Sleepwalking / Somnambulism

Author: Antonio Maroccia
Date: 26/12/2012


Sleepwalking, also known as somnambulism , is a sleep disorder belonging to the parasomnia family. Sleepwalkers arise from the slow wave sleep stage in a state of low consciousness and perform activities which are usually performed during a state of full consciousness. These activities can be as benign as sitting up in bed, walking to the bathroom, and cleaning, or as hazardous as cooking, driving, violent gestures, grabbing at hallucinated objects, or even homicide.
Although generally sleepwalking cases consist of simple, repeated behaviours, there are occasionally reports of people performing complex behaviours while asleep, although their legitimacy is often disputed. In 2004, sleep medicine experts in Australia claimed to have successfully treated a woman who said she had sex with strangers in her sleep. In December 2008, reports were published about a woman who sent semi-coherent emails while sleepwalking, including one inviting a friend around for dinner and drinks. Sleepwalkers often have little or no memory of the incident, as their consciousness has altered into a state in which it is harder to recall memories. Although their eyes are open, their expression is dim and glazed over. Sleepwalking may last as little as 30 seconds or as long as 30 minutes. Link Wikipedia

Clinical definition

Patients affected by this disorder carry out automatic motor activities that range from simple to complex. Individuals may walk, urinate inappropriately, eat, or exit from their home while remaining only partially aware. Full arousal may be difficult, and individuals may rarely respond to attempted awakening with agitation or even violence.
There are five stages of sleep. Stages 1, 2, 3 and 4 are characterized as non-rapid eye movement (NREM) sleep. REM (rapid eye movement) sleep is the sleep cycle associated with dreaming as well as surges of important hormones essential for proper growth and metabolism. Each sleep cycle (stages 1,2,3,4 and REM) last about 90-100 minutes and repeats throughout the night. The average person experiences four to five complete sleep cycles per night. Sleepwalking characteristically occurs during the first or second sleep cycles, during stages 3 and 4. Sleepwalking arises from slow-wave sleep (NREM stage N3 sleep), usually in the first 2 h of the night, and it's most common in children and adolescents, when these sleep stages are most robust. Episodes are usually isolated but may be recurrent in 1–6% of patients. The cause is unknown, though it has a familial basis in roughly one-third of cases. Upon waking the sleepwalker has no memory of his or her behaviors.

Genetic factors

Sleepwalking may be transmitted as an autosomal dominant trait with reduced penetrance. The first genetic locus for sleepwalking was found on chromosome 20q12-q13.12.
Genome-wide multipoint parametric linkage analysis for sleepwalking revealed a maximum logarithm of the odds score of 3.44 at chromosome 20q12-q13.12 between 55.6 and 61.4 cM.
This part of genome is correlated to the HLA-DQB1 genes system and it's already known that these kinds of genes are involved in disorders of motor control during sleep. Autoimmune diabetes is also linked to mutations on HLA-DQB1 genes but there is no certified association with somnambulism.

Environmental factors

Sleep deprivation, chaotic sleep schedules, fever, stress, magnesium deficiency, and alcohol intoxication can trigger sleepwalking. Drugs, for example, sedative/hypnotics (drugs that promote sleep), neuroleptics (drugs used to treat psychosis), minor tranquilizers (drugs that produce a calming effect), stimulants (drugs that increase activity), and antihistamines (drugs used to treat symptoms of allergies) can cause sleepwalking.

Physiologic factors

Physiologic factors that may contribute to sleepwalking include:

  • the length and depth of slow wave sleep, which is greater in young children, may be a factor in the increased frequency of sleepwalking in children. In fact, after a long period of sleep deprivation, we can see an increase in depth and length of the slow-wave sleep with a relative increase of states 3 and 4 on states 1 and 2.
  • conditions such as pregnancy and menstruation are known to increase the frequency of sleepwalking;
  • arrhythmias (abnormal heart rhythms);
  • fever: cytokines involved in inflammatory events may stop the function of colinergic neurons that maintain active the cerebral cortex (this is why we have to sleep when we are ill)
  • gastroesophageal reflux (acid reflux)
  • nighttime asthma;
  • nighttime seizures (convulsions);
  • obstructive sleep apnea (condition in which breathing stops temporarily while sleeping); and
    psychiatric disorders, for example, posttraumatic stress disorder, panic attacks, or dissociative states (for example, multiple personality disorder)

