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Polysomnography
James D. Geyer, MD
Director, Sleep Program
Associate Professor of Neurology and Sleep Medicine
Alabama Neurology and Sleep Medicine
Tuscaloosa, Alabama
Paul R. Carney, MD
Wilder Professor and Chief
Division of Pediatric Neurology
Director, Comprehensive Pediatric Epilepsy Program
Departments of Pediatrics and Neurology
McKnight Brain Institute
University of Florida College of Medicine
Gainesville, Florida
Troy A. Payne, MD
Medical Director
St Cloud Hospital Sleep Center
St Cloud, Minnesota
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vi
Sleep medicine continues to evolve rapidly as a subspecialty 20 Hz may be sufficient; for rapidly varying signals, such as
with numerous disorders now recognized and an ever-changing EEG and EMG, the sampling rate must be much higher, usually
set of diagnostic criteria and protocols. As with any medical 250 Hz or more. If the sampling rate is inadequate, waveforms
discipline, accurate diagnosis is an essential prerequisite for are distorted and scoring and interpretation may be erroneous.
a rational approach to management. Polysomnography, the For example, if the sampling rate for eye movement channels is
recording of multiple physiologic functions during sleep, was too low, the sharp deflection associated with a rapid eye move-
developed in the 1970s and is the most important laboratory ment may appear as a slower deflection characteristic of a slow
test used in sleep medicine. Polysomnography complements eye movement.
the clinical evaluation and assists with diagnosis and manage- Because of the differences in signal acquisition and display
ment of a variety of sleep disorders.1 parameters, not all digital recordings have the same appear-
Digital amplifiers and computerized signal processing are ance. In addition, although transducers used for the recording
now the standard of care and provide many advantages over of EEG, EOG, and EMG are largely standardized, EEG and EOG
older analog amplifiers and paper recording. This is especially montages vary among laboratories. Furthermore, transducers
true for the evaluation of brief electroencephalographic (EEG) and recording techniques for the assessment of respiration dur-
transients such as epileptiform sharp waves and spikes and their ing sleep vary widely among sleep laboratories.2 For example,
differentiation from artifacts and benign EEG waveforms. This airflow can be monitored directly with a pneumotachograph,
section of the book has been significantly expanded. Digitized thermistor, or thermocouple or indirectly with the recordings
data can also be displayed using a variety of montages depend- of tracheal sound or by the summation of signals from tho-
ing on the purpose at hand; for example, the display can be racic and abdominal inductance recordings. Respiratory effort
limited to EEG, electro-oculogram (EOG), and chin electro- can be assessed with respiratory inductance plethysmography,
myogram (EMG) during sleep staging and then expanded to stretch sensitive transducers (strain gauges), diaphragmatic
include respiratory and leg movement channels during scoring EMG, intrathoracic (esophageal) pressure, or nasal pressure.
of these functions. Filters and sensitivities can be altered during Scoring of sleep stages has been standardized for many years3
review to assist with interpretation of the study. and has recently been updated.4 The new scoring and staging
While digital polysomnography provides a number of criteria are discussed in detail in the text and the waveforms are
advantages as described above, features related to signal acquisi- presented in appropriate chapters.
tion, display resolution, and printer resolution must be under- As a result of these variations, the overall appearance of the
stood by the technologist and the interpreter. For digital signal polysomnographic display may be markedly different from one
acquisition, the analog signal generated by the transducer must laboratory to the next. No atlas can provide examples of nor-
be converted to digitized information. A critical variable is the mal and abnormal polysomnography using all of the displays
rate at which the signal is sampled and digitized. For slowly and transducers used in accredited sleep laboratories. For this
varying signals, such as thoracic motion, a sampling rate of atlas, the illustrations were prepared from several sleep centers
vii
and electrodiagnostic/neurophysiology laboratories in order to 3. Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Tech-
introduce the reader to several of the possible formats. niques, and Scoring System for Sleep Stages of Human Subjects. Los Angeles:
Brain Information Service/Brain Research Institute, 1968.
This atlas is designed to aid the sleep medicine specialist 4. Iber C, Ancoli-Israel S, Chesson A, Quan SF. The AASM Manual for the
and those training in sleep medicine. It also serves as a refer- Scoring of Sleep and Associated Events: Rules, Terminology and Technical Speci-
ence and training tool for technologists. The atlas covers nor- fications. 1st Ed. Westchester, Illinois: American Academy of Sleep Medi-
mal polysomnographic features of wakefulness and the various cine, 2007.
stages of sleep as well as polysomnographic findings character-
istic of sleep-related breathing disorders, sleep-related move-
ments, and parasomnias. In addition, examples of cardiac
arrhythmias, nocturnal seizures, and artifacts are included.
A variety of time scales are used to illustrate their value.
REFERENCES
1. American Academy of Sleep Medicine. International Classification of Sleep
Disorders. 2nd Ed. Diagnostic and coding manual. Westchester, Illinois:
American Academy of Sleep Medicine, 2005.
2. Parisi RA, Santiago TV. Respiration and respiratory function: Technique
of recording and evaluation. In: Chokroverty S, ed. Sleep Disorders Medi-
cine: Basic Sciences, Technical Considerations, and Clinical Aspects. Boston:
Butterworth-Heinemann, 1994:127139.
