Primary Insomnia The most common form No underlining cause(physiological/psychological Caused by maladaptive learnt behaviours Clinical characteristics suffered for at least a month not linked with any other sleep disorder or psychopathology Secondary Insomnia Has a specific cause Factors affecting insomnia Environmental Factors Stress Sleep hygiene/bedtime behaviour Illness Sleep Apnoea Obstructive Central Personality

Sleep Apnoea Obstructive brief interruptions during sleep = collapsed airway stopping breathing snoring loudly more common in obese people but is seen in children linked to impaired cognition Kumar found a reduction in brain tissue in the part of the brain responsible for memory circuits using MRI Macey found a small but significant reduction in brain neurons = oxygen deprivation Linked to cardiovascular function Goldbart found that in children aged months who had OSA suffered from cardiovascular strain leading to impaired function which improved with the removal of the adenoids In children enlarged tonsils and adenoids are linked to OSA Mitchel found that after removal children who had previously had 40 episodes a night only had 5/6 episodes a night Central periods of not breathing during sleep = faulty mechanism in the brainstem not sending signals to the diaphragm and intercostals which are needed to breath White found that oxygen therapy has been found to reduce the effects and show mild improvement

Environmental Factors external stimuli interfere with the brains normal calming down of brain activity unfamiliar surrounding can increase brain activity therefore interfere with the calming down of the brain activity high altitudes mean that there is decreased oxygen levels than normal causing physiological distress increasing brain activity Sleep hygiene/ bedtime behaviour sleep hygiene = behaviours that promote the calming down of the brain ready for sleep poor sleep hygiene = behaviours which hinder this increasing the brain activity consuming alcohol, nicotine, caffeine sleep area is associated with stimulating activities such as watching tv prolonging sleep e.g. Another story, reading Stress Acute stress activate the SNS(stress response SAM) increasing brain activity. Normal brain activity should resume when stressor goes away Chronic stress – stressor persistists – SAM/HPA/Exhaustion(selye) insomnia persists and physiological harm may be caused

Personality People who are more likely to have a stress like personality are more likely to have insomnia Vergontaz found a link to insomnia and stress hormones, due to chronic stress HPA – hyperarousal of CNS interferes with the decreasing of brain activity leading up to sleep Straub hypothesised that serotonin activity linked to temperament and insomnia. They found a +ve link to sleep latency and harm avoidance Leblanc found a link to insomnia and several psychological disorders such as depression Suggests that maybe treatment of these psychological disorders may have a knock on effect on sleep Monc found similar findings using a personality inventory, that neuroticism was linked to increased sleep latency Fatal Familial insomnia Strikes during middle age, no sleep A mutation in the brain leads to the formation of prions in the thalamus of the brain, causing it to form a sponge like structure and death within a year

Sample bias. The problem with research into obstructive sleep apnoea (OSA) is that the sample size is small, especially as the frequency of OSA in the Western world is only 5%. This means that there will always be methodological issues with interpreting the data and generalising it to the population of those with the disorder. Direction of effect. The problem with research into the factors affecting insomnia is that it is mainly correlational and so we cannot be sure of the direction of effect. Thus, rather than high stress hormone levels and CNS activity causing insomnia, it could be suggested that insomnia is causing the stress and arousal. Similarly, rather than day-time napping causing insomnia, the insomnia may be causing the day-time napping. In fact these relationships are likely to be two- directional, in that both the factors and the insomnia influence each other. Cause and effect. As the research into the factors is correlational it does not establish cause and effect. Thus, we cannot say that the factors cause insomnia only that they are linked, which limits the conclusions that can be made. Reductionism of correlations. Correlations are oversimplified because they only examine two variables when there may be other factors that affect the insomnia. Using normal samples instead of insomniacs. The participants in Monk et al.’s (2007) study into personality were not insomniacs but normal working adults, which limits what the study can tell us about insomnia! Self-report criticisms. The questionnaires in Monket al.’s (2007) study were all self-report, mail- in ones. The anonymity of the questionnaire can encourage greater accuracy of answers, and so internal validity (truth). However self-report is also subject to participant reactivity, which reduces internal validity because participants may have been influenced by what they supposed the researchers were looking for (demand characteristics) or by what they felt was socially desirable or even perhaps macho.

Sleep walking people assume that they sleepwalk with their eyes closed, but actually eyes open people are still able to function to an extent Fenwick et al. Found that people have been reported driving, and doing other dangerous stuff occurs in stage 3-4 of sleep early childhood going into puberty people often dont remember what they have done several factors have been linked to sleep-walking Horne found a genetic link to sleep walking Palambini investigated genetic link between RLS and sleepwalking. RLS is a genetic trait passed down, and sleepwalking was found to associate with it therefore suggesting the sleepwalking has a genetic cause Hublin investigated the genetic link through twin studies Finnish twins – prevalence of sleepwalking increased into adulthood with males but decreased with females from childhood Pilon found that anger and too much sleep were also linked as well as alcohol and caffiene There is a high percentage of injury and a low percentage of killing another person

Narcolepsy short naps between mins Linked with cataplexy = loss of muscle tone The neurotransmitter hypocretin thought to be linked with wakefulness Mignot found a mutation in narcoleptics for the receptor for hypocretin(a neurotransmitter which maintains wakefulness) Thannickal et al found that narcoleptics have over 80% less hypocretin neurones Narcolepsy may be caused by a genetic fault Mignot found in a twin study MZ twins has a 30% concordance rate with a much lower rate in first relatives There may be other neurotransmitters involved with narcolepsy Kim et al. Found that GABA lvl in narcoleptics were higher than that of the control group in the prefrontal cortex It has been linked with a mutation of the immune system Honda et al. Found an increased frequency of one type of antigen on the surface of WBC Mignot found that this wasn’t present in the majority of narcoleptics Biological explanations seem like the only explanation for narcolepsy, however some unsuccessful psychological explanations have been put forward Wiess et al. Suggested that the sudden bouts of sleepiness were to disguise sexual fantasies