University of Zagreb, School of Medicine
Somnambulism, also known as sleepwalking, is a sleep disorder that affects approximately 2.5% of adult population and has slightly higher prevalence in children. The main characteristic of this disorder is the coexistence of both sleep elements and elements of wakefulness. Sleepwalkers have a disrupted sleep pattern, which can cause specific changes in electroencephalogram (EEG) recordings such as cyclic alternating pattern (CAP) change and increased slow wave activity. A few hypotheses claim that a change in serotoninergic and dopaminergic transmission is responsible for sleepwalking, but scientific proof is yet to be found. Various clinical cases show correlation between different drugs (zolpidem, quetiapine) or chemical substances (alcohol, caffeine) and sleepwalking. A positive family history is another known risk factor for somnambulism. Since sleepwalking is most often correlated with various sleep-breathing disorders, the main type of treatment is surgical removal of the tissue causing this problem. Other treatment protocols may include psychiatric help, drugs or changes in sleep routine. Diagnosis is based on anamnestic data and EEG recordings.
KEYWORDS: alcohol, clinical approach, quetiapine, sleepwalking, slow wave activity (SWA), zolpidem
The aim of this article is to briefly present somnambulism, or sleepwalking, as a sleep disorder grouped with other parasomnias that are characterized by a variety of actions not normally seen in sleep. 1 During the episode of sleepwalking different actions such as eating, driving, talking or various violent acts are done unconsciously. 1,2 Crimes committed during the sleepwalking episode have been a law problem for decades because the episode cannot be proven retrospectively and up until now no absolute solution was found. With the advancement of sleep medicine, certain EEG changes are found only in sleepwalkers and are used as a diagnostic parameter and as proof that one has mentioned affliction. Episodes of sleepwalking occur most often in prepubertal children, but can also be seen in adults with decreasing frequency of cases in older age groups.1 Up to 25% of children who have experienced sleepwalking during their childhood are troubled with same problem in adulthood.3 These cases represent almost 90% of sleepwalking cases in adults.4 Somnambulism attacks can be precipitated by taking drugs, alcohol abuse, other sleep disorders or sleep disturbances, but in many cases the cause is unknown. When caused by known factors, somnambulism is not treated directly, but through treatment of the precipitating cause.3 Other situations require supportive treatment or, rarely, medications.5
Mechanisms of somnambulism
The sleep cycle lasts approximately 90 min,1 and is divided into two major phases NREM (non-rapid eye movement) and REM (rapid eye movement). The NREM sleep phase is subdivided into 4 stages from 1 to 4 with increasing depth of sleep. Somnambulism occurs during the first sleep cycle in stages 3 and 4 of NREM sleep, 6,7 and rarely in stage 2.7 Sleepwalkers have a different, more disrupted, sleep pattern when compared to healthy individuals. Disruption is seen as microarousals, wake after sleep onset (WASO), arousals, awakenings, or an abnormal amount of cyclic alternating pattern (CAP A2 and A3).2 In NREM sleep, EEG recordings show high amplitude and low frequency Δ waves whose changes can be seen in patients suffering from sleepwalking as well as CAP changes. The primary change seen in a sleepwalker’s brain is consistent CAP change which is always present in EEG recordings, whereas a second measured parameter known as slow wave activity (SWA) is not as consistent.2 The first measured changes were described as hypersynchronous delta activity (HSD), but subsequent research showed that this parameter cannot be used for precise classification of somnambulism.7 SWA is an EEG-measured parameter used for describing sleep dynamics and it describes sleep depth and intensity. Researchers have shown that prior to the onset of a sleepwalking episode a patient’s EEG will show increased SWA that is different for every individual.7 The reason for this increased activity is still unknown, but may be related to other changes present in the body during the episode. During both major sleep phases sensations and motor functions are inhibited in order to prevent unfortunate events. Since a sleepwalking episode is characterized by different types of movement, varying from simple hand movements up to running or driving, it is reasonable to assume that motor function is disinhibited and fully active as in wakefulness. 1On the other hand, during the episode the person is completely unconscious and once woken up is unable to remember any events from that time. Scientists theorize that the coexistence of wake and sleep elements, often described as a dissociative state,4 can be explained by changes in dopamine and serotonin signaling systems. Dopamine pathways regulate consciousness throughout projections in the cerebrum and cerebral cortex, but also have important projections in the raphe nuclei located in the brainstem. Impairment between the two serotonin pathways, one arising from the nuclei raphe in order to regulate consciousness and other descending towards the spinal cord to regulate motor activity, is thought to be responsible for sleepwalking.8 This hypothesis is based on case reports of sleepwalking among patients with Parkinson’s disease or ones whose treatment includes dopamine and serotonin antagonists.8,9 Furthermore, different studies have shown involvement of the brain stem and cerebellum in initiation of movement. Confirmation of these findings came from SPECT image of sleepwalkers which have shown activity in mentioned parts of the brain, but negligible activity in cerebrum and cerebral cortex responsible for consciousness.1
Chemical substances and risk factors
