Biological Rhythms

Definitions A rhythm is something which is repeated regularly. All living organisms have some kind of biorhythm which exists on a constant basis-

hibernation/migration/sleep/temperature etc. Each biorhythm is repeated over different intervals (yearly/monthly/daily) and it depends on

the rhythm itself how often it repeats itself. Biological rhythms are governed by a combination of exogenous zeitgebers and endogenous

pacemakers. A bodily rhythm is a cyclical variation over some period of time in physiological or

psychological processes. Environmental factors such as light-dark cycles, noise, clocks and so on give clues as to

external cycles and exogenous zeitgebers. In the absence of any zeitgeber, behaviours that show rhythmicity are driven by internal

timing devices; internal biological clocks which are known as endogenous pacemakers Patterns of physiological or psychological processes that are repeated over periods of time We both have them and are affected by them. Grouped according to their period and duration.

Ultradian Rhythms Ultradian biorhythms occur more often than once a day. Found in most mammals. An example can be found in sleep, as it is divided into several separate stages of approx. 90

minutes that repeat themselves. Linked to a controlling mechanism in the medulla. This ‘clock’ seems to control a pattern of regular changes in our alertness and associated

activity during the day, as well as NREM and REM sleep cycles at night. Ultradian rhythms start to function in the womb A rhythm of CNS activity has been observed in foetuses at 20 weeks, and EEG rhythms have

been recorded in pre-term neonates.Infradian Rhythms

There are biorhythms that occur less often than once a day and more often than once a year, such as the menstrual cycle.

Have cycles longer than 24 hours along with a regular repeating pattern. Control mechanisms range from the influence of pheromones, the influence of day/night

cycle and the direct influence of the suprachiasmatic nucleus Reinberg (1967)

o Exogenous light cues have an impact on infradian rhythms.o Documented the menstrual cycle of a woman who lived in a cave for three months

with no EZ’s (exogenous zeitgebers)o Her menstrual cycle became much shorter.

Russell et al o Pheromones allow women’s menstrual cycles to synchronise with each other.o Can be argued this allows for an evolutionary advantage for women and men.

Infradian rhythms include bird migration, hibernation, menstrual cycle and most reproductive cycles. Seasonal rhythms which last approx. 1 year are known as circannual rhythms- usually associated with long-lived plants and animals.

Circadian Rhythms These biorhythms repeat themselves roughly every 24 hours, such as the sleep wake cycle or

body temperature cycle. Green (1994)

o Suggested that mammals possess about 100 different biological rhythms A theory as to why these cycles are 24 hours long is that they are a) influenced by exogenous

zeitgebers such as the day/night cycle-each dawn follows 24 hours after the last or b) controlled by an endogenous pacemaker that maintains and internal 24 hour repeating cycle.

Sifreo Case studyo Studied for 7 months underground with no contact to daylight and no other clues

about what time is was.o He quickly settled into a regular cycle of sleeping and waking at a regular 24.9 hour

rhythm.o The sleep-wake cycle is something that we are born with and which is biologically

determined, and functions without external zeitgebers. Aschaff and Wever

o Isolated participants in an underground WW2 bunker in the absence of environmental time cues for 3-4 weeks.

o All participants followed a circadian rhythm with a sleep wake cycle of about 25 hours.

o Experimental changes in room temperature had no effect on their cycle. These studies use very few participants- often only a single individual and findings may not

be generalizable to a wider population, as there may be a specific factors about these individuals [age/gender/personality] which account for the results.

Individual differences. The main endogenous pacemaker for circadian rhythms is the suprachiasmatic nucleus

(SCN) a small group of cells found jut above the optic chiasm. This provides evidence for a connection between exogenous and endogenous controls) Endogenous pacemaker: The internal 24/25 hr cycle is the result of protein synthesis

(melatonin and serotonin) Once a day, the SCN stimulates the pineal gland to produce melatonin, which causes us to

fall asleep. As the melatonin level peaks, the SCN produces serotonin and as melatonin levels drop, we

wake up. Exogenous zeitgeber: the SCN is located directly next to the optic chiasm, allowing it to

directly detect the current light levels, synchronising the internal body clock so that it is in sync with the day-night cycle.

The SCN uses both of these cues in its control of the sleep-wake cycle and does so via the pineal gland.

Once in a 24 hour cycle the SCN stimulates the pineal gland to remove the neurotransmitter serotonin from the synapses and synthesise it into melatonin which makes us sleepy.

When the levels of melatonin gets too high, the SCN stops the pineal gland synthesising melatonin and we wake up.

Schochat et alo Made use of an ultra-short sleep wake paradigm, in which 6 male participants spent

29 hours in a sleep lapo They attempted to sleep for 7 minutes in every 20.o Levels of melatonin were measured via blood sample taken 3 times an hour.

o Found a close and precise temporal relationship between the circadian rhythms of sleep propensity and the levels of melatonin- melatonin = sleep.

o Correlational Morgan (1995)

o Removed the SCN from hamsters and found that they lost their circadian rhythms.o These rhythms returned when the SCN was restored.o Animal research/ethics.

