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Chapter 1. Why We Sleep: Structure, Function, and Sleep Deprivation Free To View

Teofilo L. Lee-Chiong, MD, FCCP
DOI: 10.1378/smbr.4th.1
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Objectives 
  • Understand the various neural processes that control sleep and wakefulness

  • Describe the physiologic changes (eg, respiratory, cardiovascular, GI, genitourinary, and endocrine) that occur during sleep

  • Identify the consequences of sleep deprivation

  • Understand the new American Academy of Sleep Medicine recommendations for scoring sleep

Sleep is a complex reversible state characterized by behavioral quiescence, as well as diminished responsiveness to external stimuli. The sleep state is generated and maintained by CNS networks using specific neurotransmitters located in specific areas of the brain.

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Function of Sleep

A grand unified theory explaining the function of sleep remains elusive.13 The scope of such a theory on the purpose of sleep should take into account its function in several areas, including (1) function across geologic history (circadian influences); (2) function across different species (phylogeny [nocturnal vs diurnal species]); (3) function across the lifespan of an individual (ontogeny); (4) function in diverse geographic areas (equatorial vs polar); (5) function of specific sleep stages (non-rapid eye movement [NREM] vs rapid eye movement [REM]); (6) function of components of specific sleep stages (eg, dreaming, penile tumescence, REM); and (7) function of sleep's effects on organ systems and processes (eg, cardiovascular, thermoregulation).

Three basic approaches have been used in understanding the function of sleep, namely, comparative physiology between sleep and wakefulness, the effects of sleep deprivation (total or selective) on physiologic processes, and the effects of sleep enhancement. It appears unlikely that sleep has no function at all (ie, an evolutionary error), given its complexity. Partial theories of sleep function have included (1) restorative and somatic growth theory (facilitation of anabolic processes, and growth hormone release during N3 sleep); (2) metabolic theory (regulation of body temperature, energy conservation, or removal of “toxins” generated during wakefulness); (3) survival theory (protective and adaptive behavior or immune defense function); and (4) neural growth and processing (neuronal synaptic plasticity, brain development, restoration, learning, and memory consolidation).

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Control of Sleep and Waking

Two intrinsic processes interact to regulate the timing of sleep and wake, namely, sleep homeostasis, which is dependent on the sleep-wake cycle, and the circadian rhythm that is independent of the sleep-wake cycle.4,5 These two processes influence sleep latency, duration, and quality. The timing of sleep is also determined by behavioral influences.

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Sleep Homeostasis

Sleep homeostasis is defined as the increase in sleep pressure that is related to the duration of previous wakefulness. This sleep pressure declines with sleep.

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Circadian System

The main role of the circadian system is to promote wakefulness during the day. There are two circadian rhythm-related peaks in wakefulness (late morning and early evening) and two periods of circadian troughs in alertness (early morning and early-midafternoon).

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Circadian Timing Systems

The suprachiasmatic nucleus is the master circadian rhythm generator in mammals.6 It is likely that other anatomic sites also harbor endogenous clocks. The activity of the suprachiasmatic nucleus is independent of the environment and fires more frequently during the daytime than at night. Actions of the suprachiasmatic nucleus include promotion of wakefulness during the day and consolidation of sleep during the night. Ablation of the suprachiasmatic nucleus results in random distribution of sleep throughout the day and night and reduction in duration of waking periods (in some).

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Neural Control of Sleep

Wake, NREM sleep, and REM sleep are each generated and maintained by different neurons and neural networks using specific neurotransmitters. Activity of aminergic neurons is increased during the wake state and decreases during both NREM and REM sleep. On the other hand, activity of cholinergic neurons is increased during both wake and REM sleep and is reduced during NREM sleep.79

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Sleep and Wake Neurotransmitters

The main neurotransmitters involved in the generation of wake include acetylcholine, dopamine, glutamate, histamine, hypocretin (orexin), norepinephrine, and serotonin. Main neurotransmitters involved in the generation of sleep include acetylcholine (REM sleep), adenosine, gamma-aminobutyric acid (GABA), and glycine.

