Physiology of sleep and polysomnography

Physiology of sleep
and polysomnography
Presenter : Dr. Saran A K
Preceptors : Dr. Kamlesh Jha and Dr. Ganashree C. P
DM Seminar | 13 September 2023
DEPT. OF PHYSIOLOGY, AIIMS PATNA 2

The Great Pyramid of Giza, Egypt.

5
Overview
● Introduction
● Sleep Active v/s Passive
● Functions of Sleep
● Stages of Sleep and Physiological Changes
● Sleep Cycle
● Physiological control of sleep
● Brain areas regulating sleep/wake
● Polysomnography
● Summary

6
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Sleep is defined as unconsciousness from which a person
can be aroused by sensory or other stimuli.

Behavioral Definition of Sleep
Sleep is defined as a reversible behavioral state of
perceptual disengagement from and unresponsiveness to
the environment.
Carskadon & Dement, 2011

• Reduced motor activity
• Reduced responsiveness to stimuli
• Stereotypic postures in humans
• Relatively easy reversible

The International Classification of Sleep Disorders (ICSD)
includes seven major categories of sleep disorders
1. Insomnia
2. Sleep-related breathing disorders
3. Central disorders of hypersomnolence
4. Circadian rhythm sleep-wake disorders
5. Parasomnias
6. Sleep-related movement disorders
7. Other sleep disorders
ICSD-3-TR

Landmarks in Sleep Medicine and Research
1924 Hans Berger First to record EEG
1935-1939 Alfred Lee Loomis, Newton Harvey,
Hallowell and Pauline Davis
First to describe the characteristic
features of non-REM sleep
1939 Nathaneil Kleltman First comprehensive sleep research
lab, depth of sleep
1953 Eugene Aserinsky, Kletman Discovered REM sleep, Eye
movements and REM Sleep
1950s William Charles Dement Proposed a classification of sleep
stages : four stages of non- REM
and REM Sleep
1967 Allan Rechtschaffen and Anthony
Kales
First consensus-based guidelines
for staging and scoring sleep - R&K
2004-2007 American Academy of Sleep
Medicine (AASM)
Sleep scoring manual - sleep
staging as well as scoring of
arousals, respiratory, cardiac and
movement events.

12
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

13
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Sleep – Active v/s Passive Process
• Passive state theory of sleep : General belief and perception -
brain is active during wakefulness and it gets tired at the end of the
day and then goes to sleep.
• Von Economo’s observations of patients with Encephalitis
lethargica provided the major scientific foundation this view.
Kumar, V.M. Sleep is neither a passive nor an active phenomenon.
Sleep Biol. Rhythms 8, 163–169 (2010).

• Moruzzi and Magoun - Electrical stimulation of the brainstem
reticular formation evokes an EEG pattern resembling
wakefulness.
• Passive occurrence of sleep was the accepted dominant
theory during the 1940s and early 1950s.

• The discovery of REM sleep in 1953 marked the beginning of
the era of the active sleep genesis concept.
• Aserinsky and Kleitman observed REMs under closed lids
in babies after the sleep onset with EEG showing low
amplitude irregular waves, like wakefulness.

• Dement working with Kleitman, established an association
between REM sleep and dreaming.
• Jouvet and colleagues described REM sleep as
“paradoxical sleep,” and demonstrated muscle atonia and
other subcortical signs with this phase in experimental
animals (cats).
Kumar, V.M. Sleep is neither a passive nor an active phenomenon.
Sleep Biol. Rhythms 8, 163–169 (2010).

