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Neuroimaging research in human MDMA users: a review
Determining whether, under what circumstances, and to what extent 3,4-methylenedioxymethamphetamine MDMA exposure produces chronic changes in human brain function is a critical public health issue. Because findings from the animal literature have indicated that specific dosage regimens of MDMA can produce long-lasting alterations in serotonergic function, existing studies of MDMA effects in humans have examined brain serotonin 5-HT transporters 5-HTT and receptors or have examined brain structures or functions potentially affected by MDMA. The objectives of this review are to provide a background for interpreting human MDMA neuroimaging research, to examine existing neuroimaging data regarding the rationale for and limitations to human MDMA research, and to provide suggestions for improving the design and interpretation of future neuroimaging approaches. Of the existing neuroimaging studies in human MDMA users, few experimental designs have been replicated across different research groups. Only investigations employing nuclear imaging methods to assay brain 5-HTT levels have been replicated across methods and research laboratories. However, the sensitivity of these methods is unknown. Future study designs might benefit from improved sample homogeneity, increased length of MDMA abstinence, longitudinal study design, test—retest measures, serotonergic specificity, and multimodal approaches. Animal studies suggesting that MDMA administration may produce long-lasting or even permanent brain changes have fueled research efforts to better understand the relationship between animal administration research and brain consequences in human MDMA users for review, see Green et al. Although the extensive animal literature on MDMA effects cannot be reviewed in detail in this manuscript, numerous animal studies have revealed that MDMA when given in sufficiently large or sufficiently frequent dosages produces long-term alterations in 5-HT function reviewed in Green et al. Findings of degenerating axons and 5-HT axon reorganization in some MDMA administration studies in animals have led to the concern that human MDMA users may suffer irreversible loss of ascending serotonergic innervation Kish ; Green et al. Further confounding the implication of animal studies for human MDMA users are recent findings in animal models indicating that loss of some 5-HT markers is not necessarily consistent with axon destruction Fantegrossi et al. In addition, the degree to which MDMA dosages and dosage regimens employed in animal research mirror those used recreationally by humans also remains unclear Lieberman and Aghajanian ; McCann and Ricaurte ; de la Torre and Farre ; Irvine et al. As such, neuroimaging studies of the acute effects of MDMA are not discussed. Before discussing current neuroimaging findings in MDMA users, several caveats are in order. First, although this review and existing human neuroimaging studies have focused on serotonergic effects of MDMA exposure, it should be made clear that MDMA is a complex pharmacological agent having a broad range of effects across multiple neurotransmitter systems e. Third, like all research in human recreational drug users, MDMA neuroimaging research based on exposure in a naturalistic setting is subject to variability introduced by many uncontrolled factors Green Given these circumstances, successful neuroimaging investigations in MDMA users face considerable challenges to their design, implementation, and interpretation. A recent review of neuroimaging in multiple drugs of abuse offers a brief overview of findings with an emphasis on ischemic effects Rojas et al. The present review has three parts: 1 this brief introduction highlighting studies that provide the foundation for human neuroimaging investigations, 2 a review of human MDMA neuroimaging research to date, and 3 a summary of the implications of existing studies and suggested future directions for MDMA neuroimaging research. Neuroimaging explorations in human MDMA users have been rooted in examining the direct or indirect pathology of the 5-HT system or in investigating neural correlates of cognitive processes demonstrated to be impaired in MDMA users. Because 5-HT alterations have been the primary focus of much of the basic and clinical literature with regard to MDMA toxicity, it is not surprising that initial neuroimaging efforts have focused on markers of serotonergic integrity. These have included the 5-HTT as a potential marker for axons Table 1 and 5-HT 2A receptors as potential indirect markers reflecting changes in 5-HT synaptic concentrations. The 5-HTT is distributed along the entire course of 5-HT axons rather than solely at the synaptic terminal Zhou et al. As a result, loss of serotonergic axons would be predicted to result in reduced levels of the 5-HTT in affected regions, providing an intriguing target marker to investigate MDMA-induced axon toxicity. Detection of 5-HT axon loss, using 5-HTT density as a surrogate, is complicated by several factors, including potential variability in 5-HTT expression associated with age Yamamoto et al. Semple et al. Reneman and colleagues