PSYA3 - Sleep

43,011 views

Published on

PSYA3 - Biological Rhythms powerpoint.
100 slides because there's a lot to know! Condensed it as much as possible.

Includes:
Biological rhythms - Circadian, Infradian, Ultradian, endogenous pacemakers, exogenous zeitgebers & consequences of disruption of said rhythms

Sleep states -
lifespan changes, restorative theory, evolutionary evaluations

Disorders of sleep - Insomnia & other sleep disorders.


There's minimal evaluation for Infradian - so do it yourself :D

0 Comments
41 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
43,011
On SlideShare
0
From Embeds
0
Number of Embeds
121
Actions
Shares
0
Downloads
463
Comments
0
Likes
41
Embeds 0
No embeds

No notes for slide

PSYA3 - Sleep

  1. 1. PSYA4 - Sleep
  2. 2. Definitions:Word DefinitionCircadian rhythm Body’s biological, internal clock. Approx.24 hours. Day/wake cycle.Ultradian rhythm Recurring function at regular intervals, inless than 24 hoursInfradian rhythm Regular occurrence in cycles of more than24 hoursEndogenous pacemakers Internal cues such as SCN(suprachiasmatic nucleus), pineal glandand melatoninExogenous zeitgebers Light, social cues, tempEntrainment Resetting the biological clock usingexogenous zeitgebers
  3. 3. Ultradian:
  4. 4. Stages of sleep: Rechtschaffen andKales (1968) (Ultradian):
  5. 5. Stages of sleep:Stage DefinitionStage 1: Drowsiness; small wave freq. (4-7hz), onEEG, NREM SleepStage 2: Asleep; EEG dominated by theta wavesbut hz increases, high energy bursts onEEG (sleep spindles), NREM SleepStage 3: Delta waves, (1-4hz), less sleep spindles,NREM SleepStage 4: Deepest stage of NREM, delta waves,hard to wake, growth hormone releasedhere, SWS (slow wave sleep)REM Sleep (paradoxical sleep) Fast desynchronised EEG, body effectivelyparalysed, dreaming more likely to occurMove back to stage 2 (approx 20 mins): Move back into REM, repeat pattern,approx every 90 minutes, 4/5 a night
  6. 6. Comparative: Jouvet (1967)• Cats and other animals• Upside-down flowerpots intank of water• Cats went into REM sleep,muscles became slack,bodies slumped, fell intowater & woke• Cats who didn’t go into REMshowed abnormal behaviourlike stress, and eventuallydied
  7. 7. Ultradian – Dement and Kleitman(1957):• Looking at relationship between REM anddreams• 9 participants (only 5 studied intensely)• Lab study – EEG’s used• Some variables controlled (noalcohol/caffeine)• All ppts showed REM every night• REM predominantly for dreaming, but notalwaysSmall sample size, subsequent studies haven’tsupported findings, lacks eco validity,objective methods, variables controlled
  8. 8. AO2 for Ultradian Rhythms:• Further evidence e.g.Friedman and Fisher (1967),who found BRAC (basic rest-activity cycle) followed 90 mincycle over 6 hr period. - May not be generalisable- Supports Ultradian Rhythms- Suggests biological mechanismto sleep Ultradian rhythm…
  9. 9. AO2 for Ultradian Rhythms:• Reductionist  - simplified form• Only looks at biology, notpsychology/social/individualdifferences• For example, people withinsomnia• They should look at broaderconcepts • Other than biological factors,perhaps the setting (lab studies)would affect people’s sleep…
  10. 10. AO2 for Ultradian Rhythms:• Ecological Validity  whether theresearch is applicable to settingoutside of the experiment• Lab study, ppts removed from naturalsleep settings• This may have affected those inDement and Kleitman’s (1957)research• Lack of eco val. could mean the studiesdon’t test what they set out to test.• Another thing which could reducevalidity may be studies conducted onanimals…
  11. 11. AO2 for Ultradian Rhythms:• Comparative research + ethicalissues • Better than human testing• May not be generalisable tohuman studies• Animals may die• E.g. Jouvet (1967)cats/flowerpots died• Though some studies arebased on science...
