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Laugh and the world laughs with you, snore and you sleep alone

Simone de Lacy
Consultant Technologist and Manager
Sleep and Respiratory Services
Guy's and St Thomas NHS Foundation Trust

All of us will experience transient sleep difficulties at some point, be it through anxiety, bereavement, intrinsic and extrinsic factors or often self-imposed sleep deprivation. Some of us, however, have chronic and severely debilitating sleep disorders that require diagnosis and treatment if quality of life is to be maintained.  
There are more than 80 ICSD (International Classification of Sleep Disorders) sleep disorders.(1) They can be divided into three broad categories:

  • The inability to initiate and or maintain sleep (insomnias).
  • Unwanted movements or behaviours during sleep (parasomnias).
  • Problems of excessive sleepiness (hypersomnias).

Of these, the complaint of insomnia is the most commonly reported.

Insomnia is a perception of inadequate or nonrestorative sleep rather than a specific sleep disorder. Approximately 30% of the adult population will experience problems with initiating or maintaining sleep in any one year. As many as half of these will find their lack of sleep so debilitating they will eventually present to the GP for advice and treatment, usually having tried numerous OTC remedies.(2) Given the average 10-minute GP consultation, it is little wonder that the patient will leave with a prescription for sleeping tablets rather than having explored the predisposing, precipitating and perpetuating factors that are the root cause (see Table 1).


Effective treatment of insomnia revolves around addressing these factors. A short-term course of sleeping tablets may be used to help overcome initial sleep difficulties, but lasting relief from symptoms is best achieved with the addition of cognitive behavioural therapy to understand and address the underlying issues, beliefs and behaviours associated with poor sleep.(3)

Delayed sleep phase syndrome
Sometimes our body clocks can be out of synchrony with the "normal" sleep-wake patterns. Our inherent "tick" is internally generated by our suprachiasmatic nucleus (SCN), a tiny collection of cells in the posterior hypothalamus. The SCN orchestrates the release of melatonin, our "dark" hormone, and is externally influenced by the amount of light hitting the retina. As the light diminishes (dusk) the production of melatonin increases and sleep is signalled. As light levels increase again (dawn), the production of melatonin is diminished. Sufferers of delayed sleep phase syndrome do not feel sleepy until the early hours of the morning and then have difficulty waking up in time for work or school. This is because their internal rhythm is shifted so that their sleep onset is delayed. Treatment may involve retraining of the SCN with the use of extrinsic melatonin three hours before desired sleep onset and/or bright light therapy at the desired wake time.

Snoring and sleep apnoea
Snoring is often ridiculed and frequently denied, and at the very least it can cause social embarrassment and marital disharmony. However, it can also be the precursor to a more serious condition: obstructive sleep apnoea (OSA), in which there is an intermittent, partial (hypopnoea) or complete collapse (apnoea) of the upper airway during sleep. The snoring sound results from the vibration of the soft palate. If the oropharyngeal opening is narrow or crowded by excess fatty tissue, floppiness of the upper airway or the skeletal anatomy, the natural reduction of muscle tone during sleep may be all that is required to allow temporary closure. This can result in a drop in oxygen levels, with a reciprocal rise in CO2 that will trigger an arousal at cortical level. These constant arousals cause sleep fragmentation and excessive daytime sleepiness, producing a higher risk of road traffic accidents than the effects of alcohol.(4) The apnoeas also put a strain on the heart, which can lead to the increased incidence of high blood pressure and stroke.(5,6)
The incidence of OSA in the adult population is between 2% and 4% (similar to that of diabetes).(7) With the current obesity epidemic there may well be a rise in reported cases. Successful treatment of OSA is achieved through maintenance of upper airway patency during sleep. At the mild end of the spectrum, dental splints, which advance the lower jaw, can be effective. For more serious cases, the airway is held open by a pneumatic splint in the form of a continuous positive airway pressure (CPAP) machine.

Restless legs syndrome and periodic limb movements disorder(8)
Restless legs syndrome (RLS) is a common and under-diagnosed sensorimotor disorder, which manifests in unpleasant sensations in the legs and sometimes arms, which can only be relieved by movement. They typically occur in the evening, and the voluntary movement in response to the uncomfortable sensations may delay sleep onset. Periodic limb movements disorder (PLMD) is a related but separate condition, which involves involuntary movement, most commonly of the legs, during sleep. People with PLMD are often unaware of these movements, which occur with a distinct periodicity (more than four in a row separated by periods of between five and 120 seconds - usually every 20-30 seconds). Most patients with RLS have PLMD; however, patients with PLMD often do not have RLS. RLS and PLMD may also be found in association with low blood ferritin levels.
Mild RLS may be best treated with lifestyle changes, especially good sleep hygiene. Dietary supplementation with iron tablets may also be required. Severe RLS and PLMD may require treatment with a variety of drugs, including licensed dopaminergic agents (ropinirole and pramipexole) or certain benzodiazepines (clonazepam).

Narcolepsy is a comparatively rare sleep disorder but is one of the most debilitating. It is a characterised by the following symptoms:

  • Excessive daytime sleepiness - often manifests as irresistible "sleep attacks" in inappropriate situations.
  • lCataplexy - a sudden partial or complete loss of muscle tone in response to an emotional stimuli, such as laughter or anger.
  • Sleep paralysis - occurs at sleep onset or on waking and involves the (often frightening) inability to move.
  • Hypnagogic hallucinations - vivid dreamlike auditory, visual or sensory experiences at sleep onset.

The cause of narcolepsy is unclear, but recent evidence links it to extremely low or nonexistent levels of the neurotransmitter hypocretin (HCRT). The latter may be due to reduced HCRT production as a result of autoimmune destruction of the HCRT-producing cells in susceptible individuals (98% of narcoleptics are positive for the HLA [human leucocyte antigen] tissue type DQB1*0602, suggesting a possible autoimmune link).
Treatment currently consists of managing the symptoms of excessive daytime sleepiness and cataplexy, but trials will soon begin on HCRT agonists.

Management of all sleep disorders should begin with attention to good sleep hygiene (see Box 1). The definitive diagnosis may require referral to a specialist sleep disorders centre.



  1. American Association of Sleep Medicine. The International Classification of Sleep Disorders: diagnostic and coding manual. Westchester, Illinois: AASM; 1990.
  2. Addison RG, Thorpy MJ, Roehrs TA, Roth T. Sleep/wake complaints in the general population. Sleep Res 1991;20:112.
  3. Stepanski EJ. Hypnotics should not be considered for the initial treatment of chronic insomnia. J  Clin Sleep Med 2005;1(2):125-8.
  4. Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnoea and the risk of traffic accidents. Cooperative Group Burgos-Santander. N Engl J Med 1999;340:847-51.
  5. Peppard P, Young T, Palta M, et al.  Prospective study of the association between sleep-disordered breathing and hypertension. New Engl J Med 2000;342:1378-84.
  6. Wolk R, Kara T, Somers V. Sleep-disordered breathing and cardiovascular disease.     Circulation 2003:108:9-12.
  7. Young T, Palta M, Dempsey J, et al.  The occurrence of sleep disordered breathing in middle-aged adults. N Engl J Med 1993:328:1230-5.
  8. Chaudhuri KR, Appiah-Kubi L, Trenkwalder C. Restless legs syndrome. J Neurol Neurosurg Psychiatry 2001;71:143-6.