Miles (1977)o Studied a man who had been blind since birth and had a 24.9 hour circadian rhythm.o External zeitgebers didn’t help (TV/clocks) and he had to use sedatives to sleep.o Suggest that light is the dominant EZ

Luce and Segal o Contrast to Miles.o Investigated people who live in the artic where in the summer months the sun

doesn’t set and found that people slept normally. Czeisler

o Disagrees with the findings of the aforementioned studies.o Claimed that isolating participants from the environment without strictly controlling

the environment isn’t sufficient to reveal the activity of the endogenous circadian pacemaker.

o Participants in earlier sleep wake cycle studies were inadvertently affected by their exposure to high levels of artificial light, which may have skewed results.

o The Sifre case however is a clear example/demonstration of an innate circadian rhythm in humans. The sleep-wake cycle is biologically determined and functions in the absence of any external cues such as daylight.

Evolutionary Explanations

Remaining hidden (predator avoidance) & conserving energy. At night prey animal can’t see predators and remaining still could be an advantage to

survival. Sleep is to provide prey with a time when they are still and less likely to be seen by predators.

Therefore: prey should only sleep at night, predators shouldn’t sleep (wrong) Meddis proposes that sleep could be a time of increased safety as animals are immobile and

therefore less likely to be noticed by predators. To be still when it is too dark to see either food or threats could therefore be an

evolutionary advantage for some animals. However, some animals do not appear to fit with this theory- animals that are nocturnal for

example. Sleep may be adaptive as it conserves energy, especially for small and new born mammals

with a high metabolism and predators who need to expend a lot of energy catching food. While sleep allowing for the conservation of energy seems correct, it has little or no

empirical evidence to support it (overall problem with the evolutionary theory. In addition to a lack of evidence, it also has anecdotal contradictions that suggest predator

avoidance and conserving energy are not the main function of sleep. According to the evolutionary explanation of sleep, the function is similar to that of

hibernation; to conserve energy when the environment is hostile. To conserve energy when we would not be very efficient and to protect us at night when we

might be vulnerable to predators. Sleep is thus an evolutionary stable strategy which increases individual and in turn species survival.

The evolutionary explanation predicts that animal species should vary in their sleep needs: animals preyed upon such as herbivores should sleep more than carnivores since sleep would protect them

However, in reality herbivores tend to sleep less than carnivores, therefore taking this approach therefore means ignoring certain contradictions.

Allison and Cicchettio Grazing animals do not fit into the theory as they sleep very little.o The nutritional value of vegetation is very poor- need to spend lots of time eating.

Siegel o Agrees that sleep may be adaptive because of its energy conservation, particularly in

smaller mammals whose high metabolic rate is linked to high energy loss, mostly heat as they have a high surface area/body volume ratio, which could result in significant/dangerous drops in body temperature.

A similar risk applies to new-borns but as they grow and reach a certain body mass, greater benefit is gained from being awake and learning

This theory suggests that sleep is an evolutionary leftover; however, we do feel lethargic and ill when we don’t sleep (sleep deprivation studies)

If protection was the only function of sleep we would expect to find that animals that are likely to be attacked sleep very little.

The theory as a whole is very difficult to see where empirical evidence could be obtained. Horne

o There are different reasons for different species, so a universal theory is pointless. Empson

o Sleep is universal among animals, even the most successful predators that should not have to waste the time asleep. Sleep is universal among animals, even the most successful predators and that sleep deprivation can be fatal; suggest sleep has some value in itself.

Disrupting Biorhythms: Jetlag

It used to be believed that jet lag occurred because travelling by plane is time consuming and tiring, however it was noticed that jet lag only occurs when travelling east-west not north-south.

The sleep wake cycle is controlled via endogenous pacemakers and external zeitgebers. When these internal and external factors are out of sync, we feel tired/awake at strange

time. Phase delay (east to west) is easier to cope with than phase advance (west to east) Jet lag is a temporary condition that can be experienced as a result of air travel across

several time zones in a short period of time. This causes the traveller’s internal biological clock to be out of sync with the external

environment. People experiencing jet lag have difficulty maintaining their internal, routine sleep wake

cycle in the new location, because exogenous zietgebers such as light and local timetables dictate a different pattern.

Psychological knowledge about out innate clocks and zeitgebers suggests that the effects of jetlag are the result of a mismatch between our inner psychological rhythms and out external cues.

Inner time conflicts produce the symptoms of jet lag. Klein

o Found that flying from Britain to America is easier to recover from than America to Britain, regardless of where participants normally lived.

o This is because West to East shortens the day, and your internal body clock can’t catch up.

Schwartzo Analysed the results of baseball games in America.o Teams who travelled west to east had fewer wins than terms that travelled east to

west. o The effects of phase advance caused a drop in performance.o Correlational not empirical data.

Choo Found a reduction in temporal lobe size and memory functioning in pilots who

regularly cross time zones especially if there is only a short turn around.o Suggests that damage caused by jet lag is not just psychologicalo Highlights the dangers of disrupting biorhythms

The stress brought on my changing time zones and the difficulty sleeping could in itself be a factor in upsetting body clocks.

Stewart and Amir (1998)o Fount that rats that have been emotionally upset are not as good at resetting their

innate clocks using light as a zeitgeber as rats that have not been emotionally stressed.

o Suggests that emotional upsets make the SCN less responsive to light. o This could be a factor in humans as well, as many people find long haul travel

stressfulo However consider issues of anthropomorphism.

Some people take longer to adjust to the new time, and some people don’t seem to experience jet lag after long travel; these people may not experience travel and changing time zones as a stressor.