Reneman et al. In a comparison of mood and 5-HTT levels, de Win et al. An additional manuscript Reneman et al. McCann et al. MDMA users had used MDMA an average of times range 70 to times and reported abstinence from the drug for a minimum of 3 weeks mean abstinence period of 19 weeks; range 3— weeks. Serum and urine drug screens were used to verify abstinence from all drugs of abuse. The findings from this report McCann et al. As critiqued by Kish and discussed in McCann et al. However, as discussed below, these results have now been largely replicated by other investigators Buchert et al. After the McCann et al. As the different manuscripts highlight slightly different aspects of the overall group, only the data from the Buchert et al. Buchert et al. Males and females were roughly balanced in each group, with a total of 59 males and 58 females participating. Similar to the initial report of McCann et al. The relationship between neuropsychiatric tests and 5-HTT status in this cohort of users was reported in Thomasius et al. This report included a detailed survey of polydrug use parameters and MDMA use patterns. While all drug-using groups i. All subjects reported drug abstinence for at least 2 weeks before the study and urine drug screens were negative at study enrollment except that marijuana positive drug screens were permitted. Brain regions having significantly reduced ligand binding included the amygdala, hippocampus, thalamus, and cortical regions frontal, occipital, orbitofrontal, parietal, anterior, and posterior cingulate. In summary, nuclear imaging studies using various methodologies and multiple ligands have demonstrated that MDMA users have reduced brain 5-HTT levels. The sensitivity of nuclear imaging methods to detect reductions in 5-HTT levels requires further clarification. In addition to the 5-HTT, 5-HT 2A receptors are important components of the serotonergic system and can be assayed in humans. Given their postsynaptic location, 5-HT 2A receptors are positioned to indirectly reflect synaptic 5-HT release and can potentially serve as a complementary measure to 5-HTT levels in determining whether MDMA has long-term functional consequences in human users Scheffel et al. The 5-HT 2A receptor largely displays activity classically associated with G-protein coupled receptors and down-regulates with sustained exposure to agonists and up-regulates in the absence of agonist reviewed in Gray and Roth ; Van Oekelen et al. The response of the 5-HT 2A receptor to antagonist exposure is less predictable and is frequently paradoxical e. MDMA administration in rodents has produced variable results with regard to 5-HT 2 receptor assays 5-HT 2 binding in neocortex is considered largely reflective of 5-HT 2A receptor status. For example, Scheffel et al. When assayed at 21 days in the Scheffel et al. Reneman and colleagues interpreted these findings as consistent with 5-HT-induced subchronic receptor downregulation followed by a denervation 5-HT-depletion -induced compensatory receptor up regulation. These diverging findings may be the result of different MDMA administration paradigms e. Sex Moses-Kolko et al. Urine drug screens were negative for all subjects at study enrollment. When ligand binding was assessed by brain region frontal, parietal, temporal, and occipital cortex , MDMA users had significantly increased expression of 5-HT 2A receptors in occipital cortex. MDMA users showed significantly reduced word recall when compared to the control group. There was no correlation between 5-HT 2A binding and word recall in controls, but within the MDMA users, increased overall receptor levels i. Given that 5-HT innervates cerebral microvessels having a mixed, but mainly vasoconstrictive effect altered 5-HT innervation to cerebral blood vessels might produce changes in resting vascular tone Cohen et al. The investigators hypothesized that low levels of 5-HT 2A receptors would correlate with vasoconstriction and decreased rCBV consistent with increased presynaptic 5-HT signaling , whereas high levels of 5-HT 2A receptors would correlate with vasodilation and increased rCBV consistent with reduced presynaptic 5-HT signaling. The final study by Reneman et al. In the aggregate data analysis, 5-HT 2A receptor binding was reduced in recent MDMA users in the three cortical regions assayed frontal, parietal, and occipital cortex when compared to controls. At present, the referenced studies of 5-HT 2A binding in human MDMA users appear consistent with classically expected G-protein coupled receptor activity of the 5-HT 2A receptor with indirect evidence for reduced receptor binding during active MDMA use but with increased receptor binding in longer-abstinent subjects—a finding potentially consistent with long-lasting reductions in 5-HT release and compensatory receptor up-regulation. As described above Reneman et al. MDMA-induced changes in neuronal volume or functional integrity might also occur due to chronic neuronal loss due to acute ischemic effects of MDMA Reneman et al. The average lifetime MDMA use was Subjects reported use of multiple recreational drugs, but denied use of drugs other than MDMA within 6 months of the study. Study-day urine drug screens were negative for