Sleep medicine is a relatively new medical subspecialty that is to EEG, electro-oculogram (EOG), and chin electromyogram
rapidly expanding as the prevalence and importance of sleep (EMG) during sleep staging and then expanded to include
disorders have become apparent. As with any medical disci- respiratory and leg movement channels during scoring of these
pline, accurate diagnosis is an essential prerequisite for a ratio- functions. Filters and sensitivities can be altered during review
nal approach to management. Polysomnography, the recording to assist with interpretation of the study.
of multiple physiologic functions during sleep, was developed In addition to digital polysomnography, several other tech-
in the 1970s and is the most important laboratory test used nical advances have improved the diagnostic value of sleep
in sleep medicine. Polysomnography complements the clini- recordings. Polysomnography can be combined with video
cal evaluation and assists with diagnosis and management of a recording (video-polysomnography); the simultaneous analy-
wide range of sleep disorders.1 sis of behavior and polysomnographic findings assists with the
As the array of sleep diagnoses has expanded, the tech- diagnosis of parasomnias, nocturnal seizures, and other sleep-
niques and equipment used for sleep recordings have become related behaviors. To assist with the diagnosis of sleep-related
more sophisticated. While sleep studies in the 1970s used ana- breathing disorders, intrathoracic pressure can be monitored
log amplifiers and bulky paper recordings that rarely consisted with intraesophageal pressure sensors that are easily inserted
of more than eight channels, computer technology of the late and well tolerated. With the availability of 16 to 32 or more
1990s permits recording of dozens of channels using sensitive channels for a recording, esophageal pH, end-tidal carbon diox-
noninvasive or minimally invasive transducers, digital ampli- ide level, and transcutaneous CO2 monitoring can be included
fiers, electronic displays, and compact data storage on magnetic in selected situations without sacrificing standard channels.
or optical media.2 While digital polysomnography provides a number of
Digital amplifiers and computerized signal processing pro- advantages as described above, features related to signal acquisi-
vide many advantages over older analog amplifiers and paper tion, display resolution, and printer resolution must be under-
recording. For example, digitized data can be displayed using stood by the technologist and the interpreter. For digital signal
a compressed time scale that makes slow rhythms more read- acquisition, the analog signal generated by the transducer must
ily identifiable, such as the regular occurrence of periodic leg be converted to digitized information. A critical variable is the
movements at 20- to 30-second intervals. Alternatively, an rate at which the signal is sampled and digitized. For slowly
expanded time scale can be used that permits easier identifica- varying signals, such as thoracic motion, a sampling rate of 20
tion of brief electroencephalographic (EEG) transients such as Hz may be sufficient; for rapidly varying signals, such as EEG
epileptiform sharp waves and spikes and their differentiation and EMG, the sampling rate must be much higher, usually 250
from artifacts and benign EEG waveforms. Digitized data can Hz or more. If the sampling rate is inadequate, waveforms are
also be displayed using a variety of montages depending on distorted and scoring and interpretation may be erroneous. For
the purpose at hand; for example, the display can be limited example, if the sampling rate for eye movement channels is too
ix
low, the sharp deflection associated with a rapid eye movement performed in the University of Michigan Electrodiagnostic
may appear as a slower deflection characteristic of a slow eye Laboratory. The studies were recorded using digital equipment
movement. manufactured by the Telefactor Corporation (Conshohocken,
Display resolution is based on the characteristics of the PA). The montages, filter settings, sensitivities, and A-D sam-
computer, the display monitor, and the software used for data pling rates used to generate the displays are specified in the
acquisition and display. The array of pixels in the screen deter- Technical Introduction.
mines the maximum resolution; for example, a 1024 x 768 The illustrations were prepared based on 1600 x 1200
display provides lower resolution than a 1600 x 1200 display. screen displays and were printed with a Hewlett-Packard Laser
While the lower resolution display may be sufficient for the Jet printer on 8.5 x 11 inch paper at 600 dot per inch resolu-
assessment of slowly varying signals such as respiration, it may tion.
be inadequate for identification of rapid EEG transients. The EEG electrodes were placed according to the Interna-
Printer resolution is based on the characteristics of the tional 1020 system.
printer, computer, and software. In some cases, waveforms that The EOG electrodes were placed 1 cm superior and lateral
are not adequately displayed on the monitor can be better ana- to the right outer canthus and 1 cm inferior and lateral to the
lyzed if a high resolution printout is obtained. left outer canthus.
Because of the differences in signal acquisition and display One chin EMG electrode was placed on the chin (mental)
parameters, not all digital recordings have the same appear- and two electrodes were placed under the chin (submental).
ance. In addition, although transducers used for the recording The submental electrode placement is generally at the mandi-
of EEG, EOG, and EMG are largely standardized, EEG and EOG ble. Generally, there is a 3-cm distance between electrodes.
montages vary among laboratories. Furthermore, transducers The EKG was recorded with one electrode each placed 2 to
and recording techniques for the assessment of respiration dur- 3 cm below the left and right clavicles midway between the
ing sleep vary widely among sleep laboratories.3 For example, shoulder and the neck..
airflow can be monitored directly with a pneumotachograph, Many of the recordings also include the second EKG chan-
thermistor, or thermocouple or indirectly with the recordings nel recorded from a left leg EMG channel and a left ear elec-
of tracheal sound or by the summation of signals from thoracic trode.
and abdominal inductance recordings. Respiratory effort can be Airflow was recorded with a single channel nasal/oral ther-
assessed with respiratory inductance plethysmography, stretch mocouple from Pro-Tech (Woodinville, WA). This thermocou-
sensitive transducers (strain gauges), diaphragmatic EMG, ple has sensors for each nostril and another that is located over
intrathoracic (esophageal) pressure, or nasal pressure. Further- the mouth.
more, although scoring of sleep stages has been standardized Thoracic and abdominal motion were recorded with respi-
for many years,4 no consensus has been reached at this writing ratory effort sensors utilizing piezoelectric crystal sensors from
concerning scoring criteria for respiratory events. EPM Systems (Midlothian, VA). These sensors are attached to a
As a result of these variations, the overall appearance of the belt that is placed around the patient.
polysomnographic display may be markedly different from For many of the recordings, an additional system was used
one laboratory to the next. No atlas can provide examples of to assess respiratory effort. This system, labeled Backup in the
normal and abnormal polysomnography using all of the dis- montages, was also recorded with piezoelectric crystal sensors
plays and transducers used in accredited sleep laboratories. For from EPM Systems (Midlothian, VA). This backup belt was
this atlas, all of the illustrations were prepared from the sleep placed between the thoracic and the abdominal belts.
studies performed at the University of Michigan Sleep Disor- Snoring sound was recorded with piezoelectric crystal sen-
ders Center, or, in a few cases, from the neonatal EEG studies sors from EPM Systems (Midlothian, VA). This sensor is placed
either 2 cm to the left or right of the trachea, midway down the REFERENCES
neck.
