Sleep Disorders

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Sleep Disorders

Poor sleep is a major cause of serious morbidity including accidents, psychiatric sequelae and reduced quality of life, and has a major economic impact

  • v Stages of Sleep and the EEG:

Non-REM sleep: (REM: Rapid Eye Movement)

  • Stage 1: mixed frequency, low voltage. Alfa ? (8-12 Hz) and Theta ? (4-6 Hz).
  • Stage 2: low voltage, slower frequencies. Contains sleep spindles (12-14 Hz) and high amplitude ‘k’ complexes
  • Stage 3 & 4: high amplitude, low frequency Delta ? (2 Hz) waves. Stage 3 characterized by < 50% ? waves with sleep spindles. Stage 4 by > 50% ? waves but no sleep spindles. Stage 3 & 4 comprise slow wave sleep (SWS). As sleep progress through stages 1 to 4 low frequencies increase at the expense of the higher frequencies which are characteristic of waking.

REM sleep (paradoxical sleep):

The EEG shows a low voltage, mixed frequency spectrum with characteristics of cortical activation. It is associated with rapid eye movements, signs of autonomic arousal and paradoxical low muscle tones, and this is when dreams occur.

Sleep architecture:

From waking, individuals pass through stages 1 to 4, then into REM sleep. REM sleep then alternates with non-REM. REM compromise 20% of total sleep time, and occurs at 80 to 90 minutes intervals. Stages 3 and 4 comprise 15-20% of total sleep time. The majority of time is spent in stage 2. SWS occurs mainly early on in sleep with REM sleep later. SWS and REM sleep are highest in neonates, and decrease in amount with increasing age.

Function of sleep:

Theories about the function of sleep include conservation of energy versus brain or body restoration. REM sleep has been proposed to reflect brain functions, and SWS to be associated with bodily functions (related to the amount of energy expanded, it is increased with exercise and decrease with hypothyroidism). It has been suggested that sleep can be core and optional sleep based on observations that:

  • Only 30% of total sleep lost is regained after sleep deprivation, especially SWS and REM.
  • Short sleepers have similar early sleep pattern to longer sleepers
  • Gradual sleep reduction down to five hours is well tolerated.

Control of sleep:

The reticular activating system is involved in arousal, and the induction of sleep is active rather than passive process. The Yerkes-Dodson curve describes the phenomena of increasing then decreasing performance with increasing arousal. The peak is reached and exceeded more quickly for difficult than easy tasks. Poor sleep affects the ability to perform simple, mundane tasks but not more complex ones which require more attention. Drugs can affect both performance (via drowsiness) and sleep, for example, antidepressants, antipsychotics, benzodiazepines, antihistamines and alcohol.

  • v Clinical Syndromes:


  • Insomnia: 30% in one year
  • Nightmares: occasional in 50% of adults, regular in 1%
  • Sleep apnoea: 4-8% of men; 2-4% of women
  • Narcolepsy: 0.15%


  • Dysomnias: poor sleep
  • Medical/psychiatric sleep disorder: i.e. secondary
  • Parasomnias: abnormalities during sleep
  • Specific sleep disorders.

1. Insomnia: this represents lack of sleep, poor quality of sleep or reduced daytime performance. It is probably the commonest complaints presented to primary health care; for example in the USA 42% prevalence. Hypnotic use is still common despite changes in guidelines (esp. in this country). Primary insomnia is rare. Causes of insomnia include:

  • Psychiatric disorders (36%)
  • Psychophysiological insomnia ‘sleeplessness phobia’ (16%). Features include: the complaint of insomnia and reduced performance when awake, trying too hard to get to sleep, tension, physical symptoms, increased sleep latency, reduced sleep efficiency and increased number of awakenings.
  • Medications, illicit drugs and alcohol (12%)
  • Periodic limb movement disorders (12%)
  • Sleep apnoea (6%)
  • Pseudo-insomnia (6%)
  • Sleep-wake schedule disorder (6%)
  • Medical disorders (6%)

However, social and personal factors are also very important in determining who present, for example women report insomnia twice as often as men, and rates are higher in the unemployed

2. Parasomnias: these are acute, undesirable, specific, episodic physical phenomena which occur during, or are exacerbated by sleep. There is an interaction between psychological (esp. stress) and biological factors. Generally treat with reassurance, education and practical advice. These occur in different stages of sleep:

  • Ø SWS: disorders of arousal; sleepwalking and night terrors. Sleepwalking is often exacerbated by excessive sleepiness. Night terrors occur early in sleep, the individual is difficult to rouse and generally has no recall.
  • Ø REM sleep: patients rouse easily. These are usually nightmares or dream anxiety attacks which are frightening, with clear recall. They may be related to psychological precipitants, fever or drug withdrawal (BDZ, antidepressant, alcohol). Other disorders are sleep-related cluster headaches and sleep related asthma; the REM sleep behaviour disorders which involve loss of the usual atonia in REM sleep so the individual acts out dreams which are often violent.
  • Ø Other Parasomnias: Enuresis (patients may have different sleep patterns and therefore not able to sense the need to urinate); bruxism (teeth-grinding); head banging; familial sleep paralysis.

3. Specific sleeps disorders:

  • Ø Narcolepsy: characterized by hypersomnolence, cataplexy, sleep paralysis and hypnogogic hallucinations (tetrad is Gelineau’s syndrome). 50% also have major affective disorder and / or personality problems. Aetiology suggests genetic cause as family history is common and HLA-DR2 found in 99%. Onset is generally in the teens or twenties. Sleep attacks are irresistible in boring situations (like this lecture!), and cataplexy is often related to emotions. There is a short REM latency. Narcolepsy can be treated with psychostimulants, and support groups are helpful.
  • Ø Periodic limb movement disorder: there are repetitive and stereotyped movement during sleep and the patient is often unaware. It may lead to poor sleep and daytime fatigue, also depression and anxiety. Found in narcolepsy, obstructive sleep apnoea, Parkinson’s disease and metabolic disorders. It can be aggravated by tricyclics and withdrawal from BDZ.
  • Ø Kline-Levine syndrome: this occurs generally in adolescent boys, and is characterized by periods of hypersomnia and overeating, often with change in libido.

