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Review
. 2009 Oct 15;5(5):471-6.

Zolpidem-induced sleepwalking, sleep related eating disorder, and sleep-driving: fluorine-18-flourodeoxyglucose positron emission tomography analysis, and a literature review of other unexpected clinical effects of zolpidem

Romy Hoque  1 , Andrew L Chesson Jr
Affiliations
Review

Zolpidem-induced sleepwalking, sleep related eating disorder, and sleep-driving: fluorine-18-flourodeoxyglucose positron emission tomography analysis, and a literature review of other unexpected clinical effects of zolpidem

Romy Hoque et al. J Clin Sleep Med. .

Abstract

Zolpidem is a hypnotic which acts at the GABAA receptor and is indicated for short-term insomnia. Sleep related disorders including somnambulism, sleep related eating and sleep-driving have been reported with zolpidem. A 51-year-old insomniac who used zolpidem 10 mg nightly starting at 44 years of age is described. A few weeks after starting zolpidem she began walking, eating, and had one episode of driving while asleep. Episodes of sleep related eating, sleepwalking, and sleeptalking occurred 3 nights per week, 1 to 2 h after sleep onset. After her evaluation, the patient's zolpidem was gradually discontinued, and all sleep related activities immediately ceased. An 18F-FDG-PET was obtained 2 months after discontinuation of zolpidem. The following day, FDG was administered 1 h after oral administration of 10 mg zolpidem, and then a second PET was performed. We report the results and a review of the literature regarding other unintended effects seen with zolpidem use.

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Figures

Figure 1
Figure 1
18-fluorine-flourodeoxyglucose-positron emission tomography (18F-FDG-PET) of a patient with zolpidem induced sleepwalking, sleep related eating disorder, and sleep-driving. A: 18F-FDG-PET off zolpidem. B: 18F-FDG-PET on zolpidem. FDG was administered to patient 1 h after ingestion of 10 mg zolpidem. Statistical parametric mapping comparison of the 2 sequences shows no significant differences.
Figure 2
Figure 2
Regional distribution of zolpidem binding, and the potential clinical consequences. Zolpidem is a benzodiazepine receptor agonist with high binding affinity for the GABAA (gamma-amino butyric acid type A) receptor expressing the α1 subunit. Benzodiazepines and benzodiazepine receptor agonists like zolpidem bind to the GABAA receptor at sites that are distinct from the GABA binding site, thereby allosterically affecting the channel. GABAA receptor sensitivity to benzodiazepines is mediated through α subunits. Zolpidem's action via synaptic GABAA receptors with α1 subunits may produce different clinical responses depending upon regional distribution of receptor subtypes. Benzodiazepines bind to all the synaptic GABAA receptors, which are expressed throughout the nervous system. Even though zolpidem is a preferred α1 agonist, α1 subunits are expressed widely throughout the CNS. Given zolpidem's many binding sites, the improvement noted across a range of neurological disorders are difficult to localize to binding at a single anatomic location. GABAA α1 subunits/ω1 benzodiazepine receptors are widely distributed throughout the central nervous system, in many more areas than indicated in this simple schematic figure.
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