Outline and evaluate research on circadian rhythms
A biological rhythm is a cyclical variation over a period of time in physiological or psychological processes. Circadian rhythms last around 24 hours, for instance the sleep/wake cycle.
Research has been conducted to try and find out what causes the rhythms. Are they related to exogenous zeitgebers e.g. light and dark? Or are they inbuilt and would persist even if external stimuli are absent. These are endogenous pacemakers. Researchers are interested in what happens when exogenous cues are removed. Siffre was a french geologist who spent 2 months in a cave with no natural light, but had food, water and could communicate but had no way of finding out the time. His physiology and behavior stayed cyclical but becomes based on a day between 25 and 30 hours. Therefore the body must have an internal clock, (endogenous pacemaker).
However Siffre’s study is a case study as it is studying one person, himself and therefore it has unique features. Due to this his behaviour may not be typical of all people and therefore means it cannot be generalised. It is possible that there was an investigator bias as he was not only the investigator and the participant.
Aschoff and Wever conducted a study in support of Siffre’s. They placed participants in an underground bunker in the absence of any environmental and social cues. They found that most participants had circadian rhythms of between 24 and 25 hours although some were longer. This shows that the circadian rhythm is about 24 hours.
A study was also conducted by Folkard et al. who isolated participants from exogenous zeitgebers for 3 weeks, manipulating the clock they had so that only 22 hours passed a day. Out of the 12 participants, only one kept pace with the clock. Showing the strength of the circadian rhythm as a free running endogenous pacemaker.
However there are individual differences with circadian rhythms. One of such differences is the cycle onset. People seem innately different in terms of when they reach their peak. For example, Duffy et al. found that morning people prefer to rise early and go to bed early, whereas evening people prefer to wake up and go to bed late. Suggesting that there are individual differences.
There are also criticisms with the methodology of the research conducted into circadian rhythms. It was thought that dim light, in contrast to daylight, would not affect the circadian rhythm.
However recent research suggests that this is not likely to be the case. Czeisler et al. altered participants’ circadian rhythms down to 22 hours and up to 28 hours just by using dim light. Suggesting that dim light does affect the circadian rhythm.
Siffre went on to suggest that the body must have an endogenous pacemaker. Such as clock in the brain. There is a structure called the suprachiasmatic nuclei (SCN) in the hypothalamus to receive information about light and dark directly from the retina which synchronises our biological rhythms to a 24 hour cycle. If the SCN is damaged, circadian rhythms disappear and they become random.
There are real world applications as since the circadian rhythm affects digestion, heart rate, hormone and other functions, this should be taken into account when taking drugs. For example, medications that act on certain hormone may have no effect if taken when target hormone levels are low but are fully effective if taken when levels are high.
Describe and evaluate research on ultradian and in
An infradian rhythm lasts longer than 24 hours, for example the menstrual cycle which on average lasts 28 days. The pituitary gland releases hormones which stimulate a follicle in one ovary to ripen an egg and also triggers the release of the female hormone oestrogen. Once the egg has ripened, the ruptured follicle starts to secrete progesterone which causes the lining of the womb to prepare for a pregnancy by increasing blood in pregnancy, progesterone is reduced and this causes the lining of the womb to be shed.
The menstrual cycle is normally governed by an endogenous system. However, it can be controlled by exogenous cues. Russell et al. 1980 took daily samples of sweat from one group of women and rubbed on to the upper lip of women in a second group. The groups were kept separate yet their menstrual cycles became synchronized, suggesting that the synchronisation of menstrual cycles can be affected by pheromones.
However, there are consequences of the menstrual cycle and PMS affects women during the week before menstruation begins. These affects include acne, depression, food cravings etc.. Dallton found that PMS was also associated with an increase in accidents, lower achievement academically, suicudes and crime.
On the other hand there may be a determinist approach to infradian biological rhythms as PMS has been used as a legal defense. It has been argued that severe PMS was similar to a mental disorder and therefore individuals should not be held for their actions. This suggests that biological rhythms may be beyond our control.
Ultradian rhythms last less than 24 hours, e.g. sleep stages. With the invention of the electroencephalograph, psychologists could investigate brain activity that occurs during sleep, concluding that it was composed of different stages.
