Sleep-wake cycle

Shift Work Disorder

What countermeasures are available?

  • leaving employment, rapid rotation schedule, clockwise rotation, permanent night work, self-selected work hours, afternoon nap before the next night shift, light exposure during the early half of the night shift, alertness-enhancing drugs

Neurobiology of the effects of caffeine

What are behavioral effects of caffeine?

What are individual differences in tolerance to shift work?

  • age, gender, personality, circadian type, DA function
  • eg. increasing age has negative impact on the ability to sleep during the day
  • eg. people with unshifted melatonin rhythm show issues (worse if too much melatonin circulates during the night shift)

What causes sleepiness in shift work?

  • circadian misalignment, sudden transitions in sleep schedule
  • circadian phase, time awake, prior sleep duration

Borbely: Two Process Model of Sleep

Sleep dependent aspects of sleep regulation

Sleep independent aspects of sleep regulation

Akerstedts Model of alertness regulation

What processes regulate the timing of sleep?

What are the effects of sleep deprivation?

lapses of consciousness may occur at high levels of sleepiness without additional warning

disrupted circadian & homeostatic sleep regulation

weakened immunity, high blood pressure, risk for diabetes, heart disease, dementia risk

Performance impairment caused by fatigue equates that due to alcohol intoxication:

  • computerized unpredictable tracking task
  • linear correlation between mean performance & hours of wakefulness, accounting for 90% of variance
  • after 24h of sustained wakefulness, performance decreased to a level equivalent to impairment observed at 0.10% blood alcohol concentration

increased risk for accidents

moody, emotional, quick-tempered -> state instability, behavioral issues

STM & LTM issues, issues with concentration, creativity, problem solving

What are physiological sleepiness indicators?

  • Karolinska Sleepiness Scale
  • EEG alpha activity
  • Standard Deviation of Heart Rate
  • slow eye movements
  • especially 5-9 Kz band
  • eye blink deviations & blink amplitude
  • frequent reductions of PFC metabolism, combined with high levels that seem to be related to efforts to fight sleepiness

report of difficulty falling asleep, staying asleep, non-restorative sleep for at least 1 month

  • affects people whose work hours overlap with typical sleep period

Mechanisms that underlie its central effects:

  • block adenosine (2a) receptors -> already at low concentrations
  • inhibition of phosphodiesterase & mobilization of intracellular calcium at higher concentrations
  • A2a receptors are found in DA-rich regions (co-localized) -> interact
  • effects of low dose caffeine can be mimicked by selective A2a antagonist
  • enhancement of postsynaptic D2 receptor transmission

EEG effects: changes towards faster frequency & lower amplitude activity (effects of caffeine similar to effects of increasing arousal), reduction in alpha band during task performance, decrease in delta & theta power

  • caffeine withdrawal: decresed alertness & increases in theta power

ERP effects:


Attention:

  • effect on latency & amplitude of early exogenous N1 component, N1 enhancement in selective search task -> increased receptivity to external stimuli, accelerated perceptual processing
  • enlargement of N2b in response to relevant stimuli -> signal-noise ratios are boosted
  • preparation mechanisms: increased negativity in ERP before a stimulus (contingent negative variation)

Arousal & Fatigue:

  • pronounced effects in situations of lower arousal o fatigue
  • more pronounced effects in degraded stimulus condition
  • enhancing mismatch negativity

Response-related Processing: effect on motor system, on movement time

How does caffeine affect the DA & ACh function?

  • transmission of D2 receptors is increased (there is an optimal range, so too much or too little results in worse PFC functioning)
  • caffeine intake increases left frontal activation more than the right (like mediating approach motivation)
  • D2 receptors modulate neural networks involved in selective & involuntary attention
  • stimulatory effect on motor behavior (DA)
  • caffeine increases firing rates in mesopontine cholinergic neurons -> role in arousal

doses above 500mg cause a decrease in performance eg. anxiety, tension

Attention System:

  • Visual Search task: increase in performance efficiency, subjects detected more targets
  • sustained attention task: subjects showed higher levels of perceptual sensitivity for relevant stimuli -> increase in hit rate without increasing FA rate

lower doses have positive effects on performance: energetic, motivated, concentrated

improvement in preparation &/or execution of motor responses

effects of caffeine on performance interact with extraversion & time of day

negative mood potentially reduced

Process S: sleep wake homeostasis

Process C: circadian process

Sleep propensity: the gap between the two processes in the figure (highest when around 11pm)

  • if awakening is extended 24h beyond, separation of the curves increases but because process S has an exponential decline, sleep duration isn't much prolonged

accumulation of sleep inducing substances in the brain eg. Adenosine

SCN as circadian oscillator

inversely related to sleep propensity: highest when sleep propensity is lowest

constantly fluctuating in the same rhythm, not depending on sleep time

coordinates the light-dark cycle of day & night

maximum in the late afternoon (body temperature highest & melatonin lowest)

slow inclination during waking and abrupt decline during sleep

causes pressure to fall asleep, drive to sleep after a certain amount of time awake

sleep-dependent, takes into account the time awake

NREM & REM ratio: determined by their propensities

  • At the sleep onset, the propensity of NREM is high vs. REM is low
  • At the end of the sleep period, they have equal propensities
  • Their cyclic alternate results from reciprocal excitatory & inhibitory interactions
  • There is decline in inhibition by Process S over the night

application of Process S & C--> Why are accident risks higher in the mornings?

major factors: circadian phase, amount of prior rime awake, amount of prior sleep

Independent Regulation/ manipulation of REM & NREM eg. selective REM deprivation followed by REM rebound

Slow wave sleep as parameter for high sleep intensity:

  • it dominates it the first part of sleep
  • it is enhanced by sleep deprivation
  • it is reduced after extended sleep
  • it has a high arousal threshold

rhythmic variations in sleepiness in accordance with circadian rhythm

Relationship between sleep & body temperature

  • in 24h environment (entrained), sleep onset starts when temperature cycle is low
  • in free running environments (non-entrained), sleep onset coincides closely with temperature minimum
  • internal desynchronization: in prolonged non-entrained schedules, the rhythms of sleep & temperature may develop different periodicities (cause body temperature has period close to 25h)

in the absence of time cues (non-entrained):

  • decreasing tendency of REM across sleep period, not rise
  • shortened REM latency
    --> REM exhibits cicradian rhythm

in the absence of external light-dark & social cycle, sleep-wake cycles remain consolidated but desynchronize from 24h (external desynchrony)

wake maintenance zone: circadian drive to stay awake increases during the day and reaches maximum at the end

  • in entrained conditions, homeostatic drive for sleep will be high at wake maintenance zone, in combination with the decrease of circadian drive for wakefulness -> increase in propensity to fall asleep

physiological & endocrine rhythms: body temperature, heart rate, cortisol, melatonin, growth hormone -> contribute to variations in sleep-wake propensity & change in association with sleep-wake cycle

during entrainment, the oscillators are synchronized (probably due to light input)

interplay of multiple external & internal oscillators eg. light-dark, social cycles

onset of melatonin secretion: opening of sleep gate (circadian pacemaker drives melatonin rhythm: melatonin receptors are present in SCN) -> feedback mechanism

Excitatory orexin system mediates circadian sleep wake propensity

Circadian pacemaker (SCN) regulates the timing & consolidation of sleep wake cycle

Homeostatic mechanism governs the accumulation of sleep debt & sleep recovery