EEG Patterns During Sleep
The Neural Origin of Sleep Spindles?
Thalamocortical oscillations in vivo. Sleep spindle oscillations are generated by synapses in the thalamus. (A, left)
Potentials recorded through a microelectrode inserted in the deafferented reticular thalamic nucleus of a cat. The
arrow points to one spindle sequence. (A, right) Spindle oscillations recorded from the thalamus of a cat with an upper
brainstem transection that created an isolated forebrain preparation. The figure shows two spindle sequences (the
second marked by an arrow) and, between them, lower frequency (delta) waves. (B) Neuronal connections involved in
the generation of spindle oscillations. (C) Intracellular recordings of one spindle sequence (see A) in three types of
neurons (cortical, reticular thalamic, and thalamocortical). Ca2+, calcium ions; IPSP, inhibitory postsynaptic potential
The Effects of Sleep Deprivation
A model of oscillatory activity
during sleep.
Who’s Active and When?
AWAKE
Slow Wave Sleep
ACh system active
ACh system inactive
sensory thalamus
facilitated
sensory thalamus
inhibited
reticular nucleus
inhibited
reticular nucleus active
thalamocortical neurons thalamocortical neurons
active
in slow rhythm
EEG desynchronous
EEG synchronous
Where is all this happening?
Another Summer of Activity
Exemplifying Different States:
This corresponds
to an awake, alert
state
Acetylcholine cannot, by itself, activate or shut down the neurons of
the thalamus. Instead it sensitizes them. By slightly depolarizing the
thalamic neurons (it does this by closing a hyperpolarizing
potassium channel), the ascending system can make the thalamus
more sensitive to sensory input.
But Wait, There’s MORE!
Now, although both areas are receiving acetylcholine, they have
different receptors and respond in different ways. Sensory
thalamus (VPL) is sensitized by acetylcholine (or "facilitated")
as described above, but the reticular nucleus is inhibited by
acetylcholine.
REMINDER:
Physiological Mechanisms of
Sleep: A Simplification
I. The occurrence of REM Sleep:
A. Controlled mostly by mechanisms located in
the brainstem (particularly the pons).
B. The components of REM are stimulated
(turned on) by acetylcholinergic mechanisms.
C. The components of REM are inhibited (turned
off) by:
a. Serotonergic neurons of the dorsal raphe
nuclei.
b. NE neurons of the locus coeruleus.
c. Both NE and 5-HT serve inhibitory functions in
that they prevent REM sleep from occurring
when they are active.
II. The components of REM:
A Desynchronized cortical EEG activity
a. Possibly produced by the pons by way of the projections from
the pontine nuclei (LDT=lateral dorsal tegmental nucleus & PPT=
pedunculopontine tegmental nucleus) to thalamic nuclei that
project broadly to various cortical areas.
B. Muscular paralysis
a. Possibly produced by ACh neurons (located in the dorsolateral
pons near the locus coeruleus) that project caudally to
magnocellular nucleus of the medial medulla and eventually to
the spinal cord.
C. Rapid Eye Movements
a. Possibly produced by pontine nuclei (LDT and PPT) that
project to superior colliculus and to the medial reticular formation.
III. Experimental evidence for mechanisms of REM:
A. Lesion PPT & LDT- decrease the amount of REM sleep
B. Increase number of ACh synapses in the brain - increase the
amount of REM sleep
C. Inhibit AChE - increase amount of REM sleep
D. Inhibit AChE - shorten intervals between periods of REM
sleep
E. Block ACh muscarinic receptors - lengthen the interval
between periods of REM sleep
IV Slow-Wave Sleep
A. The nucleus of the solitary tract in the medulla is involved in
slow-wave sleep.
B. Slow-wave sleep may be induced by the basal forebrain region
(rostral to the hypothalamus, including the pre-optic region).
V. Experimental evidence for mechanisms of slow-wave sleep
A. Stimulate the nucleus of the solitary tract (in the medulla) produce EEG synchrony that looks like slow-wave sleep
B. Record from the nucleus of the solitarty tract in the cat - see
increased firing during slow-wave sleep.
a. you do not see an increase in firing before slow-wave sleep.
So, it is theorized that the nucleus of the solitary tract is involved
in slow-wave sleep, but not in the induction of slow-wave sleep.
C. Stimulate particular areas of the basal forebrain region - see
EEG synchrony and sleep.
VI. Substances and activities that modulate sleepiness or
amounts of sleep.
A. Eating protein - facilitates the secretion of somatostatin increases REM sleep.
B. Eating Carbohydrates - facilitates the secretion of insulin –
increases slow-wave sleep.
