Dyssomnias: problems with the amount, quality or timing of sleep, including insomnia and narcolepsy.
Parasomnias: Behavioural or physiological events that occur duing sleep, including sleep walking and nightmares. Parasomnias are rarely associated with daytime tiredness.
Generally, insomnia involves problems in falling asleep, maintaining sleep, and reduction in sleep quality - meaning it can lead to daytime tiredness which can then affect work and social functioning.
Is chronic insomnia in the absence of any psychological or physical condition that might explain the disorder. The most severe form is idopathic insomnia which begins in childhood and is lifelong, but is extremely rare. It doesn't seem to be linked with anxiety or arousal and people learn to live with it reasonably well. It is sometimes associated with high levels of depression.
Primary insomnia is more common in people with higher than average levels of anxiety. Anxiety can affect a sensitive sleep control system and therefore lead to insomnia. Arousal is incompatible with sleep. High levels of arousal probably interfere with the brain's complex sleep mechanisms. Vgontzas et al found that insomniacs have increased levels of ACTH and cotisol (linked to long term stress).
With this, you cannot establish cause and effect. Techniques to reduce arousal are usually effective.
Brain mechanisms of sleep
Sleep mechanisms are complicated and involve an interaction between endogenous pacemakers and exogenous zeitgebers as well as the release of neurotransmitters e.g. melatonin which help us to control our sleep patterns.
Secondary insomnia is chronic insomnia that can be explained by a pre-existing psychological or physical condition. Other sleep related phenomena such as sleepwalking and sleep apnoea can lead to insomnia.
Explanations for secondary insomnia:
- Psychological disorders: e.g. depression, anxiety states and schizophrenia. 40% of patients seeking treatment for insomnia have an associated psychological disorder (Morin et al)
- Heart failure, asthma and Parkinson's disease can lead to insomnia. Some treatments can lead to insomnia e.g. the use of steroids for treating asthma
- Drug use can lead to insomnia e.g. amphetamines and alcohol (stimulants) and overuse of sleeping pills can lead to disrupted sleep patterns and increased insomnia
- Fatal familia insomnia: a rare genetic condition where a person sleeps normally until around middle age, then severe insomnia develops which eventually leads to death. It is associated with the loss of brain neurons.
- Neuroticism: is significantly corellated with anxiety. Vahtera et al found that vulnerability to sleep disorders following traumatic life events e.g. divorce is highly correlated with the personality trait of anxiety
- Chronotype: some people are aroused, alert and functioning well in the morning (larks) and others function well in the evenings (owls). The difference between these two types is probably genetic and based in the biological circadian rhythm of sleep and waking. The circadian rhythm of larks is 2 hours ahead of owls (Kerkhod and Van Dongen). As circadian rhythms, controlled by our endogenous pacemakers, control our sleep walking behaviour, arousal levels and alertness, larks and owls will peak and different times of the day.
These patterns are stable over time and represent a distinctive personality trait. These patterns are controlled by our biological clocks, which in turn, are controlled by our 'clock' genes on our chromosomes.
The chronotype is probably genetically determined. How much you sleep, your N/REM cycle, vulnerability to narcolepsy and nightmares, although may be genetic, research suggests there may be environmental influence (Van Dongen et al). However, if your inbuilt tendency is to be a lark/owl, it is best to go with it rather than fight against it, as this could then lead to sleep disorders.
Apnoea is a disorder where a person stops breathing while asleep. The pauses may last from a few seconds to minutes, and may occur 5 – 30 times an hour, therefore having a major disruptive effect on sleep, causing someone to keep waking throughout the night and leading to daytime sleepiness - insomnia. Obstructive Sleep Apnoea is caused by airways being obstructed in some way – narrowing airways or enlarged tissue at the back of the mouth or tonsils. OSA is also linked with obesity (narrows airways). Mild bouts of sleep apnoea are very common in people who snore. Central Sleep Apnoea is linked with heart problems and is probably caused by a malfunction in the brain’s control of the respiratory and heart functions.
Research into Insomnia
Gregory et al 2006 carried out a longitudinal study in New Zealand to investigate the relationship between family conflict and later development of insomnia.
1,000 children born in 1972 were followed up from birth to 2006. One of the variables studied was level of family conflict. This was assessed using questionnaires measuring tension, hostility, distress and experiences such as separation and divorce. Factors such as socio-economic status, gender, health and depression were controlled.
Gregory et al found the amount of family conflict experienced between age 9 and 15 was significantly correlated with the frequency of insomnia at age 18.
They concluded that there is a possible relationship between family conflict and later sleep problems. They suggested that insecurity may lead to high levels of anxiety and a tendency to focus on family difficulties – which fits in with research that shows insomnia is often linked to high levels of anxiety.
- As the study began when the children were born, parental consent would have been needed. Once they were 16, they could give their own informed consent.