Psychologically and physiologically, the way to minimize the effects of jetlag are said to be to keep well hydrated, avoid alcohol and caffeine (which are said to interfere with the brain’s normal functioning) and to fit in to local zeitgebers (having meals at the correct times.

Logically this ought to make adjustments easier, but there is no empirical data to support this.

Treatment for jetlag includes using melatonin to rest the endogenous ‘clock’; trialled n aircrew but few results.

Disrupting Bio-Rhythms: Shift work

It is estimated that 20% of people in the USA work shifts; defined as work which occurs outside the arbitrary hours of 7am and 6pm.

Most industrial accidents happen at night when people are working shifts. Monk and Folkard

o Identified two main types of shift worko Rapidly rotating o Slowly rotating

There are problems with both types of shift work. Rapidly rotating shift work is the least damaging, as it lets workers keep their circadian rhythms fairly constant.

Hawkins et al (1978)o Fount that it takes individuals about a week to change their circadian rhythms.o Rapidly rotating shifts will mean the sleep wake cycle is always out of sink

Slowly rotating shift work forces your circadian sleep wake cycle to change in line with your shifts (i.e. sleep during the day).

While you can get used to the new cycle, changing back can cause issues due to the lack of daylight and social withdrawal.

Dawson and Campbell (1991)o Exposed shift workers to four hours of very bright light, which helped their circadian

rhythms change quicker.o Real life application to psychological research.

Czeisler et al (1982)o Found that workers recover quicker if they use phase delay rather than phase

advance.o The extra hour makes the working day longer not shorter, with late finished not

earlier starts.o Managers found that productivity increased and workers made fewer errors.o Czeisler’s research into shift workers in Utah led to managers introducing a phase

delay system of shifts, where shifts rotate forward in time.o Shift rotations were also altered to every 21 days rather than every 7 days.o Nine months later workers were healthier, happier and work output was up.o Illustrates again practical application.

Humans often try to disobey their internal clock by living a 24 hour lifestyle. Workers on a night shift have significantly higher rates of heart disease and diseases of the

digestive system. It’s estimated that 20% of shift workers report falling asleep during work, increasing the risk

of industrial accidents and decreasing economic gain/productivity. Shift workers don’t get enough sleep. Night time shifts affect the body’s natural sleep-wake

pattern, making it difficult to stay awake during the day. This harms health, on the job safety, task performance, memory and mood, as well as having

social costs related to time spent and family. In shift work change exogenous zeitgebers such as daytime and night-time are never

permanently synchronised with the start and end of shifts. This means that their cycle is governed by consistently mistimed circadian rhythms and

alternating external cues. A person may work the night shift for five nights, followed by two days off. During the two days off, the person resumes a normal daytime (diurnal) activity with family

or friends. This disrupts the person’s previously adjusted circadian rhythm, and they must then readjust

their sleep wake pattern when they got back to work. Without a constant pattern biological rhythms remain continually out of synch. Many industries depend on shift work to keep going 24 hours a day. Out innate biological clocks are reset at least daily by environmental stimuli (zeitgebers) The most powerful zeitgeber is light which puts endogenous clock mechanisms in tune with

the environment. Additional zeitgebers include mealtimes and other markers of daily/nightly routines, such as

clocks and TV. Innate rhythms of metabolic rate and body temperature do not vary with either zeitgebers

or altered daily shifts. There could therefore be conflict between the brain working to one rhythm and the body to

another. You cannot assume that all individuals will experience the same problems. Webb (1975)

o Some people are more alert in the morning and others in the afternoon. One problem with shift work is often mild sleep deprivation. Akerstedt

o Showed that people on shift work slept 1-4 hours less than when they could sleep at ‘normal’ times.

o They had a particular deficit in REM sleep; if REM sleep provides psychological restoration shift work leads to a lack of this.

Burch et al o Fount that night shift workers had disrupted circadian melatonin production and

that this was associated with disrupted sleep, fatigue, increased risk of accidents and even chronic diseases.

Furlan et alo Highlighted that night shift work is associated with an increase of heart disease.

Insomnia

Accounts for 65% of all patients attending sleep clinics. It is categorised byo Sleep onset latency (time taken to fall asleep) of more than 30 minutes.o Sleep efficiency (time in bed actually asleep) of less than 85%o Several night time awakenings

One way to look at insomnia is to gauge its severityo Mild: little effect on work or social functioningo Moderate: negative effect on work and social functioningo Severe: major effect on daily functioningo Acute: an episode of poor sleep lasting only a few dayso Chronic: the problem sleep lasts for months or longer; may continue in childhood

and continue through to adulthood Primary insomnia is the most common form of insomnia and has no clear underlying cause. There is a sleep problem but there is no physiological or psychiatric cause and it is likely that

the sleep problem is the result of maladaptive behaviours or learning. The clinical characteristics are that for at least a month the individual would have suffered

insomnia, but this would not be linked with any other sleep disorder, such as parasomnia or narcolepsy, nor with another psychopathology such as clinical depression, nor with medication or substance abuse.

Sleeplessness that is not attributed to a medical, psychiatric or environmental cause. Secondary insomnia is insomnia that has a specific cause. Examples of such causes include: sleep apnoea, restless leg syndrome (RLS0 circadian

rhythms disorders and various other medical/substance abuse/emotional problems, such as depression.

o Hormonal changes in womeno Decreased melatonino Dementiao PTSDo Environment

Sleep apnoea is characterised by frequent interruptions of breathing when asleep followed by choking and gasping for breath and is usually associated with loud snoring.

