Zolpidem withdrawal delirium, seizure, and acute psychosis: Case reports and literature review

Abstract

Zolpidem, a non-benzodiazepine hypnotic drug, shows a high affinity for the BZ1 (ω1) subtypes of the modulatory sites within the GABAA receptor complex, but classical benzodiazepines (diazepam, lorazepam) have a non-specific affinity profile at ω1 and ω2 subtypes of the GABAA receptor. Therefore, zolpidem is thought to be safer than benzodiazepines. We present five cases with withdrawal delirium, seizure, acute psychosis and orofacial dyskinesia that developed following cessation of zolpidem. Adverse effects such as withdrawal seizure and withdrawal delirium have been rarely reported in relation to zolpidem. Chemically unrelated to benzodiazepines, zolpidem is thought to have fewer adverse effects, but shares a pharmacokinetic profile with the benzodiazepines. It is advised that the normal criteria for the prescription of benzodiazepines also be used when prescribing non-benzodiazepine sedatives and hypnotics, as they act upon the same receptor, namely, the benzodiazepine-GABA-chloride complex. However, at higher than recommended doses for extended periods of time, the addictive potential of zolpidem may be similar to that of the benzodiazepines. It is possible that zolpidem abandons its selectivity for the BZ1 receptors and demonstrates all the actions of classic benzodiazepines.

• Zolpidem
• benzodiazepines
• BZ1 (ω1) receptor, GABAA receptor
• withdrawal delirium
• seizure, orofacial dyskinesia