Parasomnia is described on wikipedia as:Parasomnias are a category of sleep disorders that involve abnormal and unnatural movements, behaviors, emotions, perceptions, and dreams that occur while falling asleep, sleeping, between sleep stages, or arousal from sleep. Most parasomnias are dissociated sleep states which are partial arousals during the transitions between wakefulness and NREM sleep, or wakefulness and REM sleep.
Objective: Epidemiologic studies from general population and clinical case series suggest association of parasomnias with mental illnesses and psychotropic medications. This cross-sectional study aimed at determining the prevalence rate of sleepwalking, sleep-related eating disorder (SRED), rapid eye movement sleep behavior-like disorder (RSBD-like disorder), and sleep-related injury (SRI) and their associated factors in an adult psychiatric outpatient clinic.
Method: Subjects aged 18 to 65 years who were attending an outpatient clinic in Hong Kong from May 2006 through June 2006 were included in this cross-sectional study. A 3-phase design was employed, including a structured questionnaire on parasomnias, followed by clinical interviews of both questionnaire-positive and -negative groups, and polysomnography for subjects having active parasomnias in recent 1 year. In addition, the principal psychiatric diagnoses, medical illnesses, and detailed drug history over recent 1 year were retrieved from the computerized records.
Results: Twelve hundred thirty-five subjects completed the phase 1 interview. The estimated prevalence of the lifetime diagnoses of sleepwalking, SRED, SRI, sleep violence, and RSBD-like disorder were 8.5%, 4.0%, 21.0%, 3.6%, and 5.8%, respectively, while the 1-year prevalence of these conditions were 2.9%, 2.4%, 8.8%, 2.5%, and 3.8%, respectively. These conditions were associated with depression and a constellation of sleep disturbances. Specific combinations of psychotropics were found to pose risk in particular parasomnias: sedative antidepressants and nonbenzodiazapine hypnotics in sleepwalking, regular zolpidem and antidepressants in SRED, and selective serotonin reuptake inhibitors in RSBD-like disorder.
Conclusions: Sleepwalking, SRED, RSBD-like disorder, and SRI were common and underrecognized among the psychiatric population in this study. Their occurrences were likely contributed by interacting effect of mental illnesses, sleep disturbances, and specific psychotropic medications. Further prospective study is warranted for clarification of the etiology and clinical management of these potentially dangerous and "hidden" parasomnias.
We have developed and validated the Munich Parasomnia Screening (MUPS) questionnaire, a self-rating instrument with 21 items assessing the lifetime prevalence and current frequency of parasomnias and nocturnal behaviors in adult persons. The MUPS was developed with psychiatric patients (total n = 74). For the validation study the MUPS was given to three large groups, i.e. psychiatric patients (n = 65), sleep-disordered patients (n = 50), and healthy controls (n = 65). In a randomly chosen subset of 20 % of these subjects the MUPS was compared to the information obtained in a detailed clinical interview with a sleep medicine expert. Validity was assessed for lifetime prevalence of any frequency for each of the 21 nocturnal behaviors. For the individual items of the MUPS sensitivity was equal to or above 90 % for all but two of 21 items and specificity was above 80 % for all items and above 90 % for 19 of 21 items. More importantly, concerning the use of the MUPS in clinical practice, positive and negative predictive values of the single items were high for the majority of items. The MUPS appears to be an easy to use and valid instrument in the recognition of nocturnal behaviors and parasomnias.
Daniel (Purcell) has floated through his life looking for something with meaning. While visiting his friend in a local drug-rehab wing of the hospital, he stumbles across two very unusual things. A beautiful young woman (Wilson) who suffers form 'parasomnia' that has kept her in a sleeping state for most of her life and a hooded serial killer named Volpe who supposedly possesses hypnotic abilities so strong he can make a person kill for him with just a stare or suggestion. When Dan becomes obsessed with his 'sleeping beauty' he kidnaps her from the hospital to prevent them from testing on her. What he discovers though is far more frightening then his new wanted status. This girl is somehow linked with Volpe through her dreams and this psycho has some very dark plans for her. There was one concept involving his cute puppy dog that shared his apartment that was quite creepy. He had just bought what he thought was a special therapeutic dog bed (it was advertised online as a "magical luxury dog bed for therapy") but it was way more than he bargained for. Whenever the pup was asleep on this bed, it would morph into a very scary creature - scary but harmless. Just the transformation of this dog was enough to creep me out, and I'm not sure why the director didn't do more with it. I think it was meant to be a dream influenced reality, but sometimes what's real and fantasy are hard to distinguish.