RLS is a condition in which the legs or feet twitch and jump, and there might also be feeling of burning, itching or pulling. This is most frequent in the evenings or at night.

Circadian rhythm disorders usually occur when an individual’s innate circadian rhythm is not matched by the environmental sleep=wake cycle/schedule e.g. in night shift workers who often have shorted than optimum hours of sleep.

Problems diagnosing secondary insomnia; it is hard to diagnose if the insomnia is the result of the disorder or the cause.

Lichstein et al

o Does depression cause insomnia or does insomnia cause depression; there is evidence that it can go either way, and that some secondary insomnia with depression as the cause could be primary insomnia in disguise.

Problems researching insomnia sleep state misperception. Many people who claim to have disrupted sleep actually have normal sleep patterns,

suggesting a psychological issue rather than a physiological one. Self-help: strategies people have taken to deal with their insomnia can often be

counterproductive (drugs and alcohol) and actually make sleep harder to achieve, causing a learned sleep disorder that makes treatment much more complicated.

Stepanskio Proved CBT has been used effectively to treat these learned sleep disorders

Insomnia is simply the inability of sleep and is extremely widespread Dement

o Estimates that at least half of all humans acknowledge that they have difficulty sleeping, but only 5-10% of sufferers actually get diagnosed with insomnia.

Psychophysiological insomnia is a form of anxiety induced insomnia and is sometimes known as learned or behavioural insomnia.

The primary components involved are intermittent period of stress, which result in poor sleep.

They also generate maladaptive behaviours, including a vicious cycle of trying harder to sleep and becoming tenser, where bedroom habits and routines condition the patient to frustration and arousal

Morin et alo Examined the role of stressful life events in the causation of primary insomnia.o Examined relationship of stress and coping skills to sleep patterns in good sleepers

and in insomniacs.o Found that both poor sleepers and good sleepers reported equivalent number of

minor stressful life eventso However, insomniacs perceived their lives as more stressful, relied more on

emotion-orientated coping strategies and reported greater pre-sleep arousal.o Concluded that a key factor in insomnia was the way people appraised stressors and

perceived lack of control over stressful events, rather than the number of stressors.o Personality factors and the way people cope with stress play a significant part in

primary insomnia. Idiopathic insomnia: occurs at a very early age, due to an abnormality in the brain

mechanisms that control the sleep-wake cycle. Neuroanatomical, neurophysiologic or neurochemical lesions exists in the sleep system, thus

rendering the sufferer unable to sleep properly. Sleep-state misperception: people sleep adequately but feel they do not; a disparity exists

between the person’s subjective description of a night’s sleep and the objective measurement of sleep obtained

Dement (1999)o Studied a patient who complained of severe insomnia and spent 10 night sin a sleep

lab.o Had to estimate each morning how long he took to fall asleepo Mean of 90 minutes, actual time taken was only on average 15 minutes.o Concluded there were discrepancies that result from an unclear perception of

consciousness and difficulty distinguishing sleep from waking. Factors affecting insomnia include:

Bedtime behaviour: energetic or exciting activities make it harder to sleep. The brain is very active and if it is still alert (daytime mode) the natural changes leading to sleep are unlikely to occur and the parasympathetic automatic nervous system will not calm the brain.

Environmental factors: Powerful stimulus (bright lights, loud noises, temperature) can all contribute to insomnia because they interfere with the brain’s natural calming of neural activity. A change in location can also boost brain activity and lead to insomnia.

Stress: acute stress can lead to insomnia as the sympathetic automatic nervous system is active. With acute stress (where the stress is transitory), once the stressor is over normal sleep should resume. Chronic stress (which results in corticosteroid activity) can produce insomnia as this changes physiological activity.

Vgontzas (2001)o Demonstrated that there is an association between insomnia and an overall increase

in stress hormones such as ACTH and cortisol secretion in a circadian pattern.o They suggest that in insomniacs there is a disorder of hyper arousal in the CNS

caused by chronic activation of the hypothalamic-pituitary-adrenal axis.o This leads to increased risk of chronic anxiety, depression and physiological damageo Real world application: therapy should therefore be based on decreasing

physiological and emotional arousal, not just sleep.o This is assuming that the high stress hormone levels and CNS activity cause the

insomnia, whereas it could be the other way round (insomnia causing stress) Bonnet & Arand (2003)

o Found that levels of anxiety rose in line with poor sleep and increasing fatigue of participants experimentally induced with insomnia.

o Suggests that an anxious personality is more susceptible to insomnia. de Sainte Hilaire (2005)

o Hypothesised that serotonin activity could relate to both temperament and sleep regulation.

o Showed that insomniacs had more anticipatory worry than controls and greater harm avoidance.

o This greater harm avoidance correlated positively with sleep latency.o Correlation is not causation, however indicates that the personality trait of harm

avoidance might be a marker for primary insomnia. Leblance et al (2007)

o Showed strong links between insomnia and high scores on depression, anxiety, neuroticism, extraversion, arousal predisposition, stress perception and emotion-orientated coping scales.

