Ecstasy impulsivity

MAO has been inhibited. As a result, transmitter accumulates in the cytoplasm and is exported into the synapse via the membrane-bound transporter. The ensuing (impulse-independent) sympathetic arousal can be disastrous, culminating in a hypertensive crisis and stroke. Although this process is a pharmacological curiosity and certainly contributed to the demise of MAOIs, it is possibly overrated (Tyrer 1979) it has been estimated that the number of deaths associated with the use of the MAOI, tranylcypromine, amounts to only 1 per 14000 patient years. However, this sequence of events echoes exactly the acute actions of methylenedioxymethamphetamine (MDMA, Ecstasy ) and undoubtedly accounts for some of the deaths attributed to this drug. 

Boot B, McGregor IS and HaU WA (2000). MDMA ("Ecstasy") neurotoxicity assessing and communicating the risks. Lancet 355,1818-1821. Butler GKL and Montgomerg AMJ (2004). Impulsivity risk taking and recreational ecstasy (MDMA) use. Drug and Alcohol Dependency 76, 55-62. 

Ecstasy may reduce subjective sedation associated with alcohol, without reversing the effects of aicohoi on impulsivity or psychomotor skiiis. Aicohoi may enhance the transient immune dysfunction associated with ecstasy. Aicohoi may slightly increase the plasma levels of ecstasy, while alcohol levels may be sightly reduced by ecstasy. 

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