all subjects. A subgroup of 10 subjects was given oral dosages of MDMA on two occasions. The second dosage of MDMA was administered 1 week to 21 days after the initial dose. The total MDMA dosage ranged from 2. Subjects who were restudied 2 to 3 weeks post-MDMA administration showed significant rCBF reductions in multiple brain regions including bilateral caudate, bilateral superior parietal cortex, and right dorsolateral prefrontal cortex. These latter findings suggested a subchronic persistent vasoconstrictive effect of MDMA administration, leading Chang et al. A subsequent investigation Reneman et al. MDMA users did not show significant differences compared to controls in frontal or occipital cortical areas. These authors interpreted the increased rCBV values in the globus pallidus as the result of loss of tonic serotonergic vasoconstrictive effects to globus pallidal arterial vessels with resulting relative vasodilation producing increased blood vessel volume. In the same study, Reneman and colleagues also conducted diffusion weighted imaging to assess for differences in the apparent diffusion coefficient ADC of water. This technique can be used to detect changes in the free movement of water and can indirectly assay loss of structural integrity, for example with regard to fiber bundles reviewed in Parker Reneman et al. Overall, the Chang et al. However, the presence of reduced blood flow at least 2—3 weeks post-MDMA administration has implications for the minimum abstinence period needed in studies directly examining blood flow or relying on methods dependent on neurovascular coupling, such as the functional magnetic resonance imaging fMRI blood oxygen level dependent BOLD technique. The study of Reneman et al. MDMA can potentially chronically influence brain gray matter integrity through several mechanisms. These include: 1 direct and indirect neuronal or glial effects 2 changes in 5-HT coupled neurotrophic factors such as brain derived nerve growth factor BDNF Duman et al. With regard to direct and indirect neuronal effects, direct toxicity of MDMA to neuronal cell bodies has not been a prominent feature of basic research reports of MDMA administration. Ricaurte et al. A single report found that MDMA administration to rats produced hyperthermia-dependent neuronal degeneration in multiple brain regions with the greatest numbers of degenerating neurons present in insular cortex and ventral thalamus Schmued MDMA administration has been reported to cause glial activation in rats under some experimental paradigms Aguirre et al. Drug use histories were collected as ranges of lifetime use episodes, so that mean use levels were not provided. MDMA users had been abstinent from MDMA for at least 3 weeks, and had significantly higher levels of polydrug exposure than the control group. Overall, MDMA users had multiple areas of reduced gray matter concentration in brainstem, cerebellum, and mostly left-sided neocortex that did not appear to be fully accounted for by other drug exposure. While there have been no additional reports using the VBM method in MDMA users, there has not been strong evidence from other methodologies to suggest reduced brain gray matter volume or concentration in MDMA-exposed humans in regions overlapping with those detected using VBM. A single study of resting metabolism in a large cohort of MDMA users reviewed below revealed significantly lower metabolic rate in bilateral caudate and putamen and left amygdala Buchert et al. Chang et al. So, it remains unclear whether MRS studies targeting those regions might produce evidence of lower NAA concentration, a potential spectroscopic correlate of neuronal volume loss Gujar et al. A single VBM study found reduced gray matter density in multiple brain regions. These findings have not been replicated. Complementary neuroimaging methods do not show evidence for altered brain gray matter in regions overlapping with those showing reduced gray matter density. Furthermore, while NAA is often cited as a neuronal specific marker Guimaraes et al. Decreased NAA may serve as a reversible marker of neuronal injury e. Levels of NAA have been demonstrated to correlate with overall neuropsychological performance, suggesting that NAA has a global role in neuronal function Jung et al. If MI is considered as a specific glial marker e. However, glial activation in terms of increased glial number, size, or metabolism after MDMA exposure is not likely solely the result of glial response to axon degeneration. MI is an important compound in cell membranes and second messenger cascades and has been implicated in psychiatric disorders such as bipolar disorder Stoll et al. Increased MI and choline due to glial proliferation have been shown in demyelinating disorders Bitsch et al. Findings from the current literature do not suggest a consistent pattern of regional brain metabolite changes in MDMA users. The estimated mean total usage of MDMA was NAA to Cr ratios did not differ from the control group in either tested region. Employing voxel placements overlapping with those used by Chang et al. In a study using proton magnetic resonance spectroscopic imaging MRSI at 1. MDMA users showed no impairment on neuropsychological assays including