Disorders of sleep

Primary insomnia is the most common form of insomnia and has no clear underlying cause. There is a sleep problem, but there is no physiological or psychiatric cause, and it is likely that the sleep problem is the result of maladaptive behaviours or learning. The clinical characteristics are that the individual has suffered from insomnia for at least a month but this would not be linked with any other sleep disorder, such as parasomnia or narcolepsy, nor with another psychopathology such as clinical depression, nor with medications or substance abuse. Worrying about the insomnia can lead to a cycle that is hard to break because the more a person focuses on their sleep problems the less likely they are to get good quality sleep.

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.

Sleepwalking - is a relatively common sleep disorder, with estimates that it affects about one in ten. Somnambulism is most likely to occur during NREM stages 3 and 4, in slow-wave sleep. It can occur in REM sleep but this is much less likely.The causes of somnambulism include a genetic predisposition, fatigue, previous lack of sleep, stress, or anxiety. In adults, alcohol and other drugs seem to act as triggers. The genetic element in somnambulism is supported by Hublin et al who used the Finnish twin cohort and found that the genetic contribution to somnambulism in childhood was 66% in men and 57% in women, and for adult somnambulism was 80% in men and 36% in women.

Narcolepsy - Narcolepsy is rare but is characterised by chronic sleepiness, and so the individual may fall asleep at any time. Short naps of 10 to 20 minutes are common, after which the sleepy feeling is temporarily reduced, only to reappear with 2 to 3 hours. Evidence for a genetic basis is provided by Mignot’s (1998) twin study. This showed a MZ 25–31% concordance rate for human narcolepsy and 1–2% for first-degree relatives of narcoleptics, which compares to a very low rate in the general population. A hypocretin (or orexin as it is also known) deficiency is definitely implicated in human narcolepsy

The sleep–wake cycle, as covered in the previous section, offers important insights into the nature of sleep such as the role of the biological clocks, the SCN and the pineal gland, and the role of biochemicals such as the melatonin released by the pineal gland when it receives electrical messages from the SCN that the light level is low. Melatonin influences the production of serotonin and this accumulates in the raphe nuclei in the hindbrain, near the pons, and stimulates the shutting down of the RAS (reticular activating system), which is closely linked with brain activity. So serotonin could be the switch to start sleep. Jouvet has also identified noradrenaline as a biochemical affecting sleep. Noradrenaline accumulates in the locus coeruleus in the pons and if this area is damaged, noradrenaline levels fall and REM sleep is impaired. This led him to conclude that different areas of the brain and the corresponding neurotransmitters controlled the two types of sleep, NREM and REM. The raphe nuclei and its serotonin pathway controls NREM sleep; the locus coeruleus and noradrenaline pathway control REM sleep. A further factor is a biochemical, adenosine. This builds up during wakefulness and is then broken down during sleep. It has been suggested (NINDS, 2007) that the build-up causes drowsiness and could switch the brain into preparing for sleep mode.