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Psychosomatics 47:86-87, February 2006
doi: 10.1176/appi.psy.47.1.86
© 2006 Academy of Psychosomatic Medicine
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Letter

Neurological and Psychopathological Sequelae Associated With a Lifetime Intake of 40,000 Ecstasy Tablets

Christos Kouimtsidis, Fabrizio Schifano, University of London, UK, Tim Sharp, Watford, UK, Lisa Ford, Justin Robinson, and Colm Magee, Slippers Hill, UK

TO THE EDITOR: The medical and psychopathological consequences of both acute and chronic "ecstasy" (MDMA, MDA, and derivatives) consumption have been extensively described, but little is known with respect to the relationship between both severity and persistence of these disturbances and lifetime number of ecstasy tablets ingested. At-risk MDMA intake seems to be related to long-term functional dysregulation in 5-HT2 pathways, resulting in altered regulation of mood, impulse control, and memory.1,2 Ecstasy consumption has spread since the late ‘80s, and the reduction in price observed over the last few years has possibly increased access to the drug. Clinicians are now meeting with a generation of patients who have been exposed to the drug for more than a decade. In this report, we describe both the transient and persisting sequelae associated with an unusual amount of ecstasy consumption.

Case Report
Mr. A, 37 years old, used ecstasy between the ages of 21 and 30. For the first 2 years, he took 5 tablets every weekend, escalating to an average daily use of 3.5 tablets for the next 3 years, and further escalation to an average of 25 tablets daily over the next 4 years. An estimate of lifetime consumption yielded a total intake of more than 40,000 tablets. At the time of his presentation, Mr. A reported current cannabis consumption, together with a previous history of polydrug misuse (i.e., solvents, benzodiazepines, amphetamines, LSD, cocaine, heroin). After three episodes of "collapsing" at parties, Mr. A finally stopped his ecstasy use. For a few months, he felt as if he was still under the influence of ecstasy and suffered several episodes of "tunnel vision." He eventually developed severe panic attacks, recurrent anxiety, depression, muscle rigidity (particularly at the neck and jaw levels), functional hallucinations, and paranoid ideation. His family and before-drug-use psychiatric history were negative. The Mini-Mental State Exam revealed disorientation to time, poor concentration, and short-term memory difficulties. Decrease in level of cannabis intake led both to disappearance of his paranoid ideas and hallucinations and reduction of his panic attacks, but remaining symptomatology persisted. Administration of the Wechsler Memory Scale (3rd Edition)3 suggested the existence of global memory-function impairment, with no subtest score being above the 10th percentile. Assessment of daily functioning skills identified major behavioral consequences of his memory loss (i.e., repeating activities several times). Although Mr. A was able to fully understand the instructions given, his concentration and attention were so impaired that he was unable to follow the sequence of the tasks required. A structural MRI brain scan revealed no focal cerebral lesions; specifically, both temporal lobes showed normal symmetrical hippocampal areas. The structural areas of the "Dealy-Brion" system were normal. There was no evidence to suggest atrophy. Mr. A was then prescribed olanzapine 10 mg and admitted to a brain-injury unit, where there was some improvement of his memory skills as a result of the use of compensatory strategies.

Comment
To our knowledge, this is the largest amount of ecstasy lifetime consumption ever described, the heaviest lifetime intake previously reported being around 2,000 tablets.2 Although much information is self-reported and might have been affected by Mr. A’s memory impairment, the history given was confirmed by notes from another service he attended just after having stopped ecstasy use.

All ecstasy misusers would develop a (mild-degree, in most cases) serotonin syndrome after acute drug intake, which is characterized by enhanced physical activity, hyperthermia and sweating, increased muscle rigidity, rhabdomyolysis, hyperreflexia, trismus, jaw-clenching, myoclonus, tremor, and nystagmus.4 An additional, non-serotonergic mechanism of MDMA activity at the neuromuscular junction-level has recently been suggested.5 Although these observations relate to acute MDMA intoxication effects, they might partly explain the persistent muscle rigidity of which Mr. A was complaining. The "tunnel vision" effect observed by Mr. A in the first few months after withdrawing from MDMA had never been reported before in this context. The neurocognitive profile here described was very similar to that shown by current heavy ecstasy users; it has been suggested that the extent of memory decline positively correlates with intensity or frequency of ecstasy consumption.6 It is also confirmed here that selective impairments of neuropsychological performance associated with regular ecstasy use are not reversed by prolonged abstinence. Contrary to results of other neuroimaging observations,7 Mr. A’s brain scan did not show any gross cerebral abnormalities, especially at the hippocampal level.

We feel that this case report adds to the existing limited knowledge of persistent sequelae associated with heavy and regular ecstasy intake.

Mr. A gave consent to his history being reported to a medical journal.

REFERENCES

  1. Green AR, Cross AJ, Goodwin GM: Review of the pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy"). Psychopharmacol (Berl) 1995; 119:247–260[CrossRef][Medline]
  2. Schifano F, Di Furia L, Forza G, et al: MDMA ("ecstasy") consumption in the context of poly-drug abuse: a report on 150 patients. Drug Alcohol Depend 1998; 52:85–90[CrossRef][Medline]
  3. Wechsler D (ed): Wechsler Memory Scale; 3rd Edition. London, UK, The Psychological Corporation, Harcourt Brace Jovanovich and Company, 1997
  4. Schifano F: A bitter pill? overview of ecstasy (MDMA; MDA)-related fatalities. Psychopharmacol (Berl) 2004; 173:242–248[CrossRef][Medline]
  5. Sparks GM, Dasari S, Cooper RL: Actions of MDMA at glutamatergic neuromuscular junctions. Neurosci Res 2004; 48:431–438[Medline]
  6. Zakzanis KK, Young DA: Memory impairment in abstinent MDMA ("ecstasy") users: a longitudinal investigation. Neurology 2001; 56:966–999[Abstract/Free Full Text]
  7. Cowan RL, Lyoo IK, Sung SM, et al: Reduced cortical gray-matter density in human MDMA (ecstasy) users: a voxel-based morphometry study. Drug Alcohol Depend 2003; 72:225–235[Medline]




This Article
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* Alert me to new issues of the journal
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* Articles by Kouimtsidis, C.
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* Articles by Kouimtsidis, C.
* Articles by Magee, C.


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