Acetylcholine is the main REM sleep neurotransmitter, whereas GABA is the main NREM neurotransmitter. Acetylcholine is both a wake and REM sleep neurotransmitter; its neurons are located primarily in the basal forebrain and pedunculopontine tegmentum and laterodorsal tegmentum in the brainstem. Acetylcholine is responsible for cortical EEG desynchronization during wake and REM sleep. Adenosine is a sleep neurotransmitter; its neurons are located primarily in the basal forebrain. Levels of adenosine progressively increase during prolonged wakefulness (homeostatic sleep drive) and decrease during sleep. Adenosine receptor blockers (eg, caffeine) increase wakefulness. Dopamine is a wake and REM sleep neurotransmitter; neurons are located primarily in the substantia nigra and ventral tegmental area of the brainstem.8 Amphetamines enhance wakefulness, in part, by increasing the release of dopamine.

GABA is a sleep neurotransmitter and is the main CNS inhibitory neurotransmitter; its neurons are located primarily in the ventrolateral preoptic area, thalamus, hypothalamus, basal forebrain, and cerebral cortex. Barbiturates, benzodiazepines, and nonbenzodiazepine benzodiazepine receptor agonists (eg, eszopiclone, zaleplon, zolpidem) act via the GABA-A receptor, whereas gamma-hydroxybutyrate (sodium oxybate) acts via the GABA-B receptor. Glutamate is the main CNS excitatory neurotransmitter. Glycine is the main inhibitory neurotransmitter in the spinal cord and is responsible for hyperpolarization (inhibition) of spinal motoneurons that causes REM sleep-related muscle atonia/hypotonia. Histamine is a wake neurotransmitter; its neurons are located primarily in the posterior hypothalamic tuberomammillary nucleus.9 First-generation histamine-1 receptor blockers cause sedation.

Hypocretin (orexin) is another wake neurotransmitter. Hypocretin neurons are located primarily in the lateral hypothalamic perifornical region, and dysfunction of this system is associated with narcolepsy-cataplexy. Norepinephrine is a wake neurotransmitter whose neurons are located primarily in the locus ceruleus. Catecholamine agonists, such as isoproterenol, enhance arousal and wakefulness. Finally, serotonin is a wake neurotransmitter, and its neurons are located primarily in the raphe nuclei and thalamus.

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Physiology During Sleep

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Autonomic Nervous System

Compared with that in the wake state, there is a reduction in sympathetic activity and an increase in parasympathetic activity during NREM sleep. There is a further decrease in sympathetic activity, as well as an increase in parasympathetic activity, during REM sleep compared with NREM sleep. Transient increases in sympathetic activity may develop during phasic REM sleep.

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Respiratory System

Respiration is under both metabolic (ie, pH, Pao2, and Paco2) and behavioral control during wakefulness. Behavioral influences are lost during sleep in which only metabolic control is present. Both hypoxic and hypercapnic ventilatory responses decrease during NREM sleep compared with that during wake and decrease further during REM sleep. There appear to be gender differences in hypoxic ventilatory responses, with a reduction in drive from wake to sleep in men but a similar drive during wake and NREM sleep in women.

During sleep compared with wakefulness, Pao2 falls by approximately 2 to 12 mm Hg, arterial oxygen saturation (Sao2) drops by 2%, and Paco2 rises by 2 to 8 mm Hg. Upper airway dilator muscle tone and activity of accessory muscles of respiration progressively fall during NREM and REM sleep compared with that in wakefulness. Tidal volume, minute ventilation, and ventilatory response to added inspiratory resistance also decrease during sleep compared with that in wakefulness.

Respiratory patterns often change during sleep, with periodic breathing and episodes of hypopneas and hyperpneas developing during stage N1 sleep. Respiration stabilizes with a regular frequency and amplitude of respiration during N3 sleep. An irregular pattern of respiration with variable respiratory rates and tidal volumes typically characterizes REM sleep. Central apneas or periodic breathing may occur during phasic REM sleep.

