PSYA3 - Sleep

PSYA4 - Sleep

Definitions:Word Definition

Circadian rhythm Body’s biological, internal clock. Approx. 24 hours. Day/wake cycle.

Ultradian rhythm Recurring function at regular intervals, in less than 24 hours

Infradian rhythm Regular occurrence in cycles of more than 24 hours

Endogenous pacemakers Internal cues such as SCN (suprachiasmatic nucleus), pineal gland and melatonin

Exogenous zeitgebers Light, social cues, temp

Entrainment Resetting the biological clock using exogenous zeitgebers

Ultradian:

Stages of sleep: Rechtschaffen and Kales (1968) (Ultradian):

Stages of sleep:Stage Definition

Stage 1: Drowsiness; small wave freq. (4-7hz), on EEG, NREM Sleep

Stage 2: Asleep; EEG dominated by theta waves but hz increases, high energy bursts on EEG (sleep spindles), NREM Sleep

Stage 3: Delta waves, (1-4hz), less sleep spindles, NREM Sleep

Stage 4: Deepest stage of NREM, delta waves, hard to wake, growth hormone released here, SWS (slow wave sleep)

REM Sleep (paradoxical sleep) Fast desynchronised EEG, body effectively paralysed, dreaming more likely to occur

Move back to stage 2 (approx 20 mins): Move back into REM, repeat pattern, approx every 90 minutes, 4/5 a night

Comparative: Jouvet (1967)

• Cats and other animals• Upside-down flowerpots in

tank of water• Cats went into REM sleep,

muscles became slack, bodies slumped, fell into water & woke

• Cats who didn’t go into REM showed abnormal behaviour like stress, and eventually died

Ultradian – Dement and Kleitman (1957):

• Looking at relationship between REM and dreams

• 9 participants (only 5 studied intensely)• Lab study – EEG’s used• Some variables controlled (no alcohol/caffeine)• All ppts showed REM every night• REM predominantly for dreaming, but not

alwaysSmall sample size, subsequent studies haven’t

supported findings, lacks eco validity, objective methods, variables controlled

AO2 for Ultradian Rhythms:

• Further evidence e.g. Friedman and Fisher (1967), who found BRAC (basic rest-activity cycle) followed 90 min cycle over 6 hr period.

- May not be generalisable- Supports Ultradian Rhythms- Suggests biological mechanism

to sleep Ultradian rhythm…


• Reductionist - simplified form• Only looks at biology, not

psychology/social/individual differences

• For example, people with insomnia• They should look at broader concepts

• Other than biological factors, perhaps the setting (lab studies) would affect people’s sleep…


• Ecological Validity whether the research is applicable to setting outside of the experiment

• Lab study, ppts removed from natural sleep settings

• This may have affected those in Dement and Kleitman’s (1957) research

• Lack of eco val. could mean the studies don’t test what they set out to test.

• Another thing which could reduce validity may be studies conducted on animals…


• Comparative research + ethical issues

• Better than human testing• May not be generalisable to

human studies• Animals may die• E.g. Jouvet (1967) cats/flowerpots

died• Though some studies are based

on science...


• Objective – based on facts• Increased replicability, due

to objective tests such as EEGs (like in Rechtschaffen and Kales (1968): Sleep Stages

• More replicable, similar results = more reliable

Infradian:

A little bit about the Infradian rhythms:

• Body rhythms which occur for periods (ha) over 24 hours.

• An example of which is the menstrual cycle

• Which is the internal control of hormones by the endocrine system

• Driven by release of oestrogen from ovaries (builds up uterine lining) which is maintained by progesterone

• Pituitary gland near hypothalamus releases FSH (follicle stimulating) and LH (luteinizing hormone) to ripen egg

• If egg isn’t implanted, then menstruation occurs

Infradian Rhythms – Russell et al (1980):

• Menstrual cycles usually controlled by hormones (Endo. Pacemakers)

• However, Russell used 2 groups of women, who were kept separately.

• Sweat from one group of women, was wiped on the upper lips of the second group of women. (ew)

• Their menstrual cycles synchronised.• Shows that cycles may be linked by

exogenous zeitgebers in the form of pheromones.

