Robin Lloyd

LiveScience.com
Sat May 10, 10:25 AM ET



If you've been recently rescued from sleepwalking, here's a possible reason why you went zombie - lack of sleep.

Sleepwalkers should keep a regular bedtime to avoid unwanted evening strolls, said Antonio Zadra Universite de Montreal, who led a team that recently investigated the link between sleep loss and sleepwalking. Somnambulism, which affects up to 4 percent of adults, can cause mental confusion, bouts of amnesia and even physical injuries in those affected as they wander.


Sleepwalking is common in kids, but usually they outgrow it, says Dr. Vishesh Kapur, director of the University of Washington Sleep Disorders Center at Harborview Medical Center.


In the February 2008 issue of the journal Annals of Neurology, Zadra, Mathieu Pilon and Jacques Montplaisir explain how they evaluated 40 suspected sleepwalkers. Each was referred to the Sleep Research Centre at Sacre-Coeur Hospital, a Universite de Montreal teaching hospital, between August 2003 and March 2007.


"Our study found that sleep deprivation can precipitate sleepwalking in predisposed individuals," Zadra said.


Zzzzzzzzzz...


Subjects who took part in the study agreed to have their baseline sleep patterns monitored during an initial all-night assessment. During a subsequent visit, patients were kept awake for the entire evening and remained under constant supervision.


Recovery sleep was allowed the next morning after patients had been awake for 25 hours. Subjects were videotaped during each sleep period as the research team evaluated their behavior, which ranged from playing with bed sheets to trying to jump over the bed rails. Subjects were evaluated on a three-point scale based on the complexity of their actions.


During baseline sleep, only half of patients exhibited some 32 of these behaviors. During recovery sleep, that figure rose to 90 percent. The research was supported by the Canadian Institutes of Health Research.


Sleepwalking is "a disorder of arousal, a kind of mixed state of being," Kapur said. There are three states of being in the world of sleep researchers - wakefulness, non-REM (rapid eye movement) sleep and REM sleep (most associated with dreams). Sleepwalking is a mixture of wakefulness and non-REM sleep, he said.


Some sort of arousal or disruption to sleep can also trigger sleepwalking, Kapur said. So people with sleep apnea (an interruption of breathing - snoring is commonly caused by apnea) sometimes sleepwalk, because apnea can create a state where someone is in between non-REM sleep and wakefulness.


Genes to jammies


Family genetics can also predispose one to sleepwalking, Kapur said, but a lot is still unknown about why some people sleepwalk and others do not.


"We know that sleepwalking happens more often in children than in adults, and the predisposing factor there might be the fact that kids have a lot more of slow-wave sleep, a deep non-REM sleep where sleepwalking often starts," Kapur said.


One of the main concerns with sleep walking is injury to oneself or others. When there is any issue of complex behavior that has someone leaving the home or potentially doing activities that could hurt them, they should be evaluated and treated, Kapur said.


Treatments for sleep walking include better sleep hygiene, keeping a regular sleep schedule (to avoid sleep deprivation) and avoiding an excess of alcohol and caffeine or maybe any at all, particularly in the evening, he said. For extreme cases, medication may be prescribed.

