Endogenous pacemakers
Many cycles follow 24-hour cycle while free running, follows that there must be internal clock (Some genetic - Miles)
Supreachisatic Nucleus
- The main EP is the SCN which generates a circadian rhythm acting as an internal clock keeping to sleep/wake cycle
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It is the product of evolution and largely genetic (Miles)
SCN (cells in hypothalamus above optic chiasm which reacts to light – influences 24 hour cycle) → regulates pineal gland →melatonin secretion = sleep induced
Morning = CLOCK + CYCLE which creates PERIOD + TIME → CC reduced, and in turn PT. This takes 24 hours within the SCN (central oscillator) and throughout the cells in the body (peripheral oscillator)
Evaluation
- After cells of SCN removed & studied in vitro, rhythm of neural activity continued
- Removal of SCN in hamsters found their circadian rhythm disappeared & not returned after transplant
- Human tumours that damaged SCN caused disorders in sleep / wake cycle (method issues)
- Now thought to be 2+ master clocks as research on animals shows some cyclical behaviour after SCN destroyed
- Although SCN has 24 hour rhythm, also involved in longer rhythms: Male hamsters have annual rhythm of testosterone dependent on light. Lesions stop testosterone secretion
Other EPs
- Locus Coeruleus (cells in pons) activate REM along with raphe nucleus
- Circadian rhythms persist in IV organs under no control of SCN
- Evidence for separate clock controlling sleep / wake cycle & temperature
- Shift work for nurses changed circadian rhythm but not their temperature cycles
- Women in cave had 24 hr temperature cycle vs. 30 hr sleep (effects similar to jet lag)
Exogenous zeitgebers – ‘entrainment’
Light
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Miles (blind man) – Shows light is the dominant cue, but can be overcome
- Shining light on knees shows role of light in other areas of the body, due to the SCN proteins being present throughout body
- Day length & light dominant EZs but others inc. seasons, weather, temperature etc.
- Arctic circle sleep for 7 hours, therefore social cues are dominant
Evaluation
- It is adaptive to have biorhythms to govern biochemical processes. Also adaptive for endogenous rhythms to be reset by external cues so in tune with environment
- Would be life threatening being solely reliant on exogenous cues, therefore endogenous are important
Other EZs
- Social cues – the liver and heart rest by eating + Eskimos rely on social cues
- Temperature – in the absence of light, temperature is used for hibernation
Interaction
Exogenous & endogenous interact to regulate the timing of biorhythms e.g. SCN + light
- Cultural factors important – Eskimos can still maintain regular sleep cycles, so cycle can’t be solely dependent on exogenous light melatonin
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Individual differences e.g. Aschoff
Disrupting the biorhythms
EPs & EZs are vital for survival, when EZ cues change; our internal clock needs to be readjusted. On average takes 3 days to adjust to a 12 hour shift in time. Artificial light can be moderately successful in resetting circadian rhythm but it takes time
Jet lag
- Effects of disrupted circadian rhythm due to dislocation of current EZ vs. body clock
- This change affects dorsal portion of SCN – takes several cycles to fully resynch
- Symptoms inc. tiredness, depression, slowed mental / physical reactions etc.
