Sleep, Dreaming and Circadian Rhythms Flashcards
Electroencephalogram (EEG)
reveals brainwaves
Electrooculogram (EOG)
Records eye movements seen during rapid eye movement (REM) sleep
Electromyogram (EMG)
Detects loss of activity in neck muscles during some sleep stages.
Emergent Stage 1 EEG:
accompanied by REM and loss of muscle tone. called REM sleep.
sleep spindles
12-14 Hz
Stage 3 and 4 also known as
slow wave sleep (SWS)
REM Sleep and Dreaming
80% of awakenings from REM lead to dream recall. External stimuli can be incorporated into dreams. Dreams run on “real time.” Virtually everyone dreams.
Sleepwalking (somnambulism), sleeptalking and bedwetting (enuresis) occur more frequently
during Stage 4 than during REM sleep, when core muscles are relaxed.
Freud’s explanation of dreams:
dreams are triggered by unacceptable repressed wishes. Our dreams (Manifest dreams) are disguised versions of our real dreams (Latent dreams). Interpreting dreams would expose the latent dreams and cure the patients.
Activation-Synthesis
Modern alternative to Freud’s explanation of dreams. Dreams due to cortex’s attempt to make sense of random brain activity.
Recuperation theories
Wakefulness causes a deviation from homeostasis, resulting in physiological and behavioral disturbances. Sleep is needed to restore homeostasis. After sleep deprivation, missed sleep will be regained.
Circadian theories
Sleep is the result of an internal timing mechanism that evolved to protect us from the dangers of the night. Missed sleep cause little or no disturbances. Little or no compensation for missed sleep.
Good correlation between the time an
animal needs to feed, and how vulnerable it is during sleep.
Conclusions of sleep
1) all animals sleep, 2) all species sleep, sleep does not serve some special higher-order human function, 3) duration of sleep varies among species, sleep is not necessarily needed in large quantities, 3) no clear correlation between sleep time and activity levels, body size, or body temp.
Circadian rhythms
about a day. Virtually all physiological, biochemical, and behavioral processes show some circadian rhythmicity (sleep, temp, hormones).
Zeitgebers
environmental cues that entrain circadian cycles (light-dark, tides).
without zeitgebers
, animals display “Free-Running Rhythms”, usually longer than 24h, ~ 25h.
Human’s free-running circadian sleep-wake cycle lasts
25.3 hrs.
Jet lag
zeitgebers are accelerated during east-bound flights (phase advance) or decelerated during west-bound flights (phase delay). Phase delays are tolerated better.
shift work
zeitgebers unchanged, but sleep-wake cycle must be altered. These changes may result in large phase shifts.
Jet lag and shift work produce
fatigue, sleep disturbances, physical & cognitive deficits.
melatonin
is synthesized in the pineal gland. not a sleep aid, but may be used to shift circadian rhythms. Melatonin levels follow circadian rhythms controlled by the Suprachiasmatic Nucleus.
Can the effects of Jet Lag be prevented or minimized?
Melatonin and Light therapy.
Pineal gland triggers
seasonal reproductive changes in fish, birds, reptiles, and amphibians – human function is unclear.
Resetting biological clock with bright lights
morning: earlier sleep, phase advance
afternoon: little effect
evening: later sleep, phase delays
Resetting biological clock with melatonin pills
morning: later sleep, phase delays
afternoon: earlier sleep, phase advance
evening: little effect
The Recuperation theory (wakefulness has a debilitating effect) predicts that sleep deprivation will cause:
1) Long periods of wakefulness will produce physiological and behavioral disturbances.
2) These disturbances will grow steadily as deprivation continues.
3) The missed sleep will be regained.
The Circadian (evolutionary) theory predicts that sleep deprivation will cause:
1) There will be no debilitating effect, except for tendency to fall asleep.
2) Tendency to sleep will be during normal sleeping time.
3) There will be little or no compensation for the loss of sleep.
3-4 hours of deprivation in one night
Increased sleepiness. Disturbances of mood. Poor performance on tests of vigilance.
2-3 days of continuous deprivation
Experience microsleeps, naps of 2-3 seconds. Micro sleeps disrupt performance on vigilance tests.
Longer periods of deprivation
No effects on motor performance. No effects of cognitive performance (IQ). May affect creativity.
Sleep-Deprivation Studies with Rats
Carousel apparatus used for sleep deprivation. When the EEG indicates sleep, the floor rotates – the sleeping rat falls into the water and wakes up.
Yoked controls – subjected to the same floor rotations.
Experimental rats typically die after several days. Postmortem studies reveal lesions indicative of extreme stress.
The circadian clock is located in the
Suprachiasmatic Nucleus. Even when isolated, it shows cycles of electrical, metabolic and biochemical activity. The Retino-
hypothalamic tract connects the retina with the Suprachiasmatic nucleus.
photoreceptors that entrain the SCN are
light-sensitive ganglion cells.
transection before the optic chiasm
eliminated the ability of light-dark cycles to entrain circadian rhythms.
transection after the optic chiasm
did not eliminate the ability of light-dark cycles to entrain circadian rhythms.
these two transections suggest that
the sensory tracts that mediate the entrainment of circadian rhythms by light-dark cycles branch off from the optic chiasm and project to the suprachiasmatic nuclei of the hypothalamus.
