doi: 10.1111/j.1472-8206.2005.00355.x CASE REPORT Topiramate prevents ecstasy consumption: a case report Shahin Akhondzadeh*, Ali Daliri Hampa Psychiatric Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran INTRODUCTION 3,4-Methylenedioxymethamphetamine (MDMA; ecstasy) is a phenethyl-amine with structural similarities to both amphetamine and mescaline, which is commonly used by young people particularly at dance parties called ‘raves’ [1]. It produces feelings of well-being, euphoria, increased extroversion, moderate derealization, slight perceptual changes as well as moderate activation of psychomotor drive, cognitive disturbances, elevated anxiety, decreased appetite and trismus [2]. MDMA is generally accepted to be a potent indirect monoaminer- gic agonist producing both carrier-mediated release and reuptake inhibition of 5-HT and dopamine. There is also evidence of a less pronounced direct agonist effect on 5-HT2, 5-HT1 and D2 receptors, which might be of importance for understanding the difference psychologi- cal profile of MDMA, amphetamine, cocaine and hallu- cinogens [2]. In animals, MDMA has also been shown to increase striatal dopamine levels [2]. Dopamine has been implicated in the mediation of euphoria induces by classical stimulants such as d-amphetamine. Therefore, increased dopaminergic activity may also contribute to MDMA-induced euphoria [3]. It has been reported that haloperidol pretreatment attenuates MDMA-induced positive and mania-like mood [3]. In addition, anticon- vulsants have repeatedly been proposed as a treatment of alcohol and benzodiazepine withdrawal, and some data exist on their utility in reducing cocaine and opiate consumption [4–7]. Topiramate is an antiepileptic drug that has a broad spectrum of antiseizure effects, which appear to be the result of several neurostabilizing pharmacological mechanisms [8]. Topiramate facilitates GABA function through a non-benzodiazepine site on the GABA-A receptor, thus decreasing extracellular release of dopamine in the midbrain, and antagonizes glutamate activity [8]. GABAergic and glutametergic neurons play a critical role in drug-reinforced behavior. Therefore, it was postulated that topiramate would be an effective treatment for reducing MDMA consumption Keywords 5-HT, dopamine, ecstasy, glutamate, topiramate Received 30 August 2004; revised 3 January 2005; accepted 13 April 2005 *Correspondence and reprints: s.akhond@neda.net ABSTRACT The last decade has witnessed a development in the phenomenon ‘ecstasy’. Several substances, with more or less the same effects, are grouped together by the term ecstasy, the best-known one being 3,4-methylenedioxymethamphetamine (MDMA). The psychopathological consequences of MDMA in humans are relatively poorly understood. In addition, the treatment approach is complicated by the lack of documented studies. Topiramate is an antiepileptic drug that has a broad spectrum of antiseizure effects, which appear to be the result of several neurostabilizing pharmacological mechanisms including facilitation of GABAergic neurotransmission and inhibition of glutametergic activity at AMPA/kainate receptors. As both GABAergic and glutametergic neurons appear to be important modulators of the brain reward system, it was postulated that topiramate would be an effective treatment for reducing MDMA consumption through the attenuation of MDMA- induced euphoria. The case of an ecstasy consumer, who started to discontinue ecstasy under topiramate treatment is presented here. Antiepileptics/mood stabilizers with glutamate inhibition activity like topiramate may present a promising new approach for challenging the consequence of drug abuse. Ó 2005 Blackwell Publishing Fundamental & Clinical Pharmacology 19 (2005) 601–602 601