Stage one is where alpha waves disappear and are replaced by low-voltage slow waves, heart rate declines and muscles relax. This is a light sleep and people are easily woken. Stage two is a deeper state, from which people are still easily woken. Short bursts of sleep spindles are noticeable, as well as sharp rises and falls in amplitude, bodily functions slows down and blood pressure, metabolism and cardiac activity decrease. Stage three is where sleep becomes increasingly deeper and people are more difficult to wake. Sleep spindles decline, being replaced by long, slow delta waves, heart rate, blood pressure and temperature decline. Finally stage four is deep sleep, where delta waves increase and metabolic rate is low, and people are difficult to wake. Growth hormones are released and incidences of sleepwalking and night terrors may occur.
Derment and Kleitman monitored electrical activity in the brain during sleep using EEG recordings and therefore could wake participants during the different stages of sleep. Participants reported their feelings, experiences and emotions. They found that people who were awakened during REM sleep reported dreaming 90% of the time, however only 7% of patents awakening from NREM sleep led to dream recall. This therefore meant that Derment and Klieitman had found the point in the cycle at which people dream.
Research conducted into this area are conducted in artificial surroundings of sleep laboratories, with electrodes etc. to be worn whilst asleep, due to the unnatural circumstances the research may lack ecological validity and therefore cannot be generalized.
Discuss the role of endogenous and exogenous zeitg
The suprachiasmatic nucleus (SCN) lies within the hypothalamus where it obtains information about light from the eye via the optic nerve, this happens even when the eye is shut. If the endogenous clock is running slow e.g. the sun rises earlier than the day before, the morning light automatically shifts the clock ahead, putting the rhythm in step with the world outside.
The role of the SCN has been demonstrated in animal studies. Morgan bred ‘mutant’ hamsters so that they had circadian rhythms of 20 hours instead of 24, and then transplanted their SCNs into the ‘normal’ hamsters. The ‘normal’ hamsters then displayed the mutant rhythms. This suggests that there is a genetic factor to the functioning of SCN.
The SCN sends signals to the pineal gland, directing it to increase production of the hormone melatonin at night. Melatonin induces sleep by inhibiting the brain mechanisms that promote wakefulness.
Folkard conducted a study where Kate Aldcroft spent time in a cave. After 25 days her temperature rhythm was a 24 hour one, yet her sleep rhythm was on a 30 hour cycle. Such desynchronisation leads to symptoms similar to jet lag.
The process of resetting the biological clock with exogenous zeitgebers is known as entrainment. The opposite of entrainment is ‘free running’ (where the biological clock operates in the absence of any exogenous cues.
Light is the dominant zeitgeber in humans. As we have seen light can reset the body’s main pacemaker, the SCN. It can also reset the other oscillators located throughout the body because the protein cryptochrome (CRP), which is part of the protein clock, is light-sensitive. This may explain why Campbell and Murphy found that if you shine a light on the back of participant’s knees this shifted their circadian rhythms.
The power of artificial lighting is that it is a dominant zeitgeber, in early studies (Siffre and Aschoff and Wever), participants were exposed to artificial lighting but it was assumed this would not be bright enough to entrain rhythms. Campbell and Murphy shifted circadian rhythms just by shining a light on the back of someone’s knees. Recent research has shown that, in general, artificial light does have an effect. For example, Bovin et al found that circadian rhythms can be entrained by ordinary dim light, although bright lighting was more effective.
If dim light does reset the biological clock, then the fact that we live in an artificially lit world may have some negative consequences. E.g. Stevens suggests that exposure to artificial lighting disrupts circadian rhythms and thus disrupts melatonin production explaining why women in industrialised societies are more likely to develop breast cancer.
Until recently it was thought that social cues were the main zeitgebers for human circadian rhythms. We eat meals at socially determined meal times, and go to bed and wake up at times designated as appropriate for our age, and so on. Our daily rhythms appear to be entrained by social convention, not internal biology.
There is a variation in the external temperature of cold blooded animals; this affects the setting of circadian rhythms as cold temperature signals a time for reduced activity. However, in warm-blooded animals recent evidence suggests that the daily changes in body temperature are governed by their own circadian clock and as these temperatures change entrain other circadian rhythms (Buhr et al).
When the biological clock fails it can cause mutations in genes which contribute to the ticking of the biological clock. Research suggests that the brain changes during adolescence, leading to a form of delayed sleep phase syndrome which would explain why some adolescents have unusual sleep patterns.