The upper airway acts much like a collapsible cylinder, with flow through it determined by the difference in upstream (ie, nasal) vs downstream pressure, as well as by airway resistance. Thus, airflow is greater with higher upstream pressure, lower downstream pressure, and decreased airway resistance. The patency of the upper airway is dependent on the balance of factors that either maintain airway opening (activation of dilator muscles) or promote airway closure (reduction in intraluminal extrathoracic airway pressure).

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Cardiovascular System

During NREM sleep, there is a decrease in heart rate, reduction in cardiac output, lowered BP, and either a reduction or no change in systemic vascular resistance compared with levels during wakefulness. Tonic REM sleep is associated with further reductions in heart rate, cardiac output, BP, and systemic vascular resistance compared with that in NREM sleep. In contrast, heart rate, cardiac output, BP, and systemic vascular resistance all increase during phasic REM sleep compared with that in NREM and tonic REM sleep, as well as during awakenings, the latter due to enhanced sympathetic tone. Nighttime systolic BP is commonly about 10% less than daytime systolic BP, referred to as the dipping phenomenon.

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GI System

Sleep is associated with a decrease in swallowing rate, diminished salivary production, and reduced esophageal motility. There is a circadian rhythmicity in basal gastric acid secretion, which peaks between 10:00 pm and 2:00 am and has a nadir between 5:00 am and 11:00 am. A decrease in intestinal motility (ie, migrating motor complex) and motor tone occurs during sleep.

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Renal System

Sleep is associated with an increase in water reabsorption, reduced glomerular filtration, and increase in renin release, which, collectively, reduces urine volume.

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Genitourinary System

Penile tumescence in men and clitoral tumescence and vaginal engorgement in women can occur during REM sleep.

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Endocrine System

Although release of growth hormone occurs primarily during N3 sleep, growth hormone secretion can also occur without N3 sleep, such as during a relaxed supine position. There is typically one peak in growth hormone secretion at sleep onset in men, whereas several peaks in growth hormone secretion occurring throughout the day and night may be seen in women. Sleep deprivation may suppress growth hormone secretion. Secretion of prolactin increases during N3 sleep and decreases during REM sleep; its secretion is suppressed by sleep fragmentation. Prolactin secretion is also influenced by circadian rhythms during wakefulness, with lower levels at noon and higher levels in the evening.

Thyroid stimulating hormone secretion is linked to both sleep and circadian rhythms; levels are low during the daytime, with a nadir between 10:00 am and 7:00 pm and increase during the night from 9:00 pm to 6:00 am, peaking prior to sleep onset. Thyroid stimulating hormone secretion is inhibited by sleep, particularly N3 sleep, and increases with awakenings and sleep deprivation. Thyroid hormone levels decrease at night.

Levels of parathyroid hormone increase during sleep.

Cortisol secretion is linked primarily to the circadian rhythm rather than to sleep. Levels of cortisol begin to rise about 2 h prior to awakening, with peak levels at 8:00 am to 9:00 am; thereafter, cortisol levels decline, with a nadir at 12:00 am. Sleep, especially N3 sleep, suppresses cortisol secretion. Secretion of cortisol increases during prolonged awakenings of > 20 min.

Levels of melatonin rise in the evening. Peak levels occur in the early morning between 2:00 am and 5:00 am; levels decline thereafter, even if no sleep occurs during the night. Synthesis and secretion of melatonin are suppressed by light exposure.

Secretion of testosterone is primarily linked to sleep. Levels increase during sleep, particularly in young adult men. Peak levels occur about 90 min prior to the first REM period.

Luteinizing hormone levels increase during sleep, mainly during NREM sleep, in adolescents and adult men. Luteinizing hormone secretion may remain unchanged or even decline during sleep in adult women, especially during the follicular phase of the menstrual cycle.

Antidiuretic hormone levels increase at night. The secretion of renin is linked to the NREM-REM sleep cycle, with greater secretion during NREM sleep; levels peak during stage N3 sleep. There is lower secretion during REM sleep. Levels are increased during recovery sleep following sleep deprivation.

Insulin levels are decreased during sleep. Insulin levels are higher in NREM sleep compared with that in REM sleep.