Oximetry was recorded with an Ohmeda model 3740 (Lou- 1. American Sleep Disorders Association. International Classification of
isville, CO). Oximetry was recorded from a finger site. Sleep Disorders. Diagnostic and coding manual, Revised. Rochester,
Many of the illustrations were obtained from studies of Minnesota: American Sleep Disorders Association, 1997.
2. Gotman J. The use of computers in analysis and display of EEG and
patients who were undergoing a treatment trial of continuous evoked potentials. In: Daly DD, Pedley TA, eds. Current Practice of Clini-
positive airway pressure (CPAP) or bilevel positive airway pres- cal Electroencephalography. 2nd Ed. New York: Raven Press, 1990:5183.
sure (BPAP) and include recordings of mask flow and tidal vol- 3. Parisi RA, Santiago TV. Respiration and respiratory function: Technique
ume. The CPAP and BPAP equipment, which generated these of recording and evaluation. In: Chokroverty S, ed. Sleep Disorders Medi-
signals, included models manufactured by Respironics, Inc. cine: Basic Sciences, Technical Considerations, and Clinical Aspects. Boston:
Butterworth-Heinemann, 1994:127139.
and Healthdyne. 4. Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Tech-
This atlas is designed to aid the sleep medicine specialist niques, and Scoring System for Sleep Stages of Human Subjects. Los Ange-
and those training in sleep medicine. It also serves as a refer- les: Brain Information Service/ Brain Research Institute, 1968.
ence and training tool for technologists. The atlas covers nor-
mal polysomnographic features of wakefulness and the various
stages of sleep as well as polysomnographic findings character-
istic of sleep-related breathing disorders, sleep-related move-
ments, and parasomnias. In addition, examples of cardiac
arrhythmias, nocturnal seizures, and artifacts are included.
While most of the figures use a 30-second time base, a variety of
shorter and longer time scales are used to illustrate their value.
As in all projects of this type, thanks must go to the technical editorial and production staff at Lippincott Williams & Wilkins
and support staff at each of our sleep centers: the DCH Sleep who provided important suggestions and support.
Center, the University of Florida, and the St.Cloud Hospital Finally, a special thanks goes to our wives and families for
Sleep Center. their unwavering support.
A special thanks goes to Leanne McMillan, Tom Gibbons,
Fran DeStefano, Lisa McAllister, and the other members of the
xii
Ronald Chervin, M.D., and Beth Malow, M.D., were invalu- As in all projects of this type, a special thanks must go to
able contributors to this project. The other faculty members the technical and support staff. In particular, we would like to
of the University of Michigan, Department of Neurology, Clini- thank Ken Morton, RPSGT, sleep laboratory supervisor at the
cal Neurophysiology Laboratory, Ivo Drury, M.B B.Ch., Ahmad University of Michigan and Brenda Livingston, clinic coordi-
Beydoun, M.D., Linda Selwa, M.D., Robert MacDonald, M.D., nator at the University of Michigan Sleep Disorders Center.
Ph.D., Jaideep Kapur, M.D., Ph.D., Erasmo Passaro, M.D., and A special thanks goes to Anne Sydor, Ph.D., and the other
Wassim Nasreddine, M.D., were vital to both the fellowship members of the editorial and production staff at Lippincott
program in sleep medicine and the production of this text. Williams & Wilkins who provided important suggestions and
The other members of the fellowship training programs in support.
sleep medicine and clinical neurophysiology provided support, Finally, a special thanks goes to our families for their unwav-
ideas, and interesting studies. We, therefore, thank and acknowl- ering support.
edge the contributions of Sarah Nath, M.D., L. John Greenfield,
M.D., Ph.D., Kirk Levy, M.D., and Willie Anderson, M.D.
xiii
Contributors vi CHAPTER 5
Preface to the Second Edition vii Limb Movement Disorders 197
Preface to the First Edition ix James D. Geyer, Troy A. Payne,
Acknowledgments to the Second Edition xii and Paul R. Carney
Acknowledgments to the First Edition xiii
CHAPTER 6
CHAPTER 1
Parasomnias 209
Introduction to Sleep and James D. Geyer, Troy A. Payne,
Polysomnography 1 and Paul R. Carney
James D. Geyer, Troy A. Payne,
Sachin Talathi, and Paul R. Carney
CHAPTER 7
CHAPTER 2 Electroencephalographic
Staging 17 Abnormalities 225
James D. Geyer, Troy A. Payne, James D. Geyer, Troy A. Payne,
and Paul R. Carney and Paul R. Carney
CHAPTER 3 CHAPTER 8
Multiple Sleep Latency Test (MSLT)/ Artifacts 251
Maintenance of Wakefulness James D. Geyer, Troy A. Payne,
Test (MWT) 89 and Paul R. Carney
James D. Geyer, Troy A. Payne,
and Paul R. Carney CHAPTER 9
CHAPTER 4
Electrocardiography 261
James D. Geyer, Troy A. Payne,
Breathing Disorders 101 and Paul R. Carney
James D. Geyer, Troy A. Payne,
and Paul R. Carney
xiv
CHAPTER 10 APPENDIX A
Calibrations 287 Electrode Placement 313
James D. Geyer, Troy A. Payne, James D. Geyer, Troy A. Payne,
and Paul R. Carney Paul R. Carney, and Julie Tsikhlakis
APPENDIX B
CHAPTER 11
Patient Calibrations for Nighttime
Actigraphy 297 Polysomnography 315
James D. Geyer, Troy A. Payne, James D. Geyer, Troy A. Payne
and Paul R. Carney Paul R. Carney, and Monica Henderson
CHAPTER 12 APPENDIX C
Technical Background 301 Multiple Sleep Latency Test (MSLT) Protocol 317
James D. Geyer, Troy A. Payne, James D. Geyer, Troy A. Payne,
and Paul R. Carney Paul R. Carney, and Betty Seals
APPENDIX D
CHAPTER 13
Maintenance of Wakefulness Test (MWT)
Recording Artifacts and Solving Protocol 321
Technical Problems with James D. Geyer, Troy A. Payne,
Polysomnography Technology 309 and Paul R. Carney
James D. Geyer, Paul R. Carney,
Troy A. Payne, and Jennifer Parr Index 323
OVERVIEW OF SLEEP STAGES AND CYCLES stage of sleep is characterized by a level on the vertical axis of
the graph with time of night on the horizontal axis. REM sleep
The monitoring of sleep is complex and requires a distinct is often highlighted by a dark bar.
