Psya3 Sleep Revision Document
Revision Notes: Sleep
Specification * Nature of sleep, including sleep stages and lifespan changes and lifespan changes in sleep. * Functions of sleep, including evolutionary explanations and restoration theory.
Nature of sleep * Sleep is a different state of consciousness where responsiveness to the external environment is diminished. * It occurs daily as circadian rhythms and is composed of an Ultradian cycle of separate stages. * With the intention of the electroencephalograph (EEG), psychologists were able to investigate brain activity occurring during sleep and concluded that it was composed of identifiably different sequential stages. (Electrical activity or brain waves). * Electro-oculograms (EOGs) measure eye movement, and Electromyograms (EMGs) measure muscle movement and have been used to distinguish the stages and cycles of sleep. * Sleep is circadian as it happens once a day however it is also Ultradian as the stages are repeated within a cycle. Each cycle is approximately 90 minutes and most people experience 5-6 cycles a night. Stages one to four are slow wave sleep (SWS) and stage five is rapid eye movement sleep (REM). * Brain is active during sleep and this activity can be measured (EEG). Different stages of sleep show different patterns alpha, delta and theta waves. * One cycle takes about 90 minutes; later in the night there is more REM sleep and less SWS.
Stages of sleep
STAGE ONE: Beginning of the sleep cycle. Alpha waves disappear and are replaced by low-voltage slow waves. Heat rate declines and muscles relax. This is a light sleep and the sleeper can easily be woken.
Brain produces high amplitude theta waves, which are very slow brain waves – lasts 5-10 minutes.
STAGE TWO: A deeper state, in which the sleep is still easily woken. Short bursts of sleep spindles are noticeable, together with sharp rises and falls in amplitude known as K-complexes. Lasts about 20 mins.
STAGE THREE: Sleep becomes increasingly deep, and the sleep difficult to wake. Sleep spindles decline, being replaced by long, slow delta waves. Heart rate, blood pressure and temperature decline.
STAGE FOUR: Deep sleep, where delta waves increase and metabolic rate are low. The sleeper is difficult to wake. Growth hormones are released and incidences of sleepwalking and night terrors may occur. 30 mins.
The sleeper spends about 30 minutes in stage 4 sleep, with about an hour passing in total from stage 1 to stage 4. Stage 3 is re-entered, then stage 2 and then the sleep enters an active stage of sleep called rapid eye movement (REM) about 90 minutes after failing asleep.
REM: Eye movements are noticeable, heart rate, respiration etc. Increase and dreaming occurs.
Another 15 minutes of REM sleep, the sleeper re-enters 2, 3 and 4 in that order then another cycle begins. It is common to go through about five Ultradian cycles in one night. As the night progresses, the sleeper spends more time in REM sleep and less time in the other stages. This pattern is fairly universal; although there are development differences.
Research support.
Dement and Kleitman (1957) * Conducted highly controlled experiments in a sleep lab using biological measurements (e.g. EEG). * 9 male participants for 61 nights. * Participants were woken at each different stage of sleep and asked a series of questions. * Those awakened during REM sleep (identified by the EEG) reported dreams 79% of the time and only 7% in NREM. * + Was an important piece of research in that it was the first piece, which objectively correlated brain states with dreaming. * - Due to artificial environment, the findings may lack ecological validity because participants in research were not allowed to experience normal sleep, they experienced sleep disturbance. Could cause REM and Stage 4 rebound effect. * - Small sample: Not representative.
EVALUATION
+ Objective evidence: EEG, EOG AND EMG illustrate psychology as a science.
+ Universality: Stages + cycles of sleep have been found across cultures.
- Artificiality of sleep laboratory – extrapolation issues.
- Individual differences – reductionist – simplifies all sleep to a set of stages + cycles – people will differ.
- A03: Weakness of the self-report method: Yields date that may be subject to social desirability bias.
Sleep and the lifespan:
Infancy: babies sleep for about 16 hours a day but not continuously. They wake up every hour or so and the cycle is shorter than an adults. They experience two types of sleep: active and quiet which are versions of REM and SWS. Approximately half is spent in active (REM) because of their need for growth. By about 6 months old most children have one main sleep-wake cycle with a few naps in the day.
Childhood: children typically sleep about 12 hours a day and EEG patterns resemble adult patterns. The amount of sleep gradually decreases. As the brain is still developing they spend approximately 3 and a half hours in REM. Parasomnias are very common in childhood (sleep walking and night terrors).
Adolescence: Sleep duration increases in adolescence. Boys often experiences orgasms and ejaculation during sleep. There is a phase delay and circadian rhythms shift so teenagers stay awake later and wake up later. Our need for sleep has decreased, as we don’t need much growth. Schools should adjust their day to fit the delayed sleep pattern syndrome.
Adulthood: adults sleep for typically 8 hours per night and 25% is spent in REM sleep. There is an increasing frequency of sleep disorders such as insomnia and sleep apnoea.
Old age: sleep patterns change and it is often more difficult to get to sleep and they wake more often. REM sleep decreases to about 20% and SWS decreases to about 5%. There is a phase advance as they go to sleep earlier and wake earlier. They also may nap during the day to satisfy sleep needs.
EVALUATION
* - Cultural differences – Tynjälä et al: your culture also affects your sleep pattern. A survey via the Internet of 11-16 year olds from 11 European countries and other non-European countries to compare. Approximately 40,000 participants. Found that teenagers in Israel slept 8.5 hours compared to other countries they slept the least. In Switzerland they slept for 9.5 hours, the most. These results were often the effect of social factors such as going out, sleeping at someone else’s house etc. In collectivist cultures they also sleep less as they have more duties and chores to do. Therefore age is not the only contributing factor. * + Developmental approach: looks and follows people as they grow and then tries to map changes. In the past the developmental approach was from new-born to adulthood. They assumed that sleep stayed the same after adulthood, which we now know not to be the case. The original form of this approach would have been a limited inadequate explanation. * - Research methods: experiments carried out in sleep labs are environmentally wrong as it is an artificial environment and therefore the results were not that reliable. Furthermore it has often been established that sleep hygiene and environment plays a part in our sleep pattern. * + Applications to real life: findings have been used to reduce the level of cot death (S.I.D.S). Infants spend a lot of time sleeping and wake up a lot. There have been methods developed to prevent it, for example sleeping on their back or side to open their airways. Dummies help them stay out of REM sleep as it keeps them partly aroused physiologically. * + Objective measurements: Research into lifespan changes in sleep has been conducted in numerous sleep laboratories throughout the world. * + Real world application: Sleep quality can be improved through the use of melatonin. Melatonin induces sleep by inhibiting the brain mechanisms that promote wakefulness. * Individual differences: Borbely (1986) warns against the use of generalisations about sleep patterns for different age groups due to the many external factors e.g., work patterns, medication etc.
Functions of sleep.
Restoration theory.
OSWALD.
SWS initiates body repair.
Growth hormone
- Important in childhood because it stimulates physical growth.
- Important throughout lifespan for protein synthesis and cell growth.
- Oswald observed that this was secreted to some extent during the day but mainly in SWS. Cauter and Plat support this in that the amount of growth hormone correlates with the amount of SWS.
REM sleep initiates brain repair.
Brain growth supports this
- Infants have a greater proportion of REM (i.e. active) sleep than adults, which suggests that REM sleep may be important to brain growth.
- Siegel suggests that the amount of REM sleep in any animal is proportionate to the immaturity in any offspring at birth. Platypus young are very immature and have about 8 hours REM, whereas dolphin young are very mature and have almost no REM sleep.
Neurotransmitter function.
- Sigel and Rogaski suggest that during REM sleep neurotransmitters are not produced, allowing neurons to regain their sensitivity.
- Stern and Morgane (1974) believed that, during REM sleep, neurotransmitter levels are replenished, supporting the idea of restorative sleep. This is backed up by the fact that anti-depressants increase neurotransmitter levels, reducing REM activity.
HORNE
- ‘Core sleep’ = SWS 4 + REM: Essential for repair/restoration of the brain.
- ‘Optimal sleep’ = SWS 1-3: Not needed at all for repair/restoration.
- Restoration of the body occurs when we are awake.
Research support
Rechtschaffne (1989)
- Rats on a turntable.
