Disorders of sleep:-
This is the area of the specification covered in this pack
 Explanations for sleep disorders, including insomnia, sleep
walking and narcolepsy
For each sleep disorder you need to know one explanation of it, so
you need to know an explanation of
1) Insomnia
2) Sleepwalking
3) narcolepsy
Narcolepsy: genes and hypocretin
AO1:
A fairly new theory links narcolepsy, genes and the neurotransmitter hypocretin.
Hypocretin (also called orexin) is a neurotransmitter that regulates arousal, wakefulness, and
appetite. The brain contains very few cells that produce orexin: in a human brain, about 10,000 to
20,000 neurons in the hypothalamus.
Some genetic variations on chromosome 6 (known as the HLA complex) predispose an individual to
narcolepsy. These variations increase the risk of an auto-immune response to neurons in the brain
that produce the neurotransmitter hypocretin (also known as orexin).
Hence people with narcolepsy often have vastly reduced numbers of neurons in their brain that
produce hypocretin, because the cells that produce it have been destroyed by the auto-immune
response.
It is also possible that for some people the auto-immune response is not caused by genes but by a
flu vaccination.
Evaluation
IDA
This explanation of narcolepsy could be deemed reductionist, because it suggests that the disorder is
caused solely by biological factors, in this case a genetic variation leading to an auto-immune
response to the neurotransmitter, hypocretin. It does not explain the environmental conditions
needed for the disorder to develop and is therefore likely to be an oversimplified theory. On the
other hand, it provides hope for people suffering from narcolepsy because it may eventually lead to
an effective treatment or even a cure.
Research evidence
Evidence 1
Mignot et al found that out of 16 pairs of mono-zygotic twins, where at least one of the pair has the
condition, 5 pairs were concordant for narcolepsy (each twin displayed the condition).
This research supports the explanation, as the concordance rate is much higher than the general
population (you have a 30% chance of narcolepsy if your identical twin has it). However, the fact it
isn’t a 100% concordance rate shows that narcolepsy isn’t entirely genetic.
Evidence 2
Broughton (1999) reported that lifestyle adjustments, such as regulated sleep schedules and relaxing
before bed, were more successful at treating the symptoms of narcolepsy than drugs.
This suggests that lifestyle plays an important role in managing narcolepsy, which means that it may
also play a role in development of the condition. The above theory overlooks the importance of
lifestyle, which means that it is insufficient to account for these data.
Evidence 3
Nishino et al found a link between low levels of hypocretin in the human cerebrospinal fluid and
narcoleptic symptoms.
This study seems to support the theory because it is the hypocretin which regulates arousal and
wakefulness, therefore if there are decreased levels of hypocretin in the cerebrospinal fluid then it is
logical to assume an equal decrease in wakefulness.
Additional evidence
Mignot et al (1999) found that dogs with narcolepsy had a defective hypocretin receptor 2 gene.
This supports the theory of a genetic cause of narcolepsy, as dogs with the gene all suffered
narcolepsy and sudden fall into REM sleep. The lack of function in hypocretin receptors could have
the same effect of destroying the cells in the hypothalamus which produce the neurotransmitterthe overall effect is that hypocretin does not have an effect.
Dement (1999) found evidence to support the hypocretin’s role in narcolepsy. They found that mice
who could not make the neurotransmitter in their brains developed symptoms of narcolepsy,
including sleep attacks and cataplexy.
This study supports the biological theory of narcolepsy because it highlights how certain failures in
brain producing specific neurotransmitters can result in symptoms similar to that of narcolepsy such
as total loss of muscle control (as in cataplexy) and the attacks of sleep synonymous with narcolepsy.
Montplaisir (2007) found abnormal numbers of hypocretinergic and dopaminergic neurons in the
brainstems of 16 narcoleptic patients.
This suggests that an imbalance of neurotransmitters is associated with narcolepsy. Furthermore it
confirms that abnormal levels of hypocretin in the brain may be responsible for the condition.
However, it also suggests the involvement of dopamine, so hypocretin alone may not be sufficient to
account for the development of narcolepsy in all cases
AO3:
The research consistently shows a link between hypocretin and narcolepsy therefore it can be seen
as reliable evidence for the theory. Also, much of the research uses scientific methods therefore
they are free from bias from the researcher which could improve the overall validity of the research
into hypocretin explanation.
The use of animal studies can’t always be generalised to humans, however in relation to Mignot’s
study the hypocretin receptor 2 gene is found in both humans and dogs. This means that the same
gene may underpin the condition in both species, though further testing would be needed to
confirm
Although Broughton’s study gives us useful information about how environmental factors may
influence narcoleptic episodes, it doesn’t give us any information about the actual cause of the
disorder.