Soehner et al (2007)o Found similar links: higher neuroticism and poorer quality of sleepo However participants in this study were not insomniacs, but normal working adults,

and assessed using self-report measures (questionnaires/social desirability bias)

Narcolepsy

Very rare condition that affects around 1 in 2000 people A neurological condition associated with a fault in the mechanisms in the brain that control

wakefulness and sleep Characterised by

o Excessive daytime sleepiness, with suffers falling rapidly into sleep episodes of 10-20 minutes several times a day, regardless of situation (sleep attacks)

o Cataplexy: sudden loss of muscle tone causing collapse, even when awake. Happens several times a day

o Hypnagogic hallucinations: auditory and visual (hypnopompic and hypnagogic).o Sleep paralysis, occurring on waking for small periods of timeo Polysomnography identifies that suffers move directly into REM with none of the

NREM build up to sleep.o Interruption of night time sleep by frequent waking periods.o Extended periods of trance like behaviours

Explained by abnormalities in the REM control mechanisms. Sleep paralysis occurs during REM and could explain cataplexy and sleep paralysis on waking. Most dreams occur during REM and could explain hallucinations. A malfunction of the sleep-wake regulating system in the brain. Whenever narcoleptics relax, they fall asleep, regardless of the activity. There is also a sudden loss of muscular control, triggered by strong emotions such as

amusement, anger, or excitement (cataplexy). Some psychoanalysts believe that such paralysis is a defence mechanism for people who are

afraid to become too emotional, since strong emotions often precipitate attack. One of the main characteristics of the condition is the intrusion of REM sleep at

inappropriate times. During REM the brain is very active and the muscles paralysed. Studies link a possible cause to the neurotransmitter orexin (also known as hypocretin). In several studies of narcoleptics levels of orexin in the cerebrospinal fluid were very low or

even undetectable There is only a 30% concordance rate for narcolepsy among Mz twins; unlikely to be an

inherited illness. Lin et al (1999)

o Some pedigree dogs are so inbred that they have a greater chance of having damage to a gene on chromosome 12

o This causes a reduction in the neurotransmitter hypocretin which has been correlated with narcolepsy

o Since uncovering the gene in dogs it has been found that humans with narcolepsy have lost 90% of their hypocretin neurons.

o Research showed that injections of hypocretin neurones reversed their narcolepsy, but this cannot be generalised to humans as the human disorder has environmental as well as genetic causes (nature nurture debate goes here.)

Overeem et al (2008)o People with narcolepsy have a reduction in hypocretin producing neurones in the

hypothalamus.o Explanations focus on the HLA (human leukocyte antigen) complex gene on

chromosome 6, which controls the immune system.o Patients with narcolepsy seem to carry a mutation in this gene which causes the

immune system to attack and destroy hypocretin neurons in the brain, causing abnormalities in REM sleep

o Some people with the mutation to the HLA complex gene do not develop narcolepsy; whilst some suffers don’t have the mutation.

Dement (1999)o Found that mice that couldn’t make orexin in their brains developed the symptoms

of narcolepsy, including sleep attacks and cataplexy. Narcolepsy Association

o The brains of narcoleptic patients have very little orexin in them and that the nerves containing orexin have degenerated

Mahowald and Schencko In humans, the absence of orexin is neither necessary nor sufficient to explain all

cases of narcolepsy Nishino et al (2000)

o Were able to confirm that orexin deficiency is definitely implicated in human narcolepsy

Thannickal et al (2000)o Narcoleptics have a reduction of about 85-95% in hypocretin neurons, whereas

melatonin neurones are unaffected, with the hypocretin loss being degenerative and perhaps autoimmune.

Longstreth et al (2007)o Confirmed the selective destruction of orexin producing cells in the lateral

hypothalamus, but only in individuals carrying one or more alleles known as human leukocyte antigens (HLA) [NATURE]

Kim et al (2008)o Showed an increase in GABA levels in the medial prefrontal cortex of narcoleptics

but this could be a physiological defence mechanism activated to reduce the nocturnal sleep disturbances in narcolepsy

Research in South China showed that narcolepsy is more common in those born in the Winter, with possible links to viral interaction as these types of infection as more common at that time

It is hard to deny the value of much animal research but must question its generalizability and the ethical cost-benefit analysis (i.e. deliberately breeding narcoleptic dogs) and questions of specism.

Although more research is needed it does seem likely that narcolepsy is the product of maladaptive HLA genes, environmental factors, degenerative neurological changes and abnormal transmitter levels

Somnambulism

3% of adults suffer from it On numerous occasions, the patient will arise and walk about, usually during the first third

of sleep. The exact cause of sleepwalking is unknown. During sleepwalking, the patient stares blankly, can be awakened with difficulty and

responds poorly to others attempts at communication. Although there may be a brief period of confusion upon first awakening, within a few

minutes the patient’s behaviour and mental activity are normal and unimpaired. After the episode or the next morning, the patient has no memory of sleep walking activity. The symptoms cause clinically important distress or impair work, social or personal function. Not directly caused by a general medical condition or substance use, including medications

or drug abuse. Environmental factors that can induce (but not cause?) sleepwalking include

o Stresso Alcoholo Sleep deprivationo Chaotic sleep scheduleso Hypnosis o Sedatives.

Genetic explanation: sleepwalking in an individual is 10% more likely if a first degree relative has a history of sleepwalking and it also occurs more frequently in identical twins.

Episodes typically occur during sleep stages 3 and 4 in slow wave sleep. Tend to happen in the first half of the night.

