Sleep disorders

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  1. Explanations of sleep disorders:
    • Insomnia
    • Sleepwalking (somnambulism)
    • Narcolepsy
  2. Insomnia:
    • Affects 10% of the population. It involves problems falling asleep, maintaining sleep and reductions in sleep quality so sleep is non-restorative.
    • Two types: - primary and secondary
  3. Primary and Secondary insomnia
    • Primary: - chronic insomnia occurring in the absence of any psychological or physical condition that might explain the disorder (a disorder in its own right)
    • Secondary: Chronic insomnia that can be explained by a pre-extisting psychological or physical (medical) conditioning (caused by another disorder) could also be a result of sleepover walkng or sleep apnea.
    • Differences: PI treat the insomnia
    • SI treat the underlying cause.
    • BUT not always clear if insomnia is just a symptom of the main cause or primary.
  4. Explanations of insomnia
    • Other sleep disorders - sleep apnoea, (abnormal pauses in breathing or instances of abnormally low breathing, during sleep), sleepwalking, snoring or teeth grinding can lead to insomnia.
    • Medical conditions (e.g. heart failure)
    • Drugs such as amphetamines, alcohol and hypotics affect brain neurotransmitters and probably lead to insomnia by disrupting the control of our complex sleep systems
    • Age - older people are more likely to get insomnia due to problems such as arthritis or diabetes
  5. Biological AO1 - insomnia
    • Refers to common observation that some people are aroused, alert and functioning well in the morning and some people in evenings (some individuals are intermediate types and function well all day)
    • Difference between extreme morning types (MT) and evening types (ET) is genetic and based on biological circadian rhythms of sleep and waking
    • These characteristics are stable over time and represent a distinctively personality trait - controlled by endogenous pacemakers due to genetics
  6. Biological AO2 - Insomnia
    • Research shows MT - circadian rhythm is 2 hours of ET
    • Lots of research supports chromosomes that effects endogenous pacemakers are genetically determined
    • Deavilleers et al 2005
  7. Deavilleers et al 2005
    • found 73% primarily insomniacs reported a family history of insomnia.
    • 24% in non-insomniacs -suggests a genetic component to the condition
  8. Cognitive A01 insomnia
    • associated with anxiety
    • Clinical anxiety - we know anxiety can be a cause of secondary insomnia
    • Associated with high level of physiological arousal acts against a tendency to sleep so more likely to suffer with insomnia
    • Clinical anxiety and depression are major causes of insomnia and even in general population a tendency towards anxiety makes insomnia more likely.
  9. Cognitive AO2 - insomnia
    • Cognitive treatments are most effective - such as muscle relaxation and CBT
    • Also supported by twin studies showing high levels of sleep disturbances (most insomnia) are associated with high levels of neuroticism a personality trait that is significantly correlated with anxiety
    • Vahlera et al (2007)
  10. Vahlera et al (2007)
    Vulnerability to sleep disorders following traumatic life events such as divorce is highly correlated with the personality trait of anxiety
  11. IDA
    • Reductionist - a holistic approach may be needed
    • Nature-nuture - Brain mechanisms V environmental factors
  12. Sleep walking:
    • May affect 10% of the population at some point in their lives
    • Around 30% 5-12years may have episodes of sleepwalking but only occurs regularly in 1-5%
    • Tends to run in families - genetic involvement
    • The person typically has their eyes open but described as a glazed or soaring in appearance
    • Typical behavior is moving around normally or just in the bed room
    • However some people have been known to drive cars and ride horses - Ebrahim and Fenwick (2008)
    • Tends to occur in stage 3+4 and therefore earlier at night since there is slow waves (less likely to happen in REM as muscles are effectively paralysed
  13. Biological Explanations AO1 - Sleepwalking
    • Tend to run in familes - led to assumption there maybe a biological (genetic) basis
    • Some research supports this - Bassetti (2002)
  14. Bassetti (2002)
    • found 50% sleepwalkers has a specific gene which is only found in 24% non-sleepwalkers
    • suggests genes may dictate the degree of vulnerability to sleepwalking
  15. Biological Explanations AO2 - Sleepwalking
    • But there is no clear biological explanation beyond the relationship with NREM
    • Lack of reliability of research suggesting a genetic link as many other studies have found NO relationship
  16. Psychodynamic Explanations AO1 - Sleepwalking
    • It has been suggested that sleep walking represents a desire to sleep where the individuals slept as a child (however this doesnt explain the wide range of activities carried out)
    • An explanation based of Fraud work suggest that we are working through unconscious anxieties during our dreams moving from REM to NREM prevents this so unconscious instinctual energies spill into NREM and are channeled into motor activities - Sleepwalking
  17. Psychodynamic Explanations AO2 - Sleepwalking
    As with most psychodynamic ideas, this explanation is impossible to test scientifically because it uses no empirical methods so unable to prove causality
  18. General AO2 - sleepwalking(SW)
    • Gender differences - boys suffer more than girls - limits generalisability from one gender to another gender
    • Pilon et al (2008) have suggested that its more likely to occur if you are fatigue and had a previous lack of sleep. Other triggas are stress, alcohol and other drugs
    • reinforced by Plazzi et al (2005) found that various factors appear to increase the likelihood of SW e.g sleep deprivation, alcohol, having a fever, stress, hormonal changes in puberty and menstruation can also be triggers
  19. IDA - sleepwalking
    • Is psychology a science? - subjective based on ideas of fraud- out of date  - not falsifiable nor empirical 
    • No medical treatmenet has yet been devised to combat SW. The disorder incurs serious accidents and distressing incidents (sexsomia) - treatment is essential
  20. Narocolepsy
    • Randomly falling asleep - when you least expect it
    • Only effects between 0.02% and 0.0005% of the western population
    • It often occurs with cataplexy (sleep hallucinations) - not at the same though
    • 4 major symptoms: - extreme daytime sleepiness
    • episodes of cataplexy
    • hypagoric hallucinations
    • Sleep paralysis
    • -> only 50% of sufferers show all four symptoms but have cataplexy and at least one other symptom
  21. Biological Explanation AO1
    • Since narcolepsy tend to co-occur with the above symptoms they may be a problem with the regulations of REM
    • Since your body is paralysed and you dream in this stage
  22. Biological Explanation AO2
    • There is strong research support evidence suggesting this is the correct explanation of narcolepsy
    • Vogel (1960)
    • Nishino et al (2000)
    • Thannickal et al (2000)
    • However the overall research is weak - research has shown it might have something to do with the brain structure
  23. Vogel (1960)
    found that REM is more likely to occur at the onset of sleep in people with narcolepsy in contract to normal people where they have REM at the end of their sleep cycle
  24. Nishino et all (2000)
    found a link between hypocretin and narcolepsy in humans
  25. Thannickal et al (2000)
    shpwed an 85-95% reduction in hypocretin neurons in people with narcolepsy BUT measuring these neurotransmitters is hard
  26. Biological explanations (gene defect) AO1:
    • A gene may be responsible for narcolepsy - shown in dogs
    • The gene is responisible for regulating brain receptors for oxexin (a neurochemical that regulates arousal, wakefullness and appetite sometimes called the hypocretin)
    • Without recpetors orexin can not function - lack of orexin/ its receptors may be the cause of narcolepsy in humans
  27. Biological explanations (gene defect) AO2:
    • Lin et al (1999) showed that dogs and mice with narcolepsy has a genetic mutant on chromosome IZ that lowers the production of hypercretin (which is a neurotransmitter that blocks messages about being awake and controls the REM)
    • Supported by other animal studies suggesting we can generalise these findings to other species - however maybe not to humans as humans have very complex brain structures
    • Nishino et al (2000) found 25-31% concordance rate for MZ twins with narcolepsy and a 1-2% rate in first order relatives - BUT the condition is not entirely inherit and therefore environmental factors must also be important
  28. IDA narcolepsy
    • Suggest psychology is a science - objective and empircal - counting neurons
    • No effective treatment exists so the explanation cannot be truely correct otherwise it would be treatable - most stimulants deal with day time tiredness - palliative nor curative
Card Set:
Sleep disorders
2014-05-31 11:02:28
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