Overall evaluation
This explanation focuses on narcolepsy being down to nature rather than nurture which has led to
practical applications in terms of treatments. Most treatments which have been developed are
biological in nature such as drug therapy (e.g. Modafinil,) to combat sleep onset during the day.
Many studies into narcolepsy are derived from animal studies, the impact of this is that the results
cannot be generalised to a human population. This is because of the differences between the
neurological makeup of humans and mice for example. A reduction in generalizability reduces the
extent to which the theory can be applicable and useful to a human population.
However the biological research into narcolepsy is generally correlational. This is an issue because
correlational studies cannot show distinctive cause and effect relationships due to the uncontrolled
nature of the studies which allows unaccounted for confounding variables to reduce the validity of
the results. However when used in accordance with animal studies they can provide a useful insight
into seemingly interlinked aspects of the brain.
Primary insomnia: predisposing, precipitating and perpetuating
factors
AO1:
Speilman and Glovinsky (1991) said that predisposing, precipitating and perpetuating factors explain
primary insomnia.
Predisposing factors include a genetic vulnerability to insomnia and the physiological state of
hyperarousal. Hyperarousal is high physiological arousal when awake or asleep and it makes it more
difficult for the individual to fall asleep.
Precipitating factors include stress or environmental change that may temporarily make it difficult to
get to sleep. Environmental change includes changing time zones. Females suffer more from
primary insomnia, as do older people so both of these factors count as precipitating factors.
Perpetuating factors maintain insomnia when the precipitating factors have gone. They include
being tense when going to sleep or the expectation of poor sleep. These perpetuating factors are
key to chronic primary insomnia.
Evaluation
IDA
The theory follows the nature nurture debate on insomnia, as the predisposing part of the theory
emphasises the nature argument towards a genetic predisposition to having insomnia, while the
precipitating part focuses on environmental factors such as stress which lead to insomnia. An
advantage of the nature side to the theory is it can easily be tested in an experimental and scientific
manner. If insomnia is due to genetic and physiological factors it is likely treatments can be
produced to prevent insomnia or reduce its symptoms. However the nurture side means we can
inform people of environments that lead to stress thus increasing likelihood of insomnia.
Research evidence
Evidence 1
Nofzinger et al (2004) found that the transition from being awake to being asleep is usually
associated with a decrease in activity in the brain stem, thalamus and prefrontal cortex. Using PET
scans, Nolfzinger et al showed that insomniacs experienced a smaller decline in such activity when
going to sleep. In fact, they found elevated level of activity in the brains of insomniacs.
This suggests that people who suffer from insomnia do so due to high physiological arousal which
supports the biological element of the explanation for insomnia.
Evidence 2
Bastien et al. (2004) found that 60% of patients with insomnia could identify a trigger for their sleep
disturbance, and these tended to be around family, work/school and health.
This study supports the idea that precipitating factors have an effect on insomnia because the stress
of external factors such family problems (divorce) may have an effect on their health resulting in
them not being able to sleep.
Evidence 3
Ohayon & Roth (2003) interviewed 14,195 participants representative of the general populations of
the UK, Italy, Portugal and Germany over the telephone about their psychiatric history and their
sleep patterns. They found that people with insomnia were six times more likely to report a mental
health problem, such as depression or anxiety, than people without insomnia.
This suggests that there are also psychological factors that can be linked to suffering from insomnia.
AO3:
The use of experimental research allows for more objective results to be gathered. Specifically,
Nofzinger used scientific equipment (PET scans) to make comparisons between people with
insomnia and people who do not have insomnia. This increases the validity of the research and
provides the explanation with strong scientific support.
However, the research into precipitating and perpetuating factors often use non-experimental, selfreport techniques to gather data which means the validity of this research can be questioned due to
issues such as social desirability bias. This means that the environmental aspects of the explanation
can be criticised as firm conclusions about how these are linked to insomnia are difficult to confirm.
Overall evaluation
As the theory has focussed on both biological and environmental factors, treatments have included
drug treatment, usually only prescribed for a short term, and cognitive behavioural therapy which
targets the mental and stress factors which contribute to insomnia.
The explanation for insomnia states there can be multiple factors which lead to insomnia; this is
useful as it takes into account many factors (holistic explanation rather than reductionist). However
it could be argued that due to this, it is very difficult to study these factors separately and to
determine which factors are the most prevalent in causing insomnia thus making it more
problematic to know what precise treatment to offer.