There are real world applications as there are enormous health, safety and economic benefits to figuring out how the circadian clock works, because desynchronised body clocks reduce alertness and can lead to major accidents.
Discuss the disruption of biological rhythms
Disruption of biological rhythms come in many forms. One of which being shift work. This is because night workers are required to be alert during the night and therefore must sleep during the day, which is not our natural rhythm and out of synch with exogenous zeitgebers.
This disruptions often causes decreased alertness, as Boivin et al. fount that night workers experience a circadian trough of decreased alertness during the night, usually between midnight when cortisol levels are at their lowest and 4.aa am when body temperature is at its lowest.
As well as sleep deprivation, as night workers have to sleep during the daytime when there are distractions such as outside noise and daylight which reduces sleep quality.
Tilly and Wilkinson found that daytime sleep is generally 2 - 3 hours shorter and REM is particularly affected. Poor quality sleep then goes on to make it harder for shift workers to stay awake during the night.
Disruptions in biological rhythms have an effect on health as Knutsson et al. found that individuals who worked shifts for more than 15 years were 3 times more likely to develop heart disease than non-shift workers. Martino et al. later went on to link shift work to a range of organ diseases, including kidney disease. It is also suspected to be due to the direct effects of desynchronisation or indirect effects, such as sleep disruption.
However shift work effects are not solely due to the disruption of biological rhythms, as there may also be due to the lack of sleep associated with having to go to bed at unusual times as well as that shift workers experience social disruption as well. This is because it is difficult to meet friends and spend time with family when working night shifts; a study by Solomon goes to show that divorce rates may be as high as 60% among all-night workers. This suggests that there are other factors involved.
A second form of disruption in biological rhythms is jet lag. Winter et al. calculated that it is the equivalent of 1 day to adjust to each hour of time change. Symptoms of jet lag include loss of appetite, nausea, fatigue, disorientation, insomnia and mild depression.
Jet lag is associated with performance decrement. A popular way to demonstrate the debilitating effects of jet lag is to study American major league baseball teams who travel from coast to coast to play games. The west coast is three hours behind the east coast so when east coast teams play on the west coast, their body clocks go backwards (phase delay). Whereas west coast team experience phase advance when they play teams on the east coast.
Rechet et al. analysed US baseball results over three years and found that teams that travelled east to west on average won 44% of their games; whereas when travelling from west to east, the percentage of the games won dropped to just 37%.
Jet lag may be affected by factors other than the disruption of biological rhythms. An example of this may be that an individual may sleep badly the night before travelling because of worry. Other factors may be drinking alcohol, low oxygen, and annoying factors can be cumulative factors. This suggests that it may not solely by the disruption of biological rhythms that cause jet lag.
Melatonin may be a cure for jet and shift lag. This is because it is a natural hormone that induces sleep. Herxheimer and Petrie reviewed 10 studies and found that where melatonin was taken near to bedtime, it was remarkably effective. However, if taken at the wrong time of day it may actually delay adaption.
Describe and evaluate lifespan changes in sleep
As humans grow from infancy to old age there are major changes in the amount and kind of sleep experienced.
At birth babies experience immature versions of SWS and REM called quite and active sleep, they will sleep for approximately 16 hours each day, 8 of which is active sleep. At 6 months a main sleep wake cycle develops meaning their circadian rhythm has been established but at the age of 1, the baby will be able to sleep through the night, often napping once or twice during the day. Their sleep will lengthen and their active sleep will reduce.
An infants increased REM sleep has been explained in terms of the relative immaturity of the infants brain related to learning. REM sleep has been linked to the production of neurotransmitters and consolidation of memories explaining why babies have a significantly greater amount of REM. This is further supported by the fact that premature babies spend 90% of their time asleep (active sleep) and their brains are even less mature.
When a child reaches the age of 5 EEG patterns look like those of an adults but they still sleep more (12 hours a day) 30% of which is REM. This is also the period of time when children may experience parasomnias including sleepwalking and sleep terrors.
During adolescents the need for sleep is around 9-10 hours a night meaning circadian rhythms change so that they feel more awake at night but will have difficulty getting up (this is an example of phase delay).
Research suggests that a chance of sleep patterns in adolescents may be linked to changes in hormone production. Hormones are primarily released at night therefore sleep patterns are disturbed, leading to sleep deprivation and thought to be similar to those typical of puberty such as irritability, moodiness and changes in motivation and school performance.