- When ever their brain patterns changed to show they were sleeping the turntable started to turn so that they woke up and exercised.
- If they didn’t they would fall into the water, rats only had 16% of usual sleep.
- Rats weak and lost weight even though it still ate as its metabolic rate had increased.
- Most of the experimental rats died between 21-33 days after the experiment began.
- Supports restoration theory as rats died because their metabolic rate was high and they needed to rest and repair.
- Difficulty extrapolating results from rats to humans. + Lab study, well controlled: can establish cause and effect. – However could be other factors? Stress? Cirelli et al (2004)
- Found that, during SWS, genes associated with the protein production that regulated synaptic connections are activated, supporting restoration theories, especially Oswald. EVALUATION: Lots of supporting research and biological support. * If sleep (SWS+REM) is restorative, total sleep deprivation should have negative effects: Case studies show some support. DJ Tripp stayed awake for 201 hours and after 5 days he experienced hallucinations and paranoia, his brain rhythms looked like he was asleep. * HOWEVER… Horne and Minard found that a series of exhausting tasks led people to get to sleep faster but not for longer. * If sleep (SWS+REM) is restorative, total sleep deprivation should have negative effects: Case studies show some support. DJ Tripp stayed awake for 201 hours and after 5 days he experienced hallucinations and paranoia, his brain rhythms looked like he was asleep. * HOWEVER… Sleep deprived individuals may actually be getting some sleep e.g. laboratory observations have found that sleep deprivation for more than 72 hours results in periods of micro sleep while participants are apparently awake (Williams et al). I.e. sleep-deprived participants are only apparently awake but experiencing some benefits of sleep. * HOWEVER… Another case study on Randy Gardener found no psychotic symptoms after 11 days without sleep and there are reports of individuals e.g. Hai Ngoc who haven’t slept for years with no ill effects. * However such individuals may be experiencing micro sleeps. * Methodological issues: Case studies relate to unique individuals and other sleep studies often use volunteers who also might have unique characteristics (e.g. less need for sleep than the norm) so results may lack Generalisability. *
Methodological issues: Non-human animal studies lack Generalisability because animals have different sleep requirements to humans. *
If SWS is important, SWS deprivation should have negative effects: Demonstrated in ‘rebound effects’ – when people are deprived of SWS they show need for more SWS on subsequent nights. * IF REM is important, REM sleep deprivation should have negative effects: This is supported by research evidence that shows that REM deprivation results in as much as 50% more REM sleep on subsequent nights.
The evolutionary approach: The main alternative to the restoration theory is the evolutionary approach, which claims that sleep has no specific benefit except for protection (to conserve energy or keep an animal safe from predators), rather than performing some specific biological function as claimed by the restoration theory. The restoration approach doesn’t explain, for example, why some species sleep one hemisphere at a time (E.g. dolphins). Nor does it explain why lack of consciousness is necessary. It looks like environmental pressures are important in shaping sleep processes, which can be explained by the evolutionary approach. * Gender bias: All of sleep deprivation research is based on male participants. EVOLUTIONARY THEORY OF SLEEP.
Sleep is adaptive. It exists to promote survival and reproduction. Any behaviour or characteristics that increase likelihood of survival and reproduction will be naturally selected and will survive as the animal evolves. Each animal adapts their sleep pattern to their environment (ecological niche) for example dolphins sleep for seconds at a time switching between hemispheres in order to survive. Energy conservation.
High expenditure of energy: Warm-blooded animals (such as birds or mammals) use energy to maintain temperature (homeostasis). This is especially true for small animals with a high metabolic rate such as mice. This linking to the benefit of sleep as sleep provides a period of enforced inactivity to conserve energy, such as hibernation; therefore small animals should sleep lots to conserve energy. This links with Webb’s hibernation theory of sleep: Active animals need large amounts of food, threatening survival during times of food scarcity. Hibernation conserves energy and increases survival. Grizzly bears hibernate though the winter, living off body fat accumulated during times of food availability. * + This theory predicts a negative correlation between body size and sleep supported by Zepelin and Rechtschaffen who found smaller animals sleep more than larger animal, although there are exceptions e.g. sloths, who are large and sleep a lot. * However, this is not supported by Capellini et al who found a positive correlation. This study used carefully selected, standardised data and therefore may be more reliable than other evidence. * + Energy only conserved in NREM sleep… In REM sleep the brain is relatively active so energy may only be conserved in NREM sleep. This suggests that only NREM (not REM) sleep is evolved for energy conservation. More primitive animals e.g. reptiles only have NREM sleep, supporting the view that NREM sleep is evolved first (for energy conservation) and REM sleep evolved later (to maintain brain activity). If this is correct we would expect a negative correlation only between body size and NREM sleep, supported by Alison and Cicchetti but not by Capellini et al. Foraging Needs Evolutionary explanations see sleep duration as affected by the amount of time needed to eat. Herbivores (e.g. cows) have to spend a lot of time eating because their food is poor in nutrients. Carnivores (e.g. lions) can afford to sleep a great deal. * + Predicts a trade-off between foraging needs and sleep: Capellini et al found that species with a greater need for foraging (because of high metabolism or diet low in energy) had lower sleep rates, supporting foraging needs as an explanation for sleep patterns. Predator avoidance Time spent asleep (conserving energy) is constrained by risk of predation (being eaten). Predators can sleep for longer. Preys are in danger when sleeping. However, if sleep is vital then it is best to be done when the animals is least vulnerable i.e. at night when they can hide. Meddis (1979) believes that sleep evolved to keep animals safely hidden from predators when usual activities, such as foraging are not required. Therefore prey animals should sleep less, being more at risk and vigilant. * + Predicts a trade-off between predation risk and sleep: Alison and Cicchetti found that species with a high risk of predation did sleep less. Though there are exceptions e.g. rabbits (high risk of predation) slept as much as moles (low risk of predation). * However Capellini et al found the relationship is complex e.g. animals that sleep socially sleep fewer hours but ought to sleep more because there is safety in numbers. Research support. * Stear (2005): Reported that sleep saves energy, keeps individuals from being lively at unnecessary times and is an adaptation to the ecological factors differing across species, supporting the evolutionary basis for sleep. * Requadt (2006): Found that animals find warm, safe places to sleep as it minimises energy requirements to maintain body temperature. This supports the evolutionary point of view. * Sigel (2008): Reported that there is less risk of injury when asleep than awake. Sleep being a safety device when essential activities are not necessary. * Pilleri (1979): Found that Indus dolphins sleep for a few seconds repeatedly, supporting the evolutionary predictions for sleep patterns in aquatic mammals. * Mukhametov (1984): Found that bottlenose dolphins have one cerebral hemisphere asleep at a time, allowing animals to be asleep, alert and breathing simultaneously. This supports evolutionary predictions for the sleep patterns of aquatic mammals. EVALUATION OF EVOLUTIONARY THEORY. * + Predators such as lions sleep longer than prey animals, such as zebras, seemingly supporting the predictions made by the evolutionary approach. * + The fact that sleep is universal to species suggests some adaptive function. * IDA: Evolutionary approach suggests that sleep must be adaptive in some way, otherwise why do all animals do it, but their patterns differ? This suggests that these patterns are in some way adaptive to the species environment. * + The ‘Phylogenetic signal’ provides key support: The fact that animals that are close on the phylogenetic scale share close similarities in their sleep patterns supports the view that such patterns have evolved through adaptation to environmental pressure. Capellini et al concluded that foraging and predation risks act as selective pressures. * Genome Lag: May have been more relevant in our evolutionary past. However, such explanations may not be true of human sleep today as predators no longer pose such a threat. It may well be that sleep patterns will change in time as evolution is a gradual process and so the patterns we have at the moment may be due to genome lag, which occurs because the environment changes more quickly than our genes. * Lacks scientific validity: Evolutionary theories have been proposed in retrospect and consequently lack empirical support, and so they lack scientific validity. Difficult to dismiss and so they are neither verifiable nor falsifiable. * Deterministic: Evolutionary theories are deterministic as they ignore free will. People can and do chose when they want too sleep. * Reductionist: Sleep is a far more complex process than proposed in the evolutionary theory. To have evolved sleep solely as protection does not explain why we have different stages and cycles of sleep or why we need to catch up on some of our missed sleep. Evolutionary theories ignore the physiological and psychological functions of sleep and so are unlikely to provide a full explanation of sleep. * Research methods: Correlational