Insulin resistance may develop during sleep deprivation. Leptin is released from peripheral adipocytes and is involved with the regulation of energy balance, primarily by reducing appetite. Secretion of leptin is influenced by both sleep and circadian rhythms, with greater secretion at night. Highest levels are from 12:00 am to 4:00 am; lowest levels, from 1:00 pm to 2:00 pm. Secretion of leptin declines during sleep restriction.

Ghrelin stimulates appetite and increases food intake; levels increase at night. In summary, levels of growth hormone are increased and levels of cortisol and adrenocorticotropic hormone decrease during the first half of the sleep period. Conversely, during the second half of the sleep period, there are lower levels of growth hormone and higher levels of cortisol and adrenocorticotropic hormone.

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Musculoskeletal System

Skeletal muscle relaxation, either hypotonia or atonia, and inhibition of deep tendon reflexes occur during sleep.

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Pupillary Changes

Pupillary constriction is seen during NREM and tonic REM sleep, whereas pupillary dilatation occurs during phasic REM sleep.

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Immunity

Proinflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α, enhance sleep. Specifically, they increase NREM sleep and delta EEG waves. Conversely, levels of IL-1β and TNF-α increase during sleep. IL-1β and TNF-α act via nuclear factor-κβ; IL-1β and TNF-α increase, and are increased by, nuclear factor-κβ in a positive-feedback-loop fashion. Nuclear factor-κβ, in turn, promotes sleep by enhancing nitric oxide synthase. Antiinflammatory cytokines, such as IL-4, IL-10, and transforming growth factor-β, suppress sleep. Acute infectious and inflammatory processes can give rise to sleepiness.

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Thermoregulation

Neurons in the preoptic and anterior hypothalamus are involved with thermoregulation. Activity of warmth-sensing neurons increases during sleep and decreases during the wake state; activity of cold-sensing neurons, on the other hand, decreases during sleep and increases during wakefulness. Core body temperature peaks in the late afternoon and early evening (6:00 pm to 8:00 pm) and falls at the onset of sleep. Temperature nadir occurs about 2 h prior to the usual wake time (4:00 am to 5:00 am).

Changes in thermoregulation occurring during sleep include (1) fall in core body temperature; (2) decline in thermal set point; (3) reduced thermoregulatory responses to thermal challenges (lower during REM sleep compared with NREM sleep); (4) decrease in metabolic heat production; (5) loss of heat production from shivering during REM sleep; and (6) increased heat loss due to sweating and peripheral vasodilatation.10

Sleep latency and architecture are influenced by changes in body temperature at bedtime. Exposure to extreme hot or cold environmental temperatures suppresses sleep onset and causes sleep disruption. Nocturnal sleep typically occurs during the falling phase of the temperature rhythm after maximum core body temperature. Awakening, on the other hand, occurs during the rising phase of the temperature rhythm after minimum core body temperature.

Initiating sleep during the falling phase of the temperature rhythm results in a shortened sleep-onset latency and increases both total sleep time and stage N3 sleep. In contrast, initiating sleep during the rising phase of the temperature rhythm will produce a more prolonged sleep onset latency, decrease in total sleep time, reduced stage N3 sleep, and increase in REM sleep.

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Metabolism

Metabolic rate decreases during NREM sleep compared with that in the wake state. Metabolic rate during REM sleep is either similar to, or greater than, that during NREM sleep.

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Dreaming

Dreaming can occur during both REM sleep (accounts for 80% of dreams) and NREM sleep (20% of dreams). In contrast to REM-related dreams, which are generally more complex and irrational, NREM dreams tend to be simpler and more realistic.

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Sleep Deprivation

Vulnerability to sleep deprivation varies within individuals across time, as well as between individuals. Consequences of total sleep deprivation appear to differ from those resulting from chronic sleep restriction. Individuals often underestimate the negative impact of sleep deprivation on cognition and performance.

