Biopsych - Sleep (Y2)

The Sleep Cycle

Chronotypes - preferences that manifest in personal sleep-wake rhythms, measured using the Munich Chronotype questionnaire (MCTQ)

  • Types -
    -> Lion - early bird; conscientious and agreeable, productive in mornings
    -> Bear - able to follow normal schedule such as office hours and follow the sun so can socialise in the evening
    -> Wolf - night owl - neuroticism and openess
    -> Dolphin - insomniacs

Measuring sleep -

  • Polysomnography - physiological information e.g. brain activity and eye movement inferences - electrodes allows researchers to measure electrophysiological activity in the brain, muscles in the face and around the eyes
  • EEG
  • Actigraphy - watch-like device measures movements - inferences about sleep are made with this information
  • Sleep diaries - completed in morning, self rated
  • Questionnaires - self, parent or observer rater
  • Smartphone applications - use high quality sensors of movements and sound to infer sleep

Questionnaires -

  • Pittsburgh Sleep Quality Index (PSQI) - 9 item self report questionnaire of sleep quality within the past month
  • Insomnia sleep index - 7 item self report questionnaire to measure insomnia

The brain during wakefulness - delta (deep), alpha (transitional), and beta (waking) waves

Sleep stages -
Sleep is not a uniform state; it is composed of different stages differentiated by patterns of brain wave activity that occur during each stage

  • These changes can be visualised using EEG and are distinguished from one another by the frequency and amplitude of brain waves
  • Divided in two general phases - REM and non-REM
  1. Rapid eye movement sleep is characterized by darting movement of the eyes under closed eyelids; brain waves in this stage appear similar to wakefulness brain waves

Waking - Alpha (8-12 Hz) - relaxed, and Beta (13-30 Hz)

  1. Stage 1 - NREM sleep, consists of theta activity (3.5-7.5 Hz)
    -> Transitional phase that occurs between wakefulness and sleep; the period during which a person drifts to sleep
  2. Stage 2 - NREM sleep, contains sleep spindles and K complexes
    -> Body goes into deep relaxation - characterised by the appearance of sleep spindles
  3. Stage 3 - slow wave sleep, consists of delta activity (< 3.5 Hz)
    -> Deep sleep characterised by low frequency, high amplitude delta waves
  4. Stage 4 - similar to stage 3
  5. REM sleep - consists of theta and beta activity - brain areas involved in during dreaming is the same one involved in waking activity; therefore, brain waves look similar to wakefulness

Brain wave characteristics -

  • Alpha wave - relativaly high freuqency, relatively low amplitude brain wave that becomes synchronised; characteristic of stage 1 sleep and rest - alpha amplitude increases when we close our eyes
  • Beta wave - high frequency, low amplitude, can be erratic, waking wave
  • Theta - transitional between waking and sleep
  • K complex - very high amplitude pattern of brain activity associated with stage 2 sleep
  • Sleep spindle - rapid burst of high frequency brain waves during stage 2 sleep that may be important for learning and memory
  • Delta wave - low frequency, high amplitude brain wave characteristic of slow wave sleep

NREM - period outside REM
REM - disorganised dreams = underused planning area of frontal lobe

The sleep cycle and characteristics

  • The sleep-wake cycle changes every 90 minutes, cycling through the stages, and the more sleep you get the longer your REM sleep gets - 1 hour in, you are at stage 3 and 4; then after REM, you progress back up to stage 2 and then back down in the cycle to peak at REM
  • Deep sleep gets shorter as the night progresses
  • Deep sleep prioritized earlier, REM prioritized later
  • Waves slow down then spike in REM, then this repeats - lower frequency waves as cycle progresses, then beta activity spikes to bring closer to waking and stage 1 sleep
  • REM sleep ->
    -> Fast, desynchronised EEG pattern
    -> Heart rate increases
    -> Body muscles are paralysed except for finger and toe twitches
    -> Rapid eye movements occur
    -> Subjects woken during REM reported dreams more often than those woken during slow wave sleep (Aserinsky and Kleitman, 1955)
    -> Penile erection or vaginal secretion
    -> Dreams

SWS sleep -

  • EEG synchrony
  • Moderate muscle tone
  • Slow or absent eye movement
  • No genital activity

