Sleep is a subject dear to all our hearts, so here is my current assignment. Please do not use this information as medical advice. It is only a brief summary of other people's research. Consult your doctor or psychologist if you have insomnia

1. Insomnia Describe the ways in which insomnia can be considered a biopsychosocial phenomenon and how its biopsychosocial phenomenology relates to its treatment in psychotherapy.

2. What is Good Sleep? Good sleep is natural. The body’s homeostatic and circadian processes default to good sleep. The good sleeper accurately interprets endogenous cues for sleep readiness (physical and mental fatigue), and these interact reciprocally with exogenous cues in the environment (e.g., darkness). Sleep occurs through physiological and cognitive de-arousal. The effective sleeper claims to sleep by ‘doing nothing’.

3. What is Insomnia? Insomnia probably arises when the natural de-arousal processes of normal sleep are inhibited. The theory is that over-arousal interacts with dysfunctional cognitions and habits to promote and maintain insomnia. 'Inhibition' is individual. It means however much inhibition outweighs the stability of the individual’s default sleep pattern. Insomniacs have higher beta and lower alpha amplitudes in their EEG. When asleep, they have more non-REM high-frequency EEG activity. Primary insomnia is the subjective difficulty (lasting for at least one month) of initiating or maintaining sleep, or of non-restorative sleep, which causes significant distress or impairment in social, occupational, or other important areas of functioning, and is not associated with another sleep, medical, or mental disorder (APA, 1994).

4. Psychological Correlates of Insomnia Factors that maintain cerebral arousal are the key correlates of insomnia. Affect-laden thinking, worry, introspection, unsuccessful emotional processing. Verbal activity, e.g., reading, problem-solving. (Mental images of the same ideas do not inhibit sleep.) Worry about sleep; trying to sleep; selective attention to noise or body sensations; attempts to ‘stop thinking’; wrong expectations about the nature of sleep.

5. Biological Correlates of Insomnia Biological factors can ‘cause’ insomnia, but probably only because they cause cerebral arousal. Insomnia is more common in the elderly. Homeostatic drive declines with age, when disturbances of the sleep-wake schedule are less well tolerated. Insomnia is often comorbid with physical illness, chronic pain, psychological illness or another parasomnia. However, comorbid insomnia does not necessarily remit with the treatment of the other disorder. The majority of insomnia patients have persistent primary insomnia.

6. Biological Correlates of Insomnia Alcohol can make it easier to fall asleep; but after the initial sedative effect diminishes, sleep becomes fragmented, shortened and shallow. Caffeine and tobacco consumption inhibits sleep. Digestion inhibits sleep, but so does going to bed hungry. The evening meal should be 3-4 hours before bedtime. Vigorous exercise close to bedtime inhibits sleep. However, cardio-vascular exercise at other times decreases sleep difficulties, decreases the time needed to fall asleep and increases the amount of time spent in deep sleep.

7. Social Correlates of Insomnia Environmental factors can inhibit sleep, but again, probably because they cause cognitive arousal. Lifestyle, e.g., late night parties or shift work. Stressful life events such as bereavement or job loss. Sensory distractions: light, noise, temperature, humidity, uncomfortable bedding. Conditioning to a non-sleep environment or to performing non-sleep activities in bed. Yet good sleepers can do all these things without losing sleep! Some people seem to have a natural predisposition to poor sleep.

8. Treatment for Insomnia: Superficial Short-term insomnia caused by situational stress, medical disorders or circadian disruption (e.g., jet lag) is treated by: Dealing with the situational stress or treating the medical disorder. Educating the client about sleep and sleep hygiene. Sometimes by a short-term course of drugs. This is usually not sufficient to treat chronic insomnia (>4 weeks).

9. Biological TreatmentDrugs For short-term insomnia (<4 weeks), drugs are effective. Non-benzodiazepines such as Zolpidem are the preferred treatment, as trials indicate they are less likely to cause dependence, rebound insomnia or medication 'hangovers'. However, drugs remove the symptoms without treating the cause. Insomnia is likely to return as soon as the drugs are discontinued unless the cognitive arousal is dealt with in some other way.

11. Do not nap during the day.

12. Go to bed at the same time every night. Refuse tasks and social engagements that require a late night.

13. Eliminate sensory distractions, e.g., noise, light, heat, cold. Make the bed comfortable, e.g., pillow correct height.