Sleep deprivation can give rise to greater morbidity, increased mortality (mechanism unknown), sleepiness, diminished vigilance, and, if severe, hypothermia.11

CNS effects of sleep deprivation consist of decreased pain tolerance, lower seizure threshold, hyperactive gag and deep tendon reflexes, nystagmus and ptosis, sluggish corneal reflexes, and decreased cerebral glucose metabolism in the subcortical frontal and midbrain regions.

The autonomic nervous system is also affected, with an increase in sympathetic activity. Cognitive performance is diminished, as is attention, working memory, executive functioning, information processing, and decision making. Response time is slowed. Children may present with hyperactivity.

Changes in the respiratory system during sleep deprivation include reductions in FEV1 and FVC. Ventilatory responsiveness is reduced.

Risk of coronary events is greater in persons whose total sleep time is habitually < 6 h. The endocrine system is also affected by sleep deprivation and often demonstrates the following changes: (1) increase in evening levels of cortisol and adrenocorticotropic hormone; (2) decrease in growth hormone level; (3) increase in ghrelin level; (4) insulin resistance with decreased glucose tolerance; (5) and reduced leptin activity.

Sleep deprivation can give rise to increased hunger and appetite, with a preference for salty, sweet, and starchy foods; with weight gain (although weight loss may develop during late stages of profound sleep deprivation due to higher metabolic rates); and with increased risk of obesity. An increase in IL-1, IL-6, C-reactive protein, and TNF-α can accompany sleep deprivation. Antibody titers to influenza and hepatitis A vaccination are reduced acutely, as is febrile response to endotoxin. Lowered resistance to infection can develop, with the presence of bacteria occasionally noted in sterile areas of the body.

Sleep deprivation has a negative impact on mood. Interestingly, remission of major depressive disorder can occur in up to 50% of patients. Finally, the frequency of medical errors and motor vehicle accidents increases with sleep deprivation.

During polysomnography, there is commonly a shortened sleep-onset latency and increase in total sleep time. Greater stage N3 sleep may be appreciated during the first recovery night after sleep deprivation, whereas REM sleep rebound often follows during the second night after sleep deprivation. Sleep architecture generally normalizes by the third night of recovery sleep. A shift to slower frequencies, such as theta and delta waves, can be seen during waking EEG. Animal models of sleep deprivation have demonstrated an increase in homeostatic sleep drive, failure of thermoregulation, weight loss despite increased food intake, increased norepinephrine levels, skin lesions, and eventually death during prolonged sleep deprivation.

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Polysomnography

Polysomnography consists of the continuous and simultaneous recording of several physiologic variables during sleep, including EEG, electrooculography (EOG), electromyography (EMG), ECG, airflow, snoring, thoracic and abdominal movement, and Sao2. Other sensors may also be used during polysomnography, such as esophageal pressure monitors, end-tidal carbon dioxide (PetCO2), transcutaneous carbon dioxide, positive airway pressure level, additional EEG channels for suspected nocturnal seizures, video monitoring, and esophageal pH sensors.

Diagnostic sleep studies have been classified into four levels based on the number of recorded channels. A level 1 study consists of an attended in-laboratory full polysomnography and is the “gold standard” for the diagnosis of obstructive sleep apnea. A level 2 study is an unattended full polysomnography or comprehensive portable polysomnography. A level 3 or cardiorespiratory sleep study consists of at least four bioparameters, such as airflow, Sao2, respiratory effort, ECG, and body position. Lastly, a level 4 study involves continuous one- or two-bioparameter recording, most commonly of Sao2 and airflow.

Polysomnography utilizes a polygraph device, which consists of a series of alternating-current and direct-current amplifiers and filters. High-frequency (fast) physiologic variables (eg, EEG, EOG, EMG, ECG) are recorded using alternating-current amplifiers, whereas low-frequency (slow) physiologic variables (eg, Sao2 and continuous positive airway pressure levels) are recorded using direct-current amplifiers. Airflow and respiratory effort are recorded using either alternating-current or direct-current amplifiers.

A derivation is the difference in voltage between two electrodes and can be either bipolar or referential. A bipolar derivation consists of two standard electrodes matched to each other. A referential derivation refers to a standard electrode matched to a reference electrode.