Hypnotic drugs
increase sleep. most commonly prescribed hyponotic drugs: benzodiazepines – Valium, Librium. Effective in the short term. Complications include: tolerance, cessation leads to insomnia, addiction, increase of stage 2 sleep, decrease of stage 4 and REM.
Antihypnotic drugs
decrease sleep. Stimulants: cocaine, amphetamine. Tricyclic antidepressants: imipramine. Both increase activity of catecholamines (norepinephrine, epinephrine, dopamine). Can suppress REM with little effect on total sleep time.
insomnia
Disorder of sleep initiation and maintenance. Often a problem of too little undisturbed sleep
Often is iatrogenic (physician-created), which is a consequence of pill use.
sleep apnea
stop breathing leads to repeated awakenings.
- Obstructive –atonia and collapse of respiratory tract.
- Central – CNS fails to maintain breathing
Patients are frequently overweight, elderly.
Restless leg syndrome
prevents sleeping
Alternative treatment of Insomnia:
sleep restriction therapy.
Hypersomnia, Narcolepsy
Severe daytime sleepiness and repeated brief daytime sleeping - “sleep attacks.” REM without atonia.
cataplexy
loss of muscle tone while awake.
sleep paralysis
paralyzed while falling asleep or upon waking.
Hypnagogic hallucinations
dreamlike experiences while awake. Possibly due to abnormalities in mechanisms triggering REM.
A 1977 study of 8 subjects who gradually reduced their nightly sleep to 4.5 - 5.5 hours found:
Daytime sleepiness when sleep was reduced to 6 hours. Increased sleep efficiency: faster falling asleep, more stage 4 sleep, fewer awakenings. In the year after the experiment, all subjects slept less than at the beginning of the experiment.
Long-term sleep reduction by napping
Leonardo da Vinci took 15 min naps every 4 hours.
circannual
cycles can last about a year. hibernation, seasonal changes in reproduction or body fat.
alert wakefulness
low amplitude, high frequency EEG waves (beta): 13-30 Hz.
just before sleep
bursts of alpha waves appear (8-12 Hz).
stage 1 (initial stage 1)
Low amplitude waves, frequency slower than alert wakefulness.
stage 2
Amplitude of waves increases and frequency slows down. K complexes appear: single positive (downward deflection) and negative wave (upward deflection). Sleep spindles appear: 1-2 sec burst of 12-14 Hz waves.
stage 3
Amplitude of waves increases and frequency slows down. Delta waves appear occasionally: 1-2 Hz
stage 4
Predominance of delta waves.
waking from non REM sleep leads to only
7% percent of dream recall
lucid dreams
Dreams in which the dreamer is aware that he/she is dreaming and can influence the course of the dreams. It is like being awake in a dream.
for reducing jet lag
Gradual shift of one’s sleep-wake cycle in the days before the trip. Light treatment early in the morning after east-bound flights facilitate the phase advance required for adjustment. Studies in hamsters suggest that a vigorous workout early in the morning may also help.
for reducing shift work
Shifts to schedules that begin later in the day produce fewer disturbances because they require phase delay. It is easier to go to bed and get up later than the reverse.
after sleep deprivation, there tends to be more
REM periods.
following REM sleep deprivation
there is a REM rebound: subjects have more REM sleep in the following 2-3 nights. if REM is replaced by a similarly long period of wakefulness, there is no REM compensation, confirming idea that wakefulness and REM sleep are equivalent in many ways.
REM sleep may:
- Maintain mental health
- Maintain motivation
- May be necessary for the processing of certain memories (consolidation)
There is some experimental support, however certain tricyclic antidepressants (imipramine) can eliminate REM without serious consequences.
individuals who are deprived of sleep become more efficient sleepers
They take less time to fall asleep. They have fewer interruptions of sleep. These subjects show a higher proportion of Slow Wave Sleep. Although total sleep is not regained, stage 4 sleep tends to be regained, with corresponding reductions in stages 1 & 2.
The idea that stage 4 may be specially important and restorative is supported by
the fact that short sleepers have as much stage 4 sleep as long sleepers. Also, waking up sleepers during stage 4 produces more sleepiness than waking them up during REM.
posterior hypothalamus promotes
wakefulness.
anterior hypothalamus promotes
sleep.
melatonin increases
sleepiness. Increased secretion of melatonin begins between 8-10 pm, and decreases during the day. Melatonin resets clock by acting on receptors of the SCN.
Nocturnal myoclonus
Periodic twitching of the legs and body leads to poor sleep.
In normal subjects, a nucleus in the caudal reticular formation (nucleus magnocellularis)
normally induces muscle relaxation during REM. Studies in a strain of narcoleptic dogs has shown that this nucleus is also active during narcoleptic attacks, which would cause the collapse of the subjects during these attacks.
orexin
Studies in these dogs also revealed the genes associated with narcolepsy. These genes encode a receptor protein that binds a neuropeptide neurotransmitter called orexin. These dogs are deficient in this protein. Orexin is synthesized in the posterior hypothalamus, which promotes wakefulness.
In humans suffering from narcolepsy
the cause of narcolepsy appears to be a hereditary disorder that stimulates the immune system to attack and destroy orexin-secreting neurons. Symptoms typically appear during adolescence. Interestingly, deficiencies in the orexin-binding protein are not only associated with narcolepsy, but also with a decrease in eating behavior.
Patients that due to injury or other reasons do not have REM sleep are often
not affected by lack of REM sleep.
Some patients experience REM sleep without
core-muscle atonia, which is thought to prevent the acting out of dreams.