McClintock and Stern (1988):• Investigate affect of women’s pheromones

(exogenous zeitgebers) on other women’s menstrual cycles

• 29 women aged (20-35 years) with irregular menstrual cycles tested

• 9 women gave pheromone samples by using cotton pads they had under their arms for 8 hours+

• Cotton pads were treated with alcohol to disguise any smells, and then frozen

• The pads were then wiped under the other 20 women’s noses

• 68% of women responded, and their cycles shortened from 1 to 14 days, or lengthened 1 to 12 days (depending on when the pheromone samples were collected)

Men have Infradian cycles too- Empson (1977):

• 21 males ppts• Body temp &

alertness measured from 49 to 102 days

• Found evidence of approx. a 20 day cycle

Infradian – SAD (Seasonal affective disorder):

• Depressed during winter months

• Due to high melatonin and reduced serotonin

• Treatment is via light box therapy

Infradian AO2 – Determinism vs Free will:

• Ms. English drove a car into her husband’s house, and blamed it on PMS (Johnson, 1987)

• Supported by Dr. Katherina, who said ‘women are not responsible for their actions on PMS’(Deterministic)

SYNOPTIC: do not analyse Born • One study found people who were told to

wake up earlier had higher levels of the stress hormone ACTH (which contributes to them waking up) causing them to wake earlier – Born et al (1999)(Free will)

Infradian AO2 - Reductionist:

• Only looking at biological aspect i.e. hormones• But that’s objective, so it’s also good • Link to endogenous/exogenous• Also it’s good for treatment? Like, for S.A.D,

getting to know how the rhythms work mean we can provide the best treatments possible

Infradian AO2 – Further research:

McClintock (1971) Found that women who work in male dominated environments have shorter menstrual cycles

Shows menstrual cycles further influenced by exogenous zeitgebers

This could be seen as an EVOLUTIONARY ADVANTAGE as it would provide more opportunities for pregnancy

Infradian AO2 – further further research:

Reinberg (1967) – showed that Infradian rhythms were also affected by LIGHT (exogenous).

Woman lived in a cave for 3 months, and her menstrual cycle changed to 26 days (average is 28 days)

Could be from the lack of natural light that she had

Circadian Rhythms:

Circa = circleDian = day

One day!

A little bit about circadian rhythms:

• Rhythms that occur on a cycle over a period of 24 hours.

• ‘Body’s biological, internal clock. Approx. 24 hours. Sleep/wake cycle.’

Introduction to Biological rhythms:The Case of Michel Siffre (1962): • Testing internal body clock• Michel Siffre spent 61 days and nights

underground in a cave• No exogenous zeitgebers

(lights/clocks/radio)• Only influence was endogenous

pacemakers (internal body clock)• Emerged 17th Sept, thought it was 20th

Aug• Natural rhythm extended to over 24

hours(Supports endogenous)

Biological rhythms:

Aschoff and Wever (1976):• Researchers placed ppts in

WW2 bunker• Removed exogenous

cues/social cues• Most people developed 24-25

hours• Some were as long as 29 hours(Supports endogenous)

Biological rhythms:

Folkard et al (1985):• Seeing the external cue time could be used

to override internal clock• 12 people lived in a cave for 3 weeks,

isolated from natural light• Woke up and went to bed when clock

showed particular time• Researchers sped up clock from 24 hour

cycles to 22 hour cycles• Volunteer’s circadian rhythms matched the

clock initially, but eventually it returned to 24 hour cycles

(Supports endogenous)

Biological Clock, Proteins – Darlington et al (1998):

• Proteins in the Drosophila fruit fly• In the morning: CLK-CYC bind• Once bound, PER-TIM are produced• Their presence decreases the amount

of CLK-CYC• Which, in turn, deceases PER-TIM.• But then it all repeats in a 24hr cycle.

This is known as NEGATIVE FEEDBACK.• In humans, the main proteins are

CLOCK-Bmal1 and PER-CRY

Things that effect circadian rhythm – Exogenous Zeitgebers:

Light: One of the most dominant

zeitgebers, it resets the body’s pacemaker through the SCN

It can reset CRY protein, which is light-sensitive

This may explain why Campbell and Murphy (1998) found that shining lights on knees caused a shift in Circadian Rhythm.

Exogenous zeitgebers:

Social cues:Eating at certain times, and the

times we sleep and wake upEntrained by social convention

rather than biologyZeitgebers for liver and heart

cells are likely to be controlled by mealtimes, as they’re reset by eating (Davidson, 2006)

Exogenous zeitgebers:

Temperature:Cold-blooded animals are

effected by weather for how active they are.

