Sleep Disorders

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  • Created by: Hope
  • Created on: 26-09-15 16:40

Insomnia AO1

Insomnia is a dysomnia. Insomnia is difficulty sleeping and staying asleep. 

It is diagnosed when the person has been experiencing it for more than one month.

It is only diagnosed if it is resulting in:

  • Daytime fatigue 
  • Severe Distress
  • When it impairs work, social life or general functioning 


Claims, at least 1/2 of all people have difficulty sleeping. BUT only 5-10% of these people actually suffer from Insomnia.

Also claims that Insomnia is not a sleep disorder but is the symptom of something else. 

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Primary Insomnia and Explainantions

  • Has no medical, psychiatric or environmental cause. 
  • Occurs on its own with no known cause. 


The control of sleep involves very complex biological networks. Many biological networks are inate and inherited from our parents. A minor imbalance could lead to primary insomnia. Support comes from the fact that some forms of primary insomnia begin very early in life and evidence it runs in familys. 

  • Doesn't explain what actually causes it. 
  • What about those people when it starts later in life? 


Insomnia is caused by a state of chronic physiological arousal. Research shows people with Insomnia have increased heart rates, cortisol levels. Also high anxiety involves high arousal. 

The chronic arousal is therefore maintained by the high anxiety about not being able to sleep.

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Secondary Insomnia

  • There is a clear, precicpatiting cause. When insomnia is caused by a psychiatric disorder (e.g. depression) or a medical disorder (e.g. chronic pain like asthsma). More common than Primary Insomnia
  • Patients with secondary insomia get treated for the underlying problem not the insomnia.

Many casues of Secondary Insomnia:

  • Medical conditions: Asthma, parkinsons, psychological disorders: Depression, anxiety, OCD, Overuse of stimulants - caffeine, alcohol, Can also be genetics or gender:


Twin studies have shown significant genetic component. It is more likely someone will develop insomnia if they are genetically vulnerable.


More woman than men are diagnosed with insomnia. Not researched a lot. May be related to fact women are found to be more stressed and have more anxiety than men. 

  • Could be no gender difference, for men it is less socially acceptable to say how their feeling.
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Evaluation of Primary Insomnia

Diagnosis is difficult:

A major issue is that is hard to diagnose and therefore is extremely difficult to researh. 

If the cause is unknown where do you begin to research? What variables do you isolate? (AO3)

How can someone be sure that they have it?

Chicken or the egg:

With the hyperarousal explanation. it is hard to establish cause and effect. Which came first - hyperarousal or insomnia. The persons insomnia may be causing the hyperarousal not the other way around. 

There is no cause and effect shown. Only shows that there is a link.

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Evaluation of Secondary Insomnia

Finding a causual explanation:

Secondary insomnia can sometimes be very easy to find the cause - As we can find cause we can conduct more research (AO3) - therefore we can gain scientific evidence. 

However, with some explanations it can be more difficult e.g. depression.

For researchers to be happy that the depression is causing the insomnia, they have to be sure the dpepression was present first and that when the depression varies is severity so will the insomnia vary in serverity. To do this they rely on self-report methods and this is difficult because they are unreliable also it is difficuult to establish cause and effect from this and is therefore unscientific. 

Precipitating or maintaining?

If is difficult to establish if a factor is causing the insomnia or is maintaining it. Anxiety often creeps in an maintains the insmonia. This 'learned anxiety' makes it harder to treat the sleep disorder. Even if the precipitating factor (e.g. depression) can be identified, the learned anxiety will maintain the problem. 

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General Evaluation of Insomnia (AO3)

External Validty of sleep studies:

Due to high control and the artificial nature of the studies, they lack ecological valdity = not generalisable. 

BUT Garcia-Borreguero Et Al (2004) found a positive correlation between rating scales and laboratory measures of the sleep disorder called 'restless leg syndrome', providing some evidence that sleep laboratory measures are good indicators of ertain sleep disorders. 

Interanl validity of research:

Due to the use of polysomnography (measures whole body e.g. blood pressure, brain waves), research is highly scientific as it is objective and can be replicated.

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General Evaluation of Insomnia (AO3)

Reliabilty and validity of sleep insomnia measures:

There is controversy over the identification of insomnia in the first place. Some people think you cannot properly diagnose it. 

Schramm Et Al (1993) examined the test-retest realiabilty of the Structured-Sleep Interview that diangoses sleep disorders. They found excellent reliabilities for almost all the current main diagnostic categories. Also using the EEG. 

The main source of disagreement between the interviewers was found in the symptom ingormation given by the patient. Suggesting that subjective slef-report should not be overly relied upon. 

HOWEVER, Vgontaz et al (1994) argued that using a number of sleep laboratory criteria is an unsatifsatory way of diagnosing insmonia. 

A study inovling 375 insomniacs and 150 non-insomniac controls found that 'sleep laboratory recordings provided little relevent information for confirmiing or exlcuding the presence of insomnia' - The lab criteria didn't say who had insomnia and who didn't.

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Sleepwalking - What is it?


  • Sleep walking is a parasomnia and occurs during SWS and stages 3 and 4 of the sleep cycle
  • A sufferer can have serveral episodes per night
  • It cannot happen during REM as the bodyies muscles are relaxed and paralysed
  • Usually, they have no recollection of the event and they usually carry out routine automatic taks, however some can be complicated.
  • 10% of people in the world sleep walk at least once
  • 30% of 5-12 year olds have episodes of sleep walking but only 1-5& it occurs regularily
  • Predominantely adolesence sleep walk more
  • There is a range of factors to accumulate to produce sleep walking e.g.: Stress related factors, chemical imbalance (increased with alcohol and drug abuse) and a multiple physical and psychological factors. 