skill set including a detailed knowledge of EEG, respiratory Sleep monitoring was traditionally by polygraph recording
monitoring, and EKG. Expertise in only one of these areas using ink-writing pens which produced tracings on paper. It was
does not confer the ability to accurately interpret the poly- convenient to divide the night into epochs of time that corre-
somnogram. spond to the length of each paper page. The usual paper speed for
Sleep is not homogeneous and is characterized by sleep sleep recording is 10 mm per second; a 30-cm page corresponds to
stages based on electroencephalographic (EEG) or electrical 30 seconds. Each segment of time represented by one page is called
brain wave activity, electrooculographic (EOG) or eye move- an epoch; sleep is staged in epochs. Today most sleep recording
ments, and electromyographic (EMG) or muscle electrical is performed digitally, but the convention of scoring sleep in
activity (13). The basic terminology and methods involved 30-second epochs or windows is still the standard. If there is a
with monitoring each of these types of activity will be discussed shift in sleep stage during a given epoch, the stage present for the
below. Sleep is composed of nonrapid eye movement (NREM) majority of the time names the epoch. When the tracings used to
and rapid eye movement (REM) sleep. NREM sleep is further stage sleep are obscured by artifact for more than one half of an
divided into stages N1, N2, and N3. Stages N3 and N4 sleep epoch, it is scored as movement time (MT). When an epoch of
were recently combined into stage N3 sleep. Stages N1 and N2 what would otherwise be considered MT is surrounded by epochs
are called light sleep and stage N3 is called deep or slow-wave of wake, the epoch is also scored as wake. Some sleep centers con-
sleep. There are usually four or five cycles of sleep, each com- sider MT to be wake and do not tabulate it separately.
posed of a segment of NREM sleep followed by REM sleep. Peri-
ods of wake may also interrupt sleep during the night. As the SLEEP ARCHITECTURE DEFINITIONS
night progresses, the length of REM sleep in each cycle usually
increases. The hypnogram is a convenient method of graphi- The term sleep architecture describes the structure of sleep.
cally displaying the organization of sleep during the night. Each Common terms used in sleep monitoring are listed in
1
Table 1-1. The total monitoring time or total recording time The normal range of the percentage of sleep spent in each
(TRT) is also called total bedtime (TBT). This is the time dura- sleep stage varies with age (2,3) and is impacted by sleep dis-
tion from lights out (start of recording) to lights on (termi- orders (Table 1-2). In adults there is a decrease in stage N3
nation of recording). The total amount of sleep stages N1, sleep with increasing age, while the amount of REM sleep
N2, N3, R, and MT is termed the total sleep time (TST). The remains fairly constant. The amount of stage N1 sleep and
time from the first sleep until the final awakening is called WASO also increases with age. In patients with severe obstruc-
the sleep period time (SPT). SPT encompasses all sleep as well tive sleep apnea (OSA) there is often no stage N3 sleep and a
as periods of wake after sleep onset and before the final awak- reduced amount of REM sleep. Chronic insomnia (difficulty
ening. This wake time is termed the WASO (wake after sleep initiating or maintaining sleep) is characterized by a long
onset). Therefore, SPT = TST + WASO. The time from the start sleep latency and increased WASO. The amount of stages N3
of sleep monitoring (or lights out) until the first epoch of and R sleep is commonly decreased as well. The REM latency
sleep is called the sleep latency. The time from the first epoch is also affected by sleep disorders and medications. A short
of sleep until the first REM sleep is called the REM latency. REM latency (usually <70 minutes) is noted in some cases of
It is useful to determine not only the total minutes of each sleep apnea, depression, narcolepsy, prior REM sleep depriva-
sleep stage, but also to characterize the relative proportion of tion, and the withdrawal of REM suppressant medications.
time spent in each sleep stage. One can characterize stages N1 An increased REM latency can be seen with REM suppressants
to N3 and REM as a percentage of total sleep time (%TST). (ethanol and many antidepressants), an unfamiliar or uncom-
Another method is to characterize the sleep stages and WASO fortable sleep environment, sleep apnea, and any process that
as a percentage of the sleep period time (%SPT). Sleep effi- disturbs sleep quality.
ciency (in percent) is usually defined as either the TST 100/
SPT or TST 100/TBT.