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Electroencephalography

Placement of EEG electrodes is based on the International 10-20 system. Each electrode is provided with a letter representing a region of the brain and a numeric subscript, namely, frontal (F), central (C), occipital (O) and mastoid (M). Odd numbers are given for left-sided electrodes, even numbers are used for right-sided electrodes, and the designation “z” is used for midline electrodes. According to the American Academy of Sleep Medicine (AASM),12 recommended electrode placements are F4M1, C4M1, and O2M1. Additional EEG electrodes can be placed if one is evaluating possible seizure activity.

The voltage recorded from EEG electrodes originates from the summed potential activity of cortical neurons, and the resultant waves can be classified, based on frequency, into delta (< 4 Hz), theta (4 to 7 Hz),47 α (8 to 13 Hz), and β (> 13 Hz). Delta waves have high amplitudes with a peak-to-peak height of > 75 microvolts (μV). On the other hand, amplitude of alpha waves is generally, < 50 μV in adults. Alpha waves can be detected when a person is relaxed and drowsy and eyes are closed; eye opening suppresses α activity. Alpha waves are most prominent in the occipital leads. Beta waves are present during alert wakefulness.

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EOG

EOG records the difference in potentials (dipole) between the cornea (positively charged) and the retina (negatively charged). This dipole changes with eye movements. A positive voltage (downward deflection) is recorded when the eye moves toward an electrode, and a negative voltage (upward deflection) accompanies an eye movement away from an electrode. The AASM-recommended12 electrode placements for EOG are E1M2 and E2M2, with E1 being 1 cm below the left outer canthus and E2 at 1 cm above the right outer canthus; M2 refers to the right mastoid process.

With this electrode arrangement, conjugate eye movements create out-of-phase deflections in the two EOG channels, and EEG artifacts produce in-phase deflections. There are two general patterns of eye movements, namely, slow rolling eye movements that occur during relaxed drowsiness with closed eyes, stage N1 sleep, or brief awakenings, and REMs that are seen during waking with open eyes (ie, eye blinks) or during REM sleep.

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EMG (Chin)

Three EMG leads are used; they are located (1) midline and 1 cm above the inferior edge of the mandible; (2) 2 cm to the right of midline and 2 cm below the inferior edge of the mandible; and (3) 2 cm to the left of midline and 2 cm below the inferior edge of the mandible. The electrode distances may be reduced to 1 cm for children.12 The derivation consists of either one of the electrodes below the mandible referred to the electrode placed above the mandible. Additional electrodes may be placed over the masseter muscle to detect bruxism.

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ECG

A single modified lead II is used for ECG. In this derivation, an electrode is placed below the right clavicle near the sternum and another electrode over the left lateral chest wall.

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Measuring Airflow

Techniques for measuring airflow consist of nasal pressure monitoring, pneumotachography, thermistors and thermocouples, or PetCO2 monitoring. According to the AASM, the oronasal thermal sensor is the recommended technique for identifying apneas, and the nasal air pressure transducer can be used as an alternative for adults. Either PetCO2 or summed calibrated inductance plethysmography can be used in children. Sensors for identifying hypopneas include the nasal air pressure transducer (recommended) and inductance plethysmography or oronasal thermal sensor (alternatives). With nasal pressure monitoring, obstructive respiratory events appear as a plateau (flattening) of the inspiratory flow signal, whereas central respiratory events are associated with reduced but rounded signals.

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Measuring Respiratory Effort

Techniques for measuring respiratory effort include esophageal pressure monitoring, surface diaphragmatic EMG, strain gauges, respiratory inductance plethysmography, and thoracic impedance. These techniques are important in distinguishing obstructive, central, and mixed apneas. The AASM-recommended12 sensors for measuring respiratory effort are esophageal manometry and inductance plethysmography.

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Measuring Oxygenation and Ventilation

The recommended sensor for Sao2 is pulse oximetry, whereas sensors for alveolar hypoventilation in children consist of transcutaneous carbon dioxide or PetCO2. Snoring can be detected using a microphone.

