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Somnambulism: Definitions of Sleepwalking and Its Effects

Updated on November 20, 2016
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What Is Somnambulism?

Somnambulism, or sleepwalking, has been studied extensively by psychologists due to its actual and potential consequences, as well as its indication of underlying cognitive disorders.

Somnambulism is classified as Non-Rapid Eye Movement (NREM) parasomnia disorder in the DSM-5, Somnambulism is characterized by non-substance-induced arousal in which the individual is relatively unresponsive; it is not explained by coexisting disorders; and there is little to no recall of dream imagery (DSM-5, 2013). Cumulatively, this condition is defined as “a series of complex behaviors that is usually initiated during arousals from slow-wave sleep and culminate in walking around with an altered state of consciousness and impaired judgment” (Bornstein, 1994). NREM sleep is differentiated from Rapid Eye Movement (REM) sleep in that it is characterized by sleep onset (N1), light sleep (N2) and deep or slow-wave sleep (N3).

The purpose of this article is to discuss the known physiology and symptoms identified with somnambulism and their consequences, possible comorbidity and heredity, treatment, and finally, the effect it can have criminal justice system in America.

Physiology and Symptomology

Characterization of somnambulism begins with identifying patients with episodes lasting from several minutes to durations longer than an hour (DSM-5, 2013). Patients are found to be unresponsive to external stimuli, have considerable misconceptions and confusion, can perceive non-existent threats and will suffer from variable retrograde amnesia in some, but not all, cases (Zadra et al., 2013). Most episodes simply include confusion and low complexity, routine behaviors but high complexity behaviors have been known to occur such as eating, engaging in conversation, leaving the building and even driving cars (DSM-5, 2013). On rare occasions, violent and aggressive behaviors have transpired, including homicidal attempts (Broughton et al., 1994), and suspected suicide attempts implicating need for further study with regards to the criminal justice system (Mahowald et al., 2003). Generally, episodes will transpire during the first third of the night during predominantly slow-wave periods of N3 NREM sleep.

The neural structures thought to be involved include: the anterior and posterior hypothalamus, basal forebrain, brainstem, cortex, thalamus, ventral tegmental area and all their neurotransmitters responsible for various interconnected and complex interactions (Zadra, 2013). Continuous airway pressure (CAP) and erratic waves, delta wave clusters and hypersynchronous delta waves have been recorded as possible, but controversial, causes in studies done by Guilleminalut et al. in 2006 when measuring child and adult sleepwalkers (Guilleminatlut et al., 2006).

Somnambulism is common in childhood at a rate of about 3% in toddlers, 11-13.5% from the ages of 7-10 years old and beginning decline at 12 years old with around 12.7% of children. However, symptoms are typically alleviated through adolescence with only 2-4% in adults but 25% of those continue symptomology into adulthood (Ohayon et al., 2012). Persistence is unclear and can there is known spontaneous occurrence in adults and is considered a disorder of arousal (Zadra, 2013).

Comorbidity and Heredity

Comorbidity has been found to include several psychological disorders such as: schizophrenia, major depressive disorder, and obsessive-compulsive disorder (DSM-5, 2013). Additionally, there has been links to associated development of neurodegenerative processes such as Parkinson’s disease and dementia and there is an approximate 25% of sleepwalkers who self-report mood and anxiety disorders (Zadra et al., 2013). Some connection to the comorbidity of migraines and sleepwalking was also identified in psychopathy and sleepwalking studies but the nature of the relation was not positively identified, only noted. Caffeine consumption was also correlated in the same study with the suggestion that it may be a trigger for predisposed patients to there was consideration for the paradoxical nature in which caffeine may be imbibed by suffers to relieve co-symptomatic exhaustion (Labelle et al., 2013)

Evidence of approximately 80% of sleepwalkers have a family member that is also affected and first-degree relatives have shown to have a ten-fold increased chance of symptomology according to twin studies (Zadra et al., 2013). In studies done on extensive familial cranial structure it was found that several family members were prone to symptoms when exhibiting a below average sized upper airway in the maxilla-mandibular anatomy such as narrow maxilla with high and narrow palate, retroposition of the mandible with a narrow hypopharynx, or a narrow nose and secondary narrow pharynx (Guilleminalut and Cao, 2010). Though the study did state that the triggering of parasomnias was still a mystery and not determinately caused by heredity in its conclusion.


Various treatments have been attempted with mixed reviews from patients on their sustainable relief of symptoms. Benzodiazepines have been widely used with positive self-reporting responses but the epistemological evidence is limited. Clonazepam seemed to show “rapid and sustained” control according to one report but it included non-sleepwalking sleep terror patients and the results were not divided. Hypnotherapy has been attempted with limited degrees of success from therapists but self-hypnosis seemed more widely self-reported as being successful (Harris & Grunstein, 2009). Continuous positive airway pressure or CPAP machines were also found to provide relief in patients that were considered to have CAP issues (Guilleminault et al., 2006).

Possible Consequences for the Criminal Justice System

Historically, sleepwalking attacks on other people have been defined as the aggressor's fault and not an excused activity, and arguments have been made thusly since the early 14th century towards. In the 17th century there was an argument made distinguishing guilt with regard to level of animosity towards the victim when the aggressor was awake being a relevant factor. In fact, the earliest trial of Colonel Cheyney Culpeper shooting both a guardsman and his horse in 1686 ultimately ended in his full pardon after over 50 witnesses testified to his “escapades” when sleeping (Umanath et al., 2011).

Today there are diagnostic tools available and substantial epistemological evidence with regards to symptomology, occurrence rates and retrograde amnesia factors. Due to this, there is now arguments relating to known sleepwalkers protectively safeguarding against injuring themselves or others lest they face liability for their actions. Another factor is the level of skepticism in which involuntary behavior during somnambulistic episodes is met with by jurors and judges during trials. Typically mental disorders are considered exceptions with regards to defendant guilt but there is no current standard for liability regarding involuntary aggression during sleepwalking episodes and much forensic research is currently being done to clarify a standard. Studies touching on the subject have been retroactively historic so they suggest deeper studies into familiar history, doctor inclusion of parasomnia symptomology on data records and self-reports, and continued research on genetics, hormones, para and neuropsychology and sleep brain imaging (Cartwright, 2004).

Final Thoughts

There has been wide evaluation of somnambulism and its effects throughout history. There is no lack of evidence that it occurs, but its causes, heredity and comorbidity remain hazy areas particularly with regards to the justice system. It is obvious that more studies are needed and will continue to be conducted in order to fully understand sleepwalking.


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