Explanations for Sleep Disorders Flashcards
What is insomnia?
This is the most prevalent sleep disorder and is characterised by inability to fall asleep, and/or waking during the night and having difficulty going back to sleep.
Discuss the genetic explanation for insomnia
Genetic factors may play a part in increasing susceptibility to such disruption. Evidence to support this idea comes from the fact that insomnia tends to run in families. For example a study in Quebec in 2007 by Beaulieu-Bonneau surveyed almost 1000 adults about their own sleep and that of close members. Those who suffered from insomnia were more likely than good sleepers to report that one or more of their family members also had sleep problems. This is consistent with the genetic explanation of insomnia.
However there are methodological problems with survey studies, as it could be that poor sleepers are simply more aware of sleep problems in others than are good sleepers. It may also be incorrect to assume that shared genes are the cause of family links in insomnia as this explanation does not take account of the myriad of other shared factors within families that could affect sleep patterns. Environmental factors such as shared night time routines or diet could play a role here. It is possible that families may share a learned insomnia effect rather than a genetic one.
One type of genetic insomnia is Fatal Familial Insomnia, which is a very rare prion disease caused by a genetic mutation. If one parent has the gene children have 50% chance of also having it. Carriers typically develop insomnia in their 40s and 50s due to accumulation of abnormal protein in the thalamus, which is involved in sleep regulation. Sufferers are unable to sleep at all, and usually dies within 18 months. Evidence for this comes from case studies, as this is such a rare disorder.
Discuss the anxiety explanation for insomnia
A further explanation for insomnia is anxiety. This may simply be the anxiety of anticipating another sleepless night and subsequent tiredness the next day. There may be a learned association between the stimulus of the bed, and the response of restlessness and anxiety, due to classical conditioning. This results from repeated pairings due to some initial insomnia, the cause of which may not be apparent.
Evidence that anxiety can explain insomnia, comes from the success of treatments which aim to break the association between bed and restlessness, such as Sleep Restriction Therapy. This works by ensuring that the individual does not sleep anywhere other than in bed, and does not go to bed until they are extremely tired. they are also required to get up at a set time each morning (usually after a very few hours in bed) even if they are sleeping. In this way a new association is set up between bed and sleeping, which is often effective in removing anxiety and therefore treating the insomnia. this provided good evidence that in these cases the insomnia can be explained by anxiety, and also shows a valuable real life application of this explanation for insomnia.
Further support for this idea comes from the finding that insomnia can result from many anxiety disorders such as OCD, and the very common experience of temporary insomnia in response to stressful situation. Therefore this explanation is high in face validity.
A longitudinal study by Gregory also provides evidence that anxiety is an important explanation for insomnia. A group of over 1000 children were followed from their birth in 1972 and it was found that there was a significant positive correlation between family conflict at ages 9 to 15 and insomnia at age 18. This seems to show that family conflict during childhood can increase anxiety and so lead to insomnia in young adulthood.
However we must be cautious in drawing firm conclusions from this study, as correlation does not show causation. It is possible that both family conflict and insomnia were caused by a third factor, such as genetics or child learning styles for example, and although the study did control for socio-economic status, health and depression, it is not possible to control for all possible factors in such correlational research. Additionally, the number of young people who did develop insomnia was small (15%) limiting our ability to draw generalised conclusions from this small sample. It is also true that although the correlation was significant it was not very strong, so we should probably conclude that anxiety may play a part in explaining insomnia, but there are almost certainly other important factors involved too.
Discuss the Circadian Rhythm Disruption for insomnia
A further explanation for some types of insomnia is circadian rhythm disorder, which is sleeplessness caused by disruption to the usual circadian patterns, often due to jet lag or shift work. Those who must work at night often struggle to sleep during the day despite extreme tiredness. The work of Czeisler has shown how this can be improved by adjusting shift patterns to phase delay rather than phase advance, and changing every three weeks. This is a valuable real life application of our understanding of this cause of insomnia which has had significant benefits (in terms of health, job satisfaction and productivity) for thousands of shift workers and the companies that they work for.
What is Narcolepsy?
The main symptom of Narcolepsy is excessive and extreme day time sleepiness. That can occur suddenly such as whilst eating or even ski-ing but is often triggered by sudden strong emotion. sleep usually last between a few seconds and around 20 minutes, although the sleep is usually easily aroused. The disorder usually starts in late teens or early adulthood.
Discuss the genetic explanation for narcolepsy
There is some evidence for a genetic explanation for Narcolepsy. Certain breeds of dog show inherited narcolepsy and so have been bred specially to research this disorder. In some Doberman Pinschers a genetic mutation on chromosome 12 can cause narcolepsy due to reduced levels of the neurotransmitter orexin. Unfortunately subsequent research has show that this genetic defect does not apply to humans. This clearly demonstrated the practical problems in attempting to develop insights into human conditions from research on animals. Even when investigating shared disorders in other mammals we can never be sure that it will be possible to generalise to humans from research carried out on other species.
Although there is some evidence for family links in narcolepsy, the fact that this seems to be the exception rather then the rule, casts doubt on the genetic explanation. Most narcoleptics do not have relatives with the disorder. A study of 16 pairs of identical twins, at least one of whom had narcolepsy found that only 4 out of the 16 co-twins were also sufferers. This low concordance rate (25%) suggests that genes may play some role in increasing susceptibility to narcolepsy, but there must also be other important environmental triggers, such as trauma or infection, probably causing damage to the hypothalamus.
discuss the neurochemical explanation for narcolepsy
A second linked explanation for narcolepsy is that it results from insufficient orexin in the brain.
