- Secondary insomnia has a medical, psychiatric or environmental cause. It is a symptom of the main problem, e.g. depression, shift work or caffeine.
- Peimary insomnia occurs on its own with no know physical cause, though the individual may feel stressed or depressed too. It may arise from bad sleep habits (e.g. sleeping with a light on) or the cause may have gone away but the insomnia persists because sleep probelms are anticipated.
- Th expectation of insmnia is self-fulfilling because trying to sleep is stressful.
- A treatment based on attribution theory shifts the insomniac's attribution of their problem from 'insomnia' to another cause (Storms and Nisbett).
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- Insomnia more often precedes than follows mood disorder (Ohayon and Roth) so treating as cause or consequence is important.
- Predisposing factors shown in twin studies as 50% of the variance in risk for insomnia appears to be genetic (Watson et al).
- Predisposition may be linked to physiological factors, as insomniacs more likely to have hyperarousal (Bonnet and Arand), making getting to sleep harder.
- Predisposing factors alone cannot explain chronic primary insomnia. The diathesis-stress model suggests environmental stressors are also needed to precipitate episodes of insomnia.
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- During SW, the EEG shows delta waves (typical of SWS) and beta waves (like being awake).
- SW may ahppen when someone is worken from deep sleep but arousal of the brain is incomplete. This abnormal arousal is probably genetic.
- Children have more SWS than adults, explaining why SW is more common when young.
- Oliviero suggests that insufficient amounts of GABA (due to underdeveloped system) means that motor activity is not inhibited during SWS. Adult sleepwalkers do appear to have less mature neural circuits that control motor exictability when awake tha controls (Oliviero et al).
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- Diathesis-stress can explain SW. Genetic predisposition provides the 'diathesis' (vulnerability) as first-degreee relatives pf sufferers are ten times more likely to SW than the population (Broughton). Also, concordance is 50% in MZ but only 10-15% in DZs, and a gene which is important in SW has been found (Lecendreux et al).
- The 'stress' is represented by environmental factors, such as frequent nightly awakenings.
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- Regulation of REM sleep was an early suggestion. This would explain symptoms such as cataplexy (like paralysis in REM) and hallucinations.
- A mutation of the immune system may be a cuase, leading to an increase of human leukocyte antigen (HLA) found in narcoleptic patients (Honda et al).
- Disrupted processing of the neurotransmitter hypocretin (orexin) may be cause, which normally helps keep us awake. Narcoleptic dogs with a mutation on chromosome 12 have disrupted hypocretin processing (Lin et al).
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- The REM hypothesis was suggested because normal sleepers enter stage 1 sleep first weheras narcoleptics fall straight into REM (Vogel).
- Recordings from the brainstems of narcoleptic dogs show that cataplexy is linked to the activation of cells normally only atcive during REM sleep (Siegel et al)
- HLA explanation isn't sufficient because not all narcoleptics have HLA variant and it is fairly common in non-narcoleptics (Mignot et al).
- Hypocretins have been found to be low in human narcoleptics (Nishino et al).
- There is no evidence that low hypocretin levels are inherited (Mignot). Low levels may be due to brain injury, infection diet, stress or an autoimmune attack. An autoimmune attack would also explain the HLA-narcolepsy link as HLA is important to the immune response (Mignot)
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