Sleep walking: a diathesis-stress model
AO1:
A diathesis-stress model recognises that there are predisposing factors (the diathesis) and
environmental causes to a disorder (the stress). It is important to realise that sleepwalking occurs in
SWS.
This model of sleepwalking says that there is a genetic predisposition to sleep walking, which is the
diathesis; this genetic predisposition is likely to be incomplete arousal – so people’s genes
predispose them to be in this state, which is a state between sleep and wakefulness. Sleepwalking
occurs in SWS and typical EEG recordings taken during sleepwalking show delta waves typical of SWS
plus higher frequency beta waves which are characteristic of an awake state. Hence it appears that
sleepwalking occurs when the person in SWS is awakened but the arousal of the brain is incomplete
so they still appear asleep.
The stress (environmental) factors that make sleepwalking more likely to occur in those with a
predisposition include sleep deprivation, drinking alcohol, fever and being a child. Children are
thought to be more vulnerable because they have more SWS than adults and it’s thought that the
mechanism that inhibits motor activity during SWS is not properly matured. Hormonal changes
during puberty and menstruation may also be triggers for sleepwalking.
Evaluation
IDA
The diathesis-stress model suggests sleepwalking has a biological basis whilst still taking into account
environmental factors that may influence this behaviour. This can be considered useful as it leads to
a less reductionist explanation of sleepwalking which could have important implications for the way
we treat people who have the disorder. It suggests that although there may be a genetic
predisposition, there may be ways in which we can help those affected manage the impact of their
biology. Therefore it is a more positive outlook for the individual than if we concentrated on the
impact of biology alone
Research evidence
Evidence 1
Ohayon researched a sample of 19,136 individuals from 15 states of the U.S. The study showed that
people with depression were 3.5 times more likely to sleepwalk than those without, and people with
alcohol abuse/dependence or obsessive-compulsive disorder were also significantly more likely to
have sleepwalking episodes.
This evidence supports the stress part of the explanation as it shows that environmental factors
increase the amount of sleepwalking that occurs in individuals for example those who drink a lot of
alcohol increased their time spent in SWS sleep which therefore could increase their chances of
sleep walking.
Evidence 2
Hublin et al (1997)
Monozygotic (1045) and dizygotic (1899) twins were interviewed about their sleepwalking habits in
childhood and adulthood. The study found that there was a link between genetics and sleepwalking.
which suggests that one can be predisposed to sleepwalking, supporting the diathesis idea.
Evidence 3
Oliviero (2008) examined the motor excitability of adult sleepwalkers during wakefulness. Compared
to normal controls, the sleepwalkers had signs of immaturity in the relevant neural circuits.
This evidence supports the diathesis-stress model, since the participants’ neural circuits were not
fully developed, therefore could not reduce motor activity. This led to a state of semi-wakefulness,
causing sleep-walking. The study also supports the finding that children sleepwalk more than adults
as their brains are still developing.
Additional evidence
Zadra et al (2008) investigated 40 patients and recorded sleepwalking for one baseline night and
during recovery sleep after 25 hours of sleep deprivation. The results show that 32 episodes were
recorded from 20 sleepwalkers (50%) at baseline whereas recovery sleep resulted in 92 episodes
being recorded from 36 patients (90%).
This study also supports the model because the participants were subject to stress caused by sleep
deprivation. Most patients who were deprived of sleep showed sleepwalking.
AO3:
Ohayon and Hublin both used a large sample which increases the population validity enabling the
results on the sleepwalking to be generalised to the wider population. increasing the extent to
which we can use the diathesis-stress model to explain why people within the wider population
sleep walk.
Research conducted in sleep labs are low in ecological validity as the environment is atypical to the
one in which the participant would normally sleep. This means the findings may be difficult to
generalise to real life situations of sleep walking. This could potentially lower the extent to which we
can explain sleepwalking using the diathesis-stress model.
Overall evaluation
This explanation doesn’t tell us why incomplete arousal occurs, and why it only occurs in some
people but not others, therefore it is more of a description of what happens during sleepwalking,
rather than an explanation of why it occurs. This could be the reason as to why no specific treatment
(at the time) is given for sleepwalking, it is mainly recommended that sufferers try to establish a
regular bed time routine in order for them to relax and get enough sleep. People who suffer from
sleepwalking could also be advised to reduce their alcohol consumption, and go to bed earlier, since
alcohol digestion and sleep deprivation have been shown to contribute to sleepwalking.