  12. 12. AO2 for Ultradian Rhythms:• Objective – based on facts• Increased replicability, dueto objective tests such asEEGs (like in Rechtschaffenand Kales (1968): SleepStages• More replicable, similarresults = more reliable
  13. 13. Infradian:
  14. 14. A little bit about the Infradianrhythms:• Body rhythms which occur for periods(ha) over 24 hours.• An example of which is the menstrualcycle• Which is the internal control ofhormones by the endocrine system• Driven by release of oestrogen fromovaries (builds up uterine lining)which is maintained by progesterone• Pituitary gland near hypothalamusreleases FSH (follicle stimulating) andLH (luteinizing hormone) to ripen egg• If egg isn’t implanted, thenmenstruation occurs
  15. 15. Infradian Rhythms – Russell et al(1980):• Menstrual cycles usually controlledby hormones (Endo. Pacemakers)• However, Russell used 2 groups ofwomen, who were keptseparately.• Sweat from one group of women,was wiped on the upper lips of thesecond group of women. (ew)• Their menstrual cyclessynchronised.• Shows that cycles may be linked byexogenous zeitgebers in the formof pheromones.
  16. 16. McClintock and Stern (1988):• Investigate affect of women’s pheromones(exogenous zeitgebers) on other women’smenstrual cycles• 29 women aged (20-35 years) with irregularmenstrual cycles tested• 9 women gave pheromone samples by usingcotton pads they had under their arms for 8hours+• Cotton pads were treated with alcohol todisguise any smells, and then frozen• The pads were then wiped under the other20 women’s noses• 68% of women responded, and their cyclesshortened from 1 to 14 days, or lengthened1 to 12 days (depending on when thepheromone samples were collected)
  17. 17. Men have Infradian cycles too-Empson (1977):• 21 males ppts• Body temp&alertness measuredfrom 49 to 102 days• Found evidence ofapprox. a 20 daycycle
  18. 18. Infradian – SAD (Seasonal affectivedisorder):• Depressed duringwinter months• Due to highmelatonin andreduced serotonin• Treatment is via lightbox therapy
  19. 19. Infradian AO2 – Determinism vs Freewill:• Ms. English drove a car into her husband’shouse, and blamed it on PMS (Johnson, 1987)• Supported by Dr. Katherina, who said ‘womenare not responsible for their actions on PMS’(Deterministic)SYNOPTIC: do not analyse Born• One study found people who were told to wakeup earlier had higher levels of the stresshormone ACTH (which contributes to themwaking up) causing them to wake earlier – Bornet al (1999)(Free will)
  20. 20. 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 meanwe can provide the best treatments possible
  21. 21. Infradian AO2 – Further research:McClintock (1971) Found thatwomen who work in maledominated environmentshave shorter menstrualcyclesShows menstrual cycles furtherinfluenced by exogenouszeitgebersThis could be seen as anEVOLUTIONARY ADVANTAGEas it would provide moreopportunities for pregnancy
  22. 22. Infradian AO2 – further furtherresearch:Reinberg (1967) – showed thatInfradian rhythms were alsoaffected by LIGHT (exogenous).Woman lived in a cave for 3months, and her menstrualcycle changed to 26 days(average is 28 days)Could be from the lack of naturallight that she had
  23. 23. Circadian Rhythms:Circa = circleDian = dayOne day!
  24. 24. A little bit about circadian rhythms:• Rhythms that occur on a cycle over a period of24 hours.• ‘Body’s biological, internal clock. Approx. 24hours. Sleep/wake cycle.’