Warm-blooded animals (like humans) suggest changes are made by their own circadian clock, and their temps entrain other circadian (Buhr et al, 2010)

Endogenous pacemakers:

• The suprachiasmatic nucleus, (SCN) is a pair of structures which lie in the hypothalamus and are located where the optic nerves from each eye cross.

• It obtains info about light even when our eyes are shut.

Endogenous pacemakers:

• The SCN sends signals to the pineal gland.

• The production of the hormone melatonin is increased at night.

• Melatonin induces (causes) sleep.

Endogenous – SCN, Albus et al 2005:

• The SCN is split in two. One in each hemisphere

• It is further split into dorsal and ventral

• Ventral is quickly reset by EXTERNAL CUES like light

• Dorsal is more resistant to being reset

Endogenous pacemakers, – Morgan et al (1995):

• ‘Role of the SCN’• Bred mutant hamsters, with

circadian rhythms of 20 hours instead of 24

• Then transplanted their SCNs into ‘normal’ hamsters

• ‘Normal’ hamsters then displayed the mutant rhythms

• Shows circadian rhythms may be controlled by the SCN

SCN

Endogenous pacemakers – DeCoursey et al (2000):

• Removed SCNs from 30 chipmunks• They were returned to natural habitat &

observed• Alongside 2 other groups: 24 surgical

controls, and 20 controls.• After 80 days, significantly more of the

SCN-lesioned chipmunks had been killed by weasels

• Probably because those chipmunks remained awake, and made noises in their burrows so weasels could hear. (Sleep = links to evolutionary)

Endogenous pacemakers, artificial lighting – Stevens (2006):

• If lights do reset the biological clock, our artificially lit world could be damaging

• Stevens (2006) suggests it disrupts our rhythm and melatonin production

AO2 for endogenous pacemakers and sleep cycles:

• Further supporting evidence • Stevens (2006) supports role of

SCN• Suggests artificial lighting disrupts

circadian rhythms, disrupting melatonin levels

• Provides further evidence SCN affected by light

• Although this research is carried out on humans… Quite a lot of research is carried out on…


• Comparative studies/generalisability• DeCoursey et al’s (2000) research on

chipmunks, Morgan et al‘s (1995) on hamsters

• Biology differs between animals and humans

• E.g. Reptiles have direct input into the pineal gland, whereas humans do not.

• Another issue, is whether or not animal testing is ethical…


• Ethical issues • Do the pros outweigh the cons?• Decoursey removed SCNs which

was detrimental to chipmunks survival

• They’re unable to say no, however we could not carry out these tests on humans

• All of the research thus far has followed a biological approach… What about evolutionary?


• What about evolution? For example hibernation? (Though humans don’t hibernate)

• SCN isn’t only control of sleep/wake cycle, temp should also be considered as temp affects hibernation

• Evolutionary approach not considered therefore reductionist


• Reductionist • Doesn’t include individual

differences/social differences/stress, anxiety, insomnia, blind people (no optic nerve)… Counter with Campbell & Murphy (1998) (kneecap light)

• Shows sleep is more complex than light/temp/biological factors

• To fully understand sleep, biological factors would have to be considered including psychological/social factors

Disrupting Biological rhythms:

Intro…

• Research has shown that endogenous pacemakers use exogenous zeitgebers to adjust the body’s biological rhythms (Czeisler et al 1982; Siffre, 1962)

• This allows our body to cope with seasonal changes slowly over time.

• However there are some faster changes such as jetlag and shift work.

Jet lag:

Phase Advance (W-E)

Phase Delay (E-W)

Jet lag – travelling long distance by plane, so exo&endo are out of sync (desynchronisation)

Phase delay:• Endogenous pacemakers

are ahead of local time

• Phase delay is considered easier to adjust to

• Moves from East to West

• When a train is delayed ‘EWWWWW’ (east to west)

Phase advance:•Endogenous pacemakers are behind local time

•Phase advance is more difficult to adjust to because our biological clocks ‘lose time’

•Moves from West to East

• When you advance down a slide ‘WEEEEEEE’ (west to east)

Consequences of jet lag – Recht et al (1995):

• Slower mental & physical reactions• Looking at performance of US baseballers• Over a 3 year period• Teams from E to W won 44% of their

games• Teams from W to E won 37% of their

games• Suggests phase delay is easier• Does not consider individual differences

(the teams may just be bad)• Longitudinal

44%

37%

Consequences of jet lag – Takahashi et al (2002):