research is often used. Correlation does not prove causation and there may have been many other factors involved. Disorders of sleep Insomnia Insomnia is a sleep disorder where sufferers have long-term problems initiating or maintaining sleep. It can take the form of an inadequate quantity or quality of sleep. Short-term insomnia: Insomnia lasting a few weeks tends to be caused by immediate worries e.g. exams or a recent death in the family. Long-term insomnia: Lasting more than four weeks (DSM definition). Long-term insomnia is divided into primary and secondary insomnia. Primary insomnia: Difficulties sleeping that are not directly associated with any other health condition or physical cause (such as drug abuse or medications). May be due to: * Bad sleeping habits e.g. drinking coffee in the evening, having naps during the day. * Expectations of sleeping problems because of previous cause e.g. depression. The original problem has disappeared but there is still an expectation of sleep problems, which acts as a self-fulfilling prophecy leading to continuing sleep problems. Secondary insomnia: Sleep difficulty is a symptom of something else i.e. insomnia is second to these other conditions, such as: * Medical e.g. heart disease, circadian rhythm disorder (leads to sleep an inappropriate times), rheumatism (makes it more difficult to sleep) or parasomnias such as sleep talking (disrupt sleep). * Psychiatric e.g. depression. * Environmental e.g. due to too much coffee, shit work. There are also risk factors that can influence insomnia: * AGE: teenagers also experience insomnia due to delayed sleep phase syndrome, a condition that is common in adolescence. Older people have increasing physical problems such as arthritis, which can disrupt sleep. * GENDER: increased incidence in women may be due to hormonal fluctuations (e.g. menopause) * SLEEP APNOEA: individual stops breathing while asleep, for a few seconds or as much as a minute. It may occur up to 30 times an hour and disrupts sleep. Chest (2001) found a significant positive correlation between insomnia and obstructive sleep apnoea suggesting a relationship. * OTHER PARASOMNIAS: sleep walking, snoring, teeth grinding are some examples. * PERSONALITY: Personality factors are implicated in research findings as being associated with the onset and continuation of insomnia. Psychasthenia, a personality disorder similar to OCD, where a sufferer is plagued with unreasonable fears and doubts, excessive anxiety and obsessive compulsions is especially implicated. Other commonly identified factors include over-sensitivity, low self-esteem, lack of autonomy and heightened emotional arousal. Lundh et al (1995) personality tested 233 persistent insomnia patients, finding that the predominant factor is Psychasthenia, with high scores on anxiety and monotony avoidance. Sufferers tend to score poorly on self-esteem and are over dependent on others. The effects of these factors are difficult in regaining sleep, daytime fatigue and lack of concentration.
Genetic explanation
- Suggest it is caused by some malfunction in our sleep control centres. E.g. A disruption of neurotransmitters (Melatonin, serotonin, noradrenaline and acetylcholine). This may be genetic. Watson et al found that MZ twin insomnia was highly correlated (0.42). DZ twin insomnia poorly at (0.15) however this correlation isn’t that high.
- Genetics: May be a genetic vulnerability to insomnia. If insomnia is genetic, it is likely that it will be passed from parent to child. Beavliev and bonneau et al (2007) reported that 34.9% of insomniacs surveyed reported having a first-degree relative with insomnia. However this isn’t 100%...
Brain Chemistry
- Insomnia may be caused by changes in brain chemistry. Winkleman et al (2008) found that people who had been suffering with insomnia for more than six months had reduced levels of the neurotransmitter GABA in their brain. This is an inhibitory neurotransmitter, which means that it reduces activity In the brain. If the insomniac has less of GABA, the brain may not be being quietened down at night and this means the insomniac is not able to sleep.
- Nofzinger et al (2004) conducted PET scans on the brain stem, thalamus and prefrontal cortex of insomniac individuals. They found that insomniacs have less decline in brain activity before sleep compared to non-suffers
Comorbidity
- Many cases of insomnia occur due to another condition.
- Physical changes: E.g. hormonal changes in women such as PMS, pregnancy and menopause.
- Psychological conditions: Mornin et al (1999) found that 40% of patients with insomnia also had a psychological depression disorder e.g. depression.
-Medical conditions: Such as Parkinson’s and asthma.
EVALUATION
- Biological Approach: this theory mainly takes a biological approach but should take an eclectic approach. The diathesis stress model says that we may inherit faulty mechanisms to produce insomnia but needs another environmental factor to produce insomnia. Research support: Kales et al (1976): Personality tested 124 insomniacs, finding that 85% had abnormal personalities characterised by Psychasthenia, elevated levels of depression and conversion hysteria. Sufferers tended to internalise psychological disturbances, producing constant emotional arousal. This suggests that a psychophysiological mechanism underpins insomnia. De Carvalho et al (2003): Found that male insomniacs tend to be impulsive characters, implying that male and female sufferers are affected by different personality traits. EVALUATION * Personality: Rather than personality traits leading to insomnia, there is a possibility that being insomniac creates changes in personality. Longitudinal studies following people at risk from their personality profile would be a good means of settling the debate. * Personality: Research suggests that treating abnormal personality traits and disorders has more success in reducing insomnia than treating insomnia to try to address personality defects. This implies that abnormal personality traits are the casual factor (However this is aetiology fallacy). * Personality: Furukawa (2009) reports success in using behavioural treatments to address personality-linked insomnia, suggesting that maladaptive learning experiences may be important factors. * Methodology: scientific and controlled but difficult to separate and assess factors. Sleep labs are in artificial environments. Furthermore an EEG can be influenced by electrical currents from other machinery and our skull can also change electrical currents, as it is very thick. Therefore conclusions may not always be accurate. * Applications to real life: cognitive behaviour therapy (CBT) changes negative thoughts about sleep, as insomniacs tend to have negative views about how well they can cope. Furthermore the therapy can educate us on good sleep hygiene. This gives hope for sleep as reduction or cure is possible. * Individual differences: Van Dongen claims that none of the research takes individual differences into account. There are four variables that aren’t considered extraneous and can become confounding. * Real world Application: The distinction between primary and secondary insomnia is important when deciding on treatment, because either you treat the insomnia (if its primary) or you should treat the underlying cause (secondary) For example, in the case of insomnia arising from depression It might be unhelpful to treat only the insomnia. * However… it is not always clear whether insomnia is simply a symptom of the main cause (i.e. secondary) or in fact primary. A survey of 15,000 Europeans found that insomnia often preceded depression i.e. was primary. This suggests that insomnia should be treated. * Insomnia is studied because it has important consequences: Such as cognitive impairment, Zammit et al found that patients experienced problems with concentration, memory and problem solving. Other problems include accidents: The national traffic administration estimates that 1500 deaths annually are due to sleepiness/fatigue. Other problems include psychological impairments. * IDA: Nature and nurture – genetics and the environment… Spielman and Glovinksy distinguished between risk facts that predispose, precipitate or perpetuate insomnia.
- Genetic factors (nature) predispose an individual to insomnia.
- Environmental stressors (nurture) trigger or precipitate primary insomnia (DSM).
- Perpetuating factors include expectations of having difficult sleeping, leading to SFP. * There is evidence to support teenage insomnia is a major problem: A survey of 4000 11-17 year olds showed that 25% experienced insomnia and 5% said it interfered with their ability to function (Roberts et al). A year later 41% reported continuing problems with insomnia. * Research complications: The large number of factors that may contribute to a persons insomnia makes it very difficult to conduct meaningful research – having so many factors lead to only small overall effects. This means that research is unlikely to uncover clear solutions to the problem. * IDA: Real world application: Attribution theory is an example of the cognitive approach in psychology. It concerns the way we think about the causes of our own (and other peoples) behaviour. In the case of insomnia, if a person believes they cannot sleep because of insomnia this produces self-fulfilling expectations. Attribution therapy suggests that an individual needs to think differently about the causes of their behaviour i.e. learn to make attribution about why they are not sleeping. Storms and Nisbett supported this in their pill study. Narcolepsy Often described as uncontrollable bouts of sleep or trouble maintaining sleep. Narcolepsy is often triggered by emotions. Clinical characteristics include: Extreme daytime sleepiness (seconds or minutes), Cataplexy (sudden loss of muscle tone), Hallucinations and Sleep paralysis. Sufferers must show cataplexy and at least one other symptom. Narcolepsy is often experienced in adolescence and early adulthood. Explanations
Psychological explanations
Lehrman and Weiss (1943) suggested that sudden attacks of sleepiness disguise sexual fantasies. * Little research support: Not generally included in explanations due to lack of evidence. Biological explanations: Malfunction of the REM system.