In adulthood sleep consists of 8 hours a night, 25% of which is REM, however, adults are more likely to have an increased frequency of sleep disorders, including insomnia and sleep apnea. As you age, sleep time stays the same but it becomes increasingly hard to go to sleep and you wake more frequently which means you have naps during the day which changes your sleep patterns (REM decreases to 20%, SWS is reduced to 5% or less and NREM increases). Older people may also experience a phase advance of circadian rhythms resulting in going to bed earlier and waking earlier.
Several studies have found an increased mortality associated with too much sleep in adulthood. Kripke et al surveyed over a million adult men and women finding that those who slept for 6-7 hours had reduced morality risk while those who slept for 8 hours on average had a 15% increase risk of death and 30% for those sleeping for 10 hours. However, the results were correlational data so do not show cause and effect therefore other variables such as underlying illness may link sleep duration with mortality.
There are real world applications for research into the nature of sleep and lifespan changes. Wilson and Carskadom suggested that teenagers should start school later due to sleep phase delay while other researchers suggest the effects of aging could be reduced by improving sleep hygiene. The habit of napping may reduce the amount of sleep experienced at night, therefore sleep hygiene may be improved by resisting naps.
A problem with research into the nature of sleep and lifespan changes is that there is a cultural bias. Most research is conducted with American and British samples meaning psychologists make assumptions about sleep behaviour ignoring cultural influences, but this may not be true. Tynjala et al looked at sleep patterns in adolescence questioning over 400,000 11-16 year olds from 11 European countries finding significant differences (13-14 year olds in Scotland sleep for more than 9 hours while in Israel they only sleep for just over 8 ½ hours). This suggests that there are contributory factors such as the number of evenings not at home, showing that sleep duration is influenced by cultural that sleep duration is influenced by cultural practices and that our view may be biased.
However, sleep patterns are not necessarily consistent but change with age. Psychologists ignore age related changes assuming that there is one sleep pattern for all. However, this link between age and sleep had lead to new understanding on some of the effects of ageing, this is the developmental approach.
Outline and evaluate restoration explanation of th
There are different stages of sleep, the main two being Slow Wave Sleep (SWS) and Rapid Eye Movement (REM) sleep. Oswald suggested that they both had different functions, SWS enables the body to repair itself and REM enables brain recovery.
In SWS a growth hormone (GH) is secreted which stimulates growth, particularly in childhood, however it is important in adulthood as it enables protein synthesis and cell growth. This is vital in the restoration of body tissue as proteins are fragile and must be constantly renewed as part of the body’s natural recovery process. A lack of sleep is associated with a decrease in immune system functioning (Krueger et al.) as the immune system consists of various protein molecules and antibodies that are regenerated during cell growth and protein synthesis in SWS.
Although the GH is secreted throughout the day, but a significant amount is at night during SWS. Sassin et al. found that when the sleep wake cycle is reversed the release of GH is also reversed which shows that the release of GH is controlled by neural mechanisms related to SWS. Research has gone on to find that the amount of GH released correlates with the amount of SWS an individual has. And the decline of GH in older age has also been associated with reduced SWS that they experience, van Cauter et al.
It is suggested that the amount of REM sleep is proportional to the immaturity of the offspring at birth as REM is associated with brain growth, for example, a platypus is immature at birth and therefore experience around 8 hours of REM sleep per day, however dolphins, which can swim at birth have almost no REM (Siegel). This suggests that there is a relationship between neural development and sleep.
Crick and Mitchison proposed that during REM sleep unwanted memories are discarded meaning that important memories are accessible. However Stickgold suggested that there was a much more complex relationship between memory and sleep as evidence suggests that REM may be important for consolidation of the procedural memory, whereas SWS is important for consolidation of semantic and episodic memory.
A weakness of the research into sleep deprivation is that case studies or observational studies are usually used, therefore participants are likely to be unique and results cannot be generalised to the wider public.
A weakness of the explanation presents itself in the form of a case study into Peter Tripp ( awake for 201 hours) became unpleasant and abusive after three days and after five, began hallucinating. However Randy Gardner (awake for 260 hours) displayed no psychotic symptoms. This suggests that there are no lasting effects into sleep deprivation.
Also, studies suggest that lack of sleep doesn’t always result in long term damaged and that there is no need for recovery of lost sleep. However when participants are deprived of more than 72 hours they experience short periods of micro sleep. This suggests that participant may be experiencing benefits from sleeping whilst appearing awake.
