Sleep disorders
Narcolepsy
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Incidence & symptoms
• 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
• These are at irregular and unexpected times
• The two main symptoms are feeling sleepy a lot of the time, and a
loss of muscular control
• Episodes are often 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
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Explanations of narcolepsy 1 – AO1
• 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 REMtype sleep and dreams intruding into the day)
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Explanations of narcolepsy 2 – AO1
• 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
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Explanations of narcolepsy 3 – AO1
• 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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AO2 (approaches)
• Most of the theories of narcolepsy stem from the biological approach as
they implicate abnormalities of genetic factors, the immune system and
biochemistry
• As such they would also advocate treatment using biological methods
such as drug therapy to try to combat sleep onset in the day, and to
combat insomnia at night
• 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 a biopsychosocial
framework to explain narcolepsy
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AO3 (refers to Res Meth issues)
• 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 & physiology of humans and animals
are different
• And also because 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 experiences 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
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AO2 (commentary)
• The most promising explanation of narcolepsy appears to be that of
low hypocretin
• Findings in dogs have been replicated in humans
• Nishino et al (2000) found that humans had low levels of hypocretin
in their CSF
• However, what might explain these low levels is unclear as human
narcolepsy does not run in families in the way that many forms of
psychopathology do (eg. schizophrenia)
• Mignot (1998) found that there was no significant increased risk of
one twin developing narcolepsy if the other twin had it
• It could be that the hypocretin abnormalities are caused by brain
injury, infection, diet, stress or an auto-immune attack
• The auto-immune aspect would link with the HLA abnormalities
found by Honda et al (1983)
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AO2 (debates)
• The explanations of narcolepsy such as those HLA and hypocretin
can be seen as reductionistic
• 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
• It would be interesting to know how patients respond to
behavioural interventions or CBT, for example
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