Phase delay – East ←West
- Delays sleep time, but easier to adjust due to natural lengthening of rhythm e.g. Siffre
- Baseball teams did better
Phase advance – West→ East
- Body clocks have to advance to catch up as the day is shortened (rhythm naturally lengthened e.g. Siffre)
- Studies suggest harder to adjust, depends upon time zone change, age (lifespan changes & Siffre) + individual differences
Evaluation
- BZs + melatonin pills help w/ jet lag by increasing melatonin and resynch body clock in SCN
- Alt reason for jet lag such as temperature clock has not reset & body is experiencing desynched rhythms like shift work + so many variables hard to measure e.g. caffeine, sleep deprivation and fasting (some EPs reset by food intake e.g. heart & liver)
Shift Work
We’re dictated by SCN but shift work goes against our natural rhythm and can lead to health issues. This is because it creates a mismatch or desynch between arousal and EZs, doesn’t allow enough time to adjust nor for long enough (shortening rather than lengthening day) + mismatch between EPs e.g. light dictates sleep but not temperature (lady in cave + nurses)
- This is even more pronounced for those with alt. shifts
- Nurses – worse on first night, but improved during the week
- These increase rates of accidents
Effects
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Decreased alertness – trough at midnight when cortisol is lowest & 4am when body temp is
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Sleep deprivation – sleeping during the day conflicts with EZs and SCN decreases sleep time and quality, and in particular REM (restoration theory link)
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Health – high correlation with shift work and organ disease due to both direct and indirect effects
Non-fluctuating shifts
- Unconventional but consistent – shift in circadian rhythm stays constant, resynch is possible
- Days off occur, become governed by mistimed circadian rhythms and always out of synch
Fluctuating shifts
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Czeisler – Preferred fluctuating shift patterns that move forward in phase delay. Benefits in health improvements, fewer accidents & more production in industrial workers
Evaluation
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Boivin - Artificial light (and melatonin pills) can help reset clock. This worked for nurses
- Harmful effects of shift work – can be caused by other issues related e.g. depression and sleep deprivation
Delayed sleep phase syndrome
Also a result of disturbance between internal clock & and EZs. Desynch in DSPS caused by having internal rhythm out of phase with the environment
Nature of sleep
Physiological measures
EEG – records neural oscillations showing awake / sleep and stages within it
EOG – measures eye movement – in REM important factor for showing dreaming
EMG – muscle activity in the chin specifically when tensed or relaxed
These techniques uncovered many facts about sleep e.g. infants 50% in REM vs. 20% for adults
Self-report –pps record length of dreams
Observation –of eye and muscle movements
Stages
During a night’s sleep you pass through different sleep cycles of 90 mins each with variance in amount of the different stages. Difference in stages is not just oscillations of depth but qualitatively different.Sleep stages alternate throughout night starting w/ rapid descent into deep sleep. Most complete 5 ultradian cycle w/ progressively less SWS & more REM towards morning
Stage 1 – ‘drift off’ relaxed state. Brain waves change from beta (awake) to alpha: greater amplitude, slower and partly irregular. Easy to wake in this stage
Stage 2 – slower, larger brain waves & occasionally quick bursts of high frequency sleep spindles + K-complexes
Stage 3 – beginning of deep sleep. Brain waves are slow and large, called delta w/ some sleep spindles. Slowing down of bodily activity
Stage 4 SWS – deepest sleep. Delta waves are slow, large and show jagged pattern on EEG. Difficult to wake and bodily functions sink to deepest state of physical rest. EMG shows muscles as relaxed. Sleep disorders + growth hormone production are associated
REM (paradoxical sleep) – similar signs of waking on EEG (why it’s paradoxical) muscles completely relaxed but eye movement is rapid. End of REM marks end of first ultradian rhythm
Dement – REM associated with dreaming through EEG, all people dream (those who don’t just forget). 80% of pps woken during REM reported dreams in vivid detail. Only 7% of awakening from NREM led to dream recall. Dreams don’t last longer than 15 mins, beyond this time people forget the beginning. Content can be affected by events experienced during the day & external stimuli
Reticular formation, locus coeruleus & raphe nuclei control REM / NREM (links w/ affective disorders & sleep)
Evaluation
- However, REM & dreaming v. different. REM = physiological state objectively measured. Dreams = subjective + problems studying scientifically
- Some studies reported 70% dreams in NREM (attributed to confusion of what is dreaming)
Physiology of sleep
Brain stem controls arousal and + sleep. Oldest part of reptilian brain, which controls vital functions
Serotonin – SCN responds to changes in light & controls production of melatonin in pineal land → production of serotonin in raphe nuclei. Increase of serotonin reduces RAS activity = onset of sleep
Noradrenalin – from locus coeruleus (part of pons) triggers REM
Functions of sleep
Evolutionary explanations
Sleep patterns evolved as an adaption. Each species has developed different sleep habits and patterns to deal w/ environment pressures e.g. predation, energy and foraging. Main assumption is that animal’s sleep pattern will be determined by its energy intake & expenditure pattern, concentrates on ecological niches