• After 11 hour flight• Doses of melatonin

reduced symptoms of jet lag by speeding up resynchronisation

• Recommended that you eat meals at the same time as locals on arrival

Shift work:• Usually found in factories and power

stations• Work one shift in a 24 hour period• People who work night shifts have

disrupted biological rhythms – Desynchronisation of endo & exo

• Some workers move a shift back each week, causing further desynchronisation

• ‘moving back’ has the same effect as phase advance

• It’s been shown a week isn’t long enough to resync

Phase advance

Consequences of shift work:

1. Poor decision making – anecdotal evidence such as:

- Chernobyl (1:30am)- Challenger space disaster

(decision to launch was made in early hours of morn)


2. Sleep deprivationWorkers on night shifts have

to sleep during the day, which is more difficult due to sunlight, bird sounds etc.

De-synced circadian rhythms

Consequences of shift work:3. Low worker satisfaction and production

(Czeisler et al, 1982)• Chemical plant, Utah, USA• Staff on short rotation shifts suffered more

health problems: difficulty sleeping & stress

• Researchers convinced the plant to put workers on a ‘Phase-delay’ shift pattern, where their shifts move forward

• Shift rotation also altered from 7 days to 21 days

• After 9 months, worker satisfaction was significantly higher


4. Gordon et al (1986):• Police in Philadelphia from

backwards to forwards rotation on 18 day cycles

• 30% reduction in sleeping on job

• 40% reduction in accidents• Officers had better sleep,

and less stress 30% 40%

Lifespan changes in sleep:

Lifespan changes in sleep:

• Little babies have the mostest sleep, and the mostest REM sleep too

• The amount of sleep you get decreases as you get older

• % amount of REM sleep decreases through life• This shows sleeping patterns are not resolute• Doesn’t account for individual differences –

those with insomnia

Lifespan changes in sleep – Ohayon et al (2004):

• Meta analysis of 65 studies• Age range: 5-102• Total sleep time decreased. Approx 8

hours at 5 years old, and 6 hours at 70 years old.

• % of 1 and 2 NREM sleep increases with age

• % of 3 and 4 NREM sleep decreases with age

• % of REM sleep decreased from 25% aged 5, to 19% aged 70.

on

Lifespan changes in sleep – Van Cauter et al (2000):

• Longitudinal study (14 years)• 149 male ppts (aged 16 to 83)• Production of growth hormone

decreases, which causes deep sleep to decrease.

• Deteriorates in 2 stages:- between 16 and 35 - between 35 and 50 years old

• Little growth hormone means ability to repair body tissue is decreased.

cauter

Evaluation for lifespan changes:

Uses EEGs to test, which are reliable as are lab studies and stuff

Supporting studies – van cauter & ohayon

But using lab studies can be bad due to unfamiliar settings which could disrupt sleeptherefore, lacks ecological validity

Does this only take night time sleep into account? What about elderly folk & babies who nap during the day?

Individual differences not considered, arguably reductionist

Evolutionary explanations:

Evolutionary explanations:

• Look at different species to determine key sleeping features

• Amount of sleep is affected by different factors:- Predator/prey- Safe place to sleep- Body & brain size- Metabolic rate

Evolutionary – Meddis (1975): (like medicine)

• Proposed that sleep is to keep animals safe when active behaviour is impossible

• For example at night, when prey animals need to hide from predators (sheep from foxes)

• For example in DeCoursey et al (2000)’s study with chipmunks, who were eaten by weasels when they couldn’t sleep & made noise

• However, it would make more sense for the animal to be awake & alert?

• It also doesn’t explain why we have 2 types of sleep

Supporting Meddis – Lesku et al (2006):

- Animals sleeping in dangerous places sleep less

- Predator (carnivores) animals sleep more than prey animalsmaybe because meat is higher in energy than say grass.

Evaluation – Lesku et al (2006):

• Correlations only show association, not cause & effect

• Many studies are in artificial environments (like zoos), are they ecologically valid?

• Takes into account the animal & their environment, so it’s not reductionist… In fact, it’s MORE holistic.