Background
Somnambulism (ie, sleepwalking) is a disorder of arousal that falls under the parasomnia group. Parasomnias are undesirable motor, verbal, or experiential events that occur during sleep. These phenomena occur as primary sleep events or secondary to systemic disease. They are categorized as those occurring in rapid eye movement (REM) sleep; those occurring during non–rapid eye movement (NREM) sleep; and miscellaneous types that do not relate to any specific sleep state.
Pathophysiology
The parasomnias have been thought to represent not pathologic cerebral functioning but rather a response to CNS activation that results in sleep-wake or REM-NREM state confusion, instability, or overlap. Recent studies, however, demonstrate differences between sleep patterns and neuronal sleep control mechanisms in individuals with parasomnias compared with those without. Normal sleep involves cyclic hypnic patterns throughout the night between wakefulness, NREM, and REM states. The CNS remains active during all sleep-wake states, although rapid changes are required in neural networks, rhythms, and neurotransmitters with state changes. The length of each cycle averages 50 minutes for a full-term newborn, increasing to approximately 90 minutes by adolescence.
Slow wave sleep (SWS) normally occurs in the first 2 hypnic cycles; younger children have an additional SWS period toward the end of the sleep period. Children typically enter their deepest sleep within 15 minutes of sleep onset, and this first SWS period lasts from 45-75 minutes. This explains why it is easy to move children without rousing them soon after sleep onset. Parasomnias occur as children are caught in a mixed state of transition from one sleep cycle to the next (eg, NREM-wakefulness). This transition state is characterized by a high arousal threshold, mental confusion, and unclear perception.
Sleepwalkers appear to have an abnormality in slow wave sleep regulation. The dissociation that occurs between body and mind sleep appears to arise from activation of thalamocingulate pathways with persisting deactivation of other thalamocortical arousal systems. The first slow wave sleep period of the night is considered to be more disturbed in somnambulistic individuals, and the entire NREM-REM sleep cycle is more fragmented. Because these disorders occur more frequently in children, these differences have been suggested as signs of CNS immaturity.
Frequency
Disorders of arousal are all more prevalent in children than adults.
In Sweden, the incidence of quiet sleepwalking is reported as 40% with a yearly prevalence of 6-17%. Only 2-3% report more than 1 episode per month, and 33% report only a single episode.
In a survey of adults in the United Kingdom, 2.2% reported having night terrors, 2.0% reported sleep walking, and 4.2% reported confusional arousals.
Mortality/Morbidity
The NREM parasomnias are rarely associated with any significant morbidity, although children can strike objects during sleepwalking and occasionally become injured. Sleep-disordered breathing and, to a lesser extent, restless legs syndrome have been associated in children, although with less frequency than reported in adults. The incidence of associated sleep disorders has been reported to be as high as 61%.
Morbidity in adolescents and adults may be more significant. More complex motor behaviors such as driving a car, cooking, eating, or playing a musical instrument have been reported. Injurious behaviors to the patient and/or bed partner may be associated with forensic medicine implications. An increased incidence of psychiatric disorders such as neuroses, panic disorder, phobias, and suicidal ideations has been reported in both these groups. Sleep-disordered breathing, including a sense of choking or blocked breathing, has also been reported. The respiratory events may have a deleterious effect on sleep by increasing arousals and sleep fragmentation.
Race
No racial predilection is known.
Sex
Sleepwalking and confusional arousals have an equal incidence in males and females. Sleep terrors are more common in boys.
Age
Sleepwalking occurs most commonly in middle childhood and preadolescence, with a peak incidence in children aged 11-12 years. Confusional arousals are most common in toddlers and preschool-aged children. Sleep terrors occur most commonly in children aged 4-12 years.
History
The most common pediatric parasomnia disorders of arousal include sleepwalking, confusional arousals, and sleep terrors. Parasomnia events have a predilection for occurring during deep sleep (stages III and IV, or SWS), are known to occur during all stages of NREM sleep, and are possible at any time during the night. As most SWS is achieved in the earlier segments of the sleep period, these phenomena usually are seen in the first one third of the sleep cycle and rarely during naps.