Sleepwalking episodes may be correlated with other sleep disturbances or an irregular sleep schedule and may be precipitated by the usage of certain medications. A study conducted on 84 symptomatic prepubertal children has shown that 51 children had various sleep problems and 29 of them had a positive family history.6 Another study included 50 symptomatic adults of which 39 had difficulties in breathing.3 Both studies used similar parameters including EEG, psychiatric evaluation, questionnaires and conversation with patients and relatives.3,6 Sleep-disordered breathing, including snoring, asthma, bruxism etc., is the most commonly seen sleep disorder underlying somnambulism in both children and adults.3,6 A group of children with an unknown underlying cause, as well as the group with known problems, had relatives who have suffered sleepwalking throughout their life.6 Recent studies describe the HLA allele DQB1, which is present in 35% of sleepwalkers, but only in 13% of people without this problem, as a gene that could explain the positive family history in sleepwalkers.1 Usage of different medications that affect the central nervous system can cause episodes of sleepwalking as a side effect. Case reports show that this side effect is seen with hypnotics, antipsychotics and antidepressants.9 Zolpidem is a hypnotic-sedative primarily used for treatment of insomnia, but can also be used for migraine relief. Its binding target is on the α1, α2 and α3 subunits of the GABAA receptor, but it has no effect on neurons expressing an α5 subunit.10 As an agonist of the above-mentioned receptors zolpidem stimulates GABA hyperpolarization of specific neurons, resulting in prolongation and preservation of the NREM sleep phase without the myorelaxant effect.4 The exact reason why some patients experience sleepwalking after taking zolpidem is still unknown, but considering everything mentioned above it seems that it is due to its selectivity for specific subunits of GABAA receptors. Zolpidem can precipitate sleepwalking episodes when used alone or in combination with other chemical substances such as alcohol, medical marijuana or various medications for example prednisone, bupropion, ergotamine etc.4,9 Quetiapine, a second-generation antipsychotic, is another drug showing a certain correlation with sleepwalking. It is primarily used for treatment of schizophrenia and bipolar disorder, but is nowadays also used in psychiatric disorders with insomnia.9 The precise mechanism of action is unknown, but quetiapine is known to be a partial agonist of the serotoninergic 5HT1A receptor and an antagonist of the dopaminergic D2, serotoninergic 5HT2A, noradrenergic α1 and histaminic H1 receptors. Some hypotheses claim that quetiapine’s activity on serotoninergic receptors is responsible for sleepwalking episodes, but the mechanism is unknown.9 Several case reports describe sleepwalking as a side effect of this drug, but an inconsistent period from the first dose to the first episode, extremely variable doses which cause this side effect, and sometimes only one episode during therapy make it impossible to establish a doubtless link.9 In the end of this section two more chemicals, alcohol and caffeine, must be mentioned due to their role in society. Various amounts of alcohol are consumed in different cultures as a part of daily routine and numerous legal cases used alcohol-induced sleepwalking as a defense for violent crimes. There is no evidence that solely consumption of acceptable alcohol amounts can influence sleep rhythm, prolong SWS or cause a sleepwalking event.11 Several clinical studies have shown that alcohol intake around bedtime can worsen sleep-breathing disorders because of its ability to decrease tonus in laryngeal musculature.11 Other cases have shown that chronic alcoholics and ones sober for longer periods of time, after consumption of alcohol, have an increased amount of SWS with greater chance of experiencing sleepwalking. Combined with various drugs that have effects on the central nervous system, alcohol increases the chance of a sleepwalking episode due to its depressant effect. Caffeine, present in coffee and some soft beverages, is an excitatory substance for the central nervous system due to its antagonism on adenosines receptors. It is used in the general population to prevent sleep at undesirable moments, but is also known for its effect on sleep. Large amounts of caffeine decrease slow wave sleep (SWS) and slow wave activity (SWA) making it hard to maintain sleep in the first sleep cycle when most sleepwalking episodes occur.2
Diagnosis of sleepwalking is based on physical examination, anamnestic data and occasionally polysomnography.3 Anamnestic data is taken from the patient and, if possible, the patient’s bed partner in order to get the best possible insight into the problem. The patient’s bed partner is the only person able to describe actions that happened during the sleepwalking episode since the sleepwalker is unconscious at the time. The sleepwalker’s complaints include daytime sleepiness, chronic fatigue and sometimes depression. One major problem is waking up in various places such as the kitchen, car, etc. with different things around them such as food leftovers, knife, etc. without the ability to explain what has happened. The underlying problem in many patients is a sleep-breathing disorder which can be discovered by physical examination and from anamnestic data.3 Once the particular problem is found, it is the basis for successful treatment of sleepwalking.3,6 Polysomnography is a method that combines EEG (electroencephalogram), ECG (electrocardiogram), EOG (electrooculogram), respiration control, measurement of oxygen levels in blood and sometimes videotaping of actions done during sleep.6 When put together, all this data give a detailed picture of the patient’s body state during regular sleep and sleepwalking episodes. Psychiatric disorders are also known to precipitate sleepwalking so, if found, they are treated to prevent further episodes.3 Whereas treatment of the underlying sleep-breathing disorder can lead to complete remission of symptoms, psychiatric and pharmacological treatment are not as successful and only lower the frequency of events. Drugs available for this indication are benzodiazepines, e.g.. clonazepam, lorazepam etc., and if depression is present different types of antidepressants are used.3
Figure 1. Painting Sleepwalker (1878) by Maximilián Pirner.
