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Author Topic: Zolpidem-Induced Sleepwalking, Sleep Related Eating Disorder and Sleep-Driving  (Read 5379 times)

Offline Chip (OP)

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Just to make you aware how dangerous Ambien can be. Some deeply technical data about GABAA receptor subunits and it's affects as when compared to traditional benzos.

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

(ee also Fludeoxyglucose (18F)Wiki and Positron emission tomographyWiki)

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.

Sleepwalking or somnambulism, is a parasomnia consisting of a series of complex behaviors usually initiated during arousals from slow wave sleep and commonly culminate in walking with an altered state of consciousness and impaired judgment.

Sleep related eating disorder (SRED) consists of recurrent episodes of involuntary eating during arousals from sleep. Parasomnias such as sleepwalking, SRED, and sleep-driving can coexist and are rare side effects of zolpidem.

In a 2005 National Institutes of Health consensus statement for the treatment of chronic insomnia in adults zolpidem was considered a hypnotic with limited risk.

Two post-marketing studies of zolpidem reported sleepwalking incidences of 7 of 1972 patients (0.3%) and 1 of 96 patients (1%).

We present a patient with zolpidem-induced sleepwalking, SRED, and sleep-driving.

Discussion (excerpt)

Zolpidem is an imidazopyridineWiki drug indicated for short-term insomnia at a dosage usually ranging from 5 to 10 mg per day.

Though considered a non-benzodiazepine since its imidazopyridine structure differs from benzodiazepine fusion of benzene and diazepine, 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 activity of the ligand-operated chloride channel.

GABA is the main inhibitory neurotransmitters in the mammalian central nervous system (CNS) but can become excitatory also.

GABAA receptors exist as pentameric protein complexes, assembled from a combination of at least 19 subunits from 7 distinct gene families (α, β, γ, δ, ϵ, θ, and π).

Synaptic GABAA receptors are responsible for modulating benzodiazepine sensitivity and typically contain α1, 2, 3, or 5, β2 or 3, and the γ2 subunits.

GABAA receptor sensitivity to benzodiazepines is mediated through α subunits.

Benzodiazepines bind to synaptic GABAA receptors containing α1, α2, α3, or α5 subunits with comparable affinity.

The GABAA receptor expressing the α1 subunit corresponds to the benzodiazepine ω1 receptor.

GABAA receptors containing the α1, α2, α3, or α5 subunits correspond to ω2 benzodiazepine receptors.

The ω3 benzodiazepine receptor is not related to the GABAA receptor. Extrasynaptic GABAA receptors are primarily composed of α4-6 subunits in combination with δ subunits, and are insensitive to benzodiazepines.

The current benzodiazepine receptor nomenclature (ω1, ω2, and ω3) replaced the previous anatomical localization classification (central benzodiazepine receptor type 1, central BZ-1; central benzodiazepine receptor type 2, central BZ-2; and peripheral benzodiazepine receptor type 3, BZ3) because of the existence of “central” benzodiazepine receptors with peripheral localization, and “peripheral” benzodiazepine receptors with central localization.

Zolpidem was developed as a drug with a structure different from benzodiazepines, allowing affinity for only a given subset of central benzodiazepine receptors resulting in hypnotic properties without additional anticonvulsant and myorelaxant properties of benzodiazepines.

In contrast to benzodiazepines like clonazepam, diazepam and flunitrazepam, which lack selectivity for the ω1, ω2, or ω3 benzodiazepine receptor subtypes; zolpidem has a high affinity for ω1.

A possible explanation for zolpidem-induced nocturnal events is that after an arousal from sleep into wakefulness, nocturnal activity (i.e., walking, eating, or driving) occurred and was subsequently not recalled after returning to sleep because of the sedation-mediated amnestic properties of zolpidem.

Another possibility is that an arousal occurred out of slow wave sleep with the parasomnia occurring in electroencephalographically verifiable sleep.

We felt our patient experienced the later, given her incoherent interactions with her husband during her nocturnal events. Patients who do not recall waking events on zolpidem are typically cognitively functional, and retain the ability to speak in coherent short phrases.

see the source link if you want to read more ...
« Last Edit: September 28, 2019, 06:23:02 AM by Chip »
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