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EMG (Anterior Tibialis)

This sensor is used to detect periodic limb movements during sleep. Additional electrodes can be placed over the extensor digitorum communis to identify REM sleep behavior disorder.

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Scoring Sleep Stages

Polysomnographic data are divided into 30-s periods or epochs. The standard paper speed used for polysomnography is 10 mm/s, or 30 cm per epoch page. Each epoch is assigned a single sleep stage that comprises the greatest percentage of the epoch.

In the wake state, > 50% of epoch has alpha EEG waves over the occipital region with eye closure. If alpha waves are absent, wakefulness is defined by the presence of any of the following: conjugate vertical eye blinks, reading eye movements that consist of a conjugate slow movement followed by a rapid movement in the opposite direction, or voluntary rapid open eye movements. There is relatively high chin EMG tone.12

An epoch is scored as stage N1 if α EEG waves are replaced by low-voltage, mixed-frequency (4 to 7 Hz) waves that occupy > 50% of the epoch. In persons who do not generate α waves, stage N1 sleep starts with the presence of 4- to 7-Hz waves, with slowing of the background EEG activity by at least 1 Hz compared with that in the wake stage. Vertex sharp waves with a duration of < 0.5 s and that are maximal over the central region may be noted. Slow eye movements, but not REMs, can occur. There are no K complexes or sleep spindles in the EEG tracings. Tonic chin EMG levels are typically lower than those during relaxed wakefulness.12

The start of stage N2 sleep is defined by the presence of K complexes (not associated with arousals) or sleep spindles during the first half of the epoch or during the last half of the previous epoch if criteria for stage N3 sleep are absent. A K complex is a high-amplitude, biphasic wave with an initial sharp negative deflection immediately followed by a positive high-voltage slow wave, which has a duration of at least 0.5 s and is seen maximally over the vertex. Sleep spindles are brief oscillations with a frequency of 12 to 14 Hz, lasting 0.5 to 1.5 s and having an amplitude that is generally < 50 μV; they are more prominent over the central leads. Sleep spindles, which are generated in the midline thalamic nuclei, are seen during stages N2 and N3 sleep. The continuation of stage N2 sleep is defined by the presence of low-amplitude, mixed-frequency EEG rhythms, and if the epoch contains or is preceded by K complexes (not associated with arousals) or sleep spindles.12

In stage N3 sleep, at least 20% of the epoch is occupied by slow-wave (0.5 to 2 Hz and > 75 μV) EEG activity that is best appreciated over the frontal regions.12 Stage REM sleep is characterized by the presence of all of the following: (1) low-amplitude, mixed-frequency EEG activity; (2) REMs; and (3) low-chin EMG tone, which is either at its lowest level in the study or at least no higher than in the other sleep stages.12 The percentage of the different sleep stages in a typical adult is N1 (5%), N2 (45%), N3 (25%), and REM (25%) sleep.

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Definitions of Polysomnographic Parameters

The following are definitions of some common polysomnographic parameters.

  1. Bedtime is the time when a person gets into bed and attempts to fall asleep.

  2. Final awakening is the time when a person awakens for the final time.

  3. Lights out is the time when sleep recording started.

  4. Lights on is the time when sleep recording ended.

  5. REM sleep latency refers to the time in minutes from the onset of sleep to the first epoch of REM sleep. REM sleep latency is about 60 to 120 min in healthy adults.

  6. Sleep efficiency is defined as the ratio of total sleep time to time in bed or (total sleep time × 100)/time in bed.

  7. Sleep onset latency is the time from lights out to sleep onset (ie, first epoch of any stage of sleep). Sleep-onset latency is generally < 15 to 30 min in healthy adults.