working memory. Although urine drug testing was not obtained, subjects reported MDMA abstinence periods ranging from 3 weeks to 4 months. More recently, Daumann et al. MDMA users had used a lifetime average of Subjects were excluded if their urine drug screens were positive for drugs other than cannabis on the study day. All subjects participated in immediate and delayed memory tests before scanning. In the memory performance comparisons, MDMA users showed significantly reduced immediate recall when compared to the control group. A single study Chang et al. In contrast, a similarly designed study by Reneman et al. Conversely, while Chang et al. Other investigators did not report reduced cortical Daumann et al. As discussed in Reneman et al. Studies to date have examined resting glucose metabolism and evoked brain activation during attentional, working memory, and episodic memory paradigms. In preliminary Obrocki et al. The comparison group was composed of oncology patients without known brain metastases who underwent FDG PET for diagnostic reasons. In the preliminary report, analysis was restricted to bilateral brain regions including the cingulate, BA 10 and 11, putamen, caudate, amygdala, and hippocampus. In two later reports which appear to be slightly different reports on the same study cohort Buchert et al. The originally reported finding Obrocki et al. Gamma et al. Subjects were also assayed for mood scores to determine whether MDMA users had increased levels of depression. Across both groups i. Regions showing decreased rCBF across both groups included bilateral medial and superior temporal lobe as well as right precuneus. MDMA users had more polydrug exposure than control subjects, were slightly younger and less educated, and showed greater evidence of depression on the mood assessments. Additionally, there were no associations between lifetime drug exposure and rCBF for any drug tested \\\\\\\\\[MDMA, cannabis, amphetamine, cocaine, lysergic acid diethylamide LSD , and magic mushrooms\\\\\\\\\]. There were also no group differences in CPT performance. Daumann et al. Both groups of users had exposure to other drugs including cannabis and amphetamines. MDMA users were asked to abstain from all drug use except cannabis for 7 days before the fMRI scans and were allowed to use cannabis up to the study day. All subjects had negative urine drug screens for drugs of abuse other than cannabis on the fMRI study day. The working memory task employed during fMRI scanning consisted of an n -back task at three levels of difficulty 0-back, 1-back, and 2-back. In this task, subjects were shown a visual presentation of a group of letters and responded when a predefined target letter was presented. For the 0-back condition, subjects responded when the target letter first appeared. For the 1-back condition, subjects responded when the same letter appeared twice in a row. For the 2-back condition, subjects responded when a letter matched one delivered two letters earlier. Of these tasks, the 2-back condition was considered the most challenging to working memory because subjects had to remember the previously presented letters for the longest period of time. In regard to task performance during fMRI scanning, reaction time and error rate were significantly increased in association with increasing levels of task difficulty across all groups of subjects. However, moderate and heavy MDMA users did not differ from each other or controls when compared on reaction time and accuracy for all three n -back tasks. Across all groups, the n -back tasks produced regional BOLD signal changes in prefrontal, parietal, occipital, and cingulate cortices. For the 0-back task, there were no group differences at any level of significance. In a separate report, Daumann et al. Seven subjects had participated in the prior study Daumann et al. With regard to performance during the fMRI task, there were no differences across groups in reaction time or accuracy. The fMRI analysis revealed no group differences during performance of the 0-back task. During the 1-back and 2-back tasks, several brain regions showed group differences in activation but the findings did not strongly overlap or show a clear pattern in the two tasks. Of the comparisons performed, the contrast between brain activation in pure MDMA users vs controls seems most pertinent to the issue of MDMA effects, per se and will be discussed in this review. Pure MDMA users showed areas of greater activation relative to controls only in the right superior parietal lobule in the 1-back task and no areas of greater activation relative to controls in the 2-back task. In contrast, pure MDMA users showed areas of lower activation relative to controls in multiple regions in the 1-back task left posterior cingulate cortex, bilateral inferior temporal gyri, and bilateral angular gyri while in the 2-back task, pure MDMA users had lower activation relative to controls only in left striate cortex. An additional study by Daumann et al. For continuing users, the mean number of MDMA tablets used was There were no differences in task performance measures of reaction time and correct response between the baseline and subsequent 18 month assessments for either