Source: Painting “Sleepwalker” by Maximilián Pirner, added by Steve McKay on Curiator.
Published January 7, 2017. Accessed September 14, 2017.
Somnambulism, or sleepwalking, is a sleep disorder which happens in the NREM stage of sleep and affects both children and adults. It is characterized by the coexistence of both sleep elements and those of wakefulness. Recent studies show that certain EEG changes can be used as confirmation criteria for this disorder, but the neuronal pathways are still unknown. Clinical studies show that different chemical substances can precipitate sleepwalking episodes. Diagnostic procedures are mostly based on anamnestic data which is supported by certain EEG findings.
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7. Jaar O, Pilon M, Carrier J, Montplaisir J, Zadra A. Analysis of slow-wave activity and slow-wave oscillations prior to somnambulism. Sleep. 2010;33(11):1511-1516. http://www.ncbi.nlm.nih.gov/pubmed/21102993. Accessed September 12, 2017.
8. Fabio D, Poryazova N, Oberholzer R, et al. Sleepwalking, REM Sleep Behaviour Disorder and Overlap Parasomnia in Patients with Parkinson’s Disease. Eur Neurol Eur Neurol. 2013;70(56):297-303. doi:10.1159/000353378.
9. Raja M, Raja S. Sleepwalking in four patients treated with quetiapine. Psychiatr Danub. 2013;25(1):80-83. http://www.hdbp.org/psychiatria_danubina/pdf/dnb_vol25_no1/dnb_vol25_no1_80.pdf. Accessed September 12, 2017.
10. Crestani F, Martin JR, Möhler H, Rudolph U. Mechanism of action of the hypnotic zolpidem in vivo. Br J Pharmacol. 2000;131(7):1251-1254. doi:10.1038/sj.bjp.0703717.
11. Pressman M, Mahowald M, Schenck C BM. Alcohol-induced sleepwalking or confusional arousal as a defense to criminal behavior: a review of scientific evidence, methods and forensic considerations. J Sleep Res. 2007;16(2):198-212. https://pdfs.semanticscholar.org/cfc9/745fc061527469c949f5df3efe93c8deb550.pdf?_ga=2.109861703.313152819.1505377611-318246257.1505377611. Accessed September 14, 2017.
Mjesečarenje ili hodanje u snu poremećaj je spavanja kojim je zahvaćeno 2,5% odrasle populacije te nešto veći postotak djece. Glavno obilježje ovog poremećaja je istovremeno postojanje elemenata spavanja i budnosti. Oboljeli imaju nepravilno i isprekidano spavanje, koje uzrokuje specifične promjene na EEG-u. Spomenute promjene su CAP promjene i povećanje frekvencije sporih valova. Postavljeno je nekoliko hipoteza koje povezuju promjene u serotoninergičkoj i dopaminergičkoj transmisiji s hodanjem u snu, ali znanstvene potvrde još nema. Različita klinička istraživanja pokazuju povezanost pojedinih lijekova (zolpidem, kvetiapin) i drugih kemikalija (alkohol, kofein) sa mjesečarenjem. Genetska podloga je dokazana. Glavni poremećaj u podlozi hodanja u snu je problem dišnih puteva te je stoga kirurški tretman takvih problema glavni način liječenja. Druge metode mogu uključivati psihijatrisko liječenje, lijekove ili promjenu u navikama spavanja. Dijagnoza se temelji na anamnezi i EEG nalazu.
KLJUČNE RIJEČI: alkohol, klinički pristup, kvetiapin, mjesečarenje, sporovalna aktivnost (SWA), zolpidem
Received September 30, 2017.
Accepted November 12, 2017.
How to cite:
Dragčević D. Somnambulism. Gyrus. 2017;4(3-4):315-318. Available at: http://gyrus.hiim.hr/index.php/2016-01-10-18-08-09/arhiva/details/3/121.