INTRODUCTION
TO ELECTROENCEPHALOGRAPHIC
TABLE 1-1 Sleep Architecture Definitions TERMINOLOGY AND MONITORING
Lights outstart of sleep recording EEG activity is characterized by the frequency in cycles per
Light onend of sleep recording second or hertz (Hz), amplitude (voltage), and the direction of
TBT (total bedtime)time from lights out to Lights on
major deflection (polarity). The classically described frequency
TST (total sleep time) = minutes of stages N1, N2, N3, and R
WASO (wake after sleep onset)minutes of wake after first
ranges are delta (<4 Hz), theta (4 to 7 Hz), alpha (8 to 13 Hz),
sleep but before the final awakening and beta (>13 Hz). Alpha waves (8 to 13 Hz) are commonly
SPT (sleep period time) = TST + WASO noted when the patient is in an awake, but relaxed, state with
Sleep latencytime from lights out until the first epoch of the eyes closed. They are best recorded over the occiput and are
sleep attenuated when the eyes are open. Bursts of alpha waves also
REM latencytime from first epoch of sleep to the first epoch are seen during brief awakenings from sleepcalled arousals.
of REM sleep Alpha activity can also be seen during REM sleep. Alpha activ-
Sleep efficiency(TST 100)/ TBT ity is prominent during drowsy eyes-closed wakefulness. This
Stage N1, N2, N3, and R as % TSTpercentage of TST activity decreases with the onset of stage N1 sleep. Near the
occupied by each sleep stage transition from stage N1 to stage N2 sleep, vertex sharp waves
Stage N1, N2, N3, and R, WASO as % SPTpercentage of SPT
high-amplitude negative waves (upward deflection on EEG
occupied by sleep stages and WASO
Arousal index
tracings) with a short durationoccur. They are more promi-
nent in central than in occipital EEG tracings. A sharp wave
is defined as deflection of 70 to 200 milliseconds in duration K complexes. Sharp waves differ from K complexes in that they
(Table 1-3). are narrower, not biphasic, and usually of lower amplitude.
Sleep spindles are oscillations of 12 to 14 Hz with a duration As sleep deepens, slow (delta) waves appear. These are
of 0.5 to 1.5 seconds. They are characteristic of stage N2 sleep. high-amplitude, broad waves. In contrast to the EEG defini-
They may persist into stage N3, but usually do not occur in tion of delta activity as less than 4 Hz, delta slow-wave activ-
stage R. The K complex is a high-amplitude, biphasic wave of ity is defined for sleep staging purposes as waves slower than
at least 0.5-second duration. As classically defined, a K com- 2 Hz (longer than 0.5-second duration) with a peak-to-peak
plex consists of an initial sharp, negative voltage (by conven- amplitude of greater than 75 mV. The amount of slow-wave
tion an upward deflection) followed by a positive-deflection activity as measured in the central EEG derivations is used
(down) slow wave. Spindles frequently are superimposed on to determine if stage N3 is present (1) (see below). Because
a K complex resembles slow-wave activity, differentiating the There are two common patterns of eye movements. Slow eye
two is sometimes difficult. However, by definition, a K com- movements (SEMs), also called slow-rolling eye movements, are
plex should stand out (be distinct) from the low-amplitude, pendular oscillating movements that are seen in drowsy (eyes-
background EEG activity. Therefore, a continuous series of closed) wakefulness and stage N1 sleep. By stage N2 sleep, SEMs
high-voltage slow (HVS) waves would not be considered to be usually have disappeared. REMs are sharper (more narrow deflec-
a series of K complexes. tions), which are typical of eyes-open wake and REM sleep.
Sawtooth waves are notched-jagged waves of frequency in In the two-tracing method of eye movement recording,
the theta range (3 to 7 Hz) that may be present during REM large-amplitude EEG activity or artifact reflected in the EOG
sleep. Although they are not part of the criteria for scoring REM tracings usually causes in-phase defections.
sleep, their presence is a clue that REM sleep is present.
ELECTROMYOGRAPHIC RECORDING
EYE MOVEMENT RECORDING
Usually, three EMG leads are placed in the mental and submental
The main purpose of recording eye movements is to identify areas. The voltage between two of these three is monitored (for
REM sleep. EOG (eye movement) electrodes typically are placed example, EMG1-EMG3). If either of these leads fail, the third
at the outer corners of the eyesat the right outer canthus (ROC) lead can be substituted. The gain of the chin EMG is adjusted so
and the left outer canthus (LOC). In a common approach, two that some activity is noted during wakefulness. The chin EMG
eye channels are recorded and the eye electrodes are referenced is an essential element only for identifying stage R sleep. In
to the opposite mastoid (ROC-A1 and LOC-A2). However, stage R, the chin EMG is relatively reducedthe amplitude is
some sleep centers use the same mastoid electrode as a reference equal to or lower than the lowest EMG amplitude in NREM
(ROC-A1 and LOC-A1). To detect vertical as well as horizontal sleep. If the chin EMG gain is adjusted high enough to show
eye movements, one electrode is placed slightly above and one some activity in NREM sleep, a drop in activity is often seen
slightly below the eyes (4,5). on transition to REM sleep. The chin EMG may also reach the
Recording of eye movements is possible because a poten- REM level long before the onset of REMS or an EEG meeting
tial difference exists across the eyeball: front positive (+), back criteria for stage R. Depending on the gain, a reduction in the
negative (). Eye movements are detected by EOG recording chin EMG amplitude from wakefulness to sleep and often a fur-
of voltage changes. When the eyes move toward an electrode, ther reduction on transition from stage N1 to N3 may be seen.
a positive voltage is recorded. By standard convention, poly- However, a reduction in the chin EMG is not required for stages
graphs are calibrated so that a negative voltage causes an N2 to N3. The reduction in the EMG amplitude during REM
upward pen deflection (negative polarity up). Thus, eye move- sleep is a reflection of the generalized skeletal-muscle hypoto-
ment toward an electrode results in a downward deflection nia present in this sleep stage. Phasic brief EMG bursts still may
(4,6). Note that movement of the eyes is usually conjugate, with be seen during REM sleep. The combination of REMs, a rela-
both eyes moving toward one eye electrode and away from the tively reduced chin EMG, and a low-voltage mixed-frequency
other. If the eye channels are calibrated with the same polarity EEG is consistent with stage R.