• However, it cannot tell us which is the more important factor determining sleep patterns

Evolutionary – Webb (1982):

• Used model of hibernation to propose that sleep is to conserve energy

• Moreso in smaller animals with higher metabolic rates

• Supported by positive correlation between metabolic rate and sleep time

• Doesn’t explain why there’s two types of sleep

• REM is highly active, and doesn’t conserve energy (it’s similar to being awake!)

• But overall, we burn less energy whilst asleep, which supports Webb’s theory.

Supporting Webb – Berger and Philips (1995):

• Empirical support:animals sleep more when food is scarce

AO2 evaluation for evolutionary:

• Holistic – Nature and environmental factors considered

• However, could also be deemed simplistic as it doesn’t take lifespan changes of sleep into account

• Why are there 2 types of sleep? (NREM & REM)• REM is still highly active, is it really conserving

energy?

AO2 evaluation for evolutionary:

• Empson (1993), describes sleep as ‘a complex function of the brain’ which has a ‘restorative function’

• Bottlenose dolphin sleeps one hemisphere of its brain at a time, so it can remain partly conscious & still breathe, shows that sleep is important, as it has had to develop this intricate sleeping method. Also links to restorative.(unihemispheric sleep)

• Shows that evolutionary should also consider than sleep has a restorative function, as sleep is there to help both the brain and the body recovery

Sleep as a restorative thing…

Oswald (1980) Restoration modelHorne (1988) Core/Optional sleep

model

Oswald (1980) Restoration Model:• High levels of brain activity during REM, reflect recovery of the

brain (EEG)• Increase in release of hormones, (like growth hormone) in SWS

(Slow wave sleep) which restore body tissues, suggesting sleep does have a restorative function

• Has not been applied to humans

Supported by:- Randy Gardner (case study) who only had mild loss of cognitive functioning- Jouvet’s study (1967), as cats without sleep died- Rechtschaffen et al (1983), rats without sleep died after 33 days

Horne (1988) – Core/Operational sleep model:

• Lab studies, showed sleep deprivation only had mild effects on cognitive functioning (Randy Gardner)

• Recovery centred on SWS Stage4 & REM• Suggested SWS and REM is core sleep needed

for brain functioning• Lighter stages (3&4) known as ‘optional sleep’• Body restoration is not purpose of sleep,

which occurs during relaxed wakefulness• Focussed on human ppts

Horne (1988) – supported by…

• Newborn baby spends 50-60% of sleep in REM compared to normal proportion of 25%, supports Horne as babies use a lot of cognitive functioning to be able to take everything in

• Horne (1988) conducted meta-analysis of 50 human sleep deprivation studies, increases reliability

• Randy Gardner (ha!) (Case study) as he lost his cognitive functioning

Oswald HorneSleep is used to restore both the BRAIN and the BODY

Core sleep is ONLY used to restore the brain

The body recovers during sleep through the release of hormones

The body recovers during periods of ‘relaxed wakefulness’

Could apply to non-humans

Could only apply to humans

Sleep deprivation studies – supports Horne:

Peter Tripp (famous DJ):- 201 hours and 10 minutes awake, mostly in a

booth in Times Square, NY- Nurses/doctors tried to keep him awake- Mean body temp declined- An EEG showed brain waves that he was asleep,

even though he was awake and talking- Followed 90min cycles of hallucinations & periods

of clarity (like Ultradian rhythms, such as REM) as though he was dreaming, even though he was awake

- Suggests that the brain has to go into this sleeping pattern to recover

Sleep deprivation studies – supports Horne:

Randy Gardner (1965):Stayed awake for 11 days and nights Reported malfunctioning cognitive

processes such as blurred vision, slurred speech, mild paranoia

Despite losing 90 hours of sleep, he only caught up 11 hours

However, caught up on more REM and Stage 4 (suggesting these are the vital stages)

Suffered no long term consequences (unlike Tripp)

Animal sleep deprivation studies – Supports Oswald:

Rechtschaffen et al (1983)Placed rats on discs over waterWhen EEG’s showed they were sleeping,

the discs would rotate, forcing the rat to walk to stay out of the water

They lost weight, had increased metabolic rates

After 33 days, all rats were deadSuggests sleep does have a restorative

functionAnimal study/not generalisable/ethical

Evaluation of restorative theories of sleep (supports):

Fatal familial insomnia – genetic defect leading to messy sleep patterns, until middle age, where they’re unable to sleep. After 2 years of sleeplessness, they die

- autopsies shown the thalamus degenerates- suggests we need sleep to recover- Cases are rare, so it’s difficult to generalise

Evaluation of restorative theories of sleep (supports):

Reductionist- Biological- Looking at nature- Doesn’t consider individual differences

Evaluation of restorative theories of sleep (refutes):

No correlation between energy expenditure and length of sleep – We’d imagine we’d sleep more after high levels of activity, and less after low activity.