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Energy conservation / hibernation theory –mammals expend a lot of energy on body temperature, particularly evident in small animals w/ high metabolism. Conserving energy at times of little resources (night) + Sleep increases when energy loss goes up (cold)
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Foraging requirements – Sleep is related to amount of time need for finding food. Herbivores require grazing and therefore cannot afford to sleep as much as carnivores (links with the predation theory + lower metabolism supports energy conservation)
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Protection from predation – Being awake is riskier than being asleep, it ensures that animals stay still (however can increase vulnerability)
Evaluation
- Helped understanding of animals but incomplete in amount of sleep stages. NREM may be functional for energy conservation compared to REM (research shows correlation between animal size and NREM but not REM). New hypothesis based on mammalian brain of reptile not evolving REM, but no research support
- Can’t apply to humans (may be more beneficial not to sleep now - genome lag)
- Comparative studies generally supports view e.g. small animals w/ high metabolism sleep more, but there are anomalies such as the sloth (energy) and rabbit (predation)
- Universal concept, species differ in sleep pattern e.g. unilateral sleeping support adaptation
- Behavioural inactivity would be a better function + snoring = vulnerability bad explanation
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Capellini – previous research flawed in methods of non-standardisation (supported in phylogeny sleep project). Found neg correlation between metabolism rate and sleep. This falsifies energy conservation but supports trade off view of foraging requirements. Also found no correlation between predation and sleep
- Fails to address restoration findings, combined approach of all 3 + restoration is supported by Horne’s core vs. optional
Restoration theory -Oswald
Sleep allows various physiological + psychological states to be recovered e.g. infancy need for brain & body growth + learning / memory consolidation
Physiological restoration
SWS – immune system + growth hormone correlation & neural control (lifespan differences)
REM – brain growth + infant neuroplasticity + correlation with brain maturity e.g. dolphins vs. newborns + restores levels of neurotransmitters after day’s activities, explains high level of brain activity & supported by SSRI reducing REM activity (links w/ affect disorders)
Horne - distinguishes between core sleep (SWS + REM for body and brain restoration) & optional sleep (made up of the other stages which aren’t necessary but can help restore) this combines evolutionary and restoration
- PPS doing psychological and physiological tests, they fell asleep more quickly but not for longer. Could be reduction in optional sleep rather than disproving hypothesis – supported by falling asleep quicker (probs reduction on 1 + 2)
Psychological restoration
Sleep deprivation -associated w/ less friendly
Sleep -associated w/ reduction of anxiety (links back to NT restoration) + memory consolidation during REM (explains high rates in neo-natal + science changing)
Deprivation Studies
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Total deprivation - DJ Trip hallucinations & paranoia, controlled by NTs (shows no N/N distinction & links with psych conditions). He had a rebound of SWS & REM and had microsleep while awake. Fatal familial insomnia, rotating rats (cognitive, physical changes + rapid death)
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Partial deprivation – pps awoken in REM. This increased every night to 2x more and had personality and cognitive change, on restoration REM increased by 10%+ cat flower pot technique (all sleep stages bar REM + rapid death)
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Marathon runners - shows discrepancies between speed / length of sleep but does show increase of SWS after a race (supports core vs. optional)
Evaluation
- Can’t really distinguish between psychological & physical due to bio basis of cognition
- Deprivation studies support Horne core vs. optional
- Death may be due to stress rather than sleep
- Comparative studies of dolphins show they have no REM
Neither theory accounts for why animals have reduced consciousness during sleep (nor how / why it turns back on). Fact that it is universal w/ particular differences suggests both theories
Lifespan changes in sleep
Infants –
- Sleep for 2/3 of day, but not continuous - suggested to be adaptive mechanism for parents to do every day activities + wouldn’t wake if hungry or cold
- As they mature, a circadian rhythm is est. and sleep becomes more consolidated at night
- Display 2 types: quiet + active sleep (immature v. of REM & SWS) High REM = brain growth + neurotransmitter production to consolidating memories. Evidence in premature babies w/ 90% REM. It is not known about dreams due to the need for subjective recall
Childhood –
- Sleep for about 10 hours with adult EEG + deeper sleep (indicate maturation of thalamalcortical systems)
- Increased rate of parasomnias
- REM 30% (increase of NREM for brain maturation and increase in activities). Evolutionary adaptive (less physical need for food searching, greater need to avoid predators + greater need to consolidate learning – theory’s of sleep link)
Adolescents –
- More sleep than adults, less than kids (9-10 hours)
- REM decrease + growth hormones released during SWS
- While quality and quantity not changed, it’s easy influenced by external pressures and can lead to change in sleep / wake cycle.