settings, eye movements produce out-of-phase deflections in the
two eye tracings (e.g., one up and one down). Because ROC is
positioned above the eyes (and LOC below), upward eye move- SLEEP STAGE CHARACTERISTICS
ments are toward ROC and away from LOC. Thus, upward eye
movement results in a downward deflection in the ROC tracing The basic rules for sleep staging are summarized in Table 1-4.
and an upward deflection in the LOC tracing. Note that some characteristics are required (bold) and some
Characteristicsa,b
Stage EEG EOG EMG
Wake (eyes open) Low-voltage, high-frequency, Eye blinks, REMs Relatively high
attenuated alpha activity
Wake (eyes closed) Low-voltage, high-frequency Slow-rolling eye movements Relatively high
>50% alpha activity
Stage N1 Low-amplitude mixed- Slow-rolling eye movements May be lower than wake
frequency < 50% alpha
activity NO spindles,
K complexes
Sharp waves near transition
to stage N2
Stage N2 At least one sleep spindle May be lower than wake May be
or K complex <20% lower than wake
Slow-wave activityb
C
Stage N3 (present) >20% slow-wave activity Usually low
C
Stage N4 (prior) >50% slow-wave activity Usually low
Stage R Low-voltage mixed- Episodic REMs Relatively reduced (equal
frequency or lower than the lowest in NREM)
Sawtooth wavesmay
be present
a
Required characteristics in bold.
b
Slow wave activity, frequency <2 Hz; peak to peak amplitude >75 V; >50% means slow wave activity present in more than 50% of the epoch;
REMs, rapid eye movements.
c
Slow waves usually seen in EOG tracings.
are helpful but not required. The typical patterns associated the epoch). Both slow scanning and more rapid irregular eye
with each sleep stage are discussed below. movements are usually present. The level of muscle tone is usu-
ally relatively high.
Stage Wake
Stage N1
During eyes-open wake, the EEG is characterized by high-
frequency low-voltage activity. The EOG tracings typically show The stage N1 EEG is characterized by low-voltage, mixed-
REM, and the chin EMG activity is relatively high allowing dif- frequency activity (4 to 7 Hz). Stage N1 is scored when less
ferentiation from Stage R sleep. During eyes-closed drowsy wake, than 50% of an epoch contains alpha waves and criteria for
the EEG is characterized by prominent alpha activity (>50% of deeper stages of sleep are not met. Slow-rolling eye movements
often are present in the eye movement tracings, and the level of amplitude > 75 mV peak-to-peak) is present for greater than 20%
muscle tone (EMG) is equal or diminished compared to that in of the epoch. Spindles may be present in the EEG. Frequently,
the awake state. Some patients do not exhibit prominent alpha the high-voltage EEG activity is transmitted to the eye leads. The
activity, making detection of sleep onset difficult. The ability of a EMG often is lower than during stages N1 and N2 sleep, but this
patient to produce alpha waves can be determined from biocali- is variable. In older patients, the slow-wave amplitude is lower
brations at the start of the study. The patient is asked to lie qui- and the total amount of slow-wave sleep is reduced. The ampli-
etly with eyes open and then with the eyes closed. Alpha activity tude of the slow waves (and amount of slow-wave sleep) is usu-
usually appears with eye closure. When patients do not pro- ally highest in the first sleep cycles. Typically, stage N3 occurs
duce significant alpha activity, differentiating wakefulness from mostly in the early portions of the night. Several parasomnias
stage N1 sleep can be difficult. Several points are helpful. First, (disorders associated with sleep) occur in stage N3 sleep and,
the presence of REMs in the absence of a reduced chin EMG therefore, can be predicted to occur in the early part of the night.
usually means the patient is still awake. However, SEMs can These include somnambulism (sleep walking) and night terrors.
be present during drowsy wake and stage N1 sleep. In this case By contrast, parasomnias occurring in REM sleep (for example,
one must differentiate wake from stage N1 by the EEG. In wake, nightmares) are more common in the early morning hours.
the EEG has considerable high-frequency activity. In stage N1,
the EEG has mixed frequency with activity in the 4 to 7 Hz theta Stage R
range. Often the easiest method to determine sleep onset in dif-
ficult cases is to find the first epoch of unequivocal sleep (usu- Stage R sleep is characterized by a low-voltage, mixed-frequency
ally stage N2) and work backward. The examiner can usually be EEG, the presence of episodic REMs, and a relatively low-am-
confident of the point of sleep onset within one or two epochs. plitude chin EMG. Sawtooth waves also may occur in the EEG.
Vertex waves are common in stage N1 sleep and are defined There usually are three to five episodes of REM sleep during
by a sharp configuration maximal over the central derivations. the night, which tend to increase in length as the night pro-
Vertex waves should be easily distinguished from the back- gresses. The number of eye movements per unit time (REM
ground activity. density) also increases during the night. Not all epochs of REM
sleep contain REMs. Epochs of sleep otherwise meeting criteria
Stage N2 for stage R and contiguous with epochs of unequivocal stage
R (REMs present) are scored as stage R (see Advanced Staging
Stage N2 sleep is characterized by the presence of one or more
Rules). Bursts of alpha waves can occur during REM sleep, but
K complexes or sleep spindles. To qualify as stage N2, an epoch
the frequency is often 1 to 2 Hz slower than during wake.
also must contain less than 20% of slow (delta) wave EEG activity
Stage R is associated with many unique, physiologic changes,
(<6 seconds of a 30-second epoch). Slow-wave activity is defined
such as widespread skeletal muscle hypotonia and sleep-related
as waves with a frequency less than 2 Hz and a minimum peak-to-
erections. Skeletal muscle hypotonia is a protective mechanism
peak amplitude of greater than 75 mV. Stage N2 occupies the great-
to prevent the acting out of dreams. In a pathologic state known
est proportion of the TST and accounts for roughly 40% to 50%
as the REM behavior disorder, muscle tone is present, and body
of sleep. Stage N2 sleep ends with a sleep stage transition (to stage
movements and even violent behavior can occur during REM
W, stage N3, stage R), an arousal, or a major body movement fol-
sleep.
