A sleep disorder is any condition that involves difficulty experienced when sleeping. Such disorders often result in daytime fatigue, causing severe distress and impairment to work and social or personal functioning. Sleep disorders can be classified as:
· Problems with falling asleep or staying asleep, ie insomnia
· Problems with staying awake, such as narcolepsy
· Problems adhering to a regular sleep schedule due to, eg shift work or jet lag
· Sleep disruptive behaviours, called parasomnias (behaviours that occur during or around sleep) such as sleep walking, night terrors and bruxism (teeth grinding)
A general definition of insomnia involves problems in falling asleep, maintaining sleep and reductions in sleep quality so that sleep is non-restorative, thus leading to daytime tiredness. This can then affect daytime work and social functioning. Insomnia is not about how many hours of sleep someone has since individual needs vary. It may be classified as transient (short-term), intermittent (occasional) or chronic (long-term).
Insomnia has important negative effects including:
Insomnia can be divided into:
PRIMARY: describes cases where insomnia occurs on its own, with no known cause (no underlying medical or physciatric condition), for more than one month. The individual may have developed poor sleeping habits, which have led to the insomnia, but insomnia is the only problem.
SECONDARY: Refers to a sleep disturbance where a specific underlying condition can be identified as the cause. It comes SECOND after the main disorder. E.g. pain that experienced with arthritis can influence sleep so the resulting insomina is secondary to the medical condition.
Explanations of primary insomnia
1) Learnt maladaptive sleep patterns
Primary insomia may be produced and maintained through problematic associations, in other words classical conditioning.
People with primary insomnia may be associating alertness, active thinking, stress, work, study, sleeplessness etc (rather than sleeping) with the bedroom they sleep in (for example - uni students in dorms)
People may repeatedly work, read, watch tv, eat in bed etc thus associating the bed with activity or stress rather than sleep. Once the insomnia occurs it may be maintained as the bed or bedroom also becomes associated with sleeplessness and axiety about sleeplessness.
AO2 practical applications
- Only have your bedroom for sleeping and resting and have separate room for work
- Only go to your bedroom when you;re actually sleepy
- Leave the room if you can't fall asleep after 20 mins
Explanations based on CC have useful practical applications
2) poor sleep hygiene
Examples of poor sleep hygiene: light, night, uncomfortable bed etc
Poor sleep habits can also account for primary insomnia, for example going to bed/waking up at irregular times, having an uncomfortable bed, not eliminating noise/light from the bedroom.
Therefore, improving sleep hygiene can reduce the chances of insomnia by establishing and maintaining more stable circadian rhythms as well as limiting sources of sleep disruption.
3) biological explanations
There's no clear explanations for primary insomnia, but its known that sleep mechanisms are very complicated, involving control centres throughtout the brain and an interplay between endogenous pacemakers (body clocks) and external zeitgebers (time-givers). Neurotransmitters such as melatonin, serotonin, noradrenaline and acetylcholine are also involved.
AO1: Primary insomnia may be caused by some BASIC MALFUNCTION IN OUR SOPHISTICATED SLEEP CONTROL SYSTEMS. This may be genetic, as there is some evidence that idiopathic insomnia (lifelong, serious insomnia beginning in childhood with no obvious cause) runs in families. One study found that nearly 35% of insomniacs surveyed indicated that they had a first degree relative with a current or recent problem with insomnia (mothers were most likely to be identified as sufferers - nearly 20%). Watson et al (2006) found that insomnia in MZ twins was highly correlated (0.47), but for DZ twins only 0.15. This suggests that genes don't predict insomnia, but do have an influence.
AO2: It's very difficult to separate environment from genetic factors in family and twin studies. Families share environments, and the increased incidence may be explained by social learning theory - observing someone with insomnia.