• General and sleep related medical history is usually sufficient to differentiate parasomnias from other disorders. Pertinent questions include the following:
•
o Detailed description of the event
o Level of consciousness before, during, and after the event
o Time of night and sleep cycle when the events occur
o Daytime sleepiness
o Associated injury
o Memory of the event
o Family history
o Any precipitating factors
• Nocturnal frontal lobe seizures and some psychiatric conditions present the most difficult diagnostic dilemmas. A history of stereotypical short attacks that repeat during the night, most frequently during stage II sleep, suggests seizures rather than a parasomnia. Onset in later childhood or adolescence, persistence into adulthood, recurring nocturnal agitation, and daytime complaints such as fatigue or sleepiness are also suggestive of a seizure disorder.
• Sleepwalking
•
o Episodes range from quiet walking about the room to agitated running or attempts to "escape." Subjects may later report attempting to escape dangerous situations or terrifying threats. Typically, the eyes are open with a glassy, staring appearance as the child quietly roams the house.
o On questioning, responses are slow or absent. If returned to bed without awakening, the child usually does not remember the event. Older children, who may awaken more easily at the end of an episode, often are embarrassed by the behavior (especially if it was inappropriate).
o Sleepwalking has no association with previous sleep problems, sleeping alone in a room or with others, achluophobia (fear of the dark), or anger outbursts.
o Some studies suggest that children who sleepwalk may have been more restless sleepers when aged 4-5 years and more restless with more frequent awakenings during the first year of life.
• Confusional arousals
•
o Episodes consist of disorientation, memory impairment, and slow mentation and often are accompanied by inconsolable crying and thrashing movements in bed. This disorder is common in younger children but decreases in frequency with age.
o In infants, episodes manifest by crying and moving about in bed.
o The eyes may be closed or opened, as in sleep terrors, but the child does not appear to feel panic.
o Events typically last from 3-13 minutes and range in frequency from 2 times per night to 2 times per year. Attempting to awaken the child often prolongs the course, and successful wakening by parents typically brings about an end to the episode.
• Sleep terrors
•
o These are the most anxiety provoking for parents. Episodes frequently begin with a "blood-curdling" scream, which is accompanied by the appearance of panic with wide-open eyes, tachycardia, tachypnea, dilated pupils, diaphoresis, and flushing.
o This may be followed by panic-driven motor activity, such as hitting the wall or running around the room.
o While typically not dangerous, the behavior is sometimes violent enough to result in injury to the patient or others; property damage also may result.
o The inability of the parent to console the child is a hallmark of the episode (which is typically shorter than confusional arousals), and amnesia for the event is usually complete.
o Sleep terrors usually resolve by adolescence, although the disorder occasionally persists into adulthood.
Physical
Physical and neurological examinations are typically normal in these children.
Causes
• Genetic
•
o Sleepwalking occurs more frequently in monozygotic twins and is 10 times more likely if a first-degree relative has a history of sleepwalking.
o An increased frequency of DQB1*04 and *05 alleles is reported. DQB1 genes have also been implicated in narcolepsy and other disorders of motor control during sleep such as REM behavior disorder.
• Environmental: Sleep deprivation, chaotic sleep schedules, fever, stress, magnesium deficiency, and chemical or drug intoxication (eg, alcohol), sedative/hypnotics (eg, Zolpidem), antidepressants (eg, bupropion, paroxetine, amitriptyline), neuroleptics (eg, lithium, reboxetine), minor tranquilizers, stimulants, antibiotics (eg, fluoroquinolone), anti-Parkinson medications (eg, levodopa), anticonvulsants (eg, topiramate), and antihistamines can trigger parasomnias.
• Physiologic
•
o The length and depth of SWS, which is greater in young children, may be a factor in the increased frequency of parasomnias in children.
o Conditions such as pregnancy and menstruation are known to increase frequency in patients with parasomnias.
• Associated medical conditions
•
o Arrhythmias
o Chronic paroxysmal hemicrania
o Migraine
o Fever
o Gastroesophageal reflux
o Nocturnal asthma
o Nocturnal seizures
o Obstructive sleep apnea: Children with obstructive sleep apnea or Tourette syndrome are at greater risk of having parasomnias along with their underlying disorder.