Breedlove (aww) et al (2007) found no relationship between length of sleep & activity levels prior to sleep.

Giant sloth will sleep up to 20 hours, and it does VERY little (lazy sod!)

Evaluating restorative theory:

• When looking at restorative theory, an explanation that could help to understand it would be the evolutionary theory of sleep, as it looks at both biological influences and influences of the environment

• So, it’s better to consider different explanations together to gain full understanding

Sleep disorders:

Narcolepsy, insomnia, sleep walking

Sleep disorder - Narcolepsy:

• It’s a disorder where people fall asleep whilst walking round.

• If triggered by an emotional experience, it’s known as ‘cataplexy’

• Lots of research suggests that it is a genetic disorder (biological link)

Three explanations for narcolepsy –

1. Rapid eye movement (1960s)REM sleep linked to eye movements, and body paralysis. Brain activity similar to if you’re awake. This explanation suggests a person experiences elements of REM sleep whilst they are awake.

Since narcoleptics often collapse (like paralysis in REM) and can dream in the brief period they are asleep


2. HLA – Human Leukocyte Antigen (1980’s)

Biological/objectiveCaused by mutation in immune

system. Best HLA marker is HLA-DQB1*0602 which is present in 90% of narcolepsy-cataplexy (Stanford school of medicine)

HLA


3. Hypocretin (yanks call it Orexin) (1990’s)

Biological/objectiveA neurotransmitter that regulates sleep,

appetite and energy conservation. It helps maintain wakefulness.

Hypocretin-1 is measured in Cerebrospinal fluid, using a lumbar puncture. Most people with narcolepsy-cataplexy have no hypocretin-1 molecules.

Evaluating hypocretin:

• People with narcolepsy have less Hypocretin-producing-cells in their brains (Thannickal et al 2000)

• People with narcolepsy have low levels of Hypocretin (Sakurai, 2007)

• Deterministic

• Not 100% concordance rates between twins, suggests there’s another factor that genes

• Reductionist – Only looks at biology, not social or psychological factors

Narcolepsy – University of Tokyo (study):

• University of Tokyo found a genetic link

• Genetic variant found in:79% chance increase of Narcolepsy in Japanese people

40% chance in other ethnic groups

Links to CPT1B and CHKB genes

Sleep disorder - Insomnia:

• Primary insomnia – No obvious psychological or physical cause

• Secondary insomnia – Result of an existing psychological or physical problem

• It affects 1/3 of American population, and a chronic problem in 1/10 Americans

Insomnia:

• Characterised by:Sleepiness, fatigue, drop in alertness,

difficulty concentrating, depression, overly emotional state

Dement argues insomnia is a symptom caused by something else. If he is correct, we should focus on what’s causing it, rather than treating the insomnia.

Primary explanations for insomnia:

Idiopathic Insomnia:- Begins in childhood & v. rare.

- Malfunction in sleep/wake cycle

- Brain: Raphe nuclei and Reticular Activating System (RAS) at fault

Idiopathic (cont.)- During sleep/wake cycle, we’re kept awake by RAS

which creates arousal in brain- In order to sleep, the RAS must be inhibited- Those with idiopathic insomnia are predisposed to

greater arousal, and struggle to switch off their RAS- Supported by Bonnet and Arand (1995) who suggest

insomniacs have higher levels of cortical activity both when awake and asleep

Primary explanations for insomnia:

Psycho-physiological insomnia:Insomnia results from learned/behavioural

conditionA) Cycle of anxiety, reduces sleep, self-

reinforcingB) Regular routines, such as brushing

teeth/getting ready for bed could create and become associated with stress, as they link to the thought of insomnia

An example of classical conditioning/phobia-like

Secondary explanations for insomnia:

• Sleeplessness caused by another disorder such as depression or a medical disorder (chronic pain)

• Much more common than primary

• Monti (2004) found that treating the CAUSE was more successful than treating the insomnia (Like Dement said!)


