Biorhythms and Sleep
Revision
in to
BAT - Ou tli ne (D) an d ev al uate (B) re se arch
of sle ep
bio rh yt hms, dis ru pt ion of sle ep, fu nc tio ns
an d sle ep dis orde rs
sleep cycles clip
http://www.psychexchange.co.uk/videos/view/
20945/
EEG
key word bingo ...
sleep-wake cycle
free - running
circadian
chronotherapeutics
primary
insomnia
Phase
delay
sleep apnoea
BRAC
endogenous pacemaker
ultradian
choose 4
NREM
unilateral
sleep
SWS
phase
advance
SAD
exogenous zeitgeber
REM
paradoxical sleep
narcolepsy
SCN
melatonin infradian
REM
rebound
* PSYA3 exam revision
AO1 = 9 marks
AO2 = 16 marks
The examiner may ‘cut up’ the questions, but this
balance will always apply
Biorhythms revision
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*Stages & cycles of sleep AO1
Most people have 5 cycles of sleep a night that last
approximately 90 minutes.
Electroencephalographs (EEGs) measure 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
1st cycle (90 min) - 1, 2, 3, 4, 3, 2, REM (10 min)
2nd cycle (90 min) 2, 3, 4, REM (10 min)
3rd cycle (90 min) - 2, REM (40 min)
4th cycle (90 min) -2, REM (60 min)
5th cycle (90 min) - 2, REM (60 min)
*
Stages & cycles of sleep AO2
Objective evidence – EEG, EOG and EMG illustrate Psychology as a
science Artificiality of sleep laboratory – extrapolation issues
Universality – stages & cycles of sleep have been found across cultures
Individual differences – reductionist – simplifies all sleep to a set range
of stages & cycles of sleep – people will differ AO3 - Weakness of the self-report method – The self-report method
yields data that may be subject to social desirability bias
*Functions of sleep: Restoration
theory AO1
Purpose of sleep is to repair and recharge the brain and body
Oswald (1980) claimed that NREM sleep restored the body and REM
sleep restored the brain Horne (1988) distinguished between core (stage 4 & REM) and optional
(stages 1 to 3) sleep and claimed that only core sleep was critical for
restoration of the brain as restoration of the body can occur during
resting wakefulness.
Stern and Morgane (1974) REM sleep allows the brain to replenish
neurotransmitters
Hartmann (1973) REM sleep is a time for synthesising noradrenaline and
dopamine *Restoration theory AO2
Case Studies - The studies of sleep deprivation in humans are mainly
case studies or small samples - difficult to extrapolate from (Randy
Gardner)
Objective measurement - The physiological measures of sleep, e.g.
REM activity and levels of neurochemicals, are objective, which means
that they are less subject to bias
Multi-perspective - The sleep deprivation research suggests that
effects are more psychological than physiological (Huber-Weidman,
1976 and the Peter Tripp case study) and so the main function of sleep
may be to recover psychological functioning.
Androcentricity – all of the sleep deprivation research is based on male
participants
Animal research – can you apply findings from Rechstaffen’s rats or
Jouvet’s cats to human behaviour?
*Functions of sleep: Evolutionary
theory AO1
Sleep may serve an adaptive rather than a restorative function - sleep
has been naturally selected because it promotes survival.
Species that sleep have survived to reproduce & carry sleep into the
next generation as an adaptive behaviour - If it was non-adaptive, i.e.
does not have an evolutionary purpose, then it should have
disappeared.
Meddis (1975) suggested that sleep is adaptive because the immobility of
sleep keeps animals safe from predators and that it occurs when normal
activities (such as feeding) are impossible.
Webb (1982) proposed the hibernation theory that suggested the
adaptive function of sleep is energy conservation.
*Evolutionary theory AO2
•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 as 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 much more quickly than the
genes.
•Low adaptive value - In some species if sleep were simply adaptive
then it should have been selected out.
•Lacks scientific validity - Evolutionary theories are post hoc, i.e. they
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 & Reductionist - Evolutionary theories are deterministic
as they ignore free will. People can and do choose when they want to
sleep. Sleep is far more complex a process to have evolved solely as
protection as this does not explain why we have the 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 for
sleep.
*Lifespan changes in sleep AO1
Sleep needs vary by age, both qualitatively (different stages of sleep) and
quantitatively (how much sleep).New-born's sleep an average of 16 to 18
hours a day. In the early months, an infants sleep is divided equally
between REM and non-REM sleep. A new-born baby will often enter REM
sleep immediately and it is not until they are 3 months old that the
sequence of NREM and REM sleep is established. By the age of 5-10 years,
the sleep stage cycle increases to approximately 70 minutes (Borbely,
1986) Between the ages of 5 and 12, total nocturnal sleep drops to about 9
-10 hours. Young adults (18-30 years) tend to start sleeping less than during
adolescence and do not experience such deep sleep. In middle age (30-45
years), people may start to notice a shallowing and shortening of sleep.