group. Interim-abstinent subjects showed no group BOLD activation differences between the baseline and follow-up scans while subjects who continued using MDMA or amphetamines showed increased task-evoked BOLD signal in parietal cortex relative to their initial baseline assessments. Notably, increased activation in the continuing drug users was positively correlated with the lifetime average MDMA dosage, but not with the degree of exposure to other drugs. These investigators Daumann et al. Citing similar findings in individuals infected with the human immunodeficiency virus HIV Chang et al. Using a visually-based working memory task that probed the function of brain regions only partially overlapping with those investigated by Daumann et al. The working memory task consisted of an immediate and delayed visual memory task in which subjects responded to a visually displayed target stimulus. In the delayed memory task DMT , distracter stimuli were interposed between the target and probe stimuli. The length of delay and the number of target stimuli thus influenced the duration of working memory and the degree of working memory load, respectively. MDMA users in this study reported a history of polydrug and alcohol use whereas control subjects reported only prior alcohol use. None of the control subjects had positive urine drug screens. Across both MDMA user and control groups, the task activated left superior frontal gyrus, right middle frontal gyrus, left superior parietal lobule, and right precuneus and insular regions. With the exception of cannabis, the pattern of increased activation in the MDMA users was similar when the data was controlled for other drug use. When controlled for prior cannabis use, the prefrontal cluster was no longer significantly different between MDMA users and controls. In a unique study, where the subjects were well-matched adolescents having minimal histories of polydrug exposure, Jacobsen et al. The participants in the study were a group of adolescents enrolled in a study of tobacco use and were daily tobacco smokers. Last use of MDMA had occurred between 1 and 12 months before the study. Using somewhat different tasks than those employed by Daumann et al. With regard to the attention tasks, MDMA users displayed accuracy comparable to that of control subjects. However, MDMA users showed significant increases in reaction times relative to controls across selective, divided, and sustained attention tasks. The hippocampus was chosen to examine regional brain activation during auditory n -back task performance at three levels of working memory load and two levels of selective attention load binaural and dichotic stimulus presentation. In the control group, the working memory task showed decreased hippocampal activation at the highest working memory load. In contrast, the MDMA group showed decreased hippocampal activation during the less demanding tasks and showed a lesser reduction during the most difficult task. Increased duration of MDMA abstinence was associated with a greater degree of decreased hippocampal BOLD signal across multiple levels of task difficulty and significantly so for the most difficult task. That is to say, with increased duration of MDMA abstinence, hippocampal activation in the MDMA user group more closely approached the pattern seen in controls, with increasingly negative BOLD signal change deactivation with increased task difficulty. Jacobsen et al. The task consisted of a learning period in which subjects were asked to encode face-profession associations in one of two profession categories artist or academic. In the recall phase, subjects were asked to match previously encoded faces with professions relative to a neutral control task. Pilot data had revealed that only the recall phase of the paradigm produced hippocampal activation so the authors reported only on data obtained during the recall phase. The study enrolled 12 MDMA users and 12 controls. MDMA users had greater daily cannabis consumption than did control subjects and 6 of the 12 MDMA users but no control subjects reported amphetamine use. MDMA users did not differ from the control group with regard to recall accuracy during performance of the face-profession association task. This apparent disassociation between performance and regional brain activation led Daumann et al. The finding by Daumann et al. However, the tasks employed by Jacobsen et al. At present, it is not possible to directly compare the findings from current functional neuroimaging studies in MDMA users across different research groups. Given the variability in task design, polydrug exposure differences, the unknown effect of different abstinence periods from MDMA, polydrugs, and cannabis, and differences in data analysis, the lack of replication of findings is not surprising. As discussed in Moeller et al. MDMA-induced alterations in local inhibitory processing have also been considered as potential etiologies for altered BOLD signal in hippocampus Jacobsen et al. Rodent and nonhuman primate models of MDMA toxicity have been criticized from the standpoint of drug administration route, dosage size, and dosing interval. A particular focus of controversy has resided in the utility of species scaling