1. Disorders of sleep

2. Links to the specification Explanations for sleep disorders, including insomnia, sleep walking and narcolepsy

3. Past exam questions Discuss explanations for insomnia and/or narcolepsy.(24 marks) Outline one explanation for narcolepsy. (4 marks) Outline one or more explanations for sleep disorders (e.g. insomnia, sleep walking, narcolepsy). (4 marks) Evaluate one or more explanations for sleep disorders.(16 marks)

4. Organisation By the end of this topic area, you will be able to: – Outline symptoms of insomnia, narcolepsy and sleepwalking – Outline explanations for insomnia, narcolepsy and sleepwalking – Evaluate explanations for insomnia, narcolepsy and sleepwalking – research evidence, methodological issues, IDA.

5. Independent work/Reaching the A* ‘Too stressed to sleep’ article Times article ‘If I collapse, a nudge from a little wet nose can save me’ Extension: A brief history of hypocretin/orexin and narcolepsy Summary questions AfL activity Cut and stick activity ‘Too stressed to sleep’ article Times article ‘If I collapse, a nudge from a little wet nose can save me’ Extension: A brief history of hypocretin/orexin and narcolepsy Summary questions AfL activity Cut and stick activity

6. Key terms/concepts InsomniaNarcolepsySomnambulismSleep Apnoea Primary insomniaSecondary insomnia CataplexySleep paralysis Hypnagogic hallucinations Restless leg syndrome ParasommniaApnoea StimulantsFatal familial insomnia GeneticNeural

7. Overview of explanations Insomnia – Hyper arousal, sleep apnoea Narcolepsy – Hypocretin and genetics Sleep walking – Genetic, neural

8. Did you know? Napoleon and Margaret Thatcher were both said to have functioned efficiently on 4-5 hours sleep per night. Albert Einstein slept around 10 hours a night. Jennifer Aniston has set off her burglar alarm with her sleepwalking

9. Insomnia (Somnabulism) Insomnia is the condition in which there are problems falling asleep and/or staying asleep, and the sleep that occurs tends not to be deep and is easily disturbed. Insomnia is also, unsurprisingly, linked with fatigue, having poor attention, impaired judgment, decreased performance, being irritable, and an increased risk of accidents. Insomnia is not a single condition as there are different forms based on the degrees of severity (mild, moderate, severe, acute, chronic) and the causes of the insomnia.

10. Primary and secondary insomnia Primary insomnia is the most common form of insomnia and has no clear underlying cause. There is a sleep problem, but there is no medical or psychiatric cause, and it is likely that the sleep problem is the result of maladaptive behaviours or learning. Secondary insomnia is insomnia that has a specific cause. Examples of such causes include sleep apnoea, restless legs syndrome (RLS), circadian rhythm disorders due to night shiftwork, and various medical, substance use, and emotional problems. Sometimes difficult to distinguish between both types.

11. Hyper arousal hypothesis This hypothesis suggests that insomniacs display a level of physiological arousal that is incompatible with the initiation and/or maintenance of sleep. In other words, their body chemicals (hormones and/or neurotransmitters) prevent them from falling asleep and/or staying asleep for the whole night.

12. Evidence for the hyper arousal hypothesis Vgontzas et al (2001) – higher levels of ACTH (a stress hormone related to arousal) in insomniacs. Nofzinger et al (2004) – the usual decrease in brain activity in some areas of the brain in sleep is not present in insomniacs so, even when asleep, insomniacs are still aroused. Winkelman et al (2008) – those with persistent insomnia showed reduced levels of GABA, (a neurotransmitter associated with reduced brain activity). They appear not to be able to ‘switch off’ at night.

13. Sleep apnoea explanation The cessation of airflow during sleep. Prevents air from entering the lungs. Caused by an obstruction which narrows the airway. Breathing may stop for up to a minute, causing blood oxygen levels to drop – person partially awakes. Possible causes include being overweight, enlarged adenoids or tonsils, excessive alcohol, sedative drugs or strong painkillers. Becomes clinically significant if lasts more than 10 seconds each time and occurs more than 10 times every hour.