4. Other sleep-related problems:

  • Ø Circadian rhythm disorders: this describes changes in the timing of sleep, for example in people on shifts and with jetlag.
  • Ø Daytime sleepiness: Narcolepsy, obstructive sleep apnoea, sleep-related motor disorders, depression, post-viral fatigue, head injury, metabolic, toxic and drug related factors, essential hyper-somnolence, and older age can all cause daytime sleepiness.
  • v Assessment
  • Patient’s description of the problem, including the onset, length and quality of sleep, and any daytime drowsiness or reduced performance
  • Objective observations by patient and spouse/relative.
  • Possible general medical, psychiatric or drug problems.
  • Details of sleep environment and hygiene
  • Drug history, both prescribed and recreational.
  • Current circumstances and stress
  • Sleep diary including caffeine, alcohol and drugs.

People often overestimate the length of time to get to sleep, even to the extent that good and poor sleepers can have similar sleep pattern. However the quantity of sleep can be relied on in assessing the presence of insomnia.

  • v Management

1. General advice:

  • Treatment of any underlying cause.
  • Education and advice on sleep hygiene.
  • Optimizing the temperature at the room
  • Encouraging a regular routine
  • Exercising late in the afternoon
  • Small food intake in the evening
  • Relaxation techniques
  • Advice about problem solving and dealing with intrusive thoughts (CBT can be used and has good evidence based results).

2. Role of drugs in sleep:

•a)    Drugs used to improve sleep:

Particularly benzodiazepines (BDZ), which can be used in short-term treatment for poor sleep associated with acute stress. BDZ reduce REM and SWS, increase stage 2. Tolerance and REM sleep rebound occur on discontinuation. Barbiturates are no longer should be used due to its narrow therapeutic window, high addictiveness, tolerance and death in overdose.

 Zopiclone (new generation partial BDZ, only used as hypnotic) increase SWS, and although early reports claimed less tolerance and dependence, recently this has been disputed.

New Melatonin derivatives medication has been just licensed for sleep, some evidence point toward better results with elderly, and may be autism. These have few side effects and do not interfere with sleep architecture.

•b)    Drugs used to reduce sleepiness:

These are for example amphetamine, pemoline and selegiline. These reduce total sleep, REM and SWS, delay sleep onset and cause fragmented sleep.

•c)     Drugs used to treat psychiatric disorders:

  • Antidepressants: some are alerting e.g. Prozac (fluxoetine), MAOI; some are sedatives, which is generally related to their anticholinergic properties (most tricyclic), or antihistaminic (Mirtazepine). In general, antidepressants suppress REM sleep. Interestingly, sleep deprivation is still used as treatment for depression and the target is to reduce REM sleep.
  • Mood-stabilizers: Lithium reduces REM sleep and delay onset. Carbamazepine reduces REM sleep and increase SWS, and can cause initial drowsiness.
  • Anti-psychotics: These reduce periods of wakefulness, increase or decrease REM sleep, depending on the dose. Total and REM sleep are reduced on stopping.

•d)    Non-psychotropic drugs:

These can affect sleep by crossing the BBB, or by causing or exacerbating a disorder which disrupt sleep (e.g. sleep apnoea). Common causes of sleep disturbance include appetite suppressants, anti-emetics, anti-histamine, corticosteroids, cardiovascular drugs and hormones.


•e)     Recreational drugs:

  • Alcohol promotes sleep in small amounts nut in larger amounts causes insomnia later in the night due to rebound and withdrawal effects. Its effect depends on the level of sleep deprivation, and interactions with other drugs.
  • Nicotine can disrupt sleep.
  • Caffeine causes an increase number of arousal and decrease REM sleep. It has a half-life of five hours. Withdrawal symptoms also occur which disrupt sleep.

•f)      Illicit drugs:

  • Cannabinoids reduce REM sleep, and increase SWS initially but decrease it after several days. Habitual use leads to excessive sleeping and lassitude, with sleep disturbance on withdrawal.
  • Narcotic analgesics cause a drowsy state followed by reduce REM and SWS. Sleep disturbance occurs on withdrawal.
  • Cocaine reduces total sleep, SWS and REM sleep. Excessive sleeping occurs on withdrawal (rebound).
  • Hallucinogens (e.g. LSD) do not affect sleep directly except by ‘ bad trips’

•g)    Drugs withdrawal:

Sedatives and hypnotics cause rebound insomnia usually for one week but can be for up to two months. Insomnia is more severe but less prolonged for drugs with shorter half-life. Chloral hydrate gives fewer problems with withdrawal but is less efficacious.

Abrupt withdrawal of antidepressant can lead to short-lived rebound insomnia and panic. Antipsychotics rarely cause dependence or withdrawal (therefore small dose, below the therapeutic dose for psychosis treatment, are used to aid sleep in some patients)


1. Shapiro C. ABC of sleep disorders. London: BMJ Publishing Group, 1993.

2. Steple D. Oxford Handbook of Psychiatry, Oxford University Press, 2006

3. Smith G et al. Key topics in Psychiatry. Bios scientific publisher limited, 1996.

4. Boyle D, Davies S. Psychiatry, Mosby’s crash course 2002

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