AO1: Another biological explanation comes from Winkelman et al (2008) who claims that insomnia may be caused by speicifc changes in brain chemistry. They found that people who had been suffering from insomnia for more than 6 months had reduced levels in their brain of the neurotransmitter GABA, an inhibitory transmitter that reduces activity in the brain. Reductions in GABA mean that the brain isnt being quietened down at night, which might account for the common complaint amongst insomniacs that they are unable to sleep because they cant 'switch off' their thoughts. AO2: The GABA neurotransmitter not reduced-is it due to insomnia or the GABA causes insomnia
This is where there is a single, underlying medical, psychiatric or environmental cause (e.g. alcohol, stress, depression, anxiety, physical injury like broken arm/leg,shift work etc). In these cases insomnia is a symptom of the main disorder, e.g. shift work or those who have circadian rhythm disorders such as phase delay symptoms (a disorder where sleep is taken at a much later time than might be expected, e.g. 4am - 11am). Finally, it may be the result of environmental factors such as too much caffeine or alcohol.
COMMON CAUSE OF SECONDARY INSOMNIA INCL.:
- AO1:PSYCHOLOGICAL DISORDERS such as depression, anxiety states and SZ; approx. 40% of patients seeking treatment for insomnia are thought to have an associated psychological disorder (morin et al 1999).
- AO2:Benca and Peterson (2008) found that depression and insomnia are so closely related that they ay share similar underlying mechanisms; e.g. genetic abnormalities in circadian pacemakers, or shared neurochemical imbalances. However, not all people with insomnia have depression and vice versa.
Consider the following study linking insomnia with high levels of anxiety;
GREGORY ET AL (2006)
Aim: to investigate the relationship between family conflict and later development of insomnia
Method: a longitudinal study following a group of new zealand children from birth in 1972 to present day. questionnaires were used to measure levels of tension, hostility and distress in the family. it also inclded events such as separation and divorce. factors such as socio-economic status, gender, health and depression were controlled.
Results: the degree of family conflict experience by the child between 9 an 15 was significantly related to the frequency of insomnia at 18.
Conclusion: researchers suggest that insecurity may lead to high levels of anxiety and a tendency to focus on family difficulties. this supports the view that insomnia is linked to high levels of anxiety.
cont..these could lead to secondary insomnia
- Medical conditions Such as heart failure, Parkinsons disease and asthma. Furthermore, treatments for medical conditions can lead to insomnia, eg the use of steroid therapy for asthma. Bardage and Isacson (2002) found that those using hypertension medication may suffer from insomnia.
- Drug use can lead to insomnia, eg stimulants such as amphetamines and alcohol, or the overuse of sleeping tablets. Philips and Danner (1995) found that smokers are more likely to be insomniacs than non smokers.
- Parasomnias - Sleep apnoea (a medical condition where sleepers have persistent pauses in breathing) and sleep walking, for example, may disrupt normal sleep.
- Brain injury - Many people are diagnosed with insomnia after brain injury. Cohen (92) found insomnia incidences of up to 72% in patients with previous brain trauma which is much higher than the general population.
Why is a distinction between primary and secondary insomnia important?: The differentiation between primary and secondary insomnia is important because of the implications for treatment. If insomnia is a symptom of another disorder, then it is important to treat the disorder rather than the insomnia.
AO2 line of argument: However, some research casts doubt on whether insomnia is just an effect- it may be the cause. Ohayon and Roth (2003) studied almost 15,000 Europeans and found that insomnia more often preceded than followed cases of mood disorder. This means that, in some cases, it might be helpful to treat insomnia regardless of whether it is a primary or secondary effect.
treatment of insomnia may give an indication of ca
- Drugs to treat depression or anxiety can reduce the secondary symptom of insomnia
- Drugs to treat insomnia, ie sleeping pills, seem to increase sleeping time, but reduce sleep quality, disrupting the normal ultradian pattern of REM and NREM sleep, demonstrating the limited nature of the biological approach.
- Stimulus control therapy - this treatments based on the idea that insomnia is a conditioned (learned) response to various cues such as night time and the envrionment of the bedroom. Because insomnia has become associated with these cues, a new association between sleep and these cues need to be learnt. Techniques used to create new associations are quite effective, supporting the role for conditioning in the development of insomnia.