  25. 25. Introduction to Biological rhythms:The Case of Michel Siffre (1962):• Testing internal body clock• Michel Siffre spent 61 days and nightsunderground in a cave• No exogenous zeitgebers(lights/clocks/radio)• Only influence was endogenouspacemakers (internal body clock)• Emerged 17th Sept, thought it was 20thAug• Natural rhythm extended to over 24hours(Supports endogenous)
  26. 26. Biological rhythms:Aschoff and Wever (1976):• Researchers placed ppts inWW2 bunker• Removed exogenouscues/social cues• Most people developed 24-25 hours• Some were as long as 29hours(Supports endogenous)
  27. 27. Biological rhythms:Folkardet al (1985):• Seeing the external cue time could beused to override internal clock• 12 people lived in a cave for 3 weeks,isolated from natural light• Woke up and went to bed when clockshowed particular time• Researchers sped up clock from 24hour cycles to 22 hour cycles• Volunteer’s circadian rhythms matchedthe clock initially, but eventually itreturned to 24 hour cycles(Supports endogenous)
  28. 28. Biological Clock, Proteins – Darlingtonet al (1998):• Proteins in the Drosophila fruit fly• In the morning: CLK-CYC bind• Once bound, PER-TIM are produced• Their presence decreases the amountof 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 areCLOCK-Bmal1 and PER-CRY
  29. 29. Things that effect circadian rhythm –Exogenous Zeitgebers:Light:One of the most dominantzeitgebers, it resets the body’spacemaker through the SCNIt can reset CRY protein, which islight-sensitiveThis may explain whyCampbell andMurphy (1998) found thatshining lights on knees caused ashift in Circadian Rhythm.
  30. 30. Exogenous zeitgebers:Social cues:Eating at certain times, and thetimes we sleep and wake upEntrained by social conventionrather than biologyZeitgebers for liver and heartcells are likely to becontrolled by mealtimes, asthey’re reset by eating(Davidson, 2006)
  31. 31. Exogenous zeitgebers:Temperature:Cold-blooded animals areeffected by weather for howactive they are.Warm-blooded animals (likehumans) suggest changes aremade by their own circadianclock, and their temps entrainother circadian(Buhr et al,2010)
  32. 32. Endogenous pacemakers:• The suprachiasmatic nucleus,(SCN) is a pair of structureswhich lie in the hypothalamusand are located where theoptic nerves from each eyecross.• It obtains info about light evenwhen our eyes are shut.
  33. 33. Endogenous pacemakers:• The SCN sends signals to thepineal gland.• The production of thehormone melatonin isincreased at night.• Melatonin induces (causes)sleep.
  34. 34. Endogenous – SCN, Albuset al 2005:• The SCN is split in two.One in each hemisphere• It is further split intodorsal and ventral• Ventral is quickly reset byEXTERNAL CUES like light• Dorsal is more resistant tobeing reset
  35. 35. Endogenous pacemakers, – Morgan etal (1995):• ‘Role of the SCN’• Bred mutant hamsters, withcircadian rhythms of 20 hoursinstead of 24• Then transplanted their SCNs into‘normal’ hamsters• ‘Normal’ hamsters then displayedthe mutant rhythms• Shows circadian rhythms may becontrolled by the SCN
  36. 36. Endogenous pacemakers –DeCourseyet al (2000):• Removed SCNs from 30 chipmunks• They were returned to naturalhabitat & observed• Alongside 2 other groups: 24 surgicalcontrols, and 20 controls.• After 80 days, significantly more ofthe SCN-lesioned chipmunks hadbeen killed by weasels• Probably because those chipmunksremained awake, and made noises intheir burrows so weasels could hear.(Sleep = links to evolutionary)
  37. 37. Endogenous pacemakers, artificiallighting – Stevens (2006):• If lights do reset thebiological clock, ourartificially lit worldcould be damaging• Stevens (2006)suggests it disruptsour rhythm andmelatoninproduction
  38. 38. AO2 for endogenous pacemakers andsleep cycles:• Further supporting evidence • Stevens (2006) supports role ofSCN• Suggests artificial lightingdisrupts circadian rhythms,disrupting melatonin levels• Provides further evidence SCNaffected by light• Although this research is carriedout on humans… Quite a lot ofresearch is carried out on…
  39. 39. AO2 for endogenous pacemakers andsleep cycles:• Comparativestudies/generalisability• DeCourseyet al’s (2000) research onchipmunks, Morgan et al‘s (1995)on hamsters• Biology differs between animals andhumans• E.g. Reptiles have direct input intothe pineal gland, whereas humansdo not.• Another issue, is whether or notanimal testing is ethical…
  40. 40. AO2 for endogenous pacemakers andsleep cycles:• Ethical issues • Do the pros outweigh the cons?• Decoursey removed SCNs whichwas detrimental to chipmunkssurvival• They’re unable to say no,however we could not carry outthese tests on humans• All of the research thus far hasfollowed a biological approach…What about evolutionary?