Biological rhythms

Basic-rest activity cycle -

  • Derment and Kleitman - violinist study about cognitive alertness - post lunch dips
  • Mammals sleep for varying amounts of the day - humans; 8 hours, horses; 3 hours, cats; 14 hours and giant sloth; 20 hours a day
  • Circadian rhythms - repeat themselves every 24 hours, various rhythms for temperature, hormones, sleep-wake cycle - exogenous zeitgebers (Siffre) and endogenous pacemakers
  • Infradian rhythms - these occur less than once a day e.g. hibernation, menstrual cycle, SAD
  • Ultradian rhythms - repeat more than once a day e.g. dream cycles, cycles of cognitive arousal during day

Biological clocks

Suprachiasmic nucleus (SCN) of hypothalamus -

  • Lesions of SCN disrupt daily activity cycles in rats (Ibuka and Kawamura, 1975) - Decoursey et al (chipmunks)
  • Fundamental functions are protected in deeper brain areas
  • Activity of SCN neurons correlates with day-night cycle (Foster and Kreitzman, 2013)
  • Neural basis of sleep - hypothalamus and brainstem interaction

Melanopsin-containing ganglion (neurons that receive and transmit light signals) -

  • Cortisol released in morning, melatonin released in light based on light signals
  • Retinohypothalamic pathway -
    -> Retinal ganglion cells containing melanopsin - night and daylight impact secretion which informs SCN
    -> Circuit for biological rhythm
  • Special photochemical - melanopsin
    -> Transmit light information from eye to rest of brain and control pupil dilation

How does the SCN work -

  • CLOCK genes encode proteins to regulate circadian rhythm (CLOCK = Circadian Locomotor Output Cycles Kaput)
  • The neuron activity that makes the clock - this is the ticking cycle
    -> The protein enters the nucleus, suppressing the gene responsible for production - no more messenger RNA is made when full
    -> Level of the protein falls, so the gene becomes active again
    -> The gene is active - messenger RNA leave the nucleus and causes production of the protein
    -> 7 genes involved in the ticking
    -> The time taken for this is the ticking

Two process model of sleep -

  • Sleep-dependent process (Process S) - shows experimental decline during sleep and increase during waking i.e. it is a function prior to waking time and when you sleep
  • Sleep independent circadian process (Process C) - controlled by circadian oscillator - how long you sleep
  • Model proposes that sleep duration and sleep propensity are driven by these two processes

Why do we sleep?

Effects of sleep deprivation -

  • Fatigue, irratability, poor performance on tasks requiring concentration, memory problems, hallucination, personality changes and rebound sleep (do not regain all sleep back)
  • Can occur from stress - lab studies confounded as sleep deprivation can be from a stressful situation of the study not just the task itself

Rechtschaffen et al, 1983 - sleep deprivation in animals -

  • Two mice in chambers on rotating platforms with water underneath
  • When the experimental mouse falls asleep, they move the carousel so the mouse falls in the water and wakes up
  • Control mouse can sleep when carousel is still
  • Everything else is controlled
  • The test rat deteriorates after 7-10 days, loses weight despite eating more, rats die in 2-3 weeks, metabolic and homeostasis failures; post mortem reveals large adrenal glands and high cortisol from stress

Record from sleep deprivation - Randy Gardener (264 hours) and Tony Wright (266 hours)

Insistent drive and needed by all animals

  1. For restoration -
  • Of the body and brain, no antidote has been developed for sleep
  • Unlike other activities, that humans can actively suppress, avoiding sleep just leads to greater sleepiness and increasingly frequent sleep onsets
  • Body restitution is not dependent on sleep - Angus et al, 1985; exercise and no exercise conditions on people who did not sleep for 60 hours, no difference in results
  • Brain restitution through sleep - high brain work increases slow wave sleep
    -> Sleep in cognitive decline
    -> Neurodevelopmental damage from sleep deprivation
    -> Brain areas that are most active the previous day show the most delta activity in sleep, suggesting they are resting

Cerebral restitution in sleep -

  • No antidote to sleep loss
  • Little inter-individual variation in SWS length
  • Limited higher level cognitive suppression
  • Amount of SWS dependent on length of prior wakefulness - recovery effects of nap determined by amount of SWS (Lumley et al, 1985)
  • SWS = brain recovery
  • REM = learning and memory consolidation - Studies have varied between conclusions of SWS and REM both improving explicit memory but some studies have suggested that memory and sleep are not linked
  1. To increases survival - is sleep an adaptation -
  • Keeps animals unobtrustive and safe
  • Sleep has evolved to enhance the survival of the species
  • Length of sleep depends on evolutionary pressues
  1. No single explanation - sleep may serve different functions in different species (Horne, 1988)
  • Horne suggests that in humans, both types of sleep are for brain repair, body repair can happen during relaxed wakefulness (day dreaming)