20
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

21
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Why do we sleep?
The true purpose of sleeping is poorly understood.
The potential functions are
1. Restorative Function
• The body repairs and revitalizes itself during the sleep state.
2. Protective behavioral adaptation
• Role in mitigating adverse consequences of stress
• Metabolic energy conservation and thermoregulation

3. Hormone regulation
• Variations in growth hormone, TSH, prolactin, cortisol, ACTH,
Melatonin associates with different stages and timings during
sleep.
4. Immune competence
• SWS enhances consolidation phase of adaptive immune
response

5. Effects on nervous system
• Restoration of natural balances among the neuronal centers
• Brain plasticity in learning and memory consolidation
• Synaptic Pruning - Targeted erasure of synapses to “forget”
unimportant information that might clutter the synaptic network
• Clearance of metabolic waste products such as adenosine
generated by neural activity in the awake brain – Glymphatic
System
• Emotion and Mood Regulation

25
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

26
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Stages of Sleep
Sleep can be classified into
• Rapid Eye Movement Sleep (REM Sleep)
• Non-Rapid Eye Movement Sleep (NREM Sleep)
27
DEPT. OF PHYSIOLOGY, AIIMS PATNA

Sleep Stages
28
RECKSHAFFEN AND KALES (R&K) AMERICAN ACADEMY OF SLEEP MEDICINE (AASM)
Combined S3 and S4 of R & K

SLOW WAVE SLEEP
OR
DEEP SLEEP
29

NREM Sleep – Physiological Changes
• Exceedingly restful
• Initially there is considerable tone in the posture muscles,
later tone decreases progressively.
• Decrease in peripheral vascular tone and other vegetative
functions → low HR, SBP, RR
• Low body temperature

• Low sympathetic activity + high parasympathetic activity
• GI activity higher
• Usually called 'dreamless sleep’
• But dreams and sometimes nightmares do occur → not
remembered because consolidation of dreams in
memory does not occur

REM Sleep – Physiological Changes
• Active form of sleep usually associated with dreaming and
active bodily muscle movements.
• Cannot be aroused easily by sensory stimulus, awaken
spontaneously in the morning during REM sleep.
• When awakened, 80-90% people report of dreaming

• Tone of skeletal muscles in the neck decreases
markedly.
• Suppression of peripheral muscle tone → locus
coeruleus dependent relative paralysis of voluntary
activity.
• Despite extreme inhibition of peripheral muscles →
irregular muscle movements + rapid saccadic / roving
eye movements.

● Concomitants of REM sleep
○ Tooth grinding (Bruxism)
○ Penile erection
○ Clitoral engorgement
● HR and RR irregular → characteristic of dream state
● SBP high
● Impaired thermoregulation

PET scan shows:
● Increased activity in visual association areas but decreased in
primary visual cortex.
● Increased activity in pontine area, amygdala and anterior cingulate
gyrus.
● Decreased activity in prefrontal and parietal cortex.
Consistent with increased emotion and operation of a closed neural
system cut off from the areas that relate brain activity to the external
world

36
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

37
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

● Of total sleep time
● 75% NREM sleep and 25% REM sleep.
● In a typical night sleep,
● a young adult first enters NREM sleep
● Passes through N1 (light sleep) to N3(deep sleep),
● Sleep then lightens and REM period follows
● This cycle is repeated at intervals of 90 minutes throughout the night
Next cycle begins with NREM sleep
Sleep Cycle

● There is less Stage N3 and more REM sleep towards morning
● Usually wake up from REM sleep
So, 4-6 REM periods occur per night
● % of REM sleep
○ Premature Infants → 80%
○ Full term neonates → 50%
○ Adults → 25%
○ Old age → further decrease in REM sleep

42
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

43
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Physiological control of Sleep
Three basic processes underlie sleep regulation
1. A Homeostatic process
2. A Circadian process
3. An Ultradian process occurring within the sleep episode -
alternation of the two basic sleep states, non-REM sleep and REM
sleep.

Two Process Model
• Proposed by Borbély, A. A
• The model posits that the interaction of its two constituent
processes, generates the timing of sleep and waking.
• A sleep/wake dependent homeostatic Process S
• Circadian Process C
Borbély, A. A. (1982). A two process model of sleep regulation. Human Neurobiology, 1(3), 195–204.

Owens, J., Gruber, R., Brown, T., Corkum, P., Cortese, S., O’Brien, L., Stein, M., & Weiss, M. (2013). Future Research
Directions in Sleep and ADHD: Report of a Consensus Working Group. Journal of Attention Disorders, 17(7), 550–564.

• Process S: The “homeostatic” process is controlled by the
sleep pressure or need that builds up during the waking period
and dissipates during sleep.
• Process C: The “circadian” process, i.e., the sleep/wake cycle
during the day and night, is controlled by a circadian
pacemaker or biologic clock.