  41. 41. AO2 for endogenous pacemakers andsleep cycles:• What about evolution? Forexample hibernation? (Thoughhumans don’t hibernate)• SCN isn’t only control ofsleep/wake cycle, temp shouldalso be considered as temp affectshibernation• Evolutionary approach notconsidered therefore reductionist
  42. 42. AO2 for endogenous pacemakers andsleep cycles:• Reductionist • Doesn’t include individualdifferences/social differences/stress,anxiety, insomnia, blind people (nooptic nerve)… Counter with Campbell& Murphy (1998) (kneecap light)• Shows sleep is more complex thanlight/temp/biological factors• To fully understand sleep, biologicalfactors would have to be consideredincluding psychological/social factors
  43. 43. Disrupting Biological rhythms:
  44. 44. Intro…• Research has shown thatendogenous pacemakers useexogenous zeitgebers to adjustthe body’s biological rhythms(Czeisleret al 1982; Siffre, 1962)• This allows our body to copewith seasonal changes slowlyover time.• However there are some fasterchanges such as jetlag and shiftwork.
  45. 45. Jet lag:Phase Advance (W-E)Phase Delay (E-W)
  46. 46. Jet lag – travelling long distance by plane, soexo&endo are out of sync (desynchronisation)Phase delay:• Endogenous pacemakersare ahead of local time• Phase delay is consideredeasier to adjust to• Moves from East to West• When a train is delayed‘EWWWWW’ (east to west)Phase advance:•Endogenous pacemakers arebehind local time•Phase advance is moredifficult to adjust to becauseour biological clocks ‘lose time’•Moves from West to East• When you advance down aslide ‘WEEEEEEE’ (west toeast)
  47. 47. Consequences of jet lag – Rechtet al(1995):• Slower mental & physical reactions• Looking at performance of USbaseballers• Over a 3 year period• Teams from E to W won 44% of theirgames• Teams from W to E won 37% of theirgames• Suggests phase delay is easier• Does not consider individualdifferences (the teams may just be bad)• Longitudinal
  48. 48. Consequences of jet lag – Takahashi etal (2002):• After 11 hour flight• Doses of melatoninreduced symptoms of jetlag by speeding upresynchronisation• Recommended that youeat meals at the sametime as locals on arrival
  49. 49. Shift work:• Usually found in factories and powerstations• Work one shift in a 24 hour period• People who work night shifts havedisrupted biological rhythms –Desynchronisation of endo&exo• Some workers move a shift back eachweek, causing furtherdesynchronisation• ‘moving back’ has the same effect asphase advance• It’s been shown a week isn’t longenough to resyncPhase advance
  50. 50. Consequences of shift work:1. Poor decision making –anecdotal evidence suchas:- Chernobyl (1:30am)- Challenger space disaster(decision to launch wasmade in early hours ofmorn)
  51. 51. Consequences of shift work:2. Sleep deprivationWorkers on night shifts haveto sleep during the day,which is more difficult dueto sunlight, bird sounds etc.De-synced circadian rhythms
  52. 52. Consequences of shift work:3. Low worker satisfaction and production(Czeisleret al, 1982)• Chemical plant, Utah, USA• Staff on short rotation shifts sufferedmore health problems: difficulty sleeping& stress• Researchers convinced the plant to putworkers on a ‘Phase-delay’ shift pattern,where their shifts move forward• Shift rotation also altered from 7 days to21 days• After 9 months, worker satisfaction wassignificantly higher
  53. 53. Consequences of shift work:4. Gordon et al (1986):• Police in Philadelphia frombackwards to forwardsrotation on 18 day cycles• 30% reduction in sleepingon job• 40% reduction in accidents• Officers had better sleep,and less stress
  54. 54. Lifespan changes in sleep:
  55. 55. Lifespan changes in sleep:
  56. 56. Lifespan changes in sleep:• Little babies have the mostest sleep, and themostest REM sleep too• The amount of sleep you get decreases as youget older• % amount of REM sleep decreases through life• This shows sleeping patterns are not resolute• Doesn’t account for individual differences –those with insomnia
  57. 57. Lifespan changes in sleep – Ohayonetal (2004):• Meta analysis of 65 studies• Age range: 5-102• Total sleep time decreased. Approx 8hours at 5 years old, and 6 hours at70 years old.• % of 1 and 2 NREM sleep increaseswith age• % of 3 and 4 NREM sleep decreaseswith age• % of REM sleep decreased from 25%aged 5, to 19% aged 70.
