Transient cocaine-induced chest pain: a case series.

OBJECTIVES: Acute chest pain and myocardial infarction are frequent complications of cocaine use. Indeed, these represent 40% of emergency department visits associated with cocaine use and 2% to 7% of all patients attending the emergency department for chest pain. Nevertheless, the prevalence of past cocaine-associated chest pain has never been evaluated in an outpatient facility for addiction. Our objective was to assess lifetime episodes of cocaine-associated chest pain in current cocaine users in an outpatient facility. METHODS: Fifty consecutive, nonselected current cocaine users were retrospectively evaluated with a standardized interview and a medical assessment. The patients and the pain characteristics are described, and clinical and biological factors associated with experiencing cocaine-associated chest pain are studied with univariate and logistic regressions analyses. RESULTS: Twenty-six subjects (52%) reported a history of chest pain associated with cocaine use. This pain was frequently described as oppressive (28%) and located in the retrosternal area (61.5%). The mean (±SD) time between cocaine use and the occurrence of the pain was 8 (±8) minutes and the mean duration was 22 (±236) minutes. Subjects who reported cocaine-associated chest pain reported an average of 12 (±7) distinct episodes. Patients describing chest pain could be predicted with one independent factor in our sample: age of onset of cocaine use (P = 0.042). CONCLUSIONS: Transient cocaine-associated chest pains are frequent in current cocaine users attending specialized addiction facilities. Cardiological explorations and monitoring and risk-reduction interventions need to be provided to this specific population.

Transient improvement in sensorimotor conversion during post-anoxic encephalopathy with bilateral medial temporal ischemia.

We report the case of a patient with sensorimotor conversion that improved transiently during post-anoxic medial temporal ischemia inducing anterograde and retrograde amnesia. Symptoms reappeared in parallel with mnesic recovery. This case raises a hypothesis concerning the role of hippocampi and amygdalae, which are involved in emotionally-associated memory. The amnesia may have modified the patient's "self," giving her a "distant" point of view. Another hypothesis is that cerebral anoxic stress may have "reset" the cerebral network that controls behavior. These findings give clues about the mechanisms of somatoform disorder and highlight the possibility of specific therapeutic strategies to induce cognitive reappraisal of emotionally-associated experiences.