It can occur in REM sleep but this is much less likely. It is most common in childhood, peaking just before or at the time of puberty and can

continue into adulthood. Other circumstances that can occur with sleep disorders include depression, decreased

concentration, fatigue, anxiety and irritability. People with chronic sleep problems tend to have other illnesses such as stomach problems,

muscle aches and headaches. Horne (1997)

o Causes of somnambulism seem to be genetic as the disorder runs in families Pilon et al (2008)

o Other triggers include fatigue, previous lack of sleep and stress or anxiety. Hublin et al (1997)

o Used the ‘Finnish twin cohort’ and found that the genetic contribution to somnambulism was:

Guilleminault et al (2003)o Suggest that in child sleepwalkers a causal factor may be other sleep disorders, such

as sleep-disordered breathing or RLS (which is a known to be a genetic disorder and might explain why sleepwalking runs in families.)

Exactly how maladaptive genes produce sleep walking isn’t known

Bassetti (2001)o Studied 74 patients who were diagnosed with adult sleepwalking and found that of

the 16 patients who underwent genetic testing, 50% of them had a specific gene that was only present in 42% of non-sleepwalkers.

Olivero (2008) o Believes that sleep disorders such as sleep walking arise when normal physiological

systems are active at inappropriate times.o Although it is not clear why the brain issues commands to the muscles during certain

phases of sleep, it has been found that these commands are usually suppressed by other neurological mechanisms.

o At times this suppression can be incomplete-because of genetic or environmental factors or physical immaturity and actions that normally occurring during wakefulness emerge in sleep.

o He proposed a possible physiological mechanism underlying sleep walking, finding that during normal sleep the chemical messenger GABA (gamma-amino butyric acid) acts as an inhibitor that prevents the activity of the brains motor system.

o In children, the neurones involved with the suppression system are still developing and hence motor activity is not fully under control.

o As a result, many children have insufficient amounts of GABE, leaving their motor neurons capable of commanding the body to move even during sleep.

o This may explain why sleepwalking begins and is more likely in childhood

Men WomenChildhood 66% 57%Adulthood 80% 36%

o The evidence is based on an anecdotal subjective hypothesis and is not backed by objective empirical research, so is therefore is not scientific.

Zadra et al (2008)o Evaluated 40 suspected sleepwalkers and found a clear link between sleep

deprivations and sleep walking. o Participants were observed in a sleep lab and had their baseline sleep patterns

monitored during an initial assessment.o During a subsequent visit, patients were kept awake for the entire evening and

remained under constant supervision.o The next morning participants were allowed ‘recovery’ sleep after being awake 25

hours. o During the first night of baseline sleep, only 50% of patients exhibited sleepwalking

behaviourso After sleep deprivation, this increased to 90%.

Lifespan Changes in Sleep

Total Sleep REMInfants 15 8Age 1-3 12 - 14 6Age 5-6 11-13 2School age 10-11 2Adolescents 9 2Adults 7-8 1 1/2

Babies spend more time in Rem than adults- has to process more of its environment/ more information.

Armstrong et al (1994) studied the sleeping habits of normal children up to 38 months of age in Australia.

Over 3000 parents were surveyed over a 1 week period, with 7 findings.o There is a wide variation of normal early childhood sleep behaviour.o Circadian rhythms are not well established until 4 months of age.o 11% of babies under 3 months of age do not have daytime sleep.o Daytime sleep becomes less regular as age increases, with a noted reduction at

around 3 months.o Frequent night time waking that disturbs parents is common from 4-12 months.o Night time setline requires more input from parents from 18 months oldo Sleeping through the night varies considerably, not only from child to child but for

any one child, and doesn’t become regular until after 24 months. Circadian rhythms are controlled by the brain and this is immature at birth, so the

development of the rhythm could well be in line with early brain development and growth. Harrison (2004)

o Found that exposure to more light in the afternoons in 6-12 week old infants promoted the development of their circadian sleep rhythm.

It is theorised that an increasing awareness of the world may also bring a need for reassurance that other people are still around and comfort is available.

Scher (1991)o Studied night waking in 100 infants

o Showed that at 3 months 46% were waking, at 6 months 39%, at 9 months 58% and at 12 months 55%.

o Not only is night waking usual, the increase at 0 months could relate to the socio emotional advances being made at the time, such as the understanding and fear of strangers.

o Ethnocentric: studies of non-Western cultures where breast feeding into the second month is common do not show the development of longer bouts of sleep at night.

Zimbardo et al o Babies spend far more time than adults in REM sleep- up to 50%.

A meta-analysis of 65 studies, representing over 3500 healthy participants showed that sleep declines with age.

o In adults, the total time asleep and the percentage of slow wave REM sleep all declined significantly with age, whereas sleep latency and the percentage of stage 1 and 2 sleep significantly increased with age.

o There were very few studies on school age children: lack of data = little can be concluded.

o Methodological limitations as much of the research uses self-reports which may be biased.

Foley et al (2007)o Studied napping in elderly people and correlated positively excessive daytime

sleepiness with depression.o This links made between reduced sleep and depression are correlation and cause

and effect cannot be inferred.o There is also the issue of self-report measures.o It is not possible to know how truthful respondents were, nor how influenced they

are by social desirability or demand characteristics.o The lack of sleep could cause depression or depression could cause lack of sleep, or

a third factor could be causing them both. Ancoli-Israrel (2008)

o Survey over 2000 women and found that normal sleep with no perceived sleep problems was linked to healthy aging- older women who slept well were significantly less likely to suffer physical problems such as cardiovascular disease and diabetes.

o Single sex study/ gynocentrico Not sleeping = worry = stress= cardio vascular problems.