  58. 58. Lifespan changes in sleep – Van Cauteret al (2000):• Longitudinal study (14 years)• 149 male ppts (aged 16 to 83)• Production of growth hormonedecreases, which causes deepsleep to decrease.• Deteriorates in 2 stages:- between 16 and 35- between 35 and 50 years old• Little growth hormone meansability to repair body tissue isdecreased.
  59. 59. Evaluation for lifespan changes: Uses EEGs to test, which arereliable as are lab studies andstuff Supporting studies – vancauter &ohayon But using lab studies can bebad due to unfamiliar settingswhich could disrupt sleeptherefore, lacks ecologicalvalidity Does this only take night timesleep into account? Whatabout elderly folk & babieswho nap during the day? Individual differences notconsidered, arguablyreductionist
  60. 60. Evolutionary explanations:
  61. 61. Evolutionary explanations:• Look at different species to determine keysleeping features• Amount of sleep is affected by differentfactors:- Predator/prey- Safe place to sleep- Body & brain size- Metabolic rate
  62. 62. Evolutionary – Meddis (1975): (like medicine)• Proposed that sleep is to keep animals safewhen active behaviour is impossible• For example at night, when prey animals needto hide from predators (sheep from foxes)• For example in DeCourseyet al (2000)’s studywith chipmunks, who were eaten by weaselswhen they couldn’t sleep & made noise• However, it would make more sense for theanimal to be awake & alert?• It also doesn’t explain why we have 2 types ofsleep
  63. 63. Supporting Meddis – Leskuet al(2006):- Animals sleeping in dangerousplaces sleep less- Predator (carnivores) animalssleep more than prey animalsmaybe because meat is higherin energy than say grass.
  64. 64. Evaluation – Leskuet 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 & theirenvironment, so it’s not reductionist… In fact,it’s MORE holistic.• However, it cannot tell us which is the moreimportant factor determining sleep patterns
  65. 65. Evolutionary – Webb (1982):• Used model of hibernation to proposethat sleep is to conserve energy• Moreso in smaller animals with highermetabolic rates• Supported by positive correlationbetween metabolic rate and sleep time• Doesn’t explain why there’s two types ofsleep• REM is highly active, and doesn’tconserve energy (it’s similar to beingawake!)• But overall, we burn less energy whilstasleep, which supports Webb’s theory.
  66. 66. Supporting Webb – Berger and Philips(1995):• Empirical support:animals sleep more whenfood is scarce
  67. 67. AO2 evaluation for evolutionary:• Holistic – Nature and environmental factorsconsidered• However, could also be deemed simplistic as itdoesn’t take lifespan changes of sleep intoaccount• Why are there 2 types of sleep? (NREM & REM)• REM is still highly active, is it really conservingenergy?
