Memory, benzodiazepines, and anxiety: integration of theoretical and clinical perspectives

Abstract

The benzodiazepines have been reported to cause anterograde amnestic effects. These impairments are likely mediated through the GABAA receptor complex, which contains the benzodiazepine receptor binding site. This GABAA receptor site is also believed to be the locus of the anxiolytic effects of the drugs as well, and recent research findings suggest that the anxiolytic and amnestic properties of the benzodiazepines may be functionally linked. Normal human memory function is extremely complex and requires the smooth integration of multiple aspects of cognition. On the basis of neuropsychological testing, the processes of memory have been divided into a variety of functions or stores that are interrelated, yet distinct. The amnestic effects of the benzodiazepines have been extensively studied within the context of this conceptual framework. Studies to date have shown that the memory deficits produced by the drugs are relatively selective and are primarily caused by impairments in the acquisition of newly learned information into long-term episodic storage. Benzodiazepines may impair other aspects of memory as well, but findings across studies have been inconsistent. The drugs clearly do not impair the recall of previously learned information, unlike anticholinergic drugs with amnestic effects, such as scopolamine. The amnestic effects of the benzodiazepines are dose-dependent, and can be predicted by pharmacokinetic/pharmacodynamic variables. In addition, multiple clinical factors may influence the likelihood of memory impairments. The amnestic effects of alprazolam are consistent with the drug effects of the benzodiazepines as a group.