Disorders of sleep
- Created by: Olivia Swain
- Created on: 15-05-13 15:52
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- Disorders of sleep
- 4. Narcolepsy - hypocretin deficiency. Linked to cataplexy. Inappropriate intrusion of REM sleep, an immunological dysfunction and low levels of neurotransmitter hypocretin. Dramatic increase in activity of the medulla.
- 8. KLS - not much is known. KLS may be caused by a problem with the immune system triggered by viruses, e.g. flu.
- 3. Insomnias - primary, secondary, fatal familial insomnia.
- STUDY 6 - Thannickal et al (found scarring in the areas of brain where narcoleptics are missing hypocretin neurones. Further suggests that narcoleptic brains have been damaged - immune system attacking?
- 7. Possible explanation for narcolepsy and cataplexy: patients versions of HLA cause their immune system to damage hypocretin neurones, resulting in low levels of hypocretin and innappropriate action of the medulla and inappropriate intrusion of REM paralysis.
- 2. Sleep disorders - hypersomnias, narcolepsy, Kleine-Levin Syndrome, hypersomnia without hypocretin deficiency.
- 1. Real world context - insomnias can affects general health, mood and cognitive capacity. Understand what's causing disorders.
- 6. Immune system - several types of immune system exist. They are controlled by a set of genes called the Human Leukocyte Antigen.
- 5. Hypocretin - produced by the hypothalamus and is involved in controlling a wide range of bodily functions e.g. weight control.
- STUDY 2 - Schenkel and Siegel (damage to the medulla causes cats to move around in their sleep. When the medulla is damaged the cats are not paralysed which shows the medulla controls movement during sleep.
- STUDY 1 - Siegel et al (the area of the medulla activated during cataplexy in dogs is the same as that activated during sleep. The medulla is involved with narcolepsy and cataplexy.
- STUDY 5 - Thannickal et al (post mortems on 16 naroleptic brains showed 10% of the normal hypocretin neurones. Explains why low levels of hypocretin are produced. Maybe you're born with it? Or were they damaged?
- STUDY 4 - Mignot et al (found that people with a mutated HLA are not all narcoleptic. Evidence that the version of the immune system is not simple as not everyone with the immune system is affected.
- STUDY 3 - Honda et al (found an unusual HLA in 100% japanese narcoleptics and the same in 40% non-narcoleptics. Results significant. Link between HLA and narolepsy, those who are narcoleptic all have the same HLA. But some people have the HLA and are non-narcoleptic so another factor must be causing the 100%
- 9. Diathesis stress - predisposing factor and a trigger. Spielman and Glovinsky = PPP.
- STUDY 1 - Watson et al (studied 1042 MZ twins and found 47% concordance rate for insomnia. 15% in DZ. Shows that insomnia is genetic amongst MZ twins but caused by other factors for DZ. Only 47% not 100%!
- STUDY 3 - Wolfson and Carskadon (adolescents' circadian rhythm is altered with the onset of sleep much later in the evening than adults. As teens start the day at the same time as adults it results in sleep deficit or insomnia. Supoprts the notion that teens are predisposed to insomnia. Non-scientific.
- STUDY 5 - Tang and Harvey (used an actigraph to show primary insomniacs that they overestimate the time taken to fall asleep. These patients became better at falling asleep. Patients who are reassured improved sleep as the perpetuating factor is gone.
- STUDY 4 - Woods et al (demonstrated that insomniacs paid far greater attention to the clock than healthy volunteers. Evidence that primary insomniacs obsess about the time and perpetuate their insomnia.
- STUDY 2 - Garfinkel et al (gave elderly insomniacs melatonin which improved sleep quality. Old age predisposes people to primary insomnia as melatonin increases sleep.
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