- Cognitive behavioural therapy (CBT) - people who suffer from insomnia often report that they become anxious at bedtime. They know they should go to sleep and stay asleep, or they may not be able to cope in their daily life. The more they try to sleep, the worse it gets. CBT is aimed at correcting these faulty cognitions. The success of this method supports a role for cognitive processes and axiety-related arousal in insomnia.
- Phototherapy (the use of very bright lights to treat disruptions to biological rhythms) can be used for circadian disruptions. Also anti-anxiety drugs and melatonin can be used, although these offer only short term solutions.
- Relaxation techniques may be used to deal with over-arousal as a cause of insomnia. ^ all practical application
More relevant IDA for above explanations of insomnia: Biological approach (link genetics)/ethical concerns for such a sensitive topic and issues when researching it/insomnia is genetic (nature) or learned (nurture)
AO2:difficulty in studying insomnia - such a complex problem with lots of factors/causes(age,gender,personality)hard to reach firm conclusion.
ao2 for insomnia
- practical applications
- learnt maladaptive sleeping patterns - only have your room for sleeping and resting and a separate room for work, only go to your bedroom if you're actually sleepy.
- poor sleep hygiene - incomplete as it does not take anything biological into account
- biological - it is holistic as takes biology (genes), environment and SLT into account
- holistic explanations overall are all holistic as they consider a range of factors (environment, genes etc)
- cause and effect - is insomnia the cause or the effect?
- biological is deterministic as saying genes determine
- validity of sleep insomnia (how we collect data) data not that accurate as we rely on data from the patient telling us, so it's also subjective
- generalisation 0 as there are many different types of insomnia its difficult to generalise causes because of the variety (so many differenty types-initial,middle,chronic)
- difficulty in studying insomnia-such a complex problem with lots of factors/causes (age,gender,personality)so hard to reach firm conclusion - individual differences
- holistic approach is best which incorporates environment, genetic, however;there currently isn't one combined at the moment-suggest this.
- people overestimate how many hours it takes to fall asleep an underestimate how many hours sleep they had
- objective data as GABA measured (for primary insomnia) and also subjective due to self report etc
- for secondary insomnia there's cause and effect problem. (e.g. depression causes insomnia, but maybe insomnia causes depression) don't know which is causing it.
- cultural differences - some wake up early (like eastern countries) so this is normal, but western may see it as terminal insomnia
- genetics explanation crictised that the concordance rate is not 100% so it's not a perfect explanation. we also don't know how the environment is playing a part
- males don't like going to the doctors, women do more. studies find it more common in women but this may be becaused women report it more
1 IDA for insomnia
Nature/nurture & generalisability
The explanations of insomnia favour both the nature and nurture side of the nature nurture debate. The biological explanation of primary insomnia is more nature as it suggests insomnia may be due to malfuntion in our sleep control systems and may be due to idiopathic insomnia (beginning in childhood, which may run in families).
A study found that nearly 35% of insomniacs indicated that they had a 1st degree relative with a current or recent problem with insomnia.
However, the maladptive sleep patterns supports the nurture side, as the associations are learnt processes, for example uni students bedrooms are associated with working as well as sleeping.
Moreover, these explanations were just on primary insomnia, there are many different types of insomnia and so generalisation is a problem due to so much variety in causes (age,gender,personality etc).
- sleepwalking is a condition in which aspects of both wakin and sleeping occur at the same time
- sleepwalking usually occurs during the first 2 hours of sleep, in stafe 3 and 4 sleep
- it affects about 20% of children, and is most common among 4 to 6 year olds (more frequent in boys)
- it affects less than 3% of adults (hubblin et al, 1997)
- sleepwalkers engage in routin behaviours such as dressing themselves, or getting themselves something to eat
- in severe cases it may have a serious effect on someones life
- it only occurs during NREM or SWS and is related to night terrors (All most commonly found in children)
- a sleep walker is not conscious and later has no memory of events during sleep walking
Explanations of sleep walking
1) SLEEP DEPRIVATION. AO1: Sleep walking can be triggered due to sleep deprivation.
AO2 R. Evidence: Zadra et al (2008)
- studied 40 self referred sleep walkers in a sleep lab. the number of times the p's walked around, played with bed sheets and dat up in bed etc were counted throughout the night
- they were observed during 1 normal nights sleep and again when deprived of sleep for 25 hours
- it was found that on the 1st night 50% of sleepwalkers had shown signs of sleep walking. after being deprived of sleep, this rose to 90%
- Zadra noted that sleep deprivation doesn't seem to cause sleep walking in normal individuals, but does in those who are genetically predisposed to the condition
AO2 evaluation points:
- sleep walking doesn't happen in those who aren't genetically predisposed to it - so sleep deprivation explanation can't be generalised to normal people that sleep walk as they may not be genetically predisposed
- individual differences - some may react different to sleep deprivation,90% did but 10% didn't
- sleep lab has low ecological validity
- 1 nights sleep may not be enough to properly study sleep walking
- self referred sleep walkers - some may not know they even sleep walk. sample may be biased and unrepresentative and so low generalisability
- practical applications, improve sleep hygiene. don't have coffee, alcohol etc and get sleeping pills if you're sleep deprived
2) Incomplete arousal
- EEG recordings made during sleep walking show a mixture of the delta waves typical of SWS, plus the higher frequency beta waves which are characteristic of the awake state.
- It looks as it sleep walking happens when someone in SWS is awakened, but the arousal of the brain is incomplete.
- This incomplete arousal seems to be the rsult of genetic factors, since sleep walking tends to run in families.
AO2 evaluation points:
- EEG recordings and data is objective and so scientific and quantitative
- Simplistic, doesn't focus on individual differences or the environment. Just the SWS and genetics briefly
3) Genetic predisposition
- The exact nature of the genes underlying sleep walking is unclear, although Bassetti (2003) suggests that it may be related to the same HLA gene abnormality associated with narcolepsy
- If sleep walking is genetic condition, it would be expected that the disorder would be more common in families and specifcally twins as they share the same genetic makeup
- Evidence to support: Broughton (1968) who found that the incidence of sleep walking in 1st degree relatives of someone with the disorder is 10x greater than in the general population
- Lecendreus et al (2003) report a 50% concordance rate in MZ twins (identical) compared to 10-15% in DZ twins
- Bassetti (2002) gene tested 16 adult sleep walkers, finding that 50% had a specific gene found in only 24% of non-sleep walking people. The gene is one of a family of genes producing proteins called HLA, involving in regulating the immune system
AO2 R. EVIDENCE:
- Hublinet et al (1997) Finnish twins, found 66% concordance rate in boys and 57% concordance rate in girls have gene suggesting genetic link
Genetic predisposition ao2 eval
- May not be representative as the sample was small in the study
- Bassetti used a volunteer sample - some sleepwalkers may not even know they sleep walk
- Objective - blood tests to find genes - replicable and consistent results = reliable
- Concordance rate not 100% so something else (Eg environment) is influential
- Deterministic - says genes control sleep walking. Focuses on biology only and you're unable to change this
- Same environment for families
- HLA gene is not in all sleepwalkers
4) other factors
AO1: Alcohol has been shown to increase the likelihood of sleep walking, as has having a fever, stress or psychiatric conditioon (Piazzi et al, 2005). Hormonal changes during puberty or menstruation may also be a cause.
AO2 EVALUATION POINTS:
- Individual differences - people may react differently to each of these factors
5) Diathesis stress model
- The diathesis (vulnerability) comes from a genetic predisposition to the disorder. There is strong evidence that suggests sleep walking is a genetic disorder e,g, Broughton (1968)
- The stress part of the model is represented either by maturity in certain key neural circuits in the brain or by the amount of SWS experienced
- One reason sleep walking is more prevalent in children is because they spend a greater amount of time in SWS than adults. The same is true for other risk factors mentioned - sleep deprivation, alcohol, fever all increase SWS and this may trigger sleep walking
AO2 EVALUATION POINTS:
- Holistic as it takes environmental and genetics into account
- Valid explanation or reason for why sleep walking more common in children
- Explanations best combined and bring in diathesis stress model
- Cause and effect issue - genetics
- 23 yrs old Canadian
- Was asleep, drove 23km to his inlaws house and assaulted his father in law and stabbed his mother in law to death
- He had financial and gambling problems
- Defefence said he has a history of sleep walking and that he wasn't aware
Narcolepsy is characterised by 4 major symptoms:
- Extreme daytime sleepiness, with repeated short episodes of sleep throughout the day
- Cataplexy: sudden, unexpected loss of muscle tone while awake. Can lead to immediate collapse (but still conscious) lasting few secs to a few mins. It can be brought on by emotional arousal
- Hypnagogic hallucinations: these are dreamlike experiences occuring during wakefulness, especially during the transitional period between sleeping and waking up
- Sleep paralysis: an inability to move often occuring when falling asleep or waking up
MALFUNCTION OF REM SLEEP
AO1: It intrudes into waking life. In the 1950's this was a popular idea because the characteristics of REM match narcolepsy. Body paralysis and hallucinations also occur. Going through REM whilst awake.
AO2 R. EVIDENCE: Vogel (1960)
- Recorded brain waves in 1 patient during narcoleptic episode and found brain waves similar to those in REM sleep
- Case study = low generalisability
AO1: Relates to genetic mutation releated to the neurotransmitter hypocretin. This neurotransmitter is involved in the brain mechanisms that promote wakefulness so it would make sense that an abnormality with this neurotransmitter would affect ability to stay awake.
AO2 R.EVIDENCE: Lin et al (1999)
- Narcoleptic dogs who had a mutation in a gene on chromosome 12 which disrupted the processing on the hypocretin.
AO2 EVALUATION POINTS:
- Problem using animals to generalise to humans however Nishino et al (2000) tested the fluid in narcoleptics spine and found low levels of hypocretin, which was done on humans.
- However, low levels of hypocretin are unlikely to be due to inherited factors because human narcolepsy doesn't run in families (Mignot 1998). The concordance rate for narcolepsy between MZ twins is only 30% showing it's not 100% inherited. This relates to nature/nurture - a stressful event (like family member death for example) is the environmental situation, which brings the narcolepsy IF there's a genetic vulnerability.
- Biological explanations may be reductionist, failing to consider the full picture.
- Application - Treatments often involve stimulants. The drug Modafinil has proved useful in treatment. It works by activating hypocretin-containing nerve cells and its success lends support to the hypocretin deficiency explanation. Mahowald and Schenck (2005) found that administering hypocretin to narcoleptic dogs led to reduced cataplexy and more normal sleep and waking durations.
E.g. of IDA
Explanations of sleep disorders often adopt a physiological approach which means that research can be carried out scientifically with accurate and objective measures of the precise physiological mechanisms involved in a sleep disorder; for example the role of hypocretin in narcolepsy.
However, such an approach raises issues of reductionism since such explanations fail to provide a holistic view. For example, explanations of sleep walking may be extremely complex and cannot be explained using one factor alone.
The diathesis stress model combines both the environment and biology in an attempt to explain why sleep walking occurs. This aims to identify the diathesis (vulnerability) as coming from a genetic predisposition to the disorder, whereas the stress could be caused by other environmental risk factors like alcohol, fever, sleep deprivatiom thus taking nurture into account. This would help to explain the results by Lecendreus et al (2003) since the concordance rate for MZ twins was just 50% and not 100%. Consequently the complexity in each sleep disorder means one explanation may not be enough.