Process S – The Homeostatic Process
• Primarily regulates the length and depth of sleep.
• Accumulation of adenosine and other sleep promoting chemicals
(somnogens) such as cytokines during wakefulness.
• Dependent on the quality and quantity of prior sleep and factors
such as individual sleep needs.

• “Sleep pressure” appears to build more quickly in infants
and young children
• The amount, timing, and density of slow-wave sleep
activity serve as markers of the homeostatic sleep drive.
• Homeostatic dysregulation - chronic insufficient sleep and/or
nonrestorative sleep.
• “Sleep debt” leads to significant neurobehavioral
impairments.

Sleep Regulating Substances (SRS)
• Kuniomi Ishimori and Henri Piéron - hypnotoxin.
• SRS includes peptides, cytokines, neurotransmitters and
some substances of lipidic nature.
• Adenosine plays a very important role in the homeostatic
mechanism.

• Neuronal activity increases SRS levels, and the levels of SRS
accumulates throughout the day.
• SRS act on neural networks controlling sleep.
• In sleep, glymphatic system facilitates the washout of accumulated
SRS.
• The level of SRS in the body comes down and the sleep pressure
dissipates.

Several SRSs act on sub-cortical sleep-regulatory circuits.
• Adenosine acts on basal forebrain (BF) neurons to promote sleep.
• GHRH, TNF and IL1 act directly on hypothalamic preoptic neurons
(VLPO) to promote NREMS.
• TNF and IL1 also act on the locus coeruleus (LC) and IL1 acts on
raphe serotonergic neurons to promote sleep.
• SRSs also act locally in the cortex to enhance sleep phenotypes.

Adenosine
A1 A2
Inhibitory Excitatory
Widely distributed both in pre
and post synaptic neurons
Striatum and Nucleus Accumbens
Inhibits wake promoting activities
in basal forebrain
Modulates neural output of Basal
Ganglia
Promotes the sleep promoting
activity of VLPO
Receptors important in sleep are A1, A2a and A2b

Silvani A, Cerri M, Zoccoli G, Swoap SJ. Is Adenosine Action
Common Ground for NREM Sleep, Torpor, and Other
Hypometabolic States? Physiology (Bethesda). 2018 May
1;33(3):182-196.
Adenosine may thus act as a “retaliatory
metabolite” that is released by cells to
retaliate against stimuli that would cause
excessive ATP breakdown.

Mechanism of action of Adenosine A1R
Adenosine release with neuronal/glial activity
↓
Adenosine feedback on presynaptic terminal and inhibit release of
glutamate
↓
Increases the G1RK channel conductance and produces
hyperpolarization.
↓
Functional deafferentation of thalamic and cortical neurons
↓
Induces slow wave sleep (SWS)

Krueger JM, Frank MG, Wisor JP, Roy S. Sleep function: Toward
elucidating an enigma. Sleep Med Rev. 2016 Aug;28:46-54.
Postsynaptic Action – A1R
Scales down the post synaptic
activity.
Post synaptic scaling is
dependent on amount of ATP
triggered by presynaptic
activity.

Lazarus, M., Huang, Z.-L., Lu, J., Urade, Y., & Chen, J.-F. (2012). How do the basal ganglia regulate
sleep–wake behavior? Trends in Neurosciences, 35(12), 723–732
A2R Receptors – NAc Model

Process C – Circadian Rhythm
• Endogenous process - sleep timing and duration of daily
sleep–wake cycles.
• Predictable patterns of circadian troughs and circadian nadirs
throughout the 24-hr day.

• The master circadian “clock” that controls sleep–wake
patterns is in the suprachiasmatic nucleus (SCN) in the
ventral hypothalamus.
• Slave “circadian clocks” control various physiologic
system in the body (e.g., cardiovascular reactivity, hormone
levels, renal and pulmonary functions).

• The human circadian clock is
slightly longer than 24 hr.
• Intrinsic circadian rhythms must be
synchronized or “entrained” to the
24-hr-day cycle by environmental
cues called “zeitgebers.”