  8. Sleep-onset REM period refers to the occurrence of REM sleep within 10 to 15 min of sleep onset.

  9. Time in bed is the duration of monitoring between “lights out” to “lights on.”

  10. Total sleep time is determined by adding all sleep stages (ie, NREM stages 1 to 3 sleep plus REM sleep) in minutes.

  11. Wake time after sleep onset is the time spent awake from sleep onset to final awakening.

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References

Benington J.  Sleep homeostasis and the function of sleep.  Sleep 2001; 23:959–-966
 
Inoue S, Honda K, Komoda Y.  Sleep as neuronal detoxification and restitution.  Behav Brain Res 1995; 69:91–-96. [PubMed] [CrossRef]
 
Rechtschaffen A.  Current perspectives on the function of sleep.  Perspect Biol Med 1998; 41:359–-390. [PubMed]
 
Borbely AA, Achermann P.  Sleep homeostasis and models of sleep regulation.  J Biol Rhythms 1999; 14:557–-568. [PubMed]
 
Silver R, Lesauter J.  Circadian and homeostatic factors in arousal.  Ann N Y Acad Sci 2008; 1129:263–-274. [PubMed] [CrossRef]
 
Markov D, Goldman M.  Normal sleep and circadian rhythms: neurobiologic mechanisms underlying sleep and wakefulness.  Psychiatr Clin North Am 2006; 29:841–-853. [PubMed] [CrossRef]
 
Van Dort CJ, Baghdoyan HA, Lydic R.  Neurochemical modulators of sleep and anesthetic states.  Int Anesthesiol Clin 2008; 46:75–-104. [PubMed] [CrossRef]
 
Monti JM, Jantos H.  The roles of dopamine and serotonin, and of their receptors, in regulating sleep and waking.  Prog Brain Res 2008; 172:625–-646. [PubMed]
 
Haas HL, Sergeeva OA, Selbach O.  Histamine in the nervous system.  Physiol Rev 2008; 88:1183–-1241. [PubMed] [CrossRef]
 
Van Someren EJ.  Mechanisms and functions of coupling between sleep and temperature rhythms.  Prog Brain Res 2006; 153:309–-324. [PubMed]
 
Mullington JM, Haack M, Toth M, et al.  Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation.  Prog Cardiovasc Dis 2009; 51:294–-302. [PubMed] [CrossRef]
 
Iber C, Ancoli-Israel S, Chesson A, et al.,  for the American Academy of Sleep Medicine.  The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications. Westchester, IL: American Academy of Sleep Medicine,  2007;
 

References

Benington J.  Sleep homeostasis and the function of sleep.  Sleep 2001; 23:959–-966
 
Inoue S, Honda K, Komoda Y.  Sleep as neuronal detoxification and restitution.  Behav Brain Res 1995; 69:91–-96. [PubMed] [CrossRef]
 
Rechtschaffen A.  Current perspectives on the function of sleep.  Perspect Biol Med 1998; 41:359–-390. [PubMed]
 
Borbely AA, Achermann P.  Sleep homeostasis and models of sleep regulation.  J Biol Rhythms 1999; 14:557–-568. [PubMed]
 
Silver R, Lesauter J.  Circadian and homeostatic factors in arousal.  Ann N Y Acad Sci 2008; 1129:263–-274. [PubMed] [CrossRef]
 
Markov D, Goldman M.  Normal sleep and circadian rhythms: neurobiologic mechanisms underlying sleep and wakefulness.  Psychiatr Clin North Am 2006; 29:841–-853. [PubMed] [CrossRef]
 
Van Dort CJ, Baghdoyan HA, Lydic R.  Neurochemical modulators of sleep and anesthetic states.  Int Anesthesiol Clin 2008; 46:75–-104. [PubMed] [CrossRef]
 
Monti JM, Jantos H.  The roles of dopamine and serotonin, and of their receptors, in regulating sleep and waking.  Prog Brain Res 2008; 172:625–-646. [PubMed]
 
Haas HL, Sergeeva OA, Selbach O.  Histamine in the nervous system.  Physiol Rev 2008; 88:1183–-1241. [PubMed] [CrossRef]
 
Van Someren EJ.  Mechanisms and functions of coupling between sleep and temperature rhythms.  Prog Brain Res 2006; 153:309–-324. [PubMed]
 
Mullington JM, Haack M, Toth M, et al.  Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation.  Prog Cardiovasc Dis 2009; 51:294–-302. [PubMed] [CrossRef]
 
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