  68. 68. AO2 evaluation for evolutionary:• Empson (1993), describes sleepas ‘a complex function of thebrain’ which has a ‘restorativefunction’• Bottlenose dolphin sleeps onehemisphere of its brain at a time,so it can remain partly conscious& still breathe, shows that sleepis important, as it has had todevelop this intricate sleepingmethod. Also links to restorative.(unihemispheric sleep)
  69. 69. • Shows that evolutionary should also considerthan sleep has a restorative function, as sleepis there to help both the brain and the bodyrecovery
  70. 70. Sleep as a restorative thing…Oswald (1980) Restoration modelHorne (1988) Core/Optional sleepmodel
  71. 71. Oswald (1980) Restoration Model:• High levels of brain activity during REM, reflect recovery ofthe brain (EEG)• Increase in release of hormones, (like growth hormone) inSWS (Slow wave sleep) which restore body tissues,suggesting sleep does have a restorative function• Has not been applied to humansSupported by:- Randy Gardner (case study) who only had mild loss ofcognitive functioning- Jouvet’s study (1967), as cats without sleep died- Rechtschaffenet al (1983), rats without sleep died after 33days
  72. 72. Horne (1988) – Core/Operational sleepmodel:• Lab studies, showed sleep deprivation onlyhad mild effects on cognitive functioning(Randy Gardner)• Recovery centred on SWS Stage4 & REM• Suggested SWS and REM is core sleepneeded for brain functioning• Lighter stages (3&4) known as ‘optionalsleep’• Body restoration is not purpose of sleep,which occurs during relaxed wakefulness• Focussed on human ppts
  73. 73. Horne (1988) – supported by…• Newborn baby spends 50-60% of sleep in REMcompared to normal proportion of 25%, supportsHorne as babies use a lot of cognitive functioningto be able to take everything in• Horne (1988) conducted meta-analysis of 50human sleep deprivation studies, increasesreliability• Randy Gardner (ha!) (Case study) as he lost hiscognitive functioning
  74. 74. Oswald HorneSleep is used to restoreboth the BRAIN and theBODYCore sleep is ONLY used torestore the brainThe body recovers duringsleep through the releaseof hormonesThe body recovers duringperiods of ‘relaxedwakefulness’Could apply to non-humansCould only apply tohumans
  75. 75. Sleep deprivation studies – supportsHorne:Peter Tripp (famous DJ):- 201 hours and 10 minutes awake, mostly in abooth 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 & periodsof clarity (like Ultradian rhythms, such as REM) asthough he was dreaming, even though he wasawake- Suggests that the brain has to go into this sleepingpattern to recover
  76. 76. Sleep deprivation studies – supportsHorne:Randy Gardner (1965):Stayed awake for 11 days and nightsReported malfunctioning cognitiveprocesses such as blurred vision,slurred speech, mild paranoiaDespite losing 90 hours of sleep, heonly caught up 11 hoursHowever, caught up on more REMand Stage 4 (suggesting these arethe vital stages)Suffered no long term consequences(unlike Tripp)
  77. 77. Animal sleep deprivation studies –Supports Oswald:Rechtschaffenet al (1983)Placed rats on discs over waterWhen EEG’s showed they were sleeping,the discs would rotate, forcing the ratto walk to stay out of the waterThey lost weight, had increasedmetabolic ratesAfter 33 days, all rats were deadSuggests sleep does have a restorativefunctionAnimal study/not generalisable/ethical
  78. 78. Evaluation of restorative theories ofsleep (supports):Fatal familial insomnia – genetic defectleading to messy sleep patterns, until middleage, where they’re unable to sleep. After 2years of sleeplessness, they die- autopsies shown the thalamus degenerates- suggests we need sleep to recover- Cases are rare, so it’s difficult to generalise
  79. 79. Evaluation of restorative theories ofsleep (supports): Reductionist- Biological- Looking at nature- Doesn’t consider individual differences
  80. 80. Evaluation of restorative theories ofsleep (refutes): No correlation between energyexpenditure and length of sleep –We’d imagine we’d sleep more afterhigh levels of activity, and less afterlow activity.Breedlove (aww) et al (2007) foundno relationship between length ofsleep & activity levels prior to sleep.Giant sloth will sleep up to 20hours, and it does VERY little (lazysod!)