lowed by SEMs and low-amplitude, mixed-frequency EEG.
shortening the total amount of sleep. However, even if arousals arousal. Because cortical EEG changes must be present to meet
are brief (1 to 5 seconds) with a rapid return to sleep, daytime the above definition, such events are also termed electrocortical
sleepiness may result, although the TST is relatively normal (7). arousals. Note that the above guidelines represent a consensus
Thus, the restorative function of sleep depends on continuity as on events likely to be of physiologic significance. The commit-
well as duration. Many disorders that are associated with exces- tee recognized that other EEG phenomena, such as delta bursts,
sive daytime sleepiness also are associated with frequent, brief also can represent evidence of arousal in certain contexts.
arousals. For example, patients with OSA frequently have arousals The frequency of arousals usually is computed as the arousal
coincident with apnea/hypopnea termination. Therefore, deter- index (number of arousals per hour of sleep). Relatively little
mination of the frequency of arousals has become a standard data is available to define a normal range for the arousal index.
part of the analysis of sleep architecture during sleep testing. Normal young adults studied after adaptation nights frequently
Movement arousals were defined in the Rechtschaffen and have an arousal index of 5 per hour or less. In one study, how-
Kales (R&K) scoring manual (1) as an increase in EMG that is ever, normal subjects of variable ages had a mean arousal index
accompanied by a change in pattern on any additional chan- of 21 per hour and the arousal index was found to increase with
nel. For EEG channels, qualifying changes included a decrease age (9). However, a respiratory arousal index (RAI) (arous-
in amplitude, paroxysmal high-voltage activity, or an increase als associated with respiratory events) as low as 10 per hour
in alpha activity. Subsequently, arousals were the object of has been associated with daytime sleepiness in some individu-
considerable research, but the criteria used to define them was als with the upper-airway resistance syndrome (UARS) (10).
variable. A report from the Atlas Task Force of the American While some have argued that patients with this disorder really
Academy of Sleep Medicine (formerly the American Sleep Dis- represent the mild end of the OSA syndrome, most would
orders Association or ASDA) has become the standard defini- agree with the concept that respiratory arousals of sufficient
tion (8). According to the ASDA Task Force, an arousal should frequency can cause daytime sleepiness in the absence of frank
be scored in NREM sleep when there is an abrupt shift in EEG apnea and arterial oxygen desaturation.
frequency, which may include theta, alpha, and/or frequencies
greater than 16 Hz, but not spindles, of 3 seconds or longer
duration. The 3-second duration was chosen for methodologi- ADVANCED SLEEP STAGING RULES
cal reasons; shorter arousals may also have physiologic impor-
tance. To be scored as an arousal, the shift in EEG frequency Staging of REM sleep also requires special rules (REM rules) to
must follow at least ten continuous seconds of any stage of define the beginning and end of REM sleep. This is necessary
sleep. Arousals in NREM sleep may occur without a concur- because REMs are episodic, and the three indicators of stage R
rent increase in the submental EMG amplitude. In REM sleep, (EEG, EOG, and EMG) may not change to (or from) the REM-
however, the required EEG changes must be accompanied by like pattern simultaneously. R&K recommend that any section
a concurrent increase in EMG amplitude for an arousal to be of the record that is contiguous with uneqivocal stage R and dis-
scored. This extra requirement was added because spontaneous plays a relatively low-voltage, mixed-frequency EEG be scored
bursts of alpha rhythm are a fairly common occurrence in REM as stage R regardless of whether REMs are present, providing
(but not NREM) sleep. Note that according to the above recom- the EMG is at the stage R level. To be REM-like, the EEG must
mendations, increases in the chin EMG in the absence of EEG not contain spindles, K complexes, or slow waves.
changes are not considered evidence of arousal in either NREM
or REM sleep. Scoring of arousal during REM does, however, Atypical Sleep Patterns
require a concurrent increase in submental EMG lasting at least
1 second. Similarly, sudden bursts of delta (slow-wave) activity Four special cases in which sleep staging is made difficult by
in the absence of other changes do not qualify as evidence of atypical EEG, EOG, and EMG patterns will be briefly mentioned.
In alpha sleep, prominent alpha activity persists into NREM of active sleep, quiet sleep, and indeterminant sleep are listed
sleep. The presence of spindles, K complexes, and slow-wave in Table 1-6. The change from active to quiet sleep is more
activity allows sleep staging despite prominent alpha activ- likely to manifest indeterminant sleep. Nonnutritive sucking
ity. Causes of the pattern include pain, psychiatric disorders, commonly continues into sleep.
chronic pain syndromes, and any cause of nonrestorative As children mature, more typically adult EEG patterns begin
sleep (11, 12). Patients taking benzodiazepines may have very to appear. Sleep spindles begin to appear at 2 months and are
prominent pseudo-spindle activity (14 to 16 Hz rather than usually seen after 3 to 4 months of age (17). K complexes usu-
the usual 12 to 14 Hz) (13). SEMs are usually absent by the ally begin to appear at 6 months of age and are fully developed
time stable stage N2 sleep is present. However, patients on by 2 years of age (18). The point at which sleep staging fol-
some serotonin reuptake inhibitors (fluoxetine and others) lows adult rules is not well defined, but usually is possible after
may have prominent slow and REMs during NREM sleep (14). age 6 months. After about 3 months, the percentage of REM
While a reduction in the chin EMG is required for staging REM sleep starts to diminish and the intensity of body movements
sleep, patients with the REM sleep behavior disorder may have during active (REM) sleep begins to decrease. The pattern of
high chin activity during what otherwise appears to be REM NREM at sleep onset begins to emerge. However, the sleep cycle
sleep (15). period does not reach the adult value of 90 to 100 minutes
until adolescence.