Makes sense because classic symptoms of narcolepsy match REM sleep characteristics such as paralysis and intrusion of REM-type sleep (hallucinations) into daytime. Therefore narcolepsy may be related to malfunction in system that regulates REM. There is some research to support the malfunction of REM: - Vogel observed sleep patterns during narcoleptic episodes in one patient, and found (as predicted) that REM patterns were present at the beginning of each episode.
- Siegel recorded activity in brain stream of narcoleptic dogs and found the same activity during cataplexy as found in REM sleep. - However generally there is little research for the REM malfunction explanation.
Biological explanations: Variant of HLA.
HLA (Human leukocyte antigen) is part of the body’s immune response. A mutation of the HLA complex gene links to hypocretin production. The mutation (on chromosome 6), which is found on white blood cells. Due to the mutation the white blood cells begin to destroy hypocretin-producing neurons in the brain (autoimmune disease). Hypocretin controls wakefulness. * Linking HLA to hypocretin: Some variants of HLA increase the likelihood of autoimmune conditions. This may result in reduced numbers of hypocretin cells in the hypothalamus, and so lead to narcolepsy (mignot). * Continues to be researched but increased HLA not found in all narcoleptics so cannot be sole explanation. * Honda found increased frequency of one type of HLA in narcoleptic patients. * Stanford Medical centre: Found more than 90% of people suffering from narcolepsy with cataplexy have been found to have the HLA variant HLA-DQB1*0602. Biological explanations: Mutation in hypocretin the neurotransmitter hypocretin plays a role in keeping people awake. Cells in the hypothalamus produce Hypocretin. In narcoleptics a large number of these hypocretin cells are missing, resulting in low levels of hypocretin. * There is research support for the role of hypocretin: Lin et al found narcoleptic dogs had a mutation on chromosome 12, which affects hypocretin production. Findings in dogs have also been confirmed in humans as Nishino et al found narcoleptics had lower levels of hypocretin in their cerebrospinal fluid. * However hypocretin loss in humans is not linked to inherited factors because narcolepsy doesn’t run in families and not concurrent in MZ twins (Mignot). Most likely due to brain injury. * IDA: Real world application: The role of hypocretin may lead to treatment for narcolepsy, although it would need to be an artificial drugs as the hypocretin molecule is unstable (broken down before reaches brain) alternatively it may be possible to transplant normal hypocretin cells. General Evaluation of Narcolepsy. * Approaches: takes a biological/physiological approach which uses scientific methods to studying the cause of narcolepsy. However, not all narcoleptics have this mutation whilst some people with the mutation do not have narcolepsy. Lehirman-Weiss tried to provide a psychodynamic explanation. Narcolepsy is due to inappropriate sexual fantasies to try and stop you experiencing the anxiety and embarrassment from it. However a psychodynamic approach cannot be falsified: if a participant lies, they are repressing it. Therefore our knowledge of narcolepsy has not advanced since biological explanations as new approaches have been unsuccessful. * Research Methods: narcoleptic dogs have been bred for the purpose of research into narcolepsy and to discover treatments for human beings. It is an emotive topic over whether this is morally right? Furthermore we are more complex than animals. However research has confirmed a significant link between HLA and hypocretin with its role of narcolepsy. * Applications to real life: raising hypocretin levels artificially should help narcoleptics. However drugs that achieve this are not available yet but would be able to test the link. Treatment often involves drugs such as Ritalin (stimulant), amphetamines and newer drugs such as modafinal. Siegel raised hypocretin levels in dogs and found it to reduce narcoleptic symptoms. Nishino however gave hypocretin intravenously to humans and found it could not go from blood to brain. * Refuting evidence: non-genetic factors are equally important. MZ twins do not show concordance for narcolepsy. However at the moment we do not know what these non-genetic or environment factors such as infections, diet or exposure to environmental toxins. * Using samples based on patient associations can cause problems with bias, as only certain types of sufferer may join the association. * The identification of genes associated with the disorder does not mean that there is a definite genetic cause and researchers stress the need to identify environmental triggers. Genes specific environments in which to express themselves. * Research has shown that injections of hypocretin of hypocretin in dogs reversed their narcolepsy, showing the influence of this neurotransmitter in the development. However these findings cannot be generalised to humans as the human condition seems to have environmental as well as genetic causes (nature/nurture debate). It is clear that environmental stimuli, in terms of emotions they trigger, seem to trigger a narcoleptic episode; it is therefore plausible to develop a diathesis stress hypothesis, stating that both predisposition to the condition (genetic factors- nurture) and an environmental trigger (emotions – nurture) cause the symptoms through their interaction. * The explanations of narcolepsy such as the HLA and hypocretin can be seen as reductionist. This is because they attempt to reduce this complex multi-system disorder too malfunctions of a specific biological system, and ignore the role of other biological variables as well as those environmental ones. * 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 voluntary control. This may be true or not true for different individuals. * Alternative explanations: Psychodynamic. * Ignores individual differences: Overlooks individual differences in that personality factors may play a part, such as the coping of strong emotions and the sudden onset of narcolepsy – some cope better than others.
Sleep walking: Sleepwalking is a parasomnia as it happens whilst we are asleep and is known as somnambulism. Mainly children suffer from it (18% of the population). It adults it is called RBD (REM behaviour sleep disorder.
Explanations:
* GENETIC: Usually runs in families, 1st degree relative – more likely to develop it. Looked at twins to discover what the concordance rate was. MZ twins 55%, DZ twins 35%. As the concordance rate is not 100% there must be another factor. * BIOLOGICAL: incomplete arousal. Sleepwalking is a disorder of arousal; the sleepwalker is asleep but engaged in tasks normally associated with being awake. EEG recordings during sleep walking show delta waves (typical of SWS) plus beta waves (typical of awake state). Person in SWS is awakened but arousal is incomplete. * ENVIRONMENTAL: things such as illness, stress, anxiety and sleep hygiene. Sleep deprivation. For females hormones also play a part. * RISK FACTORS: Sleepwalking is increased by sleep deprivation, having a fever, stress, alcohol, and psychiatric conditions. (Pizzazz et al.) Hormonal changes in puberty and menstruation may also be triggers but possibly only for genetically vulnerable individuals. * CHILDREN: Children tend to have more SWS or because the system that usually inhibits motor activity in SWS isn’t fully developed in children (and may be undeveloped in some adults). One study has found that adult sleepwalkers showed signs of immaturity in the relevant neural circuits.
AO2 Evaluative Points: * Supportive research: Lecendreux – 60 participants who had a history of sleepwalking in their family and a matched control group of non-sleepwalkers. They found the sleepwalking group all had the HLA gene in common so they now think you can inherit the malfunctioning gene. Therefore this suggests a plausible biological explanation. * Approaches: the explanations are mainly biological. As these biological explanations dominate psychological research other psychologists have tried to find other explanations. One psychodynamic explanation is that sleepwalking allows us to work through our worries; this means that we are less likely to use a defence mechanism. * Methodology: scientific evidence which is very reliable. However the data may not be as reliable as we think from EEG’s 1) skull is very thick an9d can disrupt impulses 2) subject to interference. Although they are supportive, research must be treated with caution. * Real world application: research into this has been useful in for the UK legal system. People were often using it as a defence as a loophole and the loophole has now vanished and it has to be backed up by medical and psychiatric evidence. This means innocent people are allowed to walk free. * Nature and nurture: genetics and the environment: Evidence for a genetic basis comes from Broughton who found that prevalence of sleep walking in first degree relatives is times greater in the general population and Lecendreux et al who found 50% concordance in MZ twins compared to the 15% DZ. The environmental component acts as a ‘stressor’ as in the DSM e.g. Sleep deprivation led to an increase in sleep walking in vulnerable individuals (i.e. those who had past experiences of sleep walking) Zadre et al. Levels of sleep walking rose from 50% to 90& after 25 hours deprivation.