  81. 81. Evaluating restorative theory:• When looking at restorative theory, anexplanation that could help to understand itwould be the evolutionary theory of sleep, asit looks at both biological influences andinfluences of the environment• So, it’s better to consider differentexplanations together to gain fullunderstanding
  82. 82. Sleep disorders:Narcolepsy, insomnia, sleep walking
  83. 83. Sleep disorder - Narcolepsy:• It’s a disorder where peoplefall asleep whilst walkinground.• If triggered by an emotionalexperience, it’s known as‘cataplexy’• Lots of research suggeststhat it is a genetic disorder(biological link)
  84. 84. Three explanations for narcolepsy –1. Rapid eye movement (1960s)REM sleep linked to eyemovements, and body paralysis.Brain activity similar to if you’reawake. This explanation suggestsa person experiences elements ofREM sleep whilst they are awake.Since narcoleptics often collapse(like paralysis in REM) and candream in the brief period theyare asleep
  85. 85. Three explanations for narcolepsy –2. HLA – Human LeukocyteAntigen (1980’s)Biological/objectiveCaused by mutation in immunesystem. Best HLA marker isHLA-DQB1*0602 which ispresent in 90% ofnarcolepsy-cataplexy(Stanford school of medicine)
  86. 86. Three explanations for narcolepsy –3. Hypocretin (yanks call it Orexin)(1990’s)Biological/objectiveA neurotransmitter that regulates sleep,appetite and energy conservation. Ithelps maintain wakefulness.Hypocretin-1 is measured inCerebrospinal fluid, using a lumbarpuncture. Most people withnarcolepsy-cataplexy have nohypocretin-1 molecules.
  87. 87. Evaluating hypocretin:• People with narcolepsyhave less Hypocretin-producing-cells in theirbrains (Thannickalet al2000)• People with narcolepsyhave low levels ofHypocretin (Sakurai,2007)• Deterministic• Not 100% concordancerates between twins,suggests there’s anotherfactor that genes• Reductionist – Only looksat biology, not social orpsychological factors
  88. 88. Narcolepsy – University of Tokyo (study):• University of Tokyo found agenetic link• Genetic variant found in:79% chance increase ofNarcolepsy in Japanese people40% chance in other ethnicgroupsLinks to CPT1B and CHKB genes
  89. 89. Sleep disorder - Insomnia:• Primary insomnia – Noobvious psychological orphysical cause• Secondary insomnia – Resultof an existing psychological orphysical problem• It affects 1/3 of Americanpopulation, and a chronicproblem in 1/10 Americans
  90. 90. Insomnia:• Characterised by:Sleepiness, fatigue, drop in alertness,difficulty concentrating, depression,overly emotional stateDement argues insomnia is asymptom caused by something else.If he is correct, we should focus onwhat’s causing it, rather thantreating the insomnia.
  91. 91. Primary explanations for insomnia:Idiopathic Insomnia:- Begins in childhood &v. rare.- Malfunction in sleep/wakecycle- Brain: Raphe nuclei andReticular Activating System(RAS) at fault
  92. 92. Idiopathic (cont.)- During sleep/wake cycle, we’re kept awake byRAS which creates arousal in brain- In order to sleep, the RAS must be inhibited- Those with idiopathic insomnia are predisposedto greater arousal, and struggle to switch off theirRAS- Supported by Bonnet and Arand (1995) whosuggest insomniacs have higher levels of corticalactivity both when awake and asleep
  93. 93. Primary explanations for insomnia:Psycho-physiological insomnia:Insomnia results from learned/behaviouralconditionA) Cycle of anxiety, reduces sleep, self-reinforcingB) Regular routines, such as brushingteeth/getting ready for bed could createand become associated with stress, asthey link to the thought of insomniaAn example of classicalconditioning/phobia-like
  94. 94. Secondary explanations for insomnia:• Sleeplessness caused byanother disorder such asdepression or a medicaldisorder (chronic pain)• Much more common thanprimary• Monti (2004) found thattreating the CAUSE wasmore successful thantreating the insomnia (LikeDement said!)