Molecular Clockwork - SCN

Melatonin acts via the MT1 and
MT2 receptors
• Through MT1 it inhibits Adenyl
cyclase and induce sleepiness
• Through MT2 receptors help to
synchronize with light dark
cycles.

Two process model – Summary
• A “sleep deficit” that slowly builds up without sleep and
dissipates with sleep
• A circadian rhythmicity in arousal.
• The difference between these processes reflects the sleep
drive.

68
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

69
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Brain stem areas regulating sleep/wake
Wake-promoting arousal systems and sleep-generating
neuronal mechanisms are responsible for wakefulness, REM
sleep and NREM sleep.

Wake Promoting Areas
The reticular activating system in the brain stem and
hypothalamus is a key component of the ascending arousal
system.

• Neurons in the reticular formation send excitatory projections to
the thalamus and hypothalamus, which in turn contributes to
global cortical activation in wakefulness.
• Conversely, there is a rapid decline in neuronal activity in all the
involved arousal systems just prior to or at sleep onset.

Wake Promoting Regions
• Locus Cerulus – Noradrenergic
• Raphe Magne - Serotonergic
• VPAG, VT - Dopaminergic
• Tuberomammillary Nucleus - Histaminergic
• Parabrachial Nucleus - Glutamatergic
• Lateral Hypothalamus - Orexinergic
• PPT and LDT – Cholinergic

Lateral Hypothalamus – Orexin
• Hypocretin 1 (Hcrt1) and hypocretin 2 (Hcrt2), also known as
Orexin A and Orexin B, respectively.
• Hcrt1 can attach to both Hcrt1 and 2 receptors, whereas Hcrt2
attaches only to Hcrt2 receptors.

• Orexin neurons send excitatory projections
• Dorsal raphe nucleus (Hrct1 and Hcrt2 receptors)
• Locus coeruleus (Hcrt1 receptors)
• Tuberomammillary nucleus (Hcrt2 receptors)
• In turn, they send inhibitory projections to Hcrt neurons.
• It appears to stabilize transitions between wake and sleep.

Sleep Promoting Regions
• Ventrolateral Preoptic (VLPO)
• Parafacial Nucleus (PZ)
• Nucleus accumbens core
• GABAergic

Wake/ Sleep - The flip–flop and bistability
The relationship between the VLPO and the major
monoamine groups concerned with wake appears to be
reciprocal.

• This reciprocal relationship is like
a type of circuit - ‘flip–flop’.
• Create a feedback loop that is
bistable.
• Only two possible stable patterns
of firing - tendency to avoid
intermediate states.
Saper CB, Chou TC, Scammell TE. The sleep switch: hypothalamic control
of sleep and wakefulness. Trends Neurosci. 2001 Dec;24(12):726-31.

Recent studies have shown that the orexin/hypocretin neurons
might influence both sides of the flip–flop circuit
• By direct projections to both the monoaminergic and
cholinergic arousal cell groups
• Projections to the VLPO region.

• Orexin/hypocretin neurons - ‘finger’,
pressing the flip–flop switch into the
‘wakeful’position preventing
inappropriate switching into the
‘sleep’position.
• Loss of orexin neuyrons - the switch
would be less stable, and more
susceptible to sudden and
inappropriate transitions. Narcolepsy

Control of REM and NREM Sleep
• REM on neurons in the Lateral
Dorsal Tegmentum (LDT) and
Pedunculopontine Tegmentum (PPT)
are inhibited during wake and NREM
by LC, DRN, TMN.
• During REM Sleep, these areas are
silent disinhibiting the REM ON
neurons

Control of REM and NREM Sleep
• These neurons activate
cholinonergic neurons in the
medial medulla and ultimately
inhibit motor neurons (atonia
of REM Sleep)
Berry, R. B. Fundamentals of Sleep Medicine. United
Kingdom: Elsevier Health Sciences. 2011

• A- The REM ON cells have positive
feedback, hence activity grows.
• D- This activity excites REM OFF cells.
• B – The REM off then inhibits the REM ON
population terminating REM episodes.
• C – The REM off have negative feedback
and as the REM off activity diminishes, the
REM ON is released from inhibition.
• Another REM episode occurs
Reciprocal Interaction Model of REM Sleep
Berry, R. B. Fundamentals of Sleep Medicine. United