o Chronic sleepwalking, especially in adults, is frequently associated with sleep-disordered breathing. Treatment of the sleep-disordered breathing with continuous positive airway pressure (CPAP) or surgery typically improves or resolves the sleepwalking. Noncompliance with CPAP is associated with persistence or recurrence of sleepwalking. Serotonin has been postulated as the physiologic link between these two disorders.
o Psychiatric disorders
o
 Posttraumatic stress disorder
 Panic attack
 Dissociative states
o Hyperthyroidism: Thyrotoxicosis has been associated with an increased incidence of sleepwalking, and achievement of euthyroidism is associated with improvement or resolution of the symptoms. Sleepwalking may occur as an early symptom, and the onset of sleepwalking in a patient out of the normal expected age range should be evaluated for hyperthyroidism. The mechanism for the sleepwalking is considered to be increased fatigue in combination with longer periods of non-REM sleep.
Investigations:
Lab Studies
• No specific laboratory studies are indicated in the workup of routine parasomnias.
Other Tests
• Polysomnogram with or without multiple sleep latency testing should be reserved for the few cases in which the diagnosis is still unclear after a careful history and physical. The abnormal behavior during SWS is generally diagnostic. Sleep deprivation can be used as a tool to induce somnambulistic episodes in the sleep laboratory.
• Microarousals and sleep state disorganization are observed frequently and often noted on EEG alone, if performed during nocturnal sleep.
• Hypersynchronous slow delta-wave activity has been observed in the sleep electroencephalogram of sleepwalkers; however, controversy remains regarding these findings on polysomnography.
Treatment
Medical Care
• General guidelines
•
o Reassurance is the mainstay of treatment. The benign nature of the events and subsequent disappearance in most cases should be emphasized.
o If environmental or predisposing factors are discovered, an attempt should be made to eliminate them. Assure adequate sleep, regulation of sleep cycle, and treatment of underlying medical conditions (eg, gastroesophageal reflux, obstructive sleep apnea, periodic leg movements, seizures).
o Avoid auditory, tactile, or visual stimuli early in the sleep cycle. These have been shown to induce events in some patients with parasomnias.
o Instruct parents to lock windows and doors, remove obstacles and sharp objects from the room, and add alarms (if necessary) to decrease the likelihood of injury during an episode.
o Depending on the situation, comforting the child and gently redirecting him or her to bed may be appropriate. Attempts to confront or wake up patients during the events frequently lengthens the parasomnia episode and may induce resistance or violence from the patient.
• Pharmacological measures may be necessary in the following situations:
o The possibility of injury is real.
o Continued behaviors are causing significant family disruption or excessive daytime sleepiness.
o Unusual symptoms are present.
o Nonpharmacological interventions have proven to be inadequate.
o Benzodiazepines, tricyclic antidepressants, and serotonin reuptake inhibitors have been shown to be useful. Clonazepam in low doses before bedtime and continued for 3-6 weeks is usually effective.
o Medication often can be discontinued after 3-5 weeks without recurrence of symptoms. Occasionally, frequency of episodes increases briefly after discontinuing the medication because of rebound sleep.
• Nonpharmacological measures
o Relaxation techniques, mental imagery, and anticipatory awakenings are preferred for long-term management. The first 2 techniques should be undertaken only with the help of an experienced behavioral therapist or hypnotist.
o Anticipatory awakenings consist of waking the child approximately 15-20 minutes before the usual time of an event and then keeping him awake through the time during which the episodes usually occur.
Medicines;
TCA
Benzodiazepines
Prognosis
• The childhood parasomnias are not associated with long-term sequelae. Although disruptive and frightening for parents in the short term, these disorders rarely cause injury. Furthermore, the prognosis for resolution with maturation is excellent.
• Prolonged disturbed sleep may be associated with school and behavioral issues. A relationship with hyperactivity is suggested but not clear.
• Adolescents with sleep terrors or sleepwalking have an increased prevalence of other sleep disorders, neurotic traits, and other psychiatric disorders.
• Rare reports describe incidences of serious injury, sexual misconduct, or violent behavior occurring during somnambulism in adults. Most serious injuries have occurred as a result of leaping through windows. Some apparent "suicides" have likely been the unfortunate result of a sleep behavior. Violent behavior toward others may also rarely occur and has been used as a legal defense. The violent behavior aspect appears to occur more frequently in men than in women.