Horne's sleep theory -

  • Core sleep -
    -> Occurs in first three cycles
    -> Is vital
    -> Consists mainly of stages 3 and 4 of sleep
    -> Function - cerebral restitution
  • Optional sleep -
    -> Occurs in second half of sleep
    -> Not vital
    -> Not made up in rebound sleep
    -> Source of individual variability
    -> Due to behavioural drive in sleep
  1. Partly different explanations across lifespan -
  • REM in infants - more premature the infant, the more REM sleep it displays (consistent across species)
  • Amount of REM sleep slowly declines through infancy and then stabilises at 25% by 2 years old - synaptic development?
  • REM deprivation results in developmental abnormalities e.g. in neonate rats (Mirimiran, 1986)
  • Autostimulation theory - REM plays a role in brain development by activating synapses (Roffwarg et al, 1996)

Sleep changes in childhood and adolescence (Gregory and Sadeh, 2015)

  • Sleep onset time becomes later and sleep duration reduces from childhood into adolescence
  • Delay in sleep onset time associated with puberty
  • Examples of other changes - SW activity moves from posterior to anterior brain regions with maturation and coherence of the EEG activity increasing with development
  • Changes in localisation, distribution and coherence of sleep from childhood into adolescence, thought to reflect sleep's role in brain maturation and information processing

Need less sleep than adults, and less in old age - REM and NREM decreases - brain development linked to sleep

How does the brain sleep?

The Flip-Flop mechanisms -

  • Awake - arousal system inhibits sleep promoting region
  • Asleep - sleep promoting region inhibits arousal system

The brain switches the direction of the inhibiting pathways action - flip flop circuit is a circuit in which one side is active and the other isn't - can only assume one of two states at one time

Neural basis of sleep -

  • Sleep promoting areas - ventrolateral preoptic nucleus (VLPO) in the anterior hypothalamus and adjacent basal forebrain
  • Wakefulness promoting areas - posterior hypothalamus and adjacent midbrain

Chemical basis of sleep - arousal controlled by circuits of neurons that secrete the following neurotransmitters

  • Involve GABAergic neurons (inhibitory neurons)
  1. Acetylcholine - pons and basal forebrain - levels of ACl in striatum, hippocampus and frontal cortex are found to relate to animal's level of activity
  • PONS, basal forebrain and medial septum
  • High in wakefulness
  • SWS levels low
  • REM levels high
  1. Norepinephrine - locus coeruleus, high in wakefulness, low in SWS and low in REM
  1. Serotonin - fires most in wakefulness, and steadily decreases through sleep until REM sleep, where it spikes again
  • Raphe nuclei
  • High in wakefulness
  • Decreasing in SWS
  • Higher in REM
  1. Histamine - tuberomammillary nucleus, high in wakefulness, low in SWS and REM
  1. Hypocretin - attacked in narcolepsy
  1. Orexin - lateral hypothalamus, high in waking and low in REM and SWS
  1. Adenosine - the longer you are awake, the more adenosine you secrete
  • Accumulates during wakefulness and is reduced during slow-wave sleep - it inhibits neural activity as the day progresses, as buildup caused drowsiness
  • Caffeine blocks the adenosine receptors preventing the inhibitory effect on neural activity and reducing the effects of sleep deprivation

How much sleep do we need?

