactly in the same way. As few studies used 1 H-MRS, DTI, and PWI to study neuronal damage in ecstasy users, little is known about the sensitivity and specificity of these techniques to detect ecstasy-induced neuronal damage. Therefore, additional studies are needed, both in animals and in heavy human ecstasy users. As expected neuronal damage after a low dose of ecstasy is relatively small, the statistical power of this study could have been insufficient for 1 H-MRS and DTI to detect changes. DTI is particularly suitable for detection of white matter lesions, while ecstasy-related neuronal damage is especially expected in basal ganglia and cerebral cortex. As these areas have low FA, the sensitivity of this parameter to detect axonal dysfunction in basal ganglia might be limited. For example, 1 H-MRS showed to be sensitive to detect changes in patients with schizophrenia, affective disorders, autism, and depression Stanley, ; Kumar et al, and substance users Ernst et al, ; Nordahl et al, ; Reneman et al, DTI showed to be sensitive in detection of early diffuse axonal injury after traumatic brain injury Arfanakis et al, and various neuropsychiatric disorders Lim and Helpern, PWI showed to be sensitive in detection of rrCBV deficits in early Alzheimer's disease Harris et al, ; Bozzao et al, and in other neuropsychiatric diseases Renshaw et al, In conclusion, with the currently used techniques we found no indications for structural neuronal damage after a low dose of ecstasy use in first time ecstasy users. Therefore, these data do not support the concern that incidental ecstasy use leads to serious axonal loss, although more studies are needed to assess the sensitivity of the currently used MR techniques to detect small ecstasy-induced neuronal changes. However, our findings of decreased rrCBV and ADC may indicate that even a low dose of ecstasy can induce sustained vasoconstriction in some brain areas, although we do not know whether these findings are permanent. Therefore, and because there may be various personal and environmental factors that play a role in the occurrence of acute and long-term effects of ecstasy, it is impossible to state, based on this study, that incidental use of ecstasy is totally safe for the brain. Diffusion tensor MR imaging in diffuse axonal injury. PubMed Google Scholar. An inventory for measuring depression. Arch Gen Psychiatry 4 : — Functional cerebral imaging by susceptibility-contrast NMR. Magn Reson Med 14 : — Bender E FDA approves study of ecstasy in some terminally ill patients. Psychiatric News 40 : Google Scholar. Eddy current correction in diffusion-weighted imaging using pairs of images acquired with opposite diffusion gradient polarity. 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Can J Psychiatry 47 : — Self-reported depressive symptomatology in community samples of polysubstance misusers who report ecstasy use: a meta-analysis. J Psychopharmacol 19 : 84— The Netherlands National Drug Monitor Annual Report Trimbos Institute: Utrecht. High intensity dependence of auditory evoked dipole source activity indicates decreased serotonergic activity in abstinent ecstasy MDMA users. Is MDMA a human neurotoxin? Diverse views from the discussants. Neuropsychobiology 42 : 42— J Psychoactive Drugs 33 : 95— Ecstasy in het uitgaanscircuit ecstasy and the Dutch rave scene: A socio-epidemiologic study on the nature and extent of, and the risks involved in using ecstasy and other party drugs at dance events. Addiction Research Institute: Utrecht. Is a single dose of MDMA harmless? Automated image registration: I. General methods and intrasubject, intramodality validation. J Comput Assist Tomogr 22 : — Zuckerman M, Kuhlman DM Personality and risk-taking: common biosocial factors. J Pers 68 : — Zuckerman M, Link K Construct validity for the sensation-seeking scale. J Consult Clin Psychol 32 : — Download references. Questionnaires on drug use were obtained by courtesy of the Addiction Research Institute of the University of Utrecht. You can also search for this author in PubMed Google Scholar. Correspondence to Maartje M L de Win. Reprints and Permissions. Neuropsychopharmacol 32, — Download citation. Received : 21 February Revised : 21 August Accepted : 28 August Published : 01 November Issue Date : 01 February Drugs: Education, Prevention and Policy Journal of Psychoactive Drugs Radiology Movement Disorders Advanced search. Skip to main content Thank you for visiting nature. Download PDF. Abstract It is debated whether ecstasy use has neurotoxic effects on the human brain and what the effects are of a low dose of ecstasy use. Image Acquisition MR imaging was performed on a 1. Figure 1. Full size image. Figure 2. Figure 3. View author publications. Rights and permissions Reprints and Permissions. About this article Cite this article de Win, M. Filatova , Anouk Schrantee , Matthan W. Caan , Frans M. Search Search articles by subject, keyword or author. Show results from All journals This journal.

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