D. Intake of or production of (due to physical activity) muramyl
peptides – (note: this is interesting because serotonin can serve
the same function) facilitates the release of interleukin 1 in the
brain - increases slow-wave sleep.
E. Intake of tryptophan rich foods - facilitates sleep induction.
Caution tryptophan supplements taken in high doses will distort
sleep patterns.
DYSSOMNIAS (Disorders of sleep or
wakefulness)
Common Circadian Rhythm Sleep Disorders
•Advanced Sleep Phase Syndrome (ASPS) - bright light
therapy
•Delayed Sleep Phase Syndrome (DSPS)
•Time Zone Change Syndrome - Jet Lag
Intrinsic Sleep Disorders (Disorders that either
originate or develop from within the body)
•Hypersomnia (Excessive Sleepiness)
•Insomnia
•Narcolepsy
•Obstructive Sleep Apnea (OSA)
•Central Sleep Apnea
•Periodic Limb Movement Disorder (PLMD)
•Restless Legs Syndrome (RLS)
Extrinsic Sleep Disorders (Disorders that either
originate or develop from causes outside the body)
•Nocturnal Eating (Drinking)Syndrome (Sleep Eating)
PARASOMNIAS (Disorder of arousal, partial
arousal or sleep stage transition)
Arousal Disorders (A parasomnia disorder presumed to
be due to an abnormal arousal mechanism)
•Confusional Arousals (Sleep inertia)
•Somnambulism (Sleepwalking) in adults
•Somnambulism (Sleepwalking) in children
•Sleep Terrors in children
•Sleep Terrors in adults
Sleep-Wake Transition Disorders
•Nocturnal Leg Cramps
•Rhythmic Movement Disorder
•Sleeptalking
Parasomnias Usually Associated with REM Sleep
•Nightmares
•Sleep Paralysis
•REM Sleep Behavior Disorder (RBD)
Other Parasomnias
•Infant Sleep Apnea
•Primary Snoring
•Sudden Infant Death Syndrome (SIDS)
•Sleep Bruxism (tooth grinding or tooth clenching)
•Sleep Enuresis (Bedwetting) in children
Proposed Sleep Disorders
•Short Sleeper
•Long Sleeper
•Subwakefuness Syndrome
•Fragmentary Myoclonus
•Sleep Hyperhidrosis (Excessive sweating)
•Menstrual-Associated Sleep Disorder
•Pregnancy-Associated Sleep Disorder
•Terrifying Hypnogogic Hallucinations
•Sleep-Related Neurogenic Tachypnea
•Sleep-Related Laryngospasm
•Sleep-Choking Syndrome
SLEEP APNEA
Central sleep apnea.
During waking, the respiratory oscillator
of the medulla receives tonic drive from
other neural structures and can
respond to voluntary and metabolic
signals to change breathing pattern.
Muscle tone keeps the oropharynx open
to the flow of air. In NREM sleep, central
drive decreases, and the rate and depth
of ventilation fall.
If the airway collapses, prolonged
apnea (lack of breathing) may result.
During REM sleep, activation of pontine
generator neurons drives the
respiratory oscillator, and
desynchronization may lead to
breathing efforts that are too frequent
or strong (hyperpnea) or that stop.
During REM sleep the oscillator also
becomes unresponsive to metabolic
signals
What are the symptoms of Narcolepsy?
-excessive sleepiness or sudden muscle weakness
cataplexy (a sudden loss in muscle tone and deep tendon reflexes
leading to --muscle weakness, temporary paralysis or a complete
postural collapse.
Cataplexy is usually brought on by an outburst of emotion - notably
laughter, anger or startle.)
-hypnagogic hallucinations
-automatic behaviors (like driving home and not remembering how
you got there!)
-disrupted major sleep episode (disruption of the longest sleep
episode that occurs on a daily basis).
EEG recording during sleep shows one or more of the
following:
-The onset of sleep is less than 10 minutes
-The onset of REM sleep is less than 20 minutes and
-A Multiple Sleep Latency Test (MSLT) that demonstrates an average
sleep onset of less than 5 minutes
Physiology shows the following:
-HLA typing demonstrates DR2 positivity (Blood contains markers for
narcolepsy)
- Lack of hypocretin – 1 in CSF
- Perhaps due to a destruction of the hypocretin (orexin) cells in the
lateral hypothalamus or a point mutation in the gene coding for
hypocretin.
Slow Wave Sleep Aids consolidation of a Motor-Learning Task