models and whether the route of administration and dosages of MDMA administered to experimental animals have relevance to human MDMA users. While these are important theoretical criticisms of the existing literature, an alternative method for examining the relevance of the experimental animal data is to examine the predictive utility of this information in the context of data from human MDMA users. In this regard, published human neuroimaging studies to date suggest that MDMA users have differences in regional brain structure to some degree consistent with those predicted by findings in animal models. Among existing reports, however, only nuclear imaging studies demonstrating reduced 5-HTT-ligand binding have been replicated across laboratories and with multiple methodologies. There have been no replications, and in some cases conflicting reports, among other imaging methods. Strikingly, there is little overlap among findings from differing experimental approaches that might be expected to provide complementary results. Several areas for improved experimental design derive from the reviewed data. These can be grouped into the general categories of increased sample homogeneity, longer abstinence periods, within-group designs, longitudinal study designs, test—retest measures, 5-HT-specific study designs, and multimodal study designs. Age, sex, hormone use, demographic matching, and genetic characterization will be increasingly important to improve homogeneity. Longitudinal designs will also be critical in examining cumulative effects of MDMA exposure and in accounting for the effects of preexisting brain differences. MDMA-abstinence periods perhaps verified by hair sampling for MDMA; Kish on the order of several months or years seem to separate long-lasting from potentially permanent effects. Given the sizeable number of external factors potentially influencing neuroimaging outcomes, a better understanding of the stability of test—retest measures seems essential. Such multimodal designs might include, for example, correlated ligand binding, volumetric, functional, and spectroscopic studies to isolate affected brain regions. In sum, it seems clear that much more research is needed before definitive conclusions can be reached regarding MDMA effects on human brain structure and function. This review focused on the existing neuroimaging findings in the context of potential confounding variables pertinent to neuroimaging research in MDMA users. While the contribution of each factor to overall variability in MDMA studies cannot be discerned, it seems clear that experimental designs that attempt to account for pertinent confounding effects will be more likely to yield informative, replicable results. April 1. Neuroreport — American Psychiatric Association Diagnostic and statistical manual of mental disorders, 4th edn. Google Scholar. 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You can also search for this author in PubMed Google Scholar. Correspondence to Ronald L. Reprints and Permissions. Cowan, R. Neuroimaging research in human MDMA users: a review. Psychopharmacology , — Download citation. Received : 02 June Accepted : 01 June Published : 18 July Issue Date : January Search SpringerLink Search. Download PDF. Abstract Rationale Determining whether, under what circumstances, and to what extent 3,4-methylenedioxymethamphetamine MDMA exposure produces chronic changes in human brain function is a critical public health issue. Objectives The objectives of this review are to provide a background for interpreting human MDMA neuroimaging research, to examine existing neuroimaging data regarding the rationale for and limitations to human MDMA research, and to provide suggestions for improving the design and interpretation of future neuroimaging approaches. Results Of the existing neuroimaging studies in human MDMA users, few experimental designs have been replicated across different research groups. Introduction Determining whether, under what circumstances, and to what extent 3,4-methylenedioxymethamphetamine MDMA exposure produces chronic changes in human brain function is a critical public health issue. Neuroimaging Neuroimaging explorations in human MDMA users have been rooted in examining the direct or indirect pathology of the 5-HT system or in investigating neural correlates of cognitive processes demonstrated to be impaired in MDMA users. Imaging the 5-HT system Because 5-HT alterations have been the primary focus of much of the basic and clinical literature with regard to MDMA toxicity, it is not surprising that initial neuroimaging efforts have focused on markers of serotonergic integrity. Discussion Rodent and nonhuman primate models of MDMA toxicity have been criticized from the standpoint of drug administration route, dosage size, and dosing interval. Acknowledgements The author would like to thank Dr. Cowan Authors Ronald L. Cowan View author publications. Rights and permissions Reprints and Permissions. About this article Cite this article Cowan, R.
The pharmacology and toxicology of “ecstasy” (MDMA) and related drugs
Купить экстази (МДМА) закладкой Танзания
The pharmacology and toxicology of “ecstasy” (MDMA) and related drugs
Закладки экстази (МДМА) Лимасол