Young suggests the more we know about the sleep patterns of different species, the more apparent it is that it is environmental pressures rather than restoration that provide understanding of sleep.
There can be fatal consequences suggested by studies of non-human animals into sleep deprivation. Rechtschaffen et al forced rats to stay physically active by rotating a disc they were standing on every time the rat began to fall asleep. The rats went on to die but this could be due to stress rather that sleep deprivation. Suggesting that the research is unethical.
The main conclusion of research conducted into the effects of sleep deprivation is that a combined approach of the restoration and evolutionary explanations would be most beneficial.
Describe and evaluate explanations of insomnia
Sleep disorders are any conditions that involve difficulty experienced when sleeping. Insomnia is a condition where there are problems falling asleep and/or staying asleep. 50% of the population sometimes experience difficulty sleeping but only 5-10% are diagnosed.
There are two types of insomnia, known as primary and secondary. Primary insomnia is split into; learned insomnia (a form of anxiety induced insomnia, where, through classical conditioning some activities are associated with sleep, and through repetition these bedtime activities trigger arousal); idiopathic insomnia ( which occurs at a young age due to abnormalities in the brain mechanisms controlling the sleep/wake cycle).
Dauvillers et al. asked primary insomniacs to complete a clinical interview, psychometric questionnaire and a questionnaire on their family history on insomnia; a control group of non-insomniacs were similarly tested. Primary insomniacs reported 72.7% familial insomnia compared to 24.1% of non-insomniacs, suggesting a link between family history and primary insomnia.
And sleep-state misperception (where people sleep adequately but feel that they do not as some overestimate the time it takes them to fall asleep). Researchers suggest this results from and unclear perception of consciousness and difficulty distinguishing sleep from waking. Dement asked a patient who suffered from sleep insomnia to sleep for 10 nights in a sleep lab and they completed a questionnaire every morning where they reported taking 1-4 hours to fall in sleep when in fact on average they took no longer than 30 minutes.
There are real world applications for research into insomnia. One of the causes of primary insomnia is the person’s belief that they are going to have difficulty sleeping; this expectation becomes self-fulfilling as the person is then tense while trying to sleep. This can be treated by convincing the individual that the course of their difficulty lays somewhere else rather than in insomnia. Storms and Nisbett's study saw insomniacs given a pill that would either stimulate of sedate them so that this who expected arousal went to sleep faster as they attributed arousal to the pill therefore relaxing.
Also there are problems with generalising. This is because there are so many different types of insomnia attributed to so many different causes that it is nearly impossible to make generalisations that describe all causes of insomnia in Amy meaningful way. This therefore suggests that there is no straight forward explanation of the causes of insomnia.
In addition there have been issues raised as to the reliability of some findings from research into insomnia. Measures such as the structured sleep interview for sleep disorders are reliable when compared to sleep lab recordings but there is a disagreement between the interviewers over the symptom information given by patients. This therefore suggests that subjective self-reports should not be relied upon as they lack validity.
There is also secondary insomnia where the sleep disturbance is associated with a mental disorder or medical condition, this form is more common. Hormonal changes are more common in women. Medical conditions such as illness, such as asthma and Parkinson’s disease can also disrupt sleep Treatment of the underlying cause usually improves sleep, although sometimes treatment for insomnia is also required. Katz et al. studied insomniacs with chronic medical conditions found that 50% suffered from insomnia, 34% from a mild form, 16% from a severe form which supports that secondary insomnia comes from other conditions. Environmental factors including such as noise, light and temperature and poor sleep hygiene such as drinking caffeine before bed have a detrimental effect on sleep.
There are implications of treatment for primary and secondary insomnia. If insomnia is classed as a symptom of another disorder, it is important to treat the disorder rather than the insomnia. However, it is not simple to work out the cause of the person’s insomnia. Ohayon and Roth studied a large group of Europeans, finding that insomnia preceded mood disorders such as depression rather than followed them. Meaning it might be helpful to treat insomnia regardless of whether it is primary or secondary.
In addition a person may develop insomnia due to predisposing factors, precipitating factors and perpetual factors. An example for predisposing factors is a genetic vulnerability, Watson et all. found that 50% of the variance could be attributed to genetic factors may also lead to the development of insomnia such as insomniacs who are more likely to experience hyper arousal which makes it difficult to go to sleep. There are also events that could trigger the disorder, two individuals may experience the same stressors but only one will develop insomnia because of the predisposing factors (these are precipitating factors). Perpetuating factors are also important as they maintain insomnia even when the causes have been treated. Spielman and Glovinsky's proposed 3p model of insomnia increased the awareness of the risk factors of insomnia.
