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. Mar-Apr 1994;20(2):147-57.

[Dependence on Benzodiazepines. Clinical and Biological Aspects]

[Article in French]
  • PMID: 7914165

[Dependence on Benzodiazepines. Clinical and Biological Aspects]

[Article in French]
A Pelissolo et al. Encephale. .


The high rate of benzodiazepines (BZD) consumption has been repeatedly confirmed by epidemiological surveys in most major western world countries. In a recent french survey 7% of chronic users of BZD (use in 5/7 days for the last 12 months) were found the general population (17% in the population aged above 65). It has been suggested that the high BZD consumption rate could be related to dependence. The existence of BZD dependence was described in the early sixties with very high dose of chlordiazepoxide but it has become a real concern for the medical community since the late seventies with increasing number of reports of withdrawal symptoms. The extend of the actual rate of withdrawal symptoms at BZD tapering is still very controversial and according to the different studies it varies from 39 to 90%. The between studies difference in parameters such as: the patient populations (psychopathology, treatment duration), the type of tapering employed (duration, nature of the medical and psychological support) and the used operational criteria for withdrawal definition most likely explain this wide variation in the rate of occurrence of withdrawal manifestations. According to the American Psychiatric Association Task Force on Benzodiazepine Dependence, Toxicity and Abuse three type of pathological events can happen after treatment discontinuation: rebound, withdrawal syndrome and recurrence. The rebound consists in the early and transitory reappearance of the anxiety symptoms pre-existing to the treatment but in an exacerbated from; the withdrawal syndrome associates the resurgence of the pre-existing anxiety symptoms and new symptoms as sensory disturbances (metallic taste, hyperosmia, cutaneous exacerbated sensitivity, photophobia...) nausea, headache, motor disturbance in some rare cases depersonalization, paranoid reaction, confusion, convulsion. Rebound or withdrawal syndrome appearance delay varies from hours to few days according mostly to compounds elimination half-life. The relapse develops later with a progressive reapparance of pre-treatment symptoms. In practice recurrence and rebound are often difficult to isolate: recurrence can follow rebound. Different operational criteria of definition for this different entities have been proposed but there is a need for a consensual position. The treatment length, a high daily dose, an alcohol abuse history, a dependent personality and the severity of the psychopathology of the patients have been found to be predictive for the occurrence of withdrawal symptoms. Behavioural therapies (individual or in group) have been proposed with some success for the treatment of benzodiazepine dependence; drug treatment with carbamazepine or imipramine have demonstrated some efficacy. Other drug as buspirone clonidine having anxiolytic properties have not demonstrated efficacy.(ABSTRACT TRUNCATED AT 400 WORDS)

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