Sleepwalking is defined by someone shifting from his or hers prior sleeping position and moving around and performing normal actions as if they were awake.

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Psychodynamic Explanation for Sleepwalking

A Freudian interpretation is that sleepwalkers are acting out their dreams - this is becasue their behaviour looks directed and purposeful.

This explanantion is discredited by the EEG's and PSG's. Usin these scientific measures we can see that sleepwalking occurs during the deeper stages of NREM, not when a person is dreaming. 

Dreams usually occur in REM. In REM the muscles in the body are effectively paralysed and it would be impossible to act out dreams. 

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Sleepwalking AO2 - Genetics


  • It tends to run in families
  • Twin studies have found that concordance rates are 55% for MZ twins and 35% DZ twins (uses MZ twins because have 100% same genes.) 


  • There are some cases where the sleepwalker has no known relative with a sleep disorder. 
  • No research has ever found 100%
  • The DZ's 35% could be due to environmental factors, e.g. they are brought up with the same stressors
  • Using twins has the problem of remocing extraneous variables - nature vs nurture debate - they're treated exactly the same
  • TheDQB1 gene is not found in all sleepwalkers if it ws down to a specific gene then all sleepwalkers would possess this gene. 
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Sleepwalking AO2- Brain Development

Brain Development -

  • Sleepwalking is more common in children
  • This suggests it may be due to delayed development of the complex networks controlling sleep
  • This explains why people may sleep walk as a child and stop when they become an adult


  • This explanation explains why sleepwalking is more ocmmon in children and why a lot of people do 'grow out' of sleep walking
  • However it cannot explain adult sleepwalkers
  • It cant explain why adults tend to sleep walk when stressed. (sleep walking gets worse with stress - if sleep walking was only due to brain development environmental factors wouldn't effect it.
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Sleepwalking - IDA's


  • The biological explanations for sleepwalking are reductionist and narrow in scope
  • They focus on only one aspect of biology and therefore are the lowest level of explanation.


  • Raise the issue of free will and determinism - raises important issues for the legal setting
  • If deterministic view is taken - sleepwalkers are not held accountable for their actions and should not be found guily of crimes they commit - sleep walking is beyond their control their biology caused it not them.
  • Jules Lowes - 32 year old man from UK tried for murder in 2003. Could not recall committing the crime and claimed he was sleepwalking. Despite being found not guilty he was indefinitely secured in an insitution.
  • Research into this area has become sociallly sensitive and has huge ramifications for the legal world.

Diathesis Stress Model 

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Narcolepsy - What is it?

  • A neurological disorder - not psychological 
  • The onset is in adolesence or early adutlhood and continues throughout someones life
  • Thought that 1 in 2000 people suffer from narcolpesy but it is difficult to get an accurate measure of incidence as some people have it worse or more mild than others


  • Sudden and uncontrollable attacks of sleep
  • Day-time sleepiness
  • Cataplexy - loss of muscular control
  • Hallucinations
  • Sleep paralysis - when they wake up but cant move their bodies - this can cause more stress which can cause another narcoleptic attack
  • Not good sleep

Episodes are often triggered by emotional arousal such as anger, fear, amusement, stress or anxiety. 

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Explanations for Narcolepsy

As technology gets better so does the understanding of Narcolepsy:

Vogel (1960)

Found REM sleep occured at the onset of sleep in narcolepstic. So they skipped straight to 5. This explained some of the symptoms for example loss of muslce tone and halluncinations.

Honda Et Al (1983)

Found increased frequency of HLA in patietns. HLA coordinate the immune response and are found on the surface of white blood cells. The current view is that the mutations in the HLA complex lead to the immune system selectively attacking and destroying hypocretin neurons in the brain. Hypocretin controls REM - so the loss of hypocretin leads to abnormalities in the REM.

Lin Et Al (1999)

Found there were low levels of the neurotransmitter hypocretin which is thought to play a role in maintaining wakefulness. Found in narcoleptic dogs there was a mutation in a gene on chromosome 12 which disrupted the way hypocretin was proessed. 

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Narcolepsy - AO2 (Approaches

Most of the theories stem from the biological approach as they implicate abnormalities in the body - so they would advoate treatment using biological methods. 

An alternative approach such as the psychoanalytic one, would explain narcolepsy differently:

Lehrman and Weiss (1943) would argue the sudden onset of sleep are ways of disguising sexual fantasies or arousal, or ways of coping with them and reducing the anxiety and distress that they may cause. 

HOWEVER, this is a minority view and generally psychoanalytic explanations are not accepted outside of psychoanalytic circles. 

Furthermroe, given that the disorder has clear psychological elements, an inclusive explanation of the disorder woudl need to refer to iological factors because there are more biological factors. 

THEREFORE it might be more useful to use biopsychosocial framework to expalin narcolepsy.

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Narcolepsy - IDA

THe explanations of narcolepsy like HLA and hypocretin are seen as reductionist. This is becasue they attempt to reduce this complex multi-system disorder to malfuunctions of a specific biologicla system. It oversimplifies the disorder in an artificial way and offers an inadequete explainations. The theory fails to explain what causes the low levels of hypcretin in the first place. It is highly probable that other non-biological factors are invovled e.g. diet and infection that cause the damage to the hypocretin neurons.

Real Life Application:

If we accept the low hypocretin hypothesis then it should be possible to develop treatments to cure/treat narcolespy. Raising the levels artificially should help but there is no treatment avalibale yet. When treatments based on this hypothesis are developed and proven successful the hypothesis can be truly seen as valid.

Research Methods Evaluation

Research uses animal samples, findings cant be extrapolated and generalised to humans becuase they are different in anatomy and physiology. Also sleep patterns are different. 

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