Sleep, Dreams and Circadian Rhythms

Part 1: What is Sleep? And why do we dream?

• Weekly Learning Outcomes:

  • Describe the four stages of sleep, with reference to the psychophysiological measures EEG, EOG and EMG.

  • Describe the theories on why we dream, and the brain regions involved.

• Sleep is a Dynamic Process

  • Measured through:

    • EEG (Brain activity)

    • EOG (Eye movements)

    • EMG (Muscle tension)

  • Polysomnography: A comprehensive recording of the biophysiological changes that occur during sleep.

• Descriptors of EEG

  • Frequency (speed) is related to wake/sleep:

    • Faster the frequency = more alertness/wakefulness

    • Slower the frequency = more drowsy/deeper sleep

  • Waves are measured by amplitude and frequency.

• Defining the Sleep Stages

  • Sleep recordings are divided into segments known as Epochs (typically 30sec).

  • Each Epoch is assigned a sleep stage based on certain characteristics of EEG/EOG/EMG.

  • Sleep Stages:

    • Wake

    • NREM1

    • NREM2

    • NREM3

    • REM

• Vigilant Wakefulness

  • Lots of EOG/EMG activity: Interacting with the environment

  • EEG:

    • Beta activity = ‘Desynchronized’

    • High frequency (15-20 Hz).

    • Low amplitude

• Stages of Sleep: NREM 1

  • EEG:

    • Low amplitude, mixed frequency

    • Predominantly theta activity (4-7 Hz)

    • Vertex sharp waves

  • EOG:

    • Slow Eye Movements (SEMs)

  • EMG:

    • Tonic activity

    • May be slight decrease from waking; maintained throughout NREM stages

  • About 2-5% of sleep period

• Stages of Sleep: NREM 2

  • EEG:

    • Low amplitude, mixed frequency

    • Predominantly theta activity (4-7 Hz)

    • K Complexes

    • Sleep Spindles

  • EOG: No eye movements present

  • EMG: Tonic activity still present, lower than wakefulness

  • About 50% of sleep period

• Stages of Sleep: NREM 3

  • EEG:

    • Slow wave rhythm: 0.5-4.0 Hz and minimum amplitude of 75 μV

  • EOG: No eye movements present

  • EMG: Tonic activity still present, lower than wakefulness

  • About 20% of sleep period

• Stages of Sleep: REM

  • EEG:

    • Low amplitude, mixed frequency EEG pattern (like N1 stage of sleep)

    • Addition of sawtooth waves

  • EOG: Bursts of EOG activity – rapid eye movements, Known as phasic REM.

  • EMG:

    • Drops to lowest level = muscle atonia

    • Reflective of inhibition of motor activity and loss of muscle tone that occurs in REM

  • About 20-25% of sleep period

• The Stages of Sleep Summary

  • NREM = Non-rapid eye movement stages of sleep

    • There are 3 of these – with stage 1 being the lightest stage of sleep, and 3 being the deepest.

  • REM = Rapid eye movement sleep

    • This is a distinct stage of sleep where rapid eye movements occur.

    • Muscle tone is at its lowest of any sleep stage = muscle atonia.

• The Temporal Organisation of Sleep

  • Sleep follows an orderly progression through the sleep stages across the night.

  • This orderly progression through the NREM stages, into REM defines one sleep cycle.

  • Normal sleep is entered through NREM

  • Episodes of NREM and REM sleep alternate about every 90 mins

  • Over the course of the night there is typically an orderly progression between stages – 5-6 sleep cycles.

  • Stage 3 (N3) more prominent in first third

  • REM more prominent in second half

• Does REM Sleep = Dreaming?

  • Dreaming can also occur during NREM sleep.

  • The qualities of NREM dreams are comparable to those of REM dreams.

  • REM sleep and dreaming can be dissociated.

• Why Do We Dream?

  • Hobson’s activation-synthesis hypothesis

    • Information provided to cortex is largely random = ‘left-overs’ from the day

  • Revonsuo’s evolutionary theory of dreams

    • Dreams stimulate threatening environments and help us better prepare when awake.

  • Revised to: Hobson’s protoconsciousness hypothesis

    • Became critical of original hypothesis – argued dreaming does serve a purpose!

    • Dreaming = evolutionary advantage

    • Unlike Revonsuo = simulating everything, not just threatening situations.

    • = ‘Training mechanism”

• The Dreaming Brain

  • Lesion/brain imaging studies implicate the Medical PFC and TPJ in dreaming.

  • Specifically: Medial Occipital Lobe = visual imagery within dreams.

Part 2: Why Do We Sleep When We Do?

• Why Do We Sleep?

  • Recuperation theories

    • Restores homeostasis

  • Adaptive theories

    • Conserve energy

    • Protect organisms

• Why Do We Sleep?

  • All animals sleep despite dangers.

  • No species has evolved to not need sleep.

  • Animals fully deprived of sleep die (biological necessity).

  • Sleep is restorative and plays a role in:

    • Growth hormone surge during sleep.

    • Brain plasticity (forming skills and memories).

    • Flushing metabolic waste from the brain via the glymphatic system.

    • Necessary for brain function.

• What Determines When We Sleep?

  • Virtually all physiological, biochemical, and behavioral processes show some circadian rhythmicity.