Specification * Nature of sleep, including sleep stages and lifespan changes and lifespan changes in sleep. * Functions of sleep, including evolutionary explanations and restoration theory.
Nature of sleep * Sleep is a different state of consciousness where responsiveness to the external environment is diminished. * It occurs daily as circadian rhythms and is composed of an Ultradian cycle of separate stages. * With the intention of the electroencephalograph (EEG), psychologists were able to investigate brain activity occurring during sleep and concluded that it was composed of identifiably different sequential stages. (Electrical activity or brain waves). * Electro-oculograms (EOGs) measure eye movement, and Electromyograms (EMGs) measure muscle movement and have been used to distinguish the stages and cycles of sleep. * Sleep is circadian as it happens once a day however it is also Ultradian as the stages are repeated within a cycle. Each cycle is approximately 90 minutes and most people experience 5-6 cycles a night. Stages one to four are slow wave sleep (SWS) and stage five is rapid eye movement sleep (REM). * Brain is active during sleep and this activity can be measured (EEG). Different stages of sleep show different patterns alpha, delta and theta waves. * One cycle takes about 90 minutes; later in the night there is more REM sleep and less SWS.
Stages of sleep
STAGE ONE: Beginning of the sleep cycle. Alpha waves disappear and are replaced by low-voltage slow waves. Heat rate declines and muscles relax. This is a light sleep and the sleeper can easily be woken.
Brain produces high amplitude theta waves, which are very slow brain waves – lasts 5-10 minutes.
STAGE TWO: A deeper state, in which the sleep is still easily woken. Short bursts of sleep spindles are noticeable, together with sharp rises and falls in amplitude known as K-complexes. Lasts about 20 mins.
STAGE THREE: Sleep becomes increasingly deep, and the sleep difficult to wake. Sleep spindles decline, being replaced by long, slow delta waves. Heart rate, blood pressure and temperature decline.
STAGE FOUR: Deep sleep, where delta waves increase and metabolic rate are low. The sleeper is difficult to wake. Growth hormones are released and incidences of sleepwalking and night terrors may occur. 30 mins.
The sleeper spends about 30 minutes in stage 4 sleep, with about an hour passing in total from stage 1 to stage 4. Stage 3 is re-entered, then stage 2 and then the sleep enters an active stage of sleep called rapid eye movement (REM) about 90 minutes after failing asleep.
REM: Eye movements are noticeable, heart rate, respiration etc. Increase and dreaming occurs.
Another 15 minutes of REM sleep, the sleeper re-enters 2, 3 and 4 in that order then another cycle begins. It is common to go through about five Ultradian cycles in one night. As the night progresses, the sleeper spends more time in REM sleep and less time in the other stages. This pattern is fairly universal; although there are development differences.
Research support.
Dement and Kleitman (1957) * Conducted highly controlled experiments in a sleep lab using biological measurements (e.g. EEG). * 9 male participants for 61 nights. * Participants were woken at each different stage of sleep and asked a series of questions. * Those awakened during REM sleep (identified by the EEG) reported dreams 79% of the time and only 7% in NREM. * + Was an important piece of research in that it was the first piece, which objectively correlated brain states with dreaming. * - Due to artificial environment, the findings may lack ecological validity because participants in research were not allowed to experience normal sleep, they experienced sleep disturbance. Could cause REM and Stage 4 rebound effect. * - Small sample: Not representative.
EVALUATION
+ Objective evidence: EEG, EOG AND EMG illustrate psychology as a science.
+ Universality: Stages + cycles of sleep have been found across cultures.
- Artificiality of sleep laboratory – extrapolation issues.
- Individual differences – reductionist – simplifies all sleep to a set of stages + cycles – people will differ.
- A03: Weakness of the self-report method: Yields date that may be subject to social desirability bias.
Sleep and the lifespan:
Infancy: babies sleep for about 16 hours a day but not continuously. They wake up every hour or so and the cycle is shorter than an adults. They experience two types of sleep: active and quiet which are versions of REM and SWS. Approximately half is spent in active (REM) because of their need for growth. By about 6 months old most children have one main sleep-wake cycle with a few naps in the day.
Childhood: children typically sleep about 12 hours a day and EEG patterns resemble adult patterns. The amount of sleep gradually decreases. As the brain is still developing they spend approximately 3 and a half hours in REM. Parasomnias are very common in childhood (sleep walking and night terrors).
Adolescence: Sleep duration increases in adolescence. Boys often experiences orgasms and ejaculation during sleep. There is a phase delay and circadian rhythms shift so teenagers stay awake later and wake up later. Our need for sleep has decreased, as we don’t need much growth. Schools should adjust their day to fit the delayed sleep pattern syndrome.
Adulthood: adults sleep for typically 8 hours per night and 25% is spent in REM sleep. There is an increasing frequency of sleep disorders such as insomnia and sleep apnoea.
Old age: sleep patterns change and it is often more difficult to get to sleep and they wake more often. REM sleep decreases to about 20% and SWS decreases to about 5%. There is a phase advance as they go to sleep earlier and wake earlier. They also may nap during the day to satisfy sleep needs.
EVALUATION
* - Cultural differences – Tynjälä et al: your culture also affects your sleep pattern. A survey via the Internet of 11-16 year olds from 11 European countries and other non-European countries to compare. Approximately 40,000 participants. Found that teenagers in Israel slept 8.5 hours compared to other countries they slept the least. In Switzerland they slept for 9.5 hours, the most. These results were often the effect of social factors such as going out, sleeping at someone else’s house etc. In collectivist cultures they also sleep less as they have more duties and chores to do. Therefore age is not the only contributing factor. * + Developmental approach: looks and follows people as they grow and then tries to map changes. In the past the developmental approach was from new-born to adulthood. They assumed that sleep stayed the same after adulthood, which we now know not to be the case. The original form of this approach would have been a limited inadequate explanation. * - Research methods: experiments carried out in sleep labs are environmentally wrong as it is an artificial environment and therefore the results were not that reliable. Furthermore it has often been established that sleep hygiene and environment plays a part in our sleep pattern. * + Applications to real life: findings have been used to reduce the level of cot death (S.I.D.S). Infants spend a lot of time sleeping and wake up a lot. There have been methods developed to prevent it, for example sleeping on their back or side to open their airways. Dummies help them stay out of REM sleep as it keeps them partly aroused physiologically. * + Objective measurements: Research into lifespan changes in sleep has been conducted in numerous sleep laboratories throughout the world. * + Real world application: Sleep quality can be improved through the use of melatonin. Melatonin induces sleep by inhibiting the brain mechanisms that promote wakefulness. * Individual differences: Borbely (1986) warns against the use of generalisations about sleep patterns for different age groups due to the many external factors e.g., work patterns, medication etc.
Functions of sleep.
Restoration theory.
OSWALD.
SWS initiates body repair.
Growth hormone
- Important in childhood because it stimulates physical growth.
- Important throughout lifespan for protein synthesis and cell growth.
- Oswald observed that this was secreted to some extent during the day but mainly in SWS. Cauter and Plat support this in that the amount of growth hormone correlates with the amount of SWS.
REM sleep initiates brain repair.
Brain growth supports this
- Infants have a greater proportion of REM (i.e. active) sleep than adults, which suggests that REM sleep may be important to brain growth.
- Siegel suggests that the amount of REM sleep in any animal is proportionate to the immaturity in any offspring at birth. Platypus young are very immature and have about 8 hours REM, whereas dolphin young are very mature and have almost no REM sleep.
Neurotransmitter function.
- Sigel and Rogaski suggest that during REM sleep neurotransmitters are not produced, allowing neurons to regain their sensitivity.
- Stern and Morgane (1974) believed that, during REM sleep, neurotransmitter levels are replenished, supporting the idea of restorative sleep. This is backed up by the fact that anti-depressants increase neurotransmitter levels, reducing REM activity.
HORNE
- ‘Core sleep’ = SWS 4 + REM: Essential for repair/restoration of the brain.
- ‘Optimal sleep’ = SWS 1-3: Not needed at all for repair/restoration.
- Restoration of the body occurs when we are awake.
Research support
Rechtschaffne (1989)
- Rats on a turntable.
- When ever their brain patterns changed to show they were sleeping the turntable started to turn so that they woke up and exercised.