14. Evidence for the sleep apnoea explanation Luyster et al (2010) – Up to 58% of patients with obstructive sleep apnoea (OSA) suffer from insomnia. When patients were treated for OSA, their insomnia improved, suggesting that it was at least partially to blame. However, a combination of treatment for OSA and CBT for psychological symptoms was most effective, suggesting that both physiological and psychological factors play a part.

15. General evaluation of insomnia research Very often diagnosis of insomnia is based on self- report. However, a lot of research suggests that patients claiming to be insomniac are in fact getting far more sleep than they believe. Lack of validity? Insomnia is very complex and unlikely to be able to be explained by one factor. So because of the large number of factors insomnia could be linked to, it makes it difficult to conduct meaningful, reliable research because research tends to find only small effects. This means research is unlikely to provide one clear explanation/solution for insomnia.

16. Narcolepsy Narcolepsy is a chronic brain disorder that involves poor control of sleep-wake cycles. People with narcolepsy experience periods of extreme daytime sleepiness and sudden, irresistible bouts of sleep that can strike at any time. These “sleep attacks” usually last a few seconds to several minutes. Narcolepsy can greatly affect daily activities. People may unwillingly fall asleep while at work or at school, when having a conversation, playing a game, eating a meal, or, most dangerously, when driving or operating other types of machinery.

17. Types of narcolepsy Narcolepsy with cataplexy – This type of narcolepsy involves a combination of excessive daytime sleepiness and cataplexy. Cataplexy is when you have attacks that cause a sudden loss of muscle tone while you are awake. It may lead to slurred speech and buckling knees, or in more severe cases complete paralysis. These events are usually triggered by strong emotions such as joy, surprise, laughter or anger.

18. Types of narcolepsy Narcolepsy without cataplexy – This type of narcolepsy occurs when you have continuous excessive sleepiness but no cataplexy. You may take a nap for a couple of hours and wake up feeling refreshed. But after a short time, you feel tired again. Sleep paralysis and hallucinations are other common symptoms of both types of narcolepsy.

19. The hypocretin explanation It is known that severe disruption of the normal sleep- wake cycle is responsible for the symptoms in narcolepsy. Abnormalities of REM or dream sleep are particularly important. A neurotransmitters known as hypocretin or orexin is normally responsible for controlling the sleep-wake cycle by maintaining stable wakefulness and preventing the onset of sleep during the day. The cells containing hypocretin are found in an area of the brain known as the hypothalamus and extend to other parts of the brain that are known to be involved in wake and sleep regulation.

20. Most narcolepsy sufferers, however, have undetectable or low levels of hypocretin which leads to the disruption of the sleep-wake cycle. Hypocretin is produced in the hypothalamus. Research suggests that the low number of cells containing hypocretin is caused by the body's immune system that normally attacks infections destroying the hypocretin cells by mistake and that narcolepsy is a so-called autoimmune disease. The hypocretin explanation

21. Evidence for the hypocretin explanation The first evidence for the role of hypocretin in narcolepsy came from narcoleptic dogs who had a mutation in a gene on Chromosome 12, which disrupted the processing of the hypocretin (Lin et al, 1999). Later research showed the injections of hypocretin in dogs reversed their narcolepsy.

22. Evidence for the hypocretin explanation Scammell et al (2001) – a case study of a 23-year- old with a damaged hypothalamus who suffered with narcolepsy showed reduced hypocretin. Nishino et al (2000) - found that human narcoleptics have lower levels of hypocretin in their cerebrospinal fluid. Siegel et al (2000) – compared brains of narcoleptics and controls (post mortem) and found that the number of brain cells containing the hypocretin was reduced by 85-95% in people with narcolepsy.