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.9
Along with sleepwalking, SRED, and sleep-driving parasomnias, zolpidem has been anecdotally reported to produce a range of unexpected beneficial effects. These include improvement in the following conditions: post-stroke Broca's aphasia; blepharospasm; quadriparesis of central pontine myelinolysis; catatonia of schizoaffective disorder; dementia with apraxia; post-anoxic minimally conscious states; bradykinesia, akinesia, and dystonia in Parkinson disease; post-levodopa dyskinesias in Parkinson disease; vertical saccadic eye movements and parkinsonism in progressive supranuclear palsy; restless legs syndrome; post-anoxic spasticity; and spinocerebellar ataxia (Table S1 summarizes the available reports of improvement in varied neurological conditions with zolpidem use). Effects were usually noted within 30 min of ingestion of the non-extended release formulation and lasted for 2 to 4 h, corresponding with a time to peak plasma contraction of approximately 1.2 h and a half-life of approximately 2.5 h.
Zolpidem effects might be mediated through its anti-anxiety effects, its benzodiazepine receptor agonist properties, its GABAergic activity, or some combination of all three. For example, symptoms of Parkinson disease worsen with anxiety. The improvement noted in Parkinson disease with zolpidem use may be secondary to its anxiolytic effect through a GABAergic effect on the limbic system or elsewhere. The improvement seen in blepharospasm, catatonia, and restless legs syndrome may be caused by the benzodiazepine ω1 receptor agonist activity of zolpidem. However, opposing this theory of purely benzodiazepine agonist mediated effects, is that parasomnias like sleepwalking are often treated with benzodiazepines like clonazepam; yet zolpidem seems to induce parasomnias in a susceptible subpopulation.
One possible explanation may be that PET is too insensitive a tool to detect subtle localized or generalized glucose metabolic rate differences on and off zolpidem in the normal brain. If such differences could be identified, then patients who are susceptible to developing parasomnias could be identified prior to use. More importantly, this may also provide insight into other extraordinary anecdotal effects of zolpidem.
A limitation of our PET analysis was that the scan was not performed in EEG verified slow wave sleep (SWS), when parasomnias are thought to emerge. Future 18F-FDG-PET studies in patients with zolpidem induced parasomnias could be attempted during EEG verified SWS on and off zolpidem to identify differences in glucose metabolic rates not seen in our analysis. However, this may prove to be difficult given the variable presence of SWS and the need to wait 1 h after FDG injection prior to the PET scan. By the time the patient receives the FDG injection and the scan is performed, the patient may no longer be in SWS. And though parasomnias tend to emerge in SWS, they can potentially arise from any NREM stage.
Future studies may also shed light on whether different susceptibilities to zolpidem induced parasomnias and its other effects may depend upon the formulation used. For example, Chiang et al. reported 2 patients who experienced zolpidem induced sleepwalking and SRED on only the extended release formulation and not the non-extended release formulation.26 Validation of these anecdotal findings and investigations into the new sublingual formulation of zolpidem may provide insight into how formulation dependent pharmacokinetics may influence an individual's susceptibility to zolpidem-induced parasomnias.27
Laura Baxter is a young woman, literally a "sleeping beauty," who suffers from a medical condition called "parasomnia." A childhood accident victim, she is actually sleeping her life away, awakening briefly on rare occasions. Art student Danny Sloan falls in love with her, unaware that her hospital neighbor, a terrifying mass murderer and mesmerist named Byron Volpe has other, more sinister plans.
During the visit, Danny sees Laura Baxter (Cherilyn Wilson) sleeping in the room next to Volpe. She suffers from a form of parasomnia in which she sleeps most of the time, and wakes occasionally for short periods of time. 041b061a72