Note that the sleep of premature infants is somewhat differ-
Sleep Staging in Infants and Children
ent from term infants (36 to 40 weeks gestation). In premature
Newborn term infants do not have the well-developed adult infants, quiet sleep usually shows a pattern of trac discontinu
EEG patterns to allow staging according to R&K rules. The fol- (19). This differs from TA as there is electrical quiescence (rather
lowing is a brief description of terminology and sleep staging than a reduction in amplitude) between bursts of high-voltage
for the newborn infant according to the state determination of activity. In addition, delta brushes (fast waves of 10 to 20 Hz) are
Anders, Emde, and Parmelee (16). Infant sleep is divided into superimposed on the delta waves. As the infant matures, delta
active sleep (corresponding to REM sleep), quiet sleep (cor- brushes disappear and TA pattern replaces trac discontinue.
responding to NREM sleep), and indeterminant sleep, which
is often a transitional sleep stage. Behavioral observations are
critical. Wakefulness is characterized by crying, quiet eyes open, RESPIRATORY MONITORING
and feeding. Sleep is often defined as sustained eye closure.
Newborn infants typically have periods of sleep lasting 3 to The three major components of respiratory monitoring during
4 hours interrupted by feeding and total sleep in 24 hours is sleep are airflow, respiratory effort, and arterial oxygen satura-
usually 16 to 18 hours. They have cycles of sleep with a 45- to tion (20, 21). Many sleep centers also find using a snore sen-
60-minute periodicity with about 50% active sleep. In new- sor to be useful. For selected cases, exhaled or transcutaneous
borns, the presence of REM (active sleep) at sleep onset is the PCO2 may also be monitored.
norm. By contrast, the adult sleep cycle is 90 to 100 minutes, Traditionally, airflow at the nose and mouth was monitored
REM occupies about 20% of sleep, and NREM sleep is noted at by thermistors or thermocouples. These devices actually detect
sleep onset. airflow by the change in the device temperature induced by a
The EEG patterns of newborn infants have been character- flow of air over the sensor. It is common to use a sensor in
ized as low-voltage irregular (LVI), trac alternant (TA), HVS, or near the nasal inlet and over the mouth (nasal-oral sensor)
and mixed (M) (Table 1-5). Eye movement monitoring is used to detect both nasal and mouth breathing. While temperature
as in adults. An epoch is considered to have high or low EMG if sensing devices may accurately detect an absence of airflow
over one half of the epoch shows the pattern. The characteristics (apnea), their signal is not proportional to flow and they have
EEG Pattern
Low-voltage irregular (LVI) Low-voltage (1435 V)a, little variation theta (58 Hz) predominates
Slow activity (15 Hz) also present
Trac alternant (TA) Bursts of high-voltage slow waves (0.53 Hz) with superimposition of rapid low-voltage
sharp waves 24 Hz
In between the high-voltage bursts (alternating with them) is low-voltage mixed-
frequency activity of 4 8 seconds in duration
High-voltage slow (HVS) Continuous moderately rhythmic medium- to high-voltage (50150 V) slow waves
(0.54 Hz)
Mixed (M) High-voltage slow- and low-voltage polyrhythmic activity
Voltage lower than in HVS
V, microvolts.
a
a slow response time (22). Therefore, they do not accurately During long periods of hypoventilation that are common in
detect decreases in airflow (hypopnea) or flattening of the air- children with sleep apnea, the end-tidal PCO2 will be elevated
flow profile (airflow limitation). Exact measurement of airflow (>45 mm Hg) (21).
can be performed by use of a pneumotachograph. This device Respiratory effort monitoring is necessary to classify respi-
can be placed in a mask over the nose and mouth. Airflow is ratory events. A simple method of detecting respiratory effort
determined by measuring the pressure drop across a linear resis- is detecting movement of the chest and abdomen. This may
tance (usually a wire screen). However, pneumotachographs are be performed with belts attached to piezoelectric transducers,
rarely used in clinical diagnostic studies. Instead, monitoring of impedance monitoring, respiratory-inductance plethysmog-
nasal pressure via a small cannula in the nose connected to a raphy (RIP), or monitoring of esophageal pressure (reflecting
pressure transducer has gained in popularity for monitoring air- changes in pleural or intrathoracic pressure). The surface EMG
flow (22, 23). The nasal pressure signal is actually proportional of the intercostal muscles or diaphragm can also be monitored
to the square of flow across the nasal inlet (24). Thus, nasal to detect respiratory effort. Probably the most sensitive method
pressure underestimates airflow at low flow rates and overes- for detecting effort is monitoring of changes in esophageal
timates airflow at high flow rates. In the midrange of typical pressure (reflecting changes in pleural pressure) associated with
flow rates during sleep, the nasal pressure signal varies fairly lin- inspiratory effort (23). This may be performed with esopha-
early with flow. The nasal pressure versus flow relationship can geal balloons or small fluid-filled catheters. Piezoelectric bands
be completely linearized by taking the square root of the nasal detect movement of the chest and abdomen as the bands are
pressure signal (25). However, in clinical practice, this is rarely stretched, and the pull on the sensors generates a signal. How-
performed. In addition to changes in magnitude, changes in the ever, the signal does not always accurately reflect the amount
shape of the nasal pressure signal can provide useful informa- of chest/abdomen expansion. In RIP, changes in the induc-
tion. A flattened profile usually means that airflow limitation is tance of coils in bands around the rib cage (RC) and abdomen
present (constant or decreasing flow with an increasing driving (AB) during respiratory movement are translated into voltage
pressure) (22, 23). The unfiltered nