Other supporting evidence include Smith et al’s study where patients with insomnia were studies, as well as a control group of normal sleepers and they were studied polysomnographically for 3 nights with whole brain scans conducted on the third night. Patients with insomnia showed consistent and significant decreases in blood flow compared to good sleepers in the frontal medial, occipital and parietal cortices.
However there are many methodological problems with sleep studies such as Smith et al’s. Sleep studies have been criticised for lacking ecological validity because they are conducted in lab experiments. This means that participants would not sleep in their normal beds and this change in environment could affect sleeping patterns and researchers do not know the extent to which the results are affected. The results from those lab experiments cannot be generalised to normal sleep as they lack mundane realism. However, Garcia-Borreguero et al. found a positive correlation between rating scales and laboratory measures of restless leg syndrome, providing some evidence that sleep laboratory measures are good indicators of certain sleep disorders.
It is also difficult to make generalisations as there are many different types of insomnia with different causes and so we should looks at it as a symptom, not a disorder. For example melatonin appears to be effective in a small group of elderly patients with insomnia but is considered ineffective in the general treatment of insomnia. Dement argues that insomnia is really a symptom of other disorders and so the treatment should be tailored to suit the causes and insomnia is not really a sleep disorder in itself.
It is important to distinguish primary and secondary insomnia because of the implications for treatment. However, recent research casts a doubt on whether insomnia is just an effect and it may be a cause. A study of almost 15000 Europeans found that insomnia more often proceeded than followed cases of mood disorder. This means that in some cases it might be helpful to treat insomnia regardless of whether it is a primary or secondary effect.
Spielman and Glovinsky proposed a useful distinction between predisposing, precipitating and perpetuating components and risk factors. Predisposing factors include a genetic vulnerability for insomnia. Research from Watson has shown that about 50% variance in the risk for insomnia can be attributed to genetic factors. Research also suggests that physiological factors may predispose a person to develop insomnia. However, predisposing factors alone are unlikely to explain chronic primary insomnia .The diathesis-stress model proposes that genetic vulnerability alone is not enough for insomnia to develop and those environmental stressors are needed to trigger the disorder in a vulnerable person.
Narcolepsy is a malfunction of the sleep-wake regulating system in the brain and it affects 1 in 2,000 individuals. The two main symptoms are feeling sleepy all the time and episodes of cataplexy which is loss of muscular control during the day. Other symptoms include hallucinations and sleep paralysis, both experienced when falling asleep and waking up, and interruption of night-time sleep by frequent waking. Narcolepsy usually begins in adolescence and the type and severity of symptoms vary from person to person and may either improve or worsen with time. An inheritable factor has been identified that can increase the likelihood of developing narcolepsy by up to ten times with the factor compared to those without it.
There are 3 explanations of narcolepsy. One of them involves REM sleep. In the 1960s, the view was that it was linked to a malfunction in the system that regulates REM sleep, which explained some of the classic symptoms of narcolepsy such as cataplexy as it accompanies REM sleep.
Research by Honda et al (1983) indicated that narcolepsy was linked to a mutation of the immune system and an increased frequency of one type of human leukocyte antigen (HLA) in narcoleptic patients.
More recent research has uncovered a link between the neurotransmitter hypocretin and narcolepsy. This is supported by Lin et. al who found that narcoleptic dogs had a gene mutations which disrupted the processing of the hypocretin.
Understanding of narcolepsy stems primarily from research involving narcoleptic dogs. It was found that these dogs have a fault receptor for hypocretin and then it was discovered that there was a similar problems in humans and that hypocretin levels were very low.
Most explanations of narcolepsy have been biological, though there have been some successful attempts to provide psychological explanations. For example, Lehrman and Weiss (1943) suggested that sudden attacks of sleepiness disguise sexual fantasies.
It is clear that there is a genetic component to narcolepsy. In dogs, it is clear that one gene can pass on the trait, whereas in humans it does not, as in humans if one twin has narcolepsy there is only a 30% chance of the other twin developing it.
Also drugs have proved useful in the treatment of narcolepsy which has been thought to activating hypocretin-containign nerve cells. The success of this drug supports the hypocretin deficiency explanation for narcolepsy.
Most research used for evidence to explain narcolepsy comes from animals, and more specifically dogs. This is not suitable for humans as findings cannot be generalised as humans and dogs have difference sleeping patterns and anatomy and so findings lack validity.
by
rose127 (student)