Stages of Sleep: Summary

Stage 1 NREM (hypnogogic state/myoclonic jerk) 15 minutes Brain waves slow from alpha to theta Parasympathetic nervous system active Heart rate slows and muscles relax Easy to be woken up

Stage 2 NREM 20 minutes Theta waves get slow and longer Sleep spindles: electrical activity also known as K-Complexes (tiny bursts of activity so

external stimuli doesn’t wake you up)

Stage 3 NREM

15 minutes Further falls in heart rate and rate of brain waves. Theta waves slow to delta waves.

Stage 4 NREM 30-40 minutes Deepest sleep Growth hormone secreted Metabolic rate is at its lowest and it is very difficult to wake up Sleep walking is likely to occur.

Stage 5 REM 10-15 minutes EEG trace spends up through stages 3 and 2 as brain becomes more active. Brainwaves desynchronise and become complex. Glucose and oxygen demands increase Cerebrally active whilst physically inactive.

Low light levels↓

Melatonin synthesis in the pineal gland↓

Influences serotonin production↓

Collects in raphe nuclei↓

Stimulates slowdown of RAS↓

Brain activity falls↓

NREM sleep

Nature of Sleep

Sleep is an ultradian biorhythm with five stages which together last about 90 minutes. A cycle of all five is repeated 5- 6 times a night. Each stage is qualitatively different and is defined by different patterns of brain activity. Sleep is an altered state of consciousness but not a state of unconsciousness- you can always

be woken up Dement and Kleitman (1957)

o Showed two types of sleep with associated brainwave patterns, but also that the two types alienate in an ultradian rhythm.

There are two types of sleep: non rapid eye movement (NREM) and rapid eye movement (REM), and each stage has its own EEG trace.

The development of the electroencephalography (EEG) was crucial for research into sleep. Without the use of EEG’s researchers had to rely on self-report, which doesn’t provide

empirical data or give us information about the physiology of sleep.

This is the reason for the stages originally being called NREM and REM, as this was all that could be observed without an EEG.

From looking at EEG’s, researchers have identified 4 stages of NREM sleep and one stage of REM sleep.

Empirical measurements are achieved using electrodes connected from an individual to a computer that receives and processes the data.

EEGs (electro-encephalograms) record brain activity from a set of electrodes temporarily attached to the head

EOG’s (electro-oculograms) record muscle movement around the eyes EMG’s (electro-myograms) electrodes are attached to the skin covering muscles. The data from these gives us a picture of overall brain activity from brainwaves to eye

movements. Empson *** *LEARN THIS STUDY* ***

o Found that after the first night, when the arrangement of sleeping is strange, participants do sleep normally

Exogenous control of sleep Morning light is received by light sensitive cells in the eyes and stimulates nerve impulses

that travel in the two optic nerves. Some impulses travel along optic nerves to the SCN, which communicates with the pineal

gland. Increased levels of light cause the pineal gland to cease producing melatonin. Low light levels detected in the SCN stimulate the pineal gland to resume serotonin

production. As the melatonin accumulates, it influences the production of serotonin (a neurotransmitter

involved in mood and sleep) Serotonin accumulates stimulating the shutting down of the reticular activating system

which is closely linked with brain activity. Serotonin therefore starts the ‘sleep clock’

Endogenous control Jouret suggested that a more important neurotransmitter is noradrenaline. If the area involved (the locus coeruleus) was damaged, noradrenaline levels fell and REM

sleep was impaired. He proposed that each area and its neurotransmitters control a different type of sleep. The raphe nuclei and serotonin = NREM sleep Locus coeruleus and noradrenaline =REM sleep.

Different types of sleep Each stage of sleep has its own corresponding EEG trace so we know there are four stages in

NREM sleep. Stage 1 sleep occurs when we are falling asleep and takes up to 15 minutes. Recordings

show brain waves slowing down from the slow alpha waves of relaxation. There patterns become synchronised and a regular pattern emerges. The parasympathetic nervous system is active and so the heart rate slows and muscles relax. It is easy to be woken up, for example, by hearing someone shout or the phone ringing. This first stage is also known as the hypnogogic state. Stage 2 lasts approx. 20 minutes and is when the breain theta waves get slower and larger

with intermittent bursts of activity known as slep spindles or K complexes (tiny bursts of electrical activity associated with external stimuli so it doesn’t wake you.

Heart rate, blood pressure and body temperature continue to fall. Stage 3 has further falls in heart rate and in the rate of breathing, and brain waves slow into

delta waves. It is now quite difficult to be woken.

Lasts approx. 15 minutes. Stage 4 is the deepest sleep and is when growth hormones are secreted. Metabolic rate is at its lowest and it is difficult to be woken asides from significant noises. This stage lasts typically for 30-40 minutes. Although it is the deepest stage of sleep, it is the stage in which sleepwalking is more likely

to occur. Jacobson and Kale

o Sleepwalking is not necessarily connected with dreaming. After approximately ½ in stage 4 sleep, the EEG trace speeds up the ‘sleep staircase’ through

stages 3 and 2, showing the brain is suddenly more active, moving into REM sleep. The brain waves desynchronise and become complex as well as faster, and the brain’s

oxygen and glucose demands increase. Although we are now cerebrally very active we are physically inactive; our bodies from the

neck down are almost paralysed. The RAS in the midbrain sets up a block which isolates the brain from the rest of the body. Only the heart and lungs seem to match the speeding up of the brain. This REM sleep lasts for 10-15 minutes and completes the first sleep cycle of the night. We then go back down through stages 2-4 again, and this cycle repeats about every 90

minutes through the night, although the time spent in stages 3 & 4 get progressively less until only stage 1 and 2 f NREM plus REM sleep are returned to by the end of the night.

