Outline and evaluate the sleep disorder Narcolepsy

by maryarrrm (student)

Narcolepsy usually begins in adolescence or early adulthood, and continues through the person’s life. It is thought that 1 in 2000 people suffer from narcolepsy but it is difficult to get an accurate measure of incidence as some people only have mild symptoms or just don’t go to their doctors. Sufferers experience sudden and uncontrollable attacks of sleep at irregular and unexpected times. The two main symptoms are feeling sleepy a lot of the time, and losses of muscular control, episodes triggered by emotional arousal such as anger, fear, amusement, stress or anxiety. Other symptoms can include hallucinations and sleep paralysis - both experienced either when falling asleep or when waking up, and frequent waking up when asleep at night.

There have been three explanations put forward for the explaining narcolepsy, in the 1960s it was considered that it occurred as a result of a malfunction in the systems which maintain REM sleep, Vogel (1960) found that REM sleep occurred at the onset of sleep in narcoleptics. This explained some of the symptoms of the disorder, such as the loss of muscle tone - found in REM sleep and the hallucinations - seen as REM-type sleep and dreams intruding into the day. A second explanation was in the 1980s research suggested that it was linked to a mutation of the immune system. Honda et al (1983) found an increased frequency of one type of human leukocyte antigen (HLA) in patients. HLA molecules coordinate the immune response and are found on the surface of white blood cells. HLA link continues to be researched though the specific HLA variant found most commonly in narcoleptics is not found in all narcoleptics and is also reasonably common in the general population. This means that HLA cannot be the sole explanation

Lastly, in the 1990s research has shown a link between low levels of hypocretin -a neurotransmitter and the disorder. Hypocretin is thought to play a role in maintaining wakefulness. Lin et al (1999) found that narcoleptic dogs had a mutation in a gene on chromosome 12 which disrupted the way that hypocretin was processed.

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Most of the theories of narcolepsy stem from the biological approach as they implicate abnormalities of genetic factors, the immune system and biochemistry. Siegal (1999) found that by recording neuron activity in the brainstem of narcoleptic dogs, they identified activity in cells during wakefulness that are usually only active in animals during REM sleep. However, research in general has not convincingly supported this. Much of the research on narcolepsy uses animal samples, especially dogs, whilst such research may be able to suggest which factors may be involved in animals, such findings cannot be extrapolated and generalised to humans. This is because the anatomy and physiology of humans and animals are different, also sleep patterns, such as when, where and how much, may be different in humans and animals. Similarly, as humans can think about things that they experience in a way which animals cannot, this may mediate and therefore moderate sleep patterns. Both of these issues mean that what is true for animals may not be true for us, findings become more reliable when they are initially achieved in animals and then replicated in humans. As Nishino et al (2000) provides the most promising lead, as the findings form narcoleptic dogs have been confirmed in human studies. For example, it was found that human narcoleptic s had lower levels of hypocretin in the cerebrospinal fluid.

An alternative approach, such as the psychoanalytic one, would explain narcolepsy quite differently. It would argue that the sudden onset of sleep are ways of disguising sexual fantasies and arousal, or ways of coping with them and reducing the anxiety and distress that they may cause. This is what Lehrman & Weiss (1943) proposed in 1943. However, this is a minority view and generally psychoanalytic explanations are not accepted outside strict psychoanalytic circles. Furthermore, given that the disorder has clear physiological elements, an inclusive explanation of the disorder would need to refer to biological factors. Therefore, it might have more explanatory value to use an eclectic l framework to explain narcolepsy.

In conclusion, the explanations of narcolepsy such as those HLA and hypocretin can be seen as reductionist. This is because they attempt to reduce this complex multi-system disorder to malfunctions of a specific biological system and ignore the role of other biological variables as well as those of environmental ones. Whilst such physiological reductionism is necessary for research purposes, where it also occurs at a theoretical level, it oversimplifies the disorder in an artificial way. These explanations can also be seen as deterministic as they suggest that if the individual has the observed abnormality of HLA or hypocretin, that they cannot bring the condition under their voluntary control. This may or may not be true for different individuals as we need to consider individual differences such as lifestyle choices. These explanations could be improved by seeing how patients respond to behavioural interventions or CBT, for example.