Biological basis of slow wave sleep - occurs when neurons in the ventrolateral preoptic (VLPO) - area becomes active

  • Destruction of the preoptic area -> total insomnia (Nautu, 1946)
  • Electrical stimulation of VLPO area -> drowsiness in cats (Sterman and Clemente, 1962)
  • VLPO contains inhibitory GABA-secreting neurons
  • Controlled by neurons in the reticular formation, an area of pons (brainstem) that secrete acetylcholine
  • The reticular formation is a complex network of brainstem nuclei and neurons
  • Projections from this area go to medial pontine reticular formation, forebrain, hypothalamus, cingulate cortex, brain stem regions that control eye movement, hippocampus, basal ganglia, thalamus and preoptic area
  • Lesions to this area of their reticular formation -> reduced REM (webster and Jones, 1988)
  • PGO - pons, geniculate and occipital - waves are first manifestation of REM sleep

REM and dreams -

  • Dreams have narratives and these often display a lack of planning, unpredictability and disorganisation if prefrontal cortex is underdeveloped
  • Cerebral blood flow is high in visual association cortex and low in primary visual cortex and prefrontal cortex
    -> Prefrontal cortex - low activity in this region during REM, reflects lack of organisation and planning that occurs in dreams
    -> Extrastriate cortex - high activity in this region during REM, reflects visual hallucinations during dreaming
    -> Striate cortex - low activity due to lack of visual input

Dreaming occurs in both NREM and REM states and the qualities of both dream states can be equated - hallucinatory and have a narrative

  • Antidepressants can diminish REM sleep without affecting dreaming
  • Some lesions can also impact dreaming without reducing REM

Average length - 7 and a quarter hours

  • Short sleepers get less than 6 hours - Horne (1988) suggested that normal sleepers can adapt to less sleep on a long term basis (Mullaney et al, 1977) and many people are naturally short sleepers (Jones and Oswald, 1968)
  • Short sleep is more efficient (induces wakefulness, stage 1 and shorter sleep onset latency than long sleep)
  • Daytime sleepiness can be counteracted by taking short (15 minute naps) e.g. Gillberg et al, 1994
  • When sleep is lost, not all made up for
  • After 36 hours of sleep deprivation, short sleepers and normal sleepers increased their sleep length by 25% and 36% respectively
  • Types of sleep recovered - 40% increase in SWS, varied increase in REM sleep (less for long sleepers); stage 2 sleep is not recovered, dispensable (Benoit et al, 1980)

Long sleepers - more than 9 hours -

  • Horne's theory is slightly outdated compared to recent studies
  • Sleep deprivation affects cognitive function and may influence aging / cognitive decline
  • Lowe et al, 2017 - meta analysis; based on 61 studies, showed that sleep deprivation affects wide range of areas of neurocognition
  • Scullin and Bliwise (2015) - review paper; sleep patterns in mid life may affect cognitive decline and aging, but evidence is mixed

Sleep disorders

Six main categories of sleep disorder - Gregory and Sadeh (2016)

  • Insomnia - persistent sleep problems - no single definition, hard to measure, occasional and regular insomnia, depression
  • Sleep related breathing disorders - Apnea
    -> Condition in which individuals cannot get air into their lungs when they sleep
    -> This causes them to wake up everytime they cannot breathe, resulting in fatigue issues of accidents, attention difficulty, irritability and other adverse effects such as stroke risk, cardiovascular risk increase and obesity as well as diabetes
  • Central disorders of hypersomnolence - excessive sleepiness
    -> Narcolepsy - a neurological disorder characterised by sleep at inappropriate times - flip flop mechanism unstable, GABAergic neurons do not function well
    -> Primary symptoms of sleep attacks and secondary symptoms of cataplexy and sleep paralysis
    -> Inherited disorder, caused by immune system attacking and destroying hypocretin-secreting neurons
    -> Treated with Ritalin and Modafinil
    -> Gene mutation discovered that produces receptor for peptide neurotransmitter called hypocretin is associated with canine narcolepsy (Lin et al, 1999)
  • Circadian rhythm sleep-wake disorders - misalignment of sleep-wake habits, autism
  • Parasomnias e.g. sleep terrors
  • Sleep related movement disorders - restless leg syndrome

Problems associated with SWS - bed wetting, night terrors (most frequent in children and in stage 3) and sleep walking

Sleep and childhood psychiatric disorders - in the DSM-5 (APA, 2013) sleep plays a major role

  • Category of sleep-wake disorders
  • A major symptom within diagnoses of many other disorders
  • Sleep problems are relevant in many disorders listed in the DSM-5

Why are sleep problems present in psychiatric disorders / neurodevelopmental conditions

  • No single explanation - depends on disorder - depression; twin studies suggest these covary in adolescence due to genetic propensity (early childhood this overlap could be environmental)
  • Trauma / abuse - often covary but mechanistic explanation needed
  • Autism - one hypothesis is that autistic individuals have less endogenous melatonin secretion (Tordjman et al, 2005)