23. Evaluation of the hypocretin explanation Drugs that increase hypocretin levels should, in theory, help treat narcolepsy, but such drugs are not yet available. Low or undetectable levels of hypocretin are found in most patients but some have normal or raised levels. Ebrahim (2002) - suggested there are two variants of narcolepsy. In most patients there seems to be a hypocretin deficiency but there may also be a form with ‘hypocretin resistance’ due to abnormal hypocretin receptors.

24. The genetic explanation Research has shown that there may be a genetic link to narcolepsy. The genetic explanation is really an extension of the hypocretin explanation for narcolepsy. In other words, it is thought that low levels of hypocretin are genetically determined – probably through a mutation in a gene on Chromosome 12, which disrupts the processing of the hypocretin (Lin et al, 1999).

25. Evaluation of the genetic explanation Nishino et al (2000) found a concordance rate of 25-31% in MZ twins, compared to a rate of approximately 0.05% of the population worldwide. But… not 100% concordance rate – role of environment? Carrying a gene for narcolepsy does not necessarily mean that a person will develop the disorder.

26. Evaluation of the genetic explanation Picchioni et al (2007) found that exposure to extreme stress and influenza, particularly before puberty, increased the risk of developing narcolepsy. Many narcoleptics do not have a family history of the disorder. Lin’s research with dogs – genetic defect on chromosome 12 not found in humans.

27. Sleepwalking Very common type of parasomnia, Latin for near sleep. Affects 1- 17% of children, some estimates up to 50%. More frequently seen in boys. Incidents of SW decrease with age. Approx 10% of adults sleep walk. Sleepwalkers unaware of their activity, and tend to be hard to wake, even though they may have their eyes open. Remember little of nothing of sleepwalking episodes. Usually occurs during deep NREM sleep (stages 3/4), early in the night.

28. Genetic explanation – Sleep walking It is suggested that sleep walking is a disorder of arousal. EEG recordings made during sleep walking show a mixture of delta waves which are typical of SWS, plus the higher frequency beta waves which are characteristic of the awake state. It looks as if sleep walking occurs when a person in SWS is awakened, but the arousal of the brain is incomplete. It is likely that this abnormal arousal is genetic.

29. Evidence for genetic explanations Bassetti (2002) – 74 patients diagnosed with adult SW. Of 16, who underwent genetic testing, 50% had a specific gene that was present in only 24% of healthy NSW people. The gene HLA DQB1*05 is one of the family of genes producing proteins called HLA, which are involved in regulating the immune system (the same gene implicated in narcolepsy).

30. Evaluation of genetic explanation In Bassetti’s study, half of the sleepwalkers did not have the HLA gene abnormality. Similarly, a quarter of his sample had the gene but were not sleepwalkers (control group). Environmental factors/diathesis stress? Zadra et al (2008) – conducted a lab study on 40 SWs. The P’s were not allowed to go to sleep. On the first night, 50% of the sleepwalkers showed signs of SW, which then increased to 90% on the second night. This suggests sleep deprivation acted as a “stressor” in individuals who had _________ for sleep walking.

31. Neural explanation Oliviero (2008) – during normal sleep the chemical messenger gamma-aminobutyric acid (GABA) acts as an inhibitor that stifles the activity of the brain’s motor system. In children the neurons that release this neurotransmitter are still developing and have not yet fully established a network of connections to keep motor activity under control.

32. Neural explanation As a result, many children have insufficient amounts of GABA, leaving their motor neurons capable of commanding the body to move even during sleep. In some, this inhibitory system may remain underdeveloped—or be rendered less effective by environmental factors—and sleepwalking can persist into adulthood – it is likely that this tendency is genetic.

33. Evaluation of the neural explanation Oliviero found that, compared to controls, sleepwalkers showed signs of immaturity in the neural circuits associated with GABA, thus supporting the suggestion that sleepwalking occurs due to impairments in the inhibitory systems in the brains of SWs. Explains why sleepwalking is more common in children.