- Information was gained through interviews and questionnaires, some of which may have included intrusive personal questions, so right to withdraw would have been given.
- Although a large study, the actual incidence of insomnia at age 18 was only 15%, mostly females. This is a relatively small group in which to study the effects of so many variables.
- The study was correlational, so cannot determine cause and effect. It could be that family conflict and insomnia are both influenced by some factor not measured in the study eg personality characteristics
Jansson-Frojmark and Lindbolm
Jansson-Frojmark and Lindbolm investigated the relationships between depression, anxiety and insomnia and discovered that there was a link, although it seems that depression and anxiety could be both a cause and an effect of insomnia.
Explanations for other sleep disorders
Sleep walking is a parasomnia – it happens during sleep but doesn’t result in severe insomnia or daytime sleepiness. Sleepwalking tends to occur in NREM 3 and 4 early in the night. It cannot happen in REM as muscles are paralysed.
This suggests that someone has a desire to sleep where they did as a child – but this doesn’t explain the automatic acts the sleepwalker carries out – making tea, cleaning etc. Freud also suggests that we have unconscious anxieties during REM sleep. When we move from REM to NREM phases we are unable to work through these anxieties, so unconscious energies spill over into NREM and are channelled into motor activities such as sleepwalking.
However this explanation cannot be experimentally tested - unfalsifiable.
Bakwin studied the frequency of sleep walking in 19 MZ and 14 DZ twins and found a concordance rate of 47% in MZ twins and 7% in DZ twins – which supports the genetic explanation, although as concordance is not 100%, there must be environmental factors involved. He also found a tendency within families for sleep walking – far more siblings of MZ sleep walkers, walked in their sleep than would be expected from the general population.
Hublin et al carried out a Finnish study of over 11,000 participants all aged between 33 and 60yrs. They each answered questions about the frequency of sleepwalking both in childhood and adulthood. They found that in males there was a genetic influence of 66% in childhood and 80% in adulthood and in females there was a genetic influence of 57% in childhood and 36% in adulthood.
Large sample size of males and females; Only Finnish; Retrospective, may not remember; Reductionist as it simplifies sleepwalking to be caused by genetic factors alone. Focus on nature and biological
Narcolepsy usually begins in adolescence or early adulthood and continues throughout life. About 1 in 2000 people are sufferers – but many people are undiagnosed where only minor symptoms are present.
REM System Malfunction:
It is thought that there may be a malfunction in the system that regulates REM sleep and that REM breaks through in to wakefulness. This explanation does help to understand some of the symptoms of narcolepsy:
- Cataplexy (loss of muscle tone whilst conscious) is something also experienced during REM sleep.
- Sleep Paralysis (involves an inability to move and occurs at the start or end of sleep and is accompanied by hypnagogic hallucinations - like awake but dreaming). During REM sleep the body is paralysed and dreaming occurs.
- Sleep Stages In addition, the sleep pattern of narcoleptics is not the same as it is for most of us. We usually go through stages before going in to REM sleep, but narcoleptics fall straight into REM.
- Extreme Daytime Tiredness This also means that they have limited NREM and therefore may also explain why narcoleptics experience extreme daytime tiredness.
Siegel has supported this explanation based on findings of studies with narcoleptic dogs. It was found that cataplexy is linked to the activation of cells that would usually only be activated in REM sleep.
- Findings based on dogs, therefore difficult to generalise such to humans.
- Reductionist to assume narcolepsy is only caused by simple activation of cells and malfunction in REM systems as it does not take in to account other important factors. Focus on nature and biological causes.
Link between orexin and narcolepsy:
It is believed that a lack of orexin (a neurotrasmitter) or its receptors may be responsible for narcolepsy in humans. Thannickal, Moore & Niehuis (2000) found that orexin producing cells in the hypothalamus are reduced in people with narcolepsy. Wickens (2005) also found that orexin is involved in controlling REM sleep.
Evidence has also come from narcoleptic dogs. Some dogs have a tendency towards cataplexy, especially when excited and they also fall straight into REM. By selective breeding it was found that a gene defect is responsible – the gene responsible for regulating brain receptors for orexin.
Nishino et al (2000) also found that narcoleptic humans had low levels of orexin in their cerebrospinal fluid.
However evidence for a genetic explanation of narcolepsy is not entirely supported. Narcolepsy usually develops during the teenage years, and whilst MZ twins have a higher concordance rate than DZ twins, it is still only 30%, which suggests there must be environmental factors involved as well.
- It is difficult to generalise findings of this research to humans, ALTHOUGH there is some supporting research on humans.
- Difficulty in determining cause and effect – does low levels of orexin lead to narcolepsy or does narcolepsy cause low levels of orexin.
- Selective breeding of animals is unethical.
- Reductionist to assume that narcolepsy is simply caused by an imbalance in a neurotransmitter. The focus is on nature as the causes are biological.