Increased signs of fatigue are a sign of middle age. In late middle age
(45-60) sleep duration drops to about 7 hours and stage 4 sleep virtually
disappears. There is a corresponding increase in lighter stages of sleep
such as stage 1.
*Lifespan changes AO2
Objective measurements - Research into lifespan changes in sleep has been
conducted in numerous sleep laboratories throughout the world - Dement
(1999) himself carried out a detailed 7 year longitudinal study called the
Stanford Summer Sleep Camp, which used twenty-four 10, 11 and 12 year
olds.
External factors and co-sleep (Reductionism) - There are numerous factors
that affect the quality and quantity of sleep experienced. Work patterns,
children, aches and pains, and medication can all affect sleep patterns.
Individual Differences - Borbely (1986) warns against the use of
generalisations about sleep patterns for different age groups. Extrapolation
could be difficult
Operationalisation of sleep - One difficulty with sleep research is to agree
when sleep occurs. Sleep onset is gradual and entails a predictable sequence
of events rather than a discrete event. If it cannot be operationalised, it
should not be measured.
Cultural traditions - In Europe and North America, adults tend to adopt a socalled monophasic pattern of sleep (that is, they sleep for one long period
during the night) and much of the research outlined would only be applicable
to these countries.
*Insomnia AO1
Primary Insomnia = chronic insomnia occurring in the absence of any
psychological or physical (medical) condition.
Secondary Insomnia = chronic insomnia that can be explained by a preexisting psychological or physical (medical) conditions.
There are numerous primary insomnia subtypes including:
Psychophysiological insomnia, Idiopathic insomnia and Sleep state
misperception.
Psychophysiological insomnia - This is a form of anxiety-induced insomnia
and is sometimes known as learned insomnia or behavioural insomnia.
The primary components involved are intermittent periods of stress,
which result in poor sleep and generate two maladaptive behaviours.
Idiopathic insomnia - This was originally called childhood-onset insomnia
because it tends to occur at a very early age. It is thought to occur due
to an abnormality in the brain mechanisms that controls the sleep-wake
cycle.
*Insomnia AO2
Physiological support - Smith et al (2002) conducted a study into
the neuro-imaging of NREM sleep in insomnia and found clear
evidence for physiological abnormalities in insomniacs.
External validity of sleep studies - Studies have examined
whether findings from sleep laboratories relate to reported sleep
disorders from patients.
Difficulty in extrapolation - Melatonin does appear to be effective
in small group of elderly patients with insomnia who have low
melatonin levels. However, it is considered ineffective in the
general treatment of insomnia, and the precise role of melatonin in
sleep still needs to be clarified.
Not a sleep disorder at all! –Dement (1999)
Reliability and validity of sleep insomnia measures: One major
obstacle to explaining the cause of insomnia is that there is
controversy over the identification of insomnia in the first place!
*Narcolepsy AO1
Narcolepsy is a disorder of the system that regulates the sleep-wake
cycle. It results in sudden and uncontrollable attacks of sleep at
irregular and unexpected times, which may last minutes or hours
The most obvious symptom of narcolepsy is a sudden loss of muscular
control (cataplexy) triggered by amusement, anger or excitement.
Narcolepsy usually begins in adolescence and may have a biological
basis. It affects 0.02% - 0.06% of the population (so is very rare).
It may be the result of a genetic abnormality (related to the HLA
complex on chromosome 6), the result of an auto-immune disease or
caused by a shortage of the neurotransmitter hypocretin.
*Narcolepsy AO2
Animal research - Understanding of narcolepsy stems primarily from
research involving narcoleptic dogs (for example, special laboratory-bred
Dobermans and Labradors).
Effective treatments and animal research: treatments for narcolepsy
often involve stimulant drugs. The drug (Provgil) has proved useful in the
treatment of narcolepsy.
Reductionism – reduces the explanation of narcolepsy to hypocretin only.
Biological approach – explains narcolepsy in terms of a physical
(biological) response
*Sleepwalking AO1
Sleepwalking affects about 20% of children and only about 1-3% of
adults (Hublin, 1997). Adolescents and adults with SW tend to have an
increased prevalence of anxiety and personality disorders.
The causes of sleep-walking are not fully known but it is thought to be
triggered by: Sleep deprivation and/or an irregular sleep schedule.
SW occurs during NREM sleep.
Research has found that SW has a significant genetic component.
Evidence comes from familial studies. For example, Broughton (1968).
They have also identified a gene that may be critical in SW – the
DQB1*05 gene.
*Sleepwalking AO2
Nature/Nurture - It remains unclear what the exact nature of the
relationship between the HLA gene and sleepwalking is.
An additional problem with the Bassetti study is that the sample of
sleepwalkers studied may not be representative of the general
population of sleepwalkers. Extrapolation issues.
Dement (1999) recognises that the possibility of sleep deprivation plays
a part in sleepwalking – however is this reductionist?
Homework
Complete one of the essays on
the list for Biorhythms and
Sleep
Plenary
Make some Taboo cards
for the topic of sleep
Then we will play the game