Sleep walking (A01)
Sleep walking is a disorder of arousal - a person who is sleep walking is partly awake in the sense that they are engaged in activities normally associated with the waking state, but they are also asleep. Most importantly the individual is in deep sleep, (slow wave sleep) with most sleep walking occuring in stages 3 and 4 of sleep, which means that it is difficult to rouse the sleep walker. Sleep walkers are therefore not acting out a dream, but performing well rehearsed automatic responses. Lavie described a 6 year old boy who got out of bed during a sleep laboratory experiment and proceeded to walk as far as the EEG monitors would allow and wave his arms in the air. It later transpired that the boy was acting out a scene from a school play where he had been the sun.
There is evidence to suggest that the tendency to sleep walk may be inherited. For example, Broughton found that the occurence of sleep walking in first degree relatives of a subject is atleast ten times greater than the general population.
There is also evidence that certain stress factors appear to increase the likelihood of sleep walking such as sleep deprivation, alcohol and stress. The fact that risk factors only trigger some people suggests that some individuals may have inherited a vulnerability for sleep walking.
Sleep walking A02 research
Twin studies have also been used; Lecendreux reported a 50% concordance rate in identical twins compared to 10-15% in non identical twins and also identified a gener that may be critical in sleep walking.
Zadra et al carried out a study involving 40 sleepwalkers at a sleep research centre. They found a strong positive correlation between the amount of sleep deprivation and the occurence of sleep walking.
This was further supported by Dement's findings; he observed that sleep walking tends to begin at around 4 years old. This is also the time that children start to stop having naps and may therefore, in effect be sleep deprives.
This is when an individual falls instantly and involuntarily to sleep. The disorder effects approximately one in two thousand people. It is often associated with a sudden loss of muscle tone causing te person to collapse, slleeping for two to twenty minute, when the person awakes they feel completely refreshed. The individual goes immediatelt into REM sleep suggesting the disorder arises from poor control of the neural mechanisms that trigger REM sleep.
A genetic influence to the disorder has been suggested; the incidence of narcolepsy varies considerably between ethnic groups, eg in Europe it affects 0.05% of the populaion byt the % is nearer to 2% in Japan. This could be considered evidence to suggest that narcolepsy is the result of genetic differences that can be passed through families.
Most recently however, research has indicates a link between the neurotransmitter hypocretin and the disorder. Normally there are 10,000-20,000 hypocretin producing cells in the hypothalamus but in many narcleptics a large number of these cells are missing, resulting in low levels of hypocretin. Chemelli produced genetically modified animals with narcoleptic symptoms caused by an absences of hypocretin.
Narcolepsy - A02 research
- The idea that there is a genetic influence in the narcoleptic disorder has been widely disputed. Mignot et al conducted a study in 1998 and found that in cases where on twin had the disorder it was not found in the other. If there was a genetic factor in the causation of narcolpesy then we would expect to see the disorder in both twins. Therefore, this reduces the reliabilty to the theory that our genes can cause nacolepsy as research is not consistent.
- Mishmina et al provides supporting research to the idea that nacolepsy is related to the neurotransmitter hypocretin. They found that there were mutations to some of the genes in narcoleptic animals and hmans which are involved in the production of receptors for hypocretin.
Insomnia - A01
Insomnia is the inability to fall asleep or stay awake. It is defined by the individual's perception of sleep quality and quantity. There are two types to insomnia, primary; where the reason for not being able to sleep in unknown and secondary; where there is a known reason for not being able to sleep.
One idea associated with primary insomnia is a type of anxiety induced insomnia where a cycle is set up. As a person tries harder to sleep, they inturn become more anxious and this only prevent them from sleeping further, so when they try and sleep the next day they immediately feel anxious about sleeping and thus the cycle continues. This type of insomnia is thought to be associated with individuals having a preoccupation with sleeping, thus cognitive factors are involved.
Seconary insomnia is thought to have many influences, one such influence is the idea that individuals have a genetic vulnerability to the disorder as so it is passed from parent to child. Another influence in the development of secondary insomnia has been associated with what food we eat. Lichstein et al asked a random sample of 772 participants to complete a sleep questionnare, to keep a sleep diary and to also report nutritional supplements that they were taking. It was found that those using vitamin supplements had poorer sleep rates of insomnia than those who did not.
Insomnia A02 research
MacMahon et al supports the idea that primary insomnia can be caused by a preoccupation with sleeping, thus cogntive factors. Using an independ group design, it was found that individuals with primary insomnia showed greater attention to sleep related stimuli that participants with deleayes sleep phase syndromes. It was concluded that cognitive factors are therefore important to this illness.
Beaulieu et al reported a 34% of insomniacs surveyed said they had a first degree relative who had, or had a history of having insomnia
Kahn found that children with a milk intolerance had increased sleep after eliminating milk from their diet.