There is very strong evidence for this explanation as 90% of narcopleptics show such low levels of orexin that is virtually undetectable. This seems to result from a reduced number of orexin producing cells in the hypothalamus. It is possible that these cells may be destroyed by an auto-immune response, possible triggered by infection, where the body’s immune system mistakenly attacks its own body cells. Evidence for this is that high levels of Human Leucocyte Antigen (HLA) gene are found in narcoleptics.
Further support comes from Gerashchenko - who destroyed certain hypothalamus cells in rats which led to reduced production of orexin and symptoms of narcolespy.
Furthermore, Parkinson’s disease sufferers also provide support for the role of orexin. they often show sleep disturbance that is very similar to narcolepsy, and post mortems have found loss of 62% of orexin containing cells in Parkinson’s sufferers’ brains. Reduced levels of orexin are also found in samples of cerebro spinal fluid from parkinson’s patients. This evidence provides very strong support for the idea that lack of orexin is an important explanation for the suddden sleepiness experienced in narcolepsy.
These physiological approaches to explaining narcolepsy could be seen as limited as they fail to consider an individual’s life style, environment and learning experiences in addition to the biochemical make up of their brain. However it may be that in the case of narcolespy it is appropriate to take this approach. So there is little if any evidence that the disorder is influenced by broader lifestyle issues.
A potential strength of the physiological appraoch is that it has important real life application in terms of treatment for narcolepsy. New research (Weinhold et al) shows that an orexin nasal spray hold promise as a treatment for common symptoms of narcolepsy. 14 narcoleptic participants received either a nasal spray containing orexin or a placebo. Those who received the orexin spray had fewer daytime sleep episodes than those who received the placebo. This early evidence holds exciting possibilities to significantly improve the lives of those who suffer with this sleep disorder.
What is sleepwalking?
Sleepwalking usually occurs early in the night, in Slow Wave (stage 3 and 4) sleep, and is more common in children than adults. The causes of sleepwalking are are not fully understood. Studies have shown that frequent sleepwalking is associated with sleep deprivation, fever, stress and taking drugs, especially sedatives, hypnotics, anti-psychotics, stimulants and antihistamines. Estimates of the prevalence of childhood sleepwalking vary from 3% to 30% and up to 4% of adults in the general population.
Explain the psychodynamic explanation for sleepwalking
Some of the earliest explanations of sleepwalking were psychodynamic, focusing on the idea that sleepwalking is the expression of repressed unconscious conflicts. The sleepwalker is, in effect ‘acting out’ repressed conflicts and may engage in institutional behaviours which their waking ego and superego would otherwise restrict. The later finding that sleepwalking occurs during SWS was seen to support this theory, since the conditions of SWS are ideal for this to happen - the likelihood of recalling such behaviours is minimal during this phase of sleep. Psychodynamic explanations for sleepwalking can look superficially convincing, particularly as anecdotal evidence suggest sleepwalkers frequently indulge in behaviours that may represent instinctive id urges whilst sleepwalking (eating, having sex, aggressive outbursts etc). Unfortunately however, the theory does not lead to hypotheses that can be tested using objective scientific methods and there is no scientific evidence to support this explanation. This is clearly a limitation of this approach and most researchers in this area now agree that the disorder is a result of underlying biological mechanisms.
Explain the genetic explanation of sleepwalking
Sleepwalking tends to run in families, suggesting a genetic cause i.e. gened may be inherited from parents which predispose an individual toward sleepwalking. There is some evidence that sleepwalking may be genetic. For example, Bakwin - studies the frequency of sleepwalking in 19 MZ and 14 DZ twins: he found a concordance rate in monozygotic twins of 47% compared with 7% in dizygotic twins. This supports a partial genetic factor in sleepwalking. He found much greater likelihood (10x) of sleepwalking in first-degree relatives of an affected individual, compared with the genetic population. However, the exact nature of the genes underlying sleepwalking is as yet unclear. Bassetti - suggests it may be related to the HLA gene, associated with narcolepsy. 50% of sleepwalkers had a particular version of this gene compared to 24% of non-sleepwalkers. However, this doesn’t explain sleepwalking in half of his participants without this variant of the gene, nor why 25% of his sample had it, but didn’t sleepwalk.
Explain the neurochemical explanation of sleepwalking
A second biological explanation for sleepwalking has been offered by neurochemical researchers. During normal sleep the neurotransmitter Gamma Amino Butyric Acid (GABA) inhibits the brain’s motor neurons and stops the sleeper from moving. Navarro et al - suggest that if there is insufficient GABA, either because the neurons that release it are under-developed (e.g. in children) or if other factors make it ineffective, motor neurons may cause the body to move even during sleep.
This was demonstrated in a study that examined the motor excitability of adult sleep walkers during wakefulness. Compared to normal controls, the sleepwalkers showed signs of immaturity in the relevant neural circuits.
A potential strength of the neurochemical explanations is that it had important real life applications in terms of treatment for sleepwalking. Benzodiazepines can be useful as they boost the action of GABA, thus inhibiting the activity of the sufferer’s brain and body and reducing sleepwalking. This can significantly reduce the risks for those who suffer with this sleep disorder.
This biological approach to explaining sleepwalking has advantages over psychodynamic explanations as it is a scientific approach where predictions can be made and tested through scientific investigation. However, the danger with this approach is that is ignores aspects of the situations that can be explained by more holistic explanations such as personality or unconscious psychodynamic factors. Therefore, this approach may offer an incomplete explanation of sleepwalking.
