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Abstract
Zolpidem, a non-benzodiazepine hypnotic, acts selectively via the α1-subunit of GABAA receptors at therapeutic doses. It is therefore thought to lack both benzodiazepine properties such as anxiolysis, anticonvulsion, muscle relaxation, and side effects such as dependency. We report a case of severe dependency of zolpidem taken because of percieved myorelaxation in a patient with multiple sclerosis and paraspasticity. The observations in the patient described here suggest that zolpidem looses α1-receptor selectivity at higher doses, thereby leading to the same risks and benefits such as benzodiazepines. This should be taken into account by doctors when prescribing higher doses. Zolpidem may improve symptoms of spasticity in high doses via affection of GABA α2-receptor and α3-receptor subunits.