Discuss explanations of narcolepsy and sleepwalkin
Individuals suffering from narcolepsy experience sudden and uncontrollable attacks of sleep at irregular and unexpected times.
A classic symptom of narcolepsy is cataplexy (loss of muscle tone) which is similar to what happens during REM sleep. At night a narcoleptics REM is abnormal therefore, the explanation that narcolepsy was caused by a malfunction in the system regulating REM was proposed.
Vogel (1960) supported this explanation through observations of REM at the onset of sleep in a narcoleptic patient, even though it occurs more commonly later on in the first cycle of sleep stages. This was further supported by neuronal activity recordings in the brainstem of narcoleptic dogs. This research showed that cataplexy co-occurred with brain cell activity that usually only occurs during REM however, support from research in general isn’t convincing.
Another explanation for narcolepsy is that of a link between the neurotransmitter - hypocretin and the sleep disorder. Sakurai (2007) states that hypocretin regulates sleep and wakefulness through interactions with systems regulating emotions and homeostasis in the hypothalamus. There are normally 10,000-20,000 hypocretin producing cells within the hypothalamus but this number decreases significantly in narcoleptics resulting in low levels of hypocretin causing the regulation of sleep and wakefulness to become unstable.
The first evidence for hypocretins was provided by narcoleptic dogs with a mutation in a gene on chromosome 12. Lin et al (1999) claims that this mutation disrupts the processing of hypocretin. Findings from narcoleptic dogs have been confirmed by human studies as human narcoleptics have lower levels of hypocretin than normal in cerebrospinal fluid. This supports the view that lower levels of hypocretin play a role in narcolepsy.
However, as these low levels of neurotransmitter are implicated as a cause there is speculation over whether a dose of hypocretins will act as a cure. On the other hand, hypocretin is an unstable molecule so when given by injection it’s broken down before reaching the brain. Therefore, researchers are trying to create an artificial drug to replace the missing hypocretin in the brains of narcoleptics.
Sleepwalking is another disorder of sleep also called somnambulism, covering activities normally associated with wakefulness that take place while asleep, for example, eating.
An explanation for this is incomplete arousal. An individual suffering with sleepwalking is partly awake and asleep therefore, are difficult to wake. Recordings of brain activity taken during sleepwalking show both Delta waves (typical of SWS) and high frequency Beta waves (typical of an awake state) meaning that it looks like sleepwalking occurs when a person in deep sleep is awakened but arousal of the brain is incomplete.
There are also risk factors such as sleep deprivation, alcohol, fever, stress or psychiatric conditions which increase the likelihood of sleepwalking. However, risk factors only act as triggers e.g. hormonal changes during puberty meaning not all people are affected by them, suggesting that individuals have inherited a vulnerability for the disorder.
This is supported by the diathesis stress model which proposes that genes provide a vulnerability for the disorder but it will only occur during periods of stress. Zadira et al (2008) studied 40 patients referred to a sleep lab preventing them from falling asleep.On the first night 50% showed signs of sleepwalking which then rose to 90% on the second night. However, sleep deprivation doesn’t lead to sleepwalking in normal individuals therefore, sleep deprivation acted as a stressor in individuals with a vulnerability to the disorder.
There is also evidence to suggest that the tendency to sleepwalk is inherited. Broughton (1968) found that the prevalence of sleepwalking in first degree relatives of sleepwalkers e.g. parents and siblings is 10 times greater than the general population. This is further supported by twin studies conducted by Lecendreux et al (2003) who reported that there was a concordance rate of 50% in monozygotic twins compared to 10-15% in dizygotic twins, emphasising the prevalence in first degree relatives.
It has also been suggested that it is more common in children as they have more SWS than adults. Oliviero (2008) suggests that the system that normally inhibits motor activity in SWS is not significantly developed in adults as compared to normal controls, sleepwalkers show signs of immaturity in relevant neural circuits.
The concept that there is a psychological cause is unlikely as sleepwalking is believed to be a result of dreams representing trauma and anxiety but it usually occurs during SWS so, is therefore unlikely to be linked with dreaming.