88
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

89
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Polysomnography
• It is the continuous monitoring and simultaneous recording of
the physiological activities during sleep.
• Simultaneous recording of
• Sleep Staging
• Eye Movements
• Electromyographic Tone
• Respiratory Parameters
• Electrocardiogram

Routine indications – PSG
1. Diagnosis of sleep related breathing disorders (SRBDs)
2. Positive Airway Pressure titration in patients with SRBDs
3. Assessment of treatment results
4. With Multiple Sleep Latency Test (MSLT) in evaluation of suspected
narcolepsy.
5. Evaluating SRBDs that are violent or otherwise potentially injurious to
patients and others
6. Atypical or unusual parasomnias

Parameter Sensors Purpose
Electroencephalography Frontal, central, occipital leads
with mastoid process reference
lead
Stage sleep, detect epileptiform activity
Electrooculography Outer canthi leads with mastoid
process reference lead
Stage sleep (specifically stage R)
Electromyography Submental surface electrodes,
Anterior tibial surface electrodes
Stage sleep (specifically stage R), detect
REM without atonia, detect periodic limb
movements and other movement
abnormalities
Airflow Nasal cannula
pressure transducer
Oronasal thermal
sensor
PAP device (titration study)
Detection of hypopneas
Detection of apneas
Snoring Microphone, piezoelectric sensor Detect snoring
Otolaryngol Clin North Am. 2020 Jun;53(3):367-383

Respiratory effort Chest and abdomen respiratory
inductance plethysmography
belts
Classify respiratory events as
obstructive, central, or mixed
Arterial
oxygen
saturation
Pulse oximetry Detect hypoxemia
Ventilation End-tidal PCO2 or transcutaneous PCO2
monitoring
Detect hypoventilation
Electrocardiogram Modified lead II Monitor cardiac rate and rhythm
Position Accelerometer, video monitors Detect position
Behaviour Audio, video monitors Detect parasomnias, abnormal behaviors,
seizures
Otolaryngol Clin North Am. 2020 Jun;53(3):367-383

Not shown - SpO2 lead and 2 leg EMG leads Arch Dis Child Educ Pract Ed. 2020 Jun;105(3):130-135

Types of monitors
Types
Type I In laboratory, technologist attending PSG
Usual channels : EEG, EOG, chin EMG, ECG, airflow, respiratory
effort and Spo2 (minimum of 7 channels as per AASM criteria)
Type II Unattended polysomnography (minimum of 7 channels, as above)
Type III Portable monitoring with three or more channels, including pulse
oximetry and heart rate (minimum of 4 channels, including
respiratory movement, airflow, heart rate, SpO2)
Type IV Portable monitoring with only one or two channels, including
pulse oximetry

Electroencephalogram
• International 10-20 System.
• A minimum of 3 EEG derivations are required - frontal, central and
occipital regions.
• M1 and M2 refer to the left and right mastoid process.
• The recommended derivations are F4-M1, C4-M1 and O2-M1
• Backup electrodes should be placed at F3, C3, O1 and M2.

Electroencephalogram
The AASM manual for the scoring of sleep and associated events,2018

Electrooculogram
• Recording of the movement of the corneo‐retinal potential
difference, not the movement of eye muscle.
• The recommended EOG derivations are E1-M2 (E1 is placed 1cm
below the left outer canthus) and E2-M2 (E2 is placed 1 cm above
the right outer canthus) Right out and up / Left out and down
E1
E2

• The acceptable derivations are E1-Fpz and E2-Fpz
• Vertical movements will show in phase deflections and
horizontal eye movements out of phase deflections.