  95. 95. Secondary explanations for insomnia:1. Sleep apnoea:Obstructive sleep apnoea – conditionwhere air stops flowing into the lungs,where breathing stops for 10+ seconds,for 5ish times a night– Lack of muscle tone in the upper airwaycauses airway to fold in & closeThis can cause people to wake up againwith a snore/snortSleep apnoea trust (2008) found thatpeople will be forced awake during thenight so are sleepy during the day
  96. 96. Causes + symptoms of sleep apnoea:• Blocked nose (various causes)• Obesity (fat people = pressure onthroat)• Drugs (tobacco/alcohol/painkillers)• Age (more common in old age)• Adenoids and tonsils (tonsillitis andall that rank stuff)Symptoms include – tiredness,reduced cognitive functioning, poorconcentration, Macey et al (2002)believes it can damage the braindue to repeated oxygen starvation
  97. 97. Secondary explanations for insomnia:2. Personality:Anxious personalitiesare more likely tosuffer from insomniaAnxiety is linked tohigher arousal whichmeans it would bemore difficult tosleep
  98. 98. Personality & Insomnia – Gregory et al(2006):• Gregory et al (2006) studied the effects of familyconflict on insomnia, which linked to high levels ofanxiety• 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 conflictexperience by child from (9-15 years) and onset ofinsomnia by 18• Could be a casual correlation between familialconflict (which leads to anxiety) and insomnia
  99. 99. Gregory et al (2006) – evaluation:• Variables well controlled• Longitudinal – lots ofinformation gathered• Longitudinal – maysuffered attrition rates• Only followed kids fromNZ (ethnocentric/culturalbias/cultural relativism?!Idk)• Questionnaires aresubjective, may also beaffected by socialdesirability bias
  100. 100. Sleep disorder – Sleep walking:• Sleepwalking is when people carry out activitiessuch as walking, weeing, or moving furniture intheir sleep – as if they were awake.• It occurs during slow-wave sleep, rather thanREM• Episodes can last from seconds to over 30mins• If left undisturbed, sleepwalkers often go back tosleep, but could fall asleep in unusual places.• Usually occurs in children aged 5-12, affecting20% of children, and 3% of adults (Hublinet al1997)
  101. 101. Sleepwalking – Bassetti (2002):• Looking at genetic evidence(biology)• Focussed on the HLA-DQB1*05 gene• Volunteer sample (somesleepwalkers may not evenknow they sleepwalk )• 74 patients (only 16genetically tested)• 8 patients had the gene (50%)• Gene present in 25% of non-sleep walking population• May not be representative
  102. 102. Bassetti (2002) – evaluation:• Objective – blood tests tofind genes, replicable +consistent results = reliable• Supporting evidence –Hublinet al (1997) Finnishtwins, found 66%concordance rates in boys,and 57% of girls have gene,suggesting genetic link• SE – Sleepwalking runs infams(Horne, 1992)• Small sample size, may notbe representative, orgeneralisable• Volunteer sample was sillybecause lots of sleepwalkersdon’t even know they do it
  103. 103. Sleep walking – Zadraet al (2008):• Investigating sleep walking &sleep deprivation• 40 ppts in lab study over 3 nights• Night one ‘normal sleep’measured – 40ppts had total of32 episodes of sleep walking• Night two – ppts kept awake for25 hours• Night three ‘Recovery sleep’measured – 40 ppts had total of92 episodes of sleep walking• Suggests tiredness can triggersleepwalking
  104. 104. Zadraet al (2008) – evaluation:• Findings not found inthose who do not sleepwalk – suggesting agenetic predisposition(link to Bassetti, 2002)• Sleepwalking common inthose with RLS (Restlessleg syndrome), which is arisk factor of insomnia,therefore excessivetiredness (SYNOPTIICCCC)• Small sample size• Lowered ecologicalvalidity, as not in theirown beds- could’ve let them sleepin the beds for a fewmore nights beforeobservations began
  105. 105. Main evaluations for sleepwalking:• Objective – scientific,based on fact, replicable +consistency = reliablee.g. blood tests in Bassetti(2002)• Deterministic – focuseson biology which is pre-determined, you’reunable to change it• Biological/reductionist –Looking at HLA DQB1*05gene in Bassetti (2002)Zadra (2008) also foundgenetic link• Research conducted in labstudy (esp sleeping) mayreduce ecological validity,may not be applicable toreal life

×