- Changes in hormone production = variation in sleep + deprivation+ wet dreams + phase delay (recommendation different school starts due to associated concentration of this)
Adult –
- Less sleep, particularly in deep sleep
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Dement – daytime sleepiness caused by same sleep required as teens but external pressures prevent it.
- Middle age marked by shallowing & shortening of sleep and increased fatigue + increased rate of sleep disorders due to increase in alcohol and caffeine intake and weight gain
Old age –
- REM and SWS decrease – no need for hormone growth + explains physical problems
- Correlation study showed increased mortality rate with too much sleep
Evaluation
- Development approach = prone to over generalisation and lack of individual difference
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Methodological issues - small sample + lab based (however, pps adjust after 1st night) + operationalisation of various stages + cultural differences all suggest individual emphasis
- Percentage of REM decreases w/ age until age of 70, when it starts increasing. Probably due to total sleep time decreasing
Sleep Disorders
Insomnia
Insomnia diagnosed when: sleep difficulties occur for 1+ month, resulting in daytime fatigue causes distress or problems with functioning. Symptoms are affective, cognitive and behavioural inc. difficulty falling asleep, staying asleep or both which can cause irritability and impaired cognition. This can be acute or chronic (10% prevalence). Dement – argues insomnia is not a disorder but a symptom
Primary Insomnia – isn’t linked to existing physical or psych condition
Genetic link shown in family study. In other cases causes may be stress and thus disappear when it is dealt with – though sometimes anxiety resulting from insomnia becomes the cause of it further. Possible causes:
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Circadian rhythm disruption - e.g. shift work + jet lag + delayed sleep wave syndrome
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Learned Insomnia - Anxiety induced insomnia. Intermittent periods of stress generate vicious cycle of trying to sleep and conditioned frustration w/ bedroom habits (shown through sleeping in situations where these aren’t present e.g. TV) can become persistent even when stress is removed. Treatments involve ‘sleep hygiene’ and attribution theory
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Idiopathic insomnia – childhood onset due to brain abnormalities in sleep / wake cycle (reticular activating system for sleep and raphe nuclei for wake)
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Sleep state misperception – sleeping adequately but don’t feel like they do due to unclear perception of consciousness and difficulty disguising sleep from waking
Secondary Insomnia –more prevalent and the result of existing condition
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Physical – diabetes, asthma etc. known cause + hormonal change in women + decrease in melatonin secretion associated with older age
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Psychological – depression can cause insomnia both through symptoms & drugs
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Stress + anxiety – anxiety leads to higher arousal creating insomnia and vicious cycle
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Medication – may be a side effect + sleep-inducing meds can have issues long time and can create dependency causing worse insomnia
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Stimulants + alcohol – increase arousal leading to insomnia which can lead to vicious cycle of frustration & anxiety + alcohol decreases deep sleep
Influencing Factors
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Sleep apnoea – temp blocked airwaves signals brain towake that occurs many times during sleep and consequently feel very sleepy during day. Diagnosed by: EEG, EMG, ECG, chest movements, airflow and audio / visual. It’s caused by various factors: jaw position, blocked nose, obesity, enlarged tonsils and drugs
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Personality – 85% showed abnormal personality and internalise distress on q. (emotional arousal is a factor), scoring higher on anger measures + link between impulsivity & insomnia (more likely ADHD link which links back to stims)