Treatment -

  • A wide variety of effective treatments for sleep disorders
  • Prevention of sleep problems in babies by offering advice booklets to parents
  • Sleep hygiene for insomnia
  • Behavioural interventions e.g. scheduled walking to avoid sleep
  • Cognitive interventions e.g. image rehearsal therapy for nightmares
  • Pharmacotherapy e.g. circadian rhythm sleep-wake disorders treated with melatonin
  • Surgery e.g. removal of adenoids and tonsils for people with obstructive sleep apnoea

Genome-wide association study of mornings and sleep length - genetic variants identified which are associated with early bird chronotype and sleep length

Hypnic jerk - The feeling of falling is known as the hypnic jerk

  • Occurs when the muscles, usually in the legs, involuntarily contract quickly like a twitch or spasm
  • Two functions -
    -> Allows a final check on our environment one last time to ensure it is safe to sleep using a startle like response
    -> Check the stability of our body position
  • Also suggested that the hypnic jerk is a symptom of our active physiological system finally giving in to our sleep drive, moving from active and volitional motor control to a state of relaxation and eventually bodily paralysis
    -> Could be a sign of the eventual switch between the brain’s reticular activating system and the ventrolateral preoptic nucleus and utilises inhibitory neurotransmitters to reduce wakefulness and promote sleep
  • Can result in sleep onset insomnia or fright about falling asleep
  • Stimulants can increase likelihood of having one, as does fatigue, sleep deprivation or erratic sleep schedules
  • Deficiencies in magnesium, calcium and iron can also increase the chances of experiencing a spontaneous hypnic jerk

Sleep paralysis - Cannot move or speak as you are waking up or falling asleep

  • Caused by insomnia, disrupted sleeping patterns, narcolepsy, PTSD, generalised anxiety disorder, panic disorder and a family history of sleep paralysis

What's the limit to how long a human can stay awake?

  • One man, Tripp, was tasked with staying awake in the 1950s and after 201 hours awake, during which he experienced hallucinations after 5 days on a similar REM cycle pattern
    -> When he finally slept, he did so for 13 hours and had one of the longest REM episodes ever recorded
    -> It was likely the Ritalin (stimulant) he took caused the hallucinations however, as others at a similar time reported sleeping longer with no ill effects
  • However, it is not fully determined how long one can go without sleep - disregarding fatal insomnia, non fatal insomnia can lead to people going decades without sleep

Sleep behaviour disorder - Muscle paralysis in REM stage is lost, and so dreams are not prevented from being acted out as they should be

  • Risk factors - Parkinson's, brain injury, Lewy body dementia, Psychiatric medicines
  • Symptoms - sleepwalking, screaming, hitting, kicking and punching

https://acamh.onlinelibrary.wiley.com/doi/full/10.1111/jcpp.12469 - more info on Gregory and Sadeh (2015)


https://docs.google.com/document/d/1pRJUdtV6vDc2bsj89_4ygApefA2TIa9DFO7eiQf9U0Y/edit - Reading also

Dreaming - REM is emotion charged, leading to dreams produced from real life stress
5 common beliefs about dreaming -

  1. External stimuli and dreams - Some stimuli more likely to be incorporated into dreams than others, such as water droplets (Dement and Wolper, 1958) and most incorporated stimuli is pressure on the legs
  2. Dream duration - similar to real time (Derment and Kleitman, 1957) - Current research suggests they run slower than real time - physical movement in a dream can take up to 40% longer than actual movement (Eriarcher et al, 2014)
  3. People who do not dream - All people dream but not all people remember them unless woken during the REM cycle (Goodenough et al, 1959) and some more recent research has mixed findings, but most are consistent with the above idea
  4. Sexual content in dreams - Erection occurs despite the content of the dream in REM
  5. Sleeptalking (soniloquy) and sleepwalking (somnambulism) - Sleeptalking is not essentially associated with REM, and often occurs in the transitionary stages and sleepwalking usually happens in SWS sleep, never during REM, when muscles are mostly relaxed

Lucid dreaming - Ability to be consciously aware that one is dreaming and be able to control the content of the dream on some occasions

  • Lucid dreaming has been proven by study; select few have them every night, but most people have them at least once in their lives
  • Certain cognitive techniques, transcranial electrical stimulation and acetylcholine administration can increase chances of lucid dreaming
  • Could negatively impact sleep as the brain is not truly resting
  • Lucid dreaming is helpful for researchers as the sensations in dreaming can be described to a higher quality level
    -> Many do not report any gustatory, olfactory and somatosensory stimuli often in their dreaming
    -> Also reported an inability to see fine visual details in dreams (Kahn and Laberge, 2011)
  • Only two studies have examined the brain changes in lucid dreaming - little consistency in results however

Why do we dream what we do?