Eye movement patterns
Fundamentals of sleep medicine

Electromyogram
A- reduction in chin EMG
C-rapid eye movements

Electrocardiogram
Single modified
lead II electrode
and torso electrode

Limb movements
Tibialis anterior
Extensor digitorum superficialis
Extensor digitorum communis

Other sensors
• Airflow Signal
• Respiratory effort signals
• Oxygen saturation
• Body position

Epochs
• Sleep Staging
• Score sleep stages in 30s, sequential epoch commencing at the start
of the study
• Assign a stage to each of the epoch
• If 2 or more stages coexist during a single epoch, assign the stage
comprising the greatest portion of the epoch.
• Respiratory events- 2min / 5min epoch
• EEG arousals- 30s epoch

SLOW WAVE SLEEP
OR
DEEP SLEEP
111

Wakefulness – W (Eyes open)
EEG → high-frequency, low-voltage activity (chiefly beta and alpha
frequencies) without the rhythmicity of alpha rhythm ⇒ indicative of
the unique activity of individual cortical neurons
EOG → Rapid eye movements (initial deflection is less than 500ms)
and eye blinks (vertical movements 0.5–2 Hz), Reading eye
movements
EMG → Chin EMG relatively increased compared with that during
sleep. moderate and variable muscle tone with muscle artifact (high-
frequency activity)
113

Wakefulness –W (Eyes closed)
● EEG → Rhythmic waves in the alpha range (8–13 Hz),
particularly over the occipital region
● EOG → Slow eye movements (SEMs) may be present
● EMG → Chin EMG activity is variable and relatively high
● Transition phase includes Alpha rhythm and Low Amplitude Mixed
Frequency waves (LAMF) with SEMs

• Time with the patient disconnected from the recording
equipment should be scored as Stage W
• Brief episodes of sleep during this time are not considered
significant for stage scoring summary.

Drowsy (before sleep onset) alpha waves, seen in EEG leads (red rectangle), occupy greater than 50% of the 30-second
epoch
Otolaryngol Clin North Am. 2016 Dec;49(6):1307-1329

N1
• Drowsy to transitions into light N1 sleep, consciousness begins to fade,
but the individual may still be awakened by minimal stimulation
• EEG → slows and shows low-amplitude mixed-frequency (LAMF) activity
(4-7 Hz) activity (more than 50% of epoch) + absence of sleep
spindles (SSs) and K complexes (KCs) not associated with arousal
• EOG → Slow roving eye movements
• EMG → less activity

Stage N1, sleep onset. Alpha waves (red rectangle) are less than 50% of the 30-second epoch

N2
• Sleep deepens and there is a further lack of sensitivity to
activation and arousal
• EEG- Low Amplitude Mixed Frequency (LAMF) - Slow activity in
the theta (0.5−4 Hz)
• Arises from cortico-cortical electrophysiological interactions

● Sleep spindles
• 10-16 Hz waxing and waning EEG oscillations lasting 1-2
seconds, typically with a gradual onset and offset
• Arise from and cortico-thalamic electrophysiological interactions
→ Opening of low-threshold Ca2+ channels, which drive a burst
of Na+ spikes in the thalamocortical neurons
• K Complexes - Large, single, biphasic slow waves

Sleep Spindle: A train of distinct waves with frequency 11-16 Hz
with a duration of ≥ 0.5 seconds usually maximal in amplitude using
central derivations

K Complex: A well delineated negative sharp wave immediately
followed by a positive component standing out from the
background EEG, with total duration ≥ 5 seconds, usually maximal
in amplitude when recorded using frontal derivations

N3
• Deep sleep - Activation and arousal occurs only if stimulus is strong
When awakened, does not report of dreams
• EEG
• Abundant, high-voltage very slow delta waves → slow wave
activity (delta 0.5-4 Hz) , ≥ 20% of epoch
• Generally unconscious of the world around them as the slow
cortical activity disrupts information processing
• Chin EMG → variable but typically less than during wake

Stage N3 or slow-wave sleep: numerous delta waves.