1. Sleep apnoea:Obstructive sleep apnoea – condition where air

stops flowing into the lungs, where breathing stops for 10+ seconds, for 5ish times a night

– Lack of muscle tone in the upper airway causes airway to fold in & close

This can cause people to wake up again with a snore/snort

Sleep apnoea trust (2008) found that people will be forced awake during the night so are sleepy during the day

Causes + symptoms of sleep apnoea:

• Blocked nose (various causes)• Obesity (fat people = pressure on

throat)• Drugs (tobacco/alcohol/painkillers)• Age (more common in old age)• Adenoids and tonsils (tonsillitis and all

that rank stuff)

Symptoms include – tiredness, reduced cognitive functioning, poor concentration, Macey et al (2002) believes it can damage the brain due to repeated oxygen starvation


2. Personality:Anxious personalities

are more likely to suffer from insomnia

Anxiety is linked to higher arousal which means it would be more difficult to sleep

Personality & Insomnia – Gregory et al (2006):

• Gregory et al (2006) studied the effects of family conflict on insomnia, which linked to high levels of anxiety

• Longitudinal• New Zealand kids followed from 1972-2006• Used questionnaires to find out about household,

recorded life events.• Extraneous variables were controlled e.g. socio-

economic status, gender, health, depression• Found a correlation between family conflict experience

by child from (9-15 years) and onset of insomnia by 18• Could be a casual correlation between familial conflict

(which leads to anxiety) and insomnia

Gregory et al (2006) – evaluation:

• Variables well controlled

• Longitudinal – lots of information gathered

• Longitudinal – may suffered attrition rates

• Only followed kids from NZ (ethnocentric/cultural bias/cultural relativism?! Idk)

• Questionnaires are subjective, may also be affected by social desirability bias

Sleep disorder – Sleep walking:• Sleepwalking is when people carry out activities

such as walking, weeing, or moving furniture in their sleep – as if they were awake.

• It occurs during slow-wave sleep, rather than REM

• Episodes can last from seconds to over 30mins

• If left undisturbed, sleepwalkers often go back to sleep, but could fall asleep in unusual places.

• Usually occurs in children aged 5-12, affecting 20% of children, and 3% of adults (Hublin et al 1997)

Sleepwalking – Bassetti (2002):• Looking at genetic evidence

(biology)• Focussed on the HLA-DQB1*05 gene• Volunteer sample (some

sleepwalkers may not even know they sleepwalk )

• 74 patients (only 16 genetically tested)

• 8 patients had the gene (50%)• Gene present in 25% of non-sleep

walking population• May not be representative

Bassetti (2002) – evaluation:

• Objective – blood tests to find genes, replicable + consistent results = reliable

• Supporting evidence – Hublin et al (1997) Finnish twins, found 66% concordance rates in boys, and 57% of girls have gene, suggesting genetic link

• SE – Sleepwalking runs in fams (Horne, 1992)

• Small sample size, may not be representative, or generalisable

• Volunteer sample was silly because lots of sleepwalkers don’t even know they do it

Sleep walking – Zadra et al (2008):• Investigating sleep walking & sleep

deprivation• 40 ppts in lab study over 3 nights• Night one ‘normal sleep’ measured –

40ppts had total of 32 episodes of sleep walking

• Night two – ppts kept awake for 25 hours

• Night three ‘Recovery sleep’ measured – 40 ppts had total of 92 episodes of sleep walking

• Suggests tiredness can trigger sleepwalking

Zadra et al (2008) – evaluation:• Findings not found in those

who do not sleep walk – suggesting a genetic predisposition (link to Bassetti, 2002)

• Sleepwalking common in those with RLS (Restless leg syndrome), which is a risk factor of insomnia, therefore excessive tiredness (SYNOPTIICCCC)

• Small sample size

• Lowered ecological validity, as not in their own beds- could’ve let them sleep in the beds for a few more nights before observations began

Main evaluations for sleepwalking:

• Objective – scientific, based on fact, replicable + consistency = reliable

e.g. blood tests in Bassetti (2002)

• Deterministic – focuses on biology which is pre-determined, you’re unable to change it

• Biological/reductionist – Looking at HLA DQB1*05 gene in Bassetti (2002)

Zadra (2008) also found genetic link

• Research conducted in lab study (esp sleeping) may reduce ecological validity, may not be applicable to real life

PSYA3 - Sleep

Education

Transcript of PSYA3 - Sleep