  • Freud - suppressed wishes; manifest and latent content; very little evidence for this
  • Reliance on self report for this topic makes the task difficult, but it is the best option
  • Two key findings - dream content is influenced by activities prior to wakefulness and the amount of anxiety experienced prior to dreaming affects emotions in dreams

Why do we dream?

  • Hobson's Activation-Synthesis Hypothesis - Information supplied to the cortex during sleep is largely random and the resulting dream is the brain’s attempt to make sense of these signals
    -> Similar to finding shapes in clouds - brain is trying to make sense of random patterns
  • Revonsou's Evolutionary Theory - Dreams serve an important biological function - has implications for Darwinian fitness of an organism and we dream to simulate threatening events such as physical attacks, social relationship threats or threats to livelihood and this simulation allows us to better predict and respond to these threats when awake (Revensou 2000 and Gauchat et al, 2015)
  • Hobson's Protoconsciousness Hypothesis - criticism of previous hypothesis - Dreaming has an evolutionary advantage - dreams simulate everything, not just threat
    -> Important to development by providing sensory simulation for underdeveloped sensory systems, especially the visual system
    -> Important for developing how to anticipate and predict events whilst awake throughout the lifespan
  • Dreaming is a training mechanism
  • Protoconsciousness is a virtual prototype of consious experience

Brain areas involved -

  • Bilateral lesions to the temporo-parietao junction and to the premedial prefrontal cortex impact dreaming
  • Additionally, lesions to the medial occipital lobe lead to a loss of visual imagery in dreams
  • These areas have increased activity during REM sleep

Studies - Kleitman, 1963 - sleep deprived students - Students experienced similar effects from sleep deprivation

  • After 1 night, they struggled at around 3:00am, and the next day could remain alert as long as not doing tasks
  • After 2 nights, this worsened but they could not do anything as their sleepiness was so severe
  • After nights 3 and 4, this worsened, but they could perform tasks in the lab as long as they were standing and moving
  • Condition did not worsen after this point

Sleep deprivation can disrupt complex cognitive function (Krause et al, 2017)

  • Only some cognitive functions appear to be susceptible - executive function is the main victim in sleep deprivation (Miller and Wallis, 2009)
  • Attention is highly impacted, negative moods are caused and there is increase in sleepiness

Physiologically - increased blood pressure, reduced body temperature, decreased immune function, hormonal changes and metabolic changes - however, these changes have little impact in the long term

  • Microsleeps - brief periods of sleep - typically 2 or 3 seconds sleep long during which the eyelids droop and volunteers become less responsive to external stimui
    -> Vigilance decreases with depression
  • Sleep deprivation is more subtle, selective and variable than deprivation of other needs

REM Deprivation effects -

  • REM rebound - more than usual amount of REM sleep for the first two or three nights
  • With each successive of deprivation, there is greater tendency for participants to initiate REM sleep
  • This suggests REM sleep is regulated separately to slow-wave sleep

Horne 2013 - REM; Brain switches between NREM, REM and wakefulness depending on the immediacy of some needs - e.g. you are woken up if in need of water or food

  • REM prepares body for natural environments as it is close to wakefulness, and therefore it prepares us for immediate activity

In zeitgeber free environments, these rhythms are free running and their duration is a free running period - very in length between all individuals (different cave studies) - around 24.2 hours

  • Do not have to be learned
  • Body temperature cycle is linked to their sleep wake - tend to sleep during falling phase of body temperature
    -> However, in lab environments, sometimes there is internal desynchronisation of these two cycles
    -> Many circadian rhythm cycles
    -> This would be incompatible with restoration theories, as the clocks do not run on the same schedules
  • Reducing jet lag - exposure to light to reset circadian rhythm (Burgess et al, 1980)

Drugs that impact sleep - hynpotics, anti-hypnotics and melatonin