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Depression + anxiety – both increase emotional arousal → physiological arousal
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Age + Gender – older people + women are more likely to suffer. Possibly due to increased prevalence of physical illnesses associated with insomnia + hormone fluctuating. Also teenagers have natural phase advance and correlation with drugs through both direct and indirect + hormone fluctuation and increases stress (lifespan links)
Evaluation…
- Important to distinguish between primary and secondary for treatment purposes. However, often precedes mood disorders, therefore treat regardless of primary or secondary effects
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Speilmen – predisposing (50% cc for insomnia), this doesn’t explain chronic primary insomnia so, predicating vulnerability (risk factors) and perpetuating (learned insomnia) explains why when original cause is treated insomnia remains
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Dement – so many different types of insomnia attributable to so many different causes, it’s impossible to generalise in a meaningful way e.g. melatonin only effective in small group
- Support for brain abnormalities from imaging studies show lack of blood to frontal media, occipital and parietal lobes
- Correlation between rating scale of insomnia and lab study show artificiality not issue
- Diagnosis excellent validity when based on objectivity, but subjective items (e.g. sleep state misconception) made any findings lack validity
Sleep walking
Everyday activities that occur during sleep w/o knowledge of doing so. SW occurs during NREM early in the night and may act as if awake but speech is nonsensical. They have no recollection and serious injury can entail. Most prevalent in children and boys. Adults who SW have increased prevalence of anxiety disorders & PDs
Genetic – family studies show 10x more prevalence in 1st degree relatives + twin studies showing 50% cc in MZ. It seems to be a genetic brain abnormality of being woken during SWS but arousal is incomplete
SWS -Children have increased SWS. Oliviero –the system that normally inhibits motor activity in SWS is not developed in children. Supported by sleep walkers having immaturity in neural circuits involved in motor excitability
Factors –psych illnesses, stress, anxiety and some drugs. Longitudinal research from sleep centre showed link between sleep deprivation and walking. Baseline showed 50% SW vs. after deprivation 90% of them did + increase in episodes (only for those w/ predisposition)
Evaluation
- Sleepwalking starts in childhood when daytime sleeping stops (this contradicts evo)
- Diathesis-stress model – genetic predisposition + maturity of neural circuits / SWS amount (which is in turn increased by other envi factors such as drugs and alcohol)
Narcolepsy
Disorder of sleep/wake cycle. Results in sudden uncontrollable attacks of REM sleep with variance in time. It involves daytime sleepiness and may not realise after microsleep they weren’t awake. The other main symptom is sudden loss of muscular control triggered by strong emotions called cataplexy. Similar to REM, everything is functional but muscle control in body is lost. Other symptoms inc. hallucinations, auto behaviour and interruption of night time sleep marked by craving of sweets and physiological arousal. Usually starts in adolescence
REM – Malfunction of REM due to association of hallucinations and muscle activity loss (cataplexy)
HLA – mutation of the immune system where an increase of HLA was found in narcoleptics
Hypocretin - Involved in regulating arousal. Dement – mice w/o hypocretin had narcolepsy + deliberate bred dogs w/ faulty hypocretin receptors also did. Levels of hypocretin in spinal fluid were near non-existent in human narcoleptics
Genetics – 25% cc rate. Suggests environment plays a role
Evaluation
- REM theory supported by neuron activity in the brainstem of narcoleptic dogs when cataplexy occurred so did neuron activation only occurred in normal dogs during REM. Is however, a lot of disputes over this theory
- The specific HLA variant found commonly in population and only minority of narcoleptics
- Hypocretin best answer, but not genetic even though narcolepsy shown to be