The 90 minute cycle is the ultradian rhythm of sleep. Dement and Kleitman

o Observed that REM sleep is associated with a highly active brain while at the same time the body’s muscles are effectively paralysed so there is virtually no movement.

o This is known as paradoxical sleep; the brain is active but the body is not.Restoration Theory

Sleep allows you to recover physiologically and psychologically after a long day. NREM is for restoring bodily functions after stress of a day. Helps reverse and/or restore biochemical +/or physiological processes that are progressively

degraded during the day. Being awake disrupts the homeostasis of the body in some way and sleep is required to

restore it. Many restorative processes-such as digestion removal of waste product and protein

synthesis do occur during sleep. Many of these also occur during waking and some occur more frequently during the day. REM is to restore brain processes (neurotransmitters) Babies spend 18hrs a day asleep and half of it is REM sleep (double that of adults). Bloch (1979)

o Rats in complex mazeso Learning and complex tasks ‘tire’ your brain by using neurochemicals. o Rats who had performed complex activates had much more REM sleepo It is surprising that the view that sleep has a vital restorative function is only weakly

supported by research. According to the restorative perspective, intense energy expenditure during the day should

increase the duration of sleep in order to restore the resources. Breedlove

o For most people, intense exercise may cause them to fall asleep more quickly but it does not cause them to sleep for longer.

Giant sloths sleep for around 20hours though its energy expenditure is small.

While REM sleep is obviously important (as shown in sleep deprivation studies) if restoration was the sole purpose of sleep we would expect consistent effects from strenuous activities (mental & physical) and sleep deprivation.

Horne (1988)o Reviewed 50 studies in which humans had been deprived of sleep.o He found that very few of these studies reported that sleep deprivation had

interfered with the participant’s ability to perform physical exercise.o Neither was there any evidence of a physiological stress response to sleep

deprivation. Sharpiro (1981)

o Found that marathon runners didn’t need more NREM sleep to recover from s tenuous physical activity

Cirelli and Tononi (2008)o Hypothesis that the new synapses generated by the day’s learning. Demonstrated in

rats by measuring synaptic neuroreceptors and found a 50% reduction after sleep; sleep allows for the reorganisation of new learning to improve efficiency.

Oswald suggested that both REM and NREM sleep serve the purpose of restoring and replenishing our bodies and brain-we sleep to restore ourselves physiologically and psychologically

NREM sleep is needed more for restoring bodily processes that have deteriorated or been worn down by the day and REM sleep helps the brain renew and replenish neurochemicals used up in the day that need to be regenerated by protein synthesis.

Babies and foetuses sleep both REM and NREM rhythms for a far greater proportion of their day than older children or adults and it is in these very early stages that both bodies and neural connection are growing fastest.

Not only do young babies spend on average about 18 hours a day sleeping, ½ of this time is spent in REM sleep as opposed to 8 hours asleep and ¼ REM in most adults.

This ties in with the larger amount of activity in the developing brain, with increased amounts of protein synthesis needed for cells and synaptic growth.

Siegel (2005)o Points out that if body or brain weight is controlled, REM sleep is most strongly

correlated with how immature the baby is at birth.o Both physical repair and synthesis of brain proteins are dependent on growth

hormones which are secreted after the first burst of delta activity in slow wave sleep.

Further support for the restoration theory comes from knowledge of patients who have had physiological assaults on the brain from drug overdoses or from ECT then spend an increase time in REM sleep, to synthesise the brain proteins that have been lost or damaged.

If restoration was the only function of sleep then we would expect to find consistent effects from sleep deprivation.

However as we saw this is not the case. People don’t need to make up the sleep they have lost, although they appear to need the

REM sleep most particularly Furthermore you would expect to find that the more active you were during the day the

more you would sleep at night. Research suggests that there is no relationship. Horne + Minard (1985)

o Engaged participants in numerous physical activities but found no increase in sleep. Carlson (1986)

o Showed that slow-wave sleep is more important for recovery after vigorous activity. Turner et al (2007)

o Found that sleep deprivation reduced working memory efficiency; after 4 days with only 26 minutes sleep per night participants working memory efficiency/span decreased by 38% compared with the control group.

Born et al (2006)o Found a link between late REM sleep and better procedural memory and better

procedural memory and between early slow wave sleep and improved procedural memory.

Horne (1988)o Concluded the sleep doesn’t provide any repair process in humans, except for the

brain.o Referred to core sleep, which he believed is essential for restoration whereas other

types of sleep are optional sleep, mainly for the purpose of energy conservation. Morgane (1974)

o Believe that REM serves the function of allowing the brain to replenish neurotransmitters that have been used during the day.

Hartmann (1973)o Suggested that REM sleep is a time for synthesising noradrenaline and dopamine to

compensate for the amount used during the day.