††††††††† While many factors have been found to correlate with sleepwalking episodes, the neural activity that underlies the phenomenon is still being investigated.† The first step is to take a look at how a sleep episode occurs.



††††††††††† NREM sleep in which sleepwalking occurs makes up about 75% of most sleep episodes, with REM occurring periodically at regular intervals (Schenck & Mahowald, 2000).† The first episode of REM sleep occurs about 90 minutes after the beginning of the sleep episode, and then recurs about every 60 to 90 minutes thereafter, lasting a short time at each occurrence.† One particularly interesting feature of REM sleep is that electroencephalography measurements (EEG) during this time are remarkably similar to when an individual is awake.† EEG measurements then transition back into the ìasleepî range when the individual abruptly resumes NREM sleep.



††††††††††† Thus, sleepwalking has been hypothesized as originating from some sort of incomplete transfer from brain functions characteristic of ìasleepî EEG frequency to those of an ìawakeî frequency.† Unfortunately, though, no specific ìasleep/awakeî control center has been identified in brain function, and localizing possible mechanisms or pathways have proven difficult† (Jones, 2000; as cited in Leo, 2003).† Brain areas have different functions based on the current state of consciousness, and different types of activity may lead to different outcomes as a result.† Essentially, sleepwalking may be triggered by an incomplete transition (or awakening) from NREM sleep to REM sleep, caused by genetic or environmental factors (Leo, 2003).



The established method of examining individuals who exhibited sleepwalking or other sleep disorders is to use the comprehensive polysomnographic evaluation (PSG).† This involves one or more overnight stays at a sleep laboratory where a number of different measures can be recorded while the individual sleeps.† These measures usually consist of respiration and blood-oxygen saturation, movements in the legs, electroencephalography (EEG) to measure brain wave activity, electrooculography (EOG) to record eye movements, electromyography (EMG) to measure muscle activity, and electrocardiography (ECG or EKG) to examine heart function (Durand & Barlow, 1997).† These measures are then analyzed together in an attempt to establish any meaningful patterns associated with sleepwalking episodes.



PSG research has yielded some interesting insights into sleepwalking, particularly regarding comorbidity with other sleep-related disorders.† Both children and adult sufferers of sleepwalking disorder often display sleep-disordered breathing (SBD) or restless leg syndrome (RLS) and, when they are treated for these disorders with conventional means such as nasal continuous positive airway pressure devices (CPAP) or prescription medication, sleepwalking and other parasomnias have been shown to completely abate in some instances (Guilleminault, Kirisoglu, Bao, Arias, Chan & Li, 2005; Guilleminault, Palombini, Pelayo, & Chervin, 2003).† This seems to imply that, at least in some cases, other illnesses could potentially be exclusively responsible for sleepwalking and other parasomnias.



The future of sleepwalking research seems to largely lie in the domain of functional imaging.† Techniques such as functional magnetic resonance imaging (fMRI), positron emission tomography (PET), and single-photon emission tomography (SPET) have made great advances in identifying brain structures involved in sleepwalking and other parasomnias.† Though there currently is a rather small number of studies in this area using these new functional imaging techniques, several great leaps have been made with a mere dozen or so studies (Otte, Nofzinger, Audenaert, Goethals, & Dierckx, 2002, for a review).† For example, the pons, thalamus, basal ganglia, and frontal cortex have been shown to initiate or become active during NREM sleep, and the pons and limbic structures have been similarly implicated in REM sleep.† One SPECT study in particular (Bassetti, Vella, Donati, Wielep, & Weder, 2000) was able to implicate thalamocingulate pathway activation during sleepwalking and thalamocortical arousal pathway deactivation during episodes of sleepwalking.† With such tremendous gains in a relatively short time, future investigations of sleepwalking using functional brain imaging look promising indeed.

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