R
• EEG
• Rapid, low voltage waves resembling alert, awake state
• Without KCs and SS
• As brain is highly active → metabolism increased by 20% -
Paradoxical
• Ponto Geniculo-occipital spikes (PGO) spikes
• EOG → rapid eye movements
• EMG → low chin EMG tone (activity)

Stage REM.REMs on the top 2 lines and low tone on chin EMG on the bottom line

Arch Dis Child 2009; 94:63–69.
Hypnogram

Hypnogram
• Compressed graphic summary of entire sleep study
• Representation of multiple variables :
• Sleep stages
• Respiratory events
• Positive airway pressure (if used)
• Motor movements
• Oximetry
• End-tidal or transcutaneous CO2,
• Heart rate variability measures
• Electroencephalographic power spectrum
• Body position
Atlas of sleep medicine

Apnea
• Drop in peak signal
excursion by ≥ 90% of
pre- event baseline
using an oronasal
thermal sensor
• Duration of ≥ 90% drop
in sensor signal lasts
≥10 seconds

Fundamentals of sleep medicine
Central sleep apnea
Obstructive sleep apnea
Mixed sleep apnea

Score an apnea as an obstructive apnea if:
• it meets apnea criteria and
• is associated with continued or increased inspiratory effort
throughout the entire period of absent airflow.
Score an apnea as a central apnea if:
• is associated with absent inspiratory effort throughout the entire
period of absent airflow.
Score an apnea as a mixed apnea if :
• is associated with absent inspiratory effort in the initial part of the
event, followed by resumption of inspiratory effort in the second
part of the event.

Hypopnea
Score a respiratory event as a hypopnea if all of the following criteria
are met:
• The peak signal excursions drop by ≥ 30% of pre-event baseline
using nasal pressure
• The duration of ≥30% drop in signal excursion is 10 seconds.
• There is a ≥3% desaturation from the pre-event baseline or the
event is associated with an arousal.

Critical limb movements
Placement of electrodes on anterior tibialis muscle for monitoring limb
movements
Movements + muscle artefact obscuring the EEG for more than half
of each epoch to the extent that sleep stage cannot be determined
Major Body movements

137
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

138
Overview
● Introduction
● Sleep Cycle
● Polysomnography
● Summary

Summary
1. Sleep is ubiquitous phenomenon across phylogeny whose functions
remain partly unelucidated.
2. Sleep is an active process involving the coordinated interaction of
various regions of the brain unlike what was believed in the 1950s.
3. AASM Criteria for Sleep Staging – W, N1, N2, N3 and R
4. The Two-process theory of sleep helps to understand the roles of
homeostatic mechanism and circadian rhythm in bringing about sleep.
139

5. The flip flop mechanism of both sleep/wake and NREM/REM is
important for stable states of sleep preventing intermediate states
as seen in narcolepsy.
6. Polysomnography serves as window to peek into the sleep, its
stages and the associated physiological changes, if deranged can
have several pathological implications.
7. Finally, as much as there are known areas, there is a wide avenue
of unknown areas - opportunities a clinical neurophysiologist.

References
1. Kryger, M. H., Roth, T., Goldstein, C. A. Kryger's Principles and Practice of Sleep
Medicine, Seventh Edition. Netherlands: Elsevier Health Sciences. 2021
2. Berry, R. B. Fundamentals of Sleep Medicine. United Kingdom: Elsevier
Health Sciences. 2011
3. AASM Manual for the scoring of sleep and associated events, 2018
4. Kandel, E. R., Principles of Neural Science, Sixth Edition. Greece: McGraw-
Hill Education. 2021
5. Barrett, D. K. E., Barman, S. M., Yuan, J., Brooks, H. L. Ganong's Review of Medical
Physiology, Twenty Sixth Edition. United States: McGraw Hill LLC. 2019
6. Hall, J. E. Guyton and Hall Textbook of Medical Physiology, 14th Edition. United
7. Saper CB, Chou TC, Scammell TE. The sleep switch: hypothalamic control of sleep and
wakefulness. Trends Neurosci. 2001 Dec;24(12):726-31.
8. Lazarus M, Oishi Y, Bjorness TE, Greene RW. Gating and the Need for Sleep: Dissociable
Effects of Adenosine A1 and A2A Receptors. Front Neurosci. 2019 Jul 17;13:740.
9. Kumar, V.M. Sleep is neither a passive nor an active phenomenon. Sleep Biol. Rhythms 8,
163–169 (2010).

THANK YOU !
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Physiology of sleep and polysomnography

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