  • The most salient of these circadian rhythms: Our sleep/wake cycle

  • Key features of circadian clocks:

    • Approximately 24 hours

    • Settable (entrainment) – LIGHT is the major synchronizer

    • Endogenous

• What Determines When We Sleep?

  • Our rhythms are ‘free-running’

  • Free-running cycles are not learned

  • Free-running rhythms

    • Circadian rhythms in constant environment

  • Internal desynchronization

    • More than one circadian mechanism?

• The Two Process Model of Sleep and Wake (Borbely, 1982)

  • Relates to sleep pressure – increasing drive for sleep accumulates with time spent awake.

  • Waking proportional to amount of Stage 3 NREM sleep.

  • The Homeostatic Process (Process S)

    • Internal (endogenous) timing that modulates periods of alertness and sleepiness throughout the day, independent of prior sleep or wakefulness.

  • The Circadian Process (Process C)

• How do these two processes work together to produce sleep/wake?

  • Homeostatic Sleep Drive's Sleep Load

  • Circadian Oscillation's Alerting Signal

  • Wake/Sleep cycle

• Regions Involved in Sleep/Wake Regulation

  • The Suprachiasmatic Nucleus (SCN) are considered the ‘master clock’:

    • Melatonin synthesis, as well as the many other rhythms in our body, are controlled by the suprachiasmatic nucleus which relies on light cues to remain synchronized.

  • Pathway from: retina – retinohypothalamic tract – SCN

    • Specialised cells in the retina called Intrinsically photosensitive retinal ganglion cells (ipRGCs) produce a photopigment called melanopsin.

    • Light activates melanopsin (photopigment).

    • This signal is transmitted to the SCN for photoentrainment.

    • Downstream effect – pineal gland = suppression of melatonin

• Regions Involved in Sleep/Wake Regulation

  • The posterior hypothalamus = wakefulness

  • The anterior hypothalamus = sleep

  • The Reticular Formation is a complex bundle of nerves in the brainstem is located in the brainstem.

    • Ascending projections to cortex regulates arousal and sleep/wake transitions

    • High levels of activation = produce wake

    • Low levels of activation = produce sleep

• Regions Involved in Sleep/Wake Regulation

  • The reticular formation and REM sleep

    1. PGO spikes (EEG spikes recorded in the pons, lateral geniculate, and occipital cortex)

    2. Cardiorespiratory changes

    3. Core-muscle relaxation

    4. Rapid eye movements

    5. Cortical EEG de-synchronization

    6. Hippocampal theta waves (hippocampal EEG waves between 5 and 8 Hertz)

    7. Twitches of extremities

  • REM sleep, slow-wave sleep, and wakefulness all result from the interaction of several mechanisms that are capable under certain conditions independently of one another.

Part 3: Insufficient Sleep: Experimental Sleep Deprivation and Sleep Disorders

• 4 in 10 Or 7.4 million Australians frequently suffer from inadequate sleep

• The Prevalence of Inadequate Sleep

• Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR)

  • Insomnia disorder

  • Hypersomnolence disorders

  • Narcolepsy

  • Breathing-related sleep disorders

  • Sleep-related hypoventilation

  • Circadian rhythm sleep-wake disorders

  • Non-rapid eye movement arousal disorders

  • Nightmare disorder

  • Rapid eye movement sleep behaviour disorder

  • Restless legs syndrome

  • Substance/medication-induced sleep disorder

• Insomnia – A Brief Overview

  • A predominant complaint of dissatisfaction with sleep quantity or quality, associated with one (or more) of the following symptoms:

    • difficulty initiating sleep,

    • maintaining sleep,

    • or early morning awakenings.

  • Insomnia can coexist with many conditions, and regardless of which came first we need to address the sleep problems in their own right.

  • Cognitive behavioural therapy for insomnia (CBT-I) is a multi-component treatment, incorporating different approaches utilised to address underlying psychological, behavioural, and physiological processes and factors that underpin and perpetuate insomnia.

• Narcolepsy – A Brief Overview

  • Defined by recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping occurring within the same day: ‘sleep attacks’

  • Other symptoms can include:

    • Episodes of cataplexy - loss of muscle tone.

    • Hypocretin (AKA orexin) deficiency, as measured using cerebrospinal fluid (CSF).

    • When hypocretin is HIGH – promotes arousal. Lack of = sleepiness

    • Sleep-onset REM (sleep is entered through NREM typically).

    • Sleep paralysis and sleep related hallucinations (hypnogogic hallucinations).

• Sleep Deprivation and Performance

  • Impairments in sustained attention are well-studied in experimental sleep deprivation protocols:

    • Ability to maintain attention and respond to stimuli over time: Psychomotor Vigilance Task (respond to timer over 10 minutes)

    • Worsening performance with time awake = increasing homeostatic sleep pressure.

    • Circadian influence on performance = recover in morning when alerting signals from the circadian process are high.

• Sleep Deprivation and Performance

  • After being awake for 17-19 hours, impairment on a simple reaction time test was comparable with impairment observed at a blood alcohol concentration of 0.05%.

  • After being awake for 21-24 hours, impairment on a simple reaction time test was comparable with impairment observed at a blood alcohol concentration of roughly 0.08-0.10%.