15. Treatment for Insomnia: CBT As the issue of insomnia is primarily psychological, it would be expected that psychological treatments would be most effective. CBT is more effective than drugs. CBT is effective over the long term. Three-quarters of insomniacs who receive CBT improve. However, the overall improvement is only 50%. The effect size of CBT for insomnia is lower than that of CBT for other psychological disorders.

16. Treatment for Insomnia: CBT CBT aims at interrupting the vicious cycle.CBT strategies include: CT for sleep-interpreting processes. BT to reduce physiological arousal. CBT to reduce cognitivearousal. Dr Jim Horne isBritain’s best-known sleep expert. Tony Wright failed to review the literature and therefore did not remain awake long enough.

17. CBT: Sleep InterpretingCognitive Restructuring Cognitive restructuring for insomnia refutes the irrational belief that poor sleep leads to devastating consequences. It also shows that worry about sleep (or anything else) does not lead to positive consequences. The client constructs a list of all potential negative consequences of poor sleep then rates the odds of each consequence actually occurring. He calculates how often sleep is poor and how often these consequences have occurred. The clinician displays the large discrepancy between beliefs and actual outcome.

18. CBT: Sleep InterpretingFrom CT to CBT Reductions in unhelpful beliefs are associated with better treatment outcome. However, studies have shown that CT alone is not as effective as cognitive-behavioural combinations. Sometimes this CT leads to a poor sleep behavioural experiment. E.g., the client deliberately sets up a bad night’s sleep such as not spending long enough in bed, to show that minor sleep deprivation doesn’t cause disaster.

19. CBT: Physiological Arousal ReductionProgressive Muscle Relaxation PMR facilitates physiological de-arousal. It meets APA criteria for an empirically validated treatment. However, its real contribution to good sleep may be that it indirectly facilitates cognitive de-arousal. Some clinicians help clients make their own relaxation tapes rather than giving them the cognitive stress of remembering the instructions.

20. CBT: Physiological Arousal ReductionBiofeedback Biofeedback is reported to produce similar reductions in sleep onset latency to PMR, i.e. it helps clients monitor their own ability to relax. Despite the APA’s conclusion that biofeedback met the criteria for a probably efficacious treatment, some studies report similar gains for pseudo-biofeedback. This suggests it may only work as a placebo.

21. CBT: Cognitive Arousal ReductionReducing the Worry These two suggestions are based on theory but have not yet been subjected to much empirical testing. Several common-sense strategies are suggested to reduce brainwave activity. Plan time for worrying well before bedtime. Do not try too hard to fall asleep or worry about sleeping. Turn the clock so the numbers are not showing. Thought stopping: Monitor your automatic thoughts and when they become non-productive, tell yourself STOP. The empirical evidence contra-indicates this strategy. Acceptance therapy: Rather than trying to suppress your automatic thoughts, let them come and accept them without analysis. Imagery training: Convert your thoughts to visual images rather than verbal processes.

22. CBT: Cognitive Arousal ReductionStimulus Control SC is a behavioural technique that meets APA criteria for empirically-supported treatments. It reinforces the association between bed and rapid sleep onset. Sleep only in the bedroom. Refrain from napping. Use the bed and bedroom only for sleep. If awake, leave the bedroom. Return to bed only when sleepy. Recognise internal cues, e.g., yawning, and go to bed when tired. Keep the same schedule every day, including weekends.

23. CBT: Cognitive Arousal ReductionParadoxical Intention PI meets APA criteria for empirically-supported treatments. It eliminates the effort to sleep and so reduces cognitive arousal. Clients deliberately try to sleep badly, e.g., to wake three times in the night. If the client is successful, it shows control over sleep, whereas ‘failure’ allows the client to sleep. Either way, the client regains control. While PI is effective for reducing night-time awakenings, it is less successful in hastening sleep onset.

24. CBT: Cognitive Arousal ReductionSleep Restriction SR consolidates sleep by limiting time in bed to actual sleep time. It meets APA criteria for a probably efficacious treatment. E.g., if a client complains of only five hours of sleep, the time in bed is deliberately limited to five hours. This slight sleep deprivation deepens and consolidates sleep. When the actual sleep time exceeds 85% of time in bed, the amount of time allowed in bed is increased by 15 to 20 minutes. If efficiency falls below 80%, time in bed is decreased by 15 to 20 minutes. Adjustments are made until the client achieves optimal sleep.

25. Sleep well!