- If they didn’t they would fall into the water, rats only had 16% of usual sleep.
- Rats weak and lost weight even though it still ate as its metabolic rate had increased.
- Most of the experimental rats died between 21-33 days after the experiment began.
- Supports restoration theory as rats died because their metabolic rate was high and they needed to rest and repair.
- Difficulty extrapolating results from rats to humans. + Lab study, well controlled: can establish cause and effect. – However could be other factors? Stress? Cirelli et al (2004)
- Found that, during SWS, genes associated with the protein production that regulated synaptic connections are activated, supporting restoration theories, especially Oswald. EVALUATION: Lots of supporting research and biological support. * If sleep (SWS+REM) is restorative, total sleep deprivation should have negative effects: Case studies show some support. DJ Tripp stayed awake for 201 hours and after 5 days he experienced hallucinations and paranoia, his brain rhythms looked like he was asleep. * HOWEVER… Horne and Minard found that a series of exhausting tasks led people to get to sleep faster but not for longer. * If sleep (SWS+REM) is restorative, total sleep deprivation should have negative effects: Case studies show some support. DJ Tripp stayed awake for 201 hours and after 5 days he experienced hallucinations and paranoia, his brain rhythms looked like he was asleep. * HOWEVER… Sleep deprived individuals may actually be getting some sleep e.g. laboratory observations have found that sleep deprivation for more than 72 hours results in periods of micro sleep while participants are apparently awake (Williams et al). I.e. sleep-deprived participants are only apparently awake but experiencing some benefits of sleep. * HOWEVER… Another case study on Randy Gardener found no psychotic symptoms after 11 days without sleep and there are reports of individuals e.g. Hai Ngoc who haven’t slept for years with no ill effects. * However such individuals may be experiencing micro sleeps. * Methodological issues: Case studies relate to unique individuals and other sleep studies often use volunteers who also might have unique characteristics (e.g. less need for sleep than the norm) so results may lack Generalisability. *
Methodological issues: Non-human animal studies lack Generalisability because animals have different sleep requirements to humans. *
If SWS is important, SWS deprivation should have negative effects: Demonstrated in ‘rebound effects’ – when people are deprived of SWS they show need for more SWS on subsequent nights. * IF REM is important, REM sleep deprivation should have negative effects: This is supported by research evidence that shows that REM deprivation results in as much as 50% more REM sleep on subsequent nights.
The evolutionary approach: The main alternative to the restoration theory is the evolutionary approach, which claims that sleep has no specific benefit except for protection (to conserve energy or keep an animal safe from predators), rather than performing some specific biological function as claimed by the restoration theory. The restoration approach doesn’t explain, for example, why some species sleep one hemisphere at a time (E.g. dolphins). Nor does it explain why lack of consciousness is necessary. It looks like environmental pressures are important in shaping sleep processes, which can be explained by the evolutionary approach. * Gender bias: All of sleep deprivation research is based on male participants. EVOLUTIONARY THEORY OF SLEEP.
Sleep is adaptive. It exists to promote survival and reproduction. Any behaviour or characteristics that increase likelihood of survival and reproduction will be naturally selected and will survive as the animal evolves. Each animal adapts their sleep pattern to their environment (ecological niche) for example dolphins sleep for seconds at a time switching between hemispheres in order to survive. Energy conservation.
High expenditure of energy: Warm-blooded animals (such as birds or mammals) use energy to maintain temperature (homeostasis). This is especially true for small animals with a high metabolic rate such as mice. This linking to the benefit of sleep as sleep provides a period of enforced inactivity to conserve energy, such as hibernation; therefore small animals should sleep lots to conserve energy. This links with Webb’s hibernation theory of sleep: Active animals need large amounts of food, threatening survival during times of food scarcity. Hibernation conserves energy and increases survival. Grizzly bears hibernate though the winter, living off body fat accumulated during times of food availability. * + This theory predicts a negative correlation between body size and sleep supported by Zepelin and Rechtschaffen who found smaller animals sleep more than larger animal, although there are exceptions e.g. sloths, who are large and sleep a lot. * However, this is not supported by Capellini et al who found a positive correlation. This study used carefully selected, standardised data and therefore may be more reliable than other evidence. * + Energy only conserved in NREM sleep… In REM sleep the brain is relatively active so energy may only be conserved in NREM sleep. This suggests that only NREM (not REM) sleep is evolved for energy conservation. More primitive animals e.g. reptiles only have NREM sleep, supporting the view that NREM sleep is evolved first (for energy conservation) and REM sleep evolved later (to maintain brain activity). If this is correct we would expect a negative correlation only between body size and NREM sleep, supported by Alison and Cicchetti but not by Capellini et al. Foraging Needs Evolutionary explanations see sleep duration as affected by the amount of time needed to eat. Herbivores (e.g. cows) have to spend a lot of time eating because their food is poor in nutrients. Carnivores (e.g. lions) can afford to sleep a great deal. * + Predicts a trade-off between foraging needs and sleep: Capellini et al found that species with a greater need for foraging (because of high metabolism or diet low in energy) had lower sleep rates, supporting foraging needs as an explanation for sleep patterns. Predator avoidance Time spent asleep (conserving energy) is constrained by risk of predation (being eaten). Predators can sleep for longer. Preys are in danger when sleeping. However, if sleep is vital then it is best to be done when the animals is least vulnerable i.e. at night when they can hide. Meddis (1979) believes that sleep evolved to keep animals safely hidden from predators when usual activities, such as foraging are not required. Therefore prey animals should sleep less, being more at risk and vigilant. * + Predicts a trade-off between predation risk and sleep: Alison and Cicchetti found that species with a high risk of predation did sleep less. Though there are exceptions e.g. rabbits (high risk of predation) slept as much as moles (low risk of predation). * However Capellini et al found the relationship is complex e.g. animals that sleep socially sleep fewer hours but ought to sleep more because there is safety in numbers. Research support. * Stear (2005): Reported that sleep saves energy, keeps individuals from being lively at unnecessary times and is an adaptation to the ecological factors differing across species, supporting the evolutionary basis for sleep. * Requadt (2006): Found that animals find warm, safe places to sleep as it minimises energy requirements to maintain body temperature. This supports the evolutionary point of view. * Sigel (2008): Reported that there is less risk of injury when asleep than awake. Sleep being a safety device when essential activities are not necessary. * Pilleri (1979): Found that Indus dolphins sleep for a few seconds repeatedly, supporting the evolutionary predictions for sleep patterns in aquatic mammals. * Mukhametov (1984): Found that bottlenose dolphins have one cerebral hemisphere asleep at a time, allowing animals to be asleep, alert and breathing simultaneously. This supports evolutionary predictions for the sleep patterns of aquatic mammals. EVALUATION OF EVOLUTIONARY THEORY. * + Predators such as lions sleep longer than prey animals, such as zebras, seemingly supporting the predictions made by the evolutionary approach. * + The fact that sleep is universal to species suggests some adaptive function. * IDA: Evolutionary approach suggests that sleep must be adaptive in some way, otherwise why do all animals do it, but their patterns differ? This suggests that these patterns are in some way adaptive to the species environment. * + The ‘Phylogenetic signal’ provides key support: The fact that animals that are close on the phylogenetic scale share close similarities in their sleep patterns supports the view that such patterns have evolved through adaptation to environmental pressure. Capellini et al concluded that foraging and predation risks act as selective pressures. * Genome Lag: May have been more relevant in our evolutionary past. However, such explanations may not be true of human sleep today as predators no longer pose such a threat. It may well be that sleep patterns will change in time as evolution is a gradual process and so the patterns we have at the moment may be due to genome lag, which occurs because the environment changes more quickly than our genes. * Lacks scientific validity: Evolutionary theories have been proposed in retrospect and consequently lack empirical support, and so they lack scientific validity. Difficult to dismiss and so they are neither verifiable nor falsifiable. * Deterministic: Evolutionary theories are deterministic as they ignore free will. People can and do chose when they want too sleep. * Reductionist: Sleep is a far more complex process than proposed in the evolutionary theory. To have evolved sleep solely as protection does not explain why we have different stages and cycles of sleep or why we need to catch up on some of our missed sleep. Evolutionary theories ignore the physiological and psychological functions of sleep and so are unlikely to provide a full explanation of sleep. * Research methods: Correlational research is often used. Correlation does not prove causation and