HLA and genetic susceptibility to sleepwalking


It is widely accepted that sleepwalking is a disorder of arousal. Arousal is a way to define the level of activation of cerebral cortex used to maintain it in a state of alertness and of correct signals reception. The arousal system is a wide web of neurons whose the most important part is
the reticular formation: it sends signals to the cortex maintaning it in a stimulation state.
Hebb suggested that each signal has two different functions:
1. arousal
2. message
In fact, each signal is transmitted on one hand to all the specific areas of the brain specifically involved to receive it and on the other hand to the reticular formation whose aim is to put the cortex in a state of arousal.
Arousal circuits widely project to the cortex, including motor cortex and a lot of neurotransmitters are involved such as: dopamine, norepinephrine, serotonin and acetylcholine. It was hypothesized that functional abnormality of these circuits could lead to changes in cortical excitability in sleepwalkers, even during wakefulness. Neurophysiological studies suggest that there are alterations in sleepwalkers consistent with an impaired efficiency of inhibitory circuits during wakefulness. This inhibitory impairment could represent the neurophysiological correlate of brain "abnormalities" of sleepwalkers such as "immaturity" of some neural circuits, synapses, or receptors.
Analysis of patients' sleep EEG over the 200 sec prior to the episodes onset revealed that the episodes were not preceded by a gradual increase in spectral power for neither delta nor slow delta over frontal, central, or parietal leads. However, time course comparisons revealed significant changes in the density of slow-wave oscillations as well as in very slow oscillations with significant increases occurring during the final 20 sec immediately preceding episode onset.

Functional involvement of cerebral cortex in adult sleepwalking

Analysis of Slow-Wave Activity and Slow-Wave Oscillations Prior to Somnambulism


There are some drugs that can be prescribed for sleepwalkers, such as a low dose of benzodiazepines, such as clonazepam, and tricyclic antidepressants. However, for most sleepwalkers, many experts advise putting away dangerous items and locking doors and windows before sleep to reduce risks of harmful activity. Good sleep hygiene and avoiding sleep deprivation is also recommended. There is no scientific evidence about the way to treat a sleepwalker, but someone suggests that waking sleepwalkers may result in their disorientation and that is not harmful.

Serotonergic hypothesis of sleepwalking

Drugs used to treat sleepwalking improve the GABA action on synapses but we may think that probably all the other neurotransmitters involved in the way of arousal may be possible targets of drugs.
Acute tryptophan depletion increases translational indices of anxiety in fact recent data suggest that serotonin can inhibit aversive responding in humans: in particular, data in rodents suggest that global serotonin depletion may specifically increase long-duration bed nucleus of the stria terminalis (BNST)-mediated aversive responses (ie, anxiety) (but there is no influence on the short-duration BNST-mediated aversise responses (ie, fear). However, there is some evidence that sleepwalking can be precipitated by sleep-disordered breathing. A hypothesis is proposed that serotonergic system may be a link between sleep-disordered breathing and sleepwalking. Serotonergic neurons meet basic requirements for such a role because they are activated by hypercapnia, they provide a tonic excitatory drive that gates afferent inputs to motoneurons, and the activity of serotonergic neurons can be dissociated from the level of arousal. So, in a state of anxiety the lack of serotonin may be the first important cause; in another way, you may suppose that lack of serotonin in a state of anxiety may lead to a sleep-disorder such as somnambulism. You might think that serotonin anti-reuptake drugs can be used for sleepwalking treatment.
In fact, a patient with a 30-year history of somnambulism and night terrors successfully recovered thanks to a selective serotonin re-uptake inhibitor.
In the end, serotoninergic neurons of dorsal raphe nucleus send more intense signals (high frequence) during wakefulness and send less intense signals during NREM stages of sleep. They stop to burn during the REM stage. A lack of serotonin may improve the intensity of NREM stages and it could lead to the rise of sleepwalking events.

Successful treatment of night terrors and somnambulism with paroxetine

Serotonin control of sleep-wake behavior


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