there may have been many other factors involved. Disorders of sleep Insomnia Insomnia is a sleep disorder where sufferers have long-term problems initiating or maintaining sleep. It can take the form of an inadequate quantity or quality of sleep. Short-term insomnia: Insomnia lasting a few weeks tends to be caused by immediate worries e.g. exams or a recent death in the family. Long-term insomnia: Lasting more than four weeks (DSM definition). Long-term insomnia is divided into primary and secondary insomnia. Primary insomnia: Difficulties sleeping that are not directly associated with any other health condition or physical cause (such as drug abuse or medications). May be due to: * Bad sleeping habits e.g. drinking coffee in the evening, having naps during the day. * Expectations of sleeping problems because of previous cause e.g. depression. The original problem has disappeared but there is still an expectation of sleep problems, which acts as a self-fulfilling prophecy leading to continuing sleep problems. Secondary insomnia: Sleep difficulty is a symptom of something else i.e. insomnia is second to these other conditions, such as: * Medical e.g. heart disease, circadian rhythm disorder (leads to sleep an inappropriate times), rheumatism (makes it more difficult to sleep) or parasomnias such as sleep talking (disrupt sleep). * Psychiatric e.g. depression. * Environmental e.g. due to too much coffee, shit work. There are also risk factors that can influence insomnia: * AGE: teenagers also experience insomnia due to delayed sleep phase syndrome, a condition that is common in adolescence. Older people have increasing physical problems such as arthritis, which can disrupt sleep. * GENDER: increased incidence in women may be due to hormonal fluctuations (e.g. menopause) * SLEEP APNOEA: individual stops breathing while asleep, for a few seconds or as much as a minute. It may occur up to 30 times an hour and disrupts sleep. Chest (2001) found a significant positive correlation between insomnia and obstructive sleep apnoea suggesting a relationship. * OTHER PARASOMNIAS: sleep walking, snoring, teeth grinding are some examples. * PERSONALITY: Personality factors are implicated in research findings as being associated with the onset and continuation of insomnia. Psychasthenia, a personality disorder similar to OCD, where a sufferer is plagued with unreasonable fears and doubts, excessive anxiety and obsessive compulsions is especially implicated. Other commonly identified factors include over-sensitivity, low self-esteem, lack of autonomy and heightened emotional arousal. Lundh et al (1995) personality tested 233 persistent insomnia patients, finding that the predominant factor is Psychasthenia, with high scores on anxiety and monotony avoidance. Sufferers tend to score poorly on self-esteem and are over dependent on others. The effects of these factors are difficult in regaining sleep, daytime fatigue and lack of concentration.
Genetic explanation
- Suggest it is caused by some malfunction in our sleep control centres. E.g. A disruption of neurotransmitters (Melatonin, serotonin, noradrenaline and acetylcholine). This may be genetic. Watson et al found that MZ twin insomnia was highly correlated (0.42). DZ twin insomnia poorly at (0.15) however this correlation isn’t that high.
- Genetics: May be a genetic vulnerability to insomnia. If insomnia is genetic, it is likely that it will be passed from parent to child. Beavliev and bonneau et al (2007) reported that 34.9% of insomniacs surveyed reported having a first-degree relative with insomnia. However this isn’t 100%...
Brain Chemistry
- Insomnia may be caused by changes in brain chemistry. Winkleman et al (2008) found that people who had been suffering with insomnia for more than six months had reduced levels of the neurotransmitter GABA in their brain. This is an inhibitory neurotransmitter, which means that it reduces activity In the brain. If the insomniac has less of GABA, the brain may not be being quietened down at night and this means the insomniac is not able to sleep.
- Nofzinger et al (2004) conducted PET scans on the brain stem, thalamus and prefrontal cortex of insomniac individuals. They found that insomniacs have less decline in brain activity before sleep compared to non-suffers
Comorbidity
- Many cases of insomnia occur due to another condition.
- Physical changes: E.g. hormonal changes in women such as PMS, pregnancy and menopause.
- Psychological conditions: Mornin et al (1999) found that 40% of patients with insomnia also had a psychological depression disorder e.g. depression.
-Medical conditions: Such as Parkinson’s and asthma.
EVALUATION
- Biological Approach: this theory mainly takes a biological approach but should take an eclectic approach. The diathesis stress model says that we may inherit faulty mechanisms to produce insomnia but needs another environmental factor to produce insomnia. Research support: Kales et al (1976): Personality tested 124 insomniacs, finding that 85% had abnormal personalities characterised by Psychasthenia, elevated levels of depression and conversion hysteria. Sufferers tended to internalise psychological disturbances, producing constant emotional arousal. This suggests that a psychophysiological mechanism underpins insomnia. De Carvalho et al (2003): Found that male insomniacs tend to be impulsive characters, implying that male and female sufferers are affected by different personality traits. EVALUATION * Personality: Rather than personality traits leading to insomnia, there is a possibility that being insomniac creates changes in personality. Longitudinal studies following people at risk from their personality profile would be a good means of settling the debate. * Personality: Research suggests that treating abnormal personality traits and disorders has more success in reducing insomnia than treating insomnia to try to address personality defects. This implies that abnormal personality traits are the casual factor (However this is aetiology fallacy). * Personality: Furukawa (2009) reports success in using behavioural treatments to address personality-linked insomnia, suggesting that maladaptive learning experiences may be important factors. * Methodology: scientific and controlled but difficult to separate and assess factors. Sleep labs are in artificial environments. Furthermore an EEG can be influenced by electrical currents from other machinery and our skull can also change electrical currents, as it is very thick. Therefore conclusions may not always be accurate. * Applications to real life: cognitive behaviour therapy (CBT) changes negative thoughts about sleep, as insomniacs tend to have negative views about how well they can cope. Furthermore the therapy can educate us on good sleep hygiene. This gives hope for sleep as reduction or cure is possible. * Individual differences: Van Dongen claims that none of the research takes individual differences into account. There are four variables that aren’t considered extraneous and can become confounding. * Real world Application: The distinction between primary and secondary insomnia is important when deciding on treatment, because either you treat the insomnia (if its primary) or you should treat the underlying cause (secondary) For example, in the case of insomnia arising from depression It might be unhelpful to treat only the insomnia. * However… it is not always clear whether insomnia is simply a symptom of the main cause (i.e. secondary) or in fact primary. A survey of 15,000 Europeans found that insomnia often preceded depression i.e. was primary. This suggests that insomnia should be treated. * Insomnia is studied because it has important consequences: Such as cognitive impairment, Zammit et al found that patients experienced problems with concentration, memory and problem solving. Other problems include accidents: The national traffic administration estimates that 1500 deaths annually are due to sleepiness/fatigue. Other problems include psychological impairments. * IDA: Nature and nurture – genetics and the environment… Spielman and Glovinksy distinguished between risk facts that predispose, precipitate or perpetuate insomnia.
- Genetic factors (nature) predispose an individual to insomnia.
- Environmental stressors (nurture) trigger or precipitate primary insomnia (DSM).
- Perpetuating factors include expectations of having difficult sleeping, leading to SFP. * There is evidence to support teenage insomnia is a major problem: A survey of 4000 11-17 year olds showed that 25% experienced insomnia and 5% said it interfered with their ability to function (Roberts et al). A year later 41% reported continuing problems with insomnia. * Research complications: The large number of factors that may contribute to a persons insomnia makes it very difficult to conduct meaningful research – having so many factors lead to only small overall effects. This means that research is unlikely to uncover clear solutions to the problem. * IDA: Real world application: Attribution theory is an example of the cognitive approach in psychology. It concerns the way we think about the causes of our own (and other peoples) behaviour. In the case of insomnia, if a person believes they cannot sleep because of insomnia this produces self-fulfilling expectations. Attribution therapy suggests that an individual needs to think differently about the causes of their behaviour i.e. learn to make attribution about why they are not sleeping. Storms and Nisbett supported this in their pill study. Narcolepsy Often described as uncontrollable bouts of sleep or trouble maintaining sleep. Narcolepsy is often triggered by emotions. Clinical characteristics include: Extreme daytime sleepiness (seconds or minutes), Cataplexy (sudden loss of muscle tone), Hallucinations and Sleep paralysis. Sufferers must show cataplexy and at least one other symptom. Narcolepsy is often experienced in adolescence and early adulthood. Explanations
Psychological explanations
Lehrman and Weiss (1943) suggested that sudden attacks of sleepiness disguise sexual fantasies. * Little research support: Not generally included in explanations due to lack of evidence. Biological explanations: Malfunction of the REM system.
Makes sense because classic symptoms of narcolepsy match REM sleep characteristics such as paralysis and intrusion of REM-type sleep (hallucinations) into daytime. Therefore narcolepsy may be related to malfunction in system that regulates REM. There is some research to support the malfunction of REM: - Vogel observed sleep patterns during narcoleptic episodes in one patient, and found (as predicted) that REM patterns were present at the beginning of each episode.
- Siegel recorded activity in brain stream of narcoleptic dogs and found the same activity during cataplexy as found in REM sleep. - However generally there is little research for the REM malfunction explanation.
Biological explanations: Variant of HLA.
HLA (Human leukocyte antigen) is part of the body’s immune response. A mutation of the HLA complex gene links to hypocretin production. The mutation (on chromosome 6), which is found on white blood cells. Due to the mutation the white blood cells begin to destroy hypocretin-producing neurons in the brain (autoimmune disease). Hypocretin controls wakefulness. * Linking HLA to hypocretin: Some variants of HLA increase the likelihood of autoimmune conditions. This may result in reduced numbers of hypocretin cells in the hypothalamus, and so lead to narcolepsy (mignot). * Continues to be researched but increased HLA not found in all narcoleptics so cannot be sole explanation. * Honda found increased frequency of one type of HLA in narcoleptic patients. * Stanford Medical centre: Found more than 90% of people suffering from narcolepsy with cataplexy have been found to have the HLA variant HLA-DQB1*0602. Biological explanations: Mutation in hypocretin the neurotransmitter hypocretin plays a role in keeping people awake. Cells in the hypothalamus produce Hypocretin. In narcoleptics a large number of these hypocretin cells are missing, resulting in low levels of hypocretin. * There is research support for the role of hypocretin: Lin et al found narcoleptic dogs had a mutation on chromosome 12, which affects hypocretin production. Findings in dogs have also been confirmed in humans as Nishino et al found narcoleptics had lower levels of hypocretin in their cerebrospinal fluid. * However hypocretin loss in humans is not linked to inherited factors because narcolepsy doesn’t run in families and not concurrent in MZ twins (Mignot). Most likely due to brain injury. * IDA: Real world application: The role of hypocretin may lead to treatment for narcolepsy, although it would need to be an artificial drugs as the hypocretin molecule is unstable (broken down before reaches brain) alternatively it may be possible to transplant normal hypocretin cells. General Evaluation of Narcolepsy. * Approaches: takes a biological/physiological approach which uses scientific methods to studying the cause of narcolepsy. However, not all narcoleptics have this mutation whilst some people with the mutation do not have narcolepsy. Lehirman-Weiss tried to provide a psychodynamic explanation. Narcolepsy is due to inappropriate sexual fantasies to try and stop you experiencing the anxiety and embarrassment from it. However a psychodynamic approach cannot be falsified: if a participant lies, they are repressing it. Therefore our knowledge of narcolepsy has not advanced since biological explanations as new approaches have been unsuccessful. * Research Methods: narcoleptic dogs have been bred for the purpose of research into narcolepsy and to discover treatments for human beings. It is an emotive topic over whether this is morally right? Furthermore we are more complex than animals. However research has confirmed a significant link between HLA and hypocretin with its role of narcolepsy. * Applications to real life: raising hypocretin levels artificially should help narcoleptics. However drugs that achieve this are not available yet but would be able to test the link. Treatment often involves drugs such as Ritalin (stimulant), amphetamines and newer drugs such as modafinal. Siegel raised hypocretin levels in dogs and found it to reduce narcoleptic symptoms. Nishino however gave hypocretin intravenously to humans and found it could not go from blood to brain. * Refuting evidence: non-genetic factors are equally important. MZ twins do not show concordance for narcolepsy. However at the moment we do not know what these non-genetic or environment factors such as infections, diet or exposure to environmental toxins. * Using samples based on patient associations can cause problems with bias, as only certain types of sufferer may join the association. * The identification of genes associated with the disorder does not mean that there is a definite genetic cause and researchers stress the need to identify environmental triggers. Genes specific environments in which to express themselves. * Research has shown that injections of hypocretin of hypocretin in dogs reversed their narcolepsy, showing the influence of this neurotransmitter in the development. However these findings cannot be generalised to humans as the human condition seems to have environmental as well as genetic causes (nature/nurture debate). It is clear that environmental stimuli, in terms of emotions they trigger, seem to trigger a narcoleptic episode; it is therefore plausible to develop a diathesis stress hypothesis, stating that both predisposition to the condition (genetic factors- nurture) and an environmental trigger (emotions – nurture) cause the symptoms through their interaction. * The explanations of narcolepsy such as the HLA and hypocretin can be seen as reductionist. This is because they attempt to reduce this complex multi-system disorder too malfunctions of a specific biological system, and ignore the role of other biological variables as well as those environmental ones. * 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 voluntary control. This may be true or not true for different individuals. * Alternative explanations: Psychodynamic. * Ignores individual differences: Overlooks individual differences in that personality factors may play a part, such as the coping of strong emotions and the sudden onset of narcolepsy – some cope better than others.
Sleep walking: Sleepwalking is a parasomnia as it happens whilst we are asleep and is known as somnambulism. Mainly children suffer from it (18% of the population). It adults it is called RBD (REM behaviour sleep disorder.
Explanations:
* GENETIC: Usually runs in families, 1st degree relative – more likely to develop it. Looked at twins to discover what the concordance rate was. MZ twins 55%, DZ twins 35%. As the concordance rate is not 100% there must be another factor. * BIOLOGICAL: incomplete arousal. Sleepwalking is a disorder of arousal; the sleepwalker is asleep but engaged in tasks normally associated with being awake. EEG recordings during sleep walking show delta waves (typical of SWS) plus beta waves (typical of awake state). Person in SWS is awakened but arousal is incomplete. * ENVIRONMENTAL: things such as illness, stress, anxiety and sleep hygiene. Sleep deprivation. For females hormones also play a part. * RISK FACTORS: Sleepwalking is increased by sleep deprivation, having a fever, stress, alcohol, and psychiatric conditions. (Pizzazz et al.) Hormonal changes in puberty and menstruation may also be triggers but possibly only for genetically vulnerable individuals. * CHILDREN: Children tend to have more SWS or because the system that usually inhibits motor activity in SWS isn’t fully developed in children (and may be undeveloped in some adults). One study has found that adult sleepwalkers showed signs of immaturity in the relevant neural circuits.
AO2 Evaluative Points: * Supportive research: Lecendreux – 60 participants who had a history of sleepwalking in their family and a matched control group of non-sleepwalkers. They found the sleepwalking group all had the HLA gene in common so they now think you can inherit the malfunctioning gene. Therefore this suggests a plausible biological explanation. * Approaches: the explanations are mainly biological. As these biological explanations dominate psychological research other psychologists have tried to find other explanations. One psychodynamic explanation is that sleepwalking allows us to work through our worries; this means that we are less likely to use a defence mechanism. * Methodology: scientific evidence which is very reliable. However the data may not be as reliable as we think from EEG’s 1) skull is very thick an9d can disrupt impulses 2) subject to interference. Although they are supportive, research must be treated with caution. * Real world application: research into this has been useful in for the UK legal system. People were often using it as a defence as a loophole and the loophole has now vanished and it has to be backed up by medical and psychiatric evidence. This means innocent people are allowed to walk free. * Nature and nurture: genetics and the environment: Evidence for a genetic basis comes from Broughton who found that prevalence of sleep walking in first degree relatives is times greater in the general population and Lecendreux et al who found 50% concordance in MZ twins compared to the 15% DZ. The environmental component acts as a ‘stressor’ as in the DSM e.g. Sleep deprivation led to an increase in sleep walking in vulnerable individuals (i.e. those who had past experiences of sleep walking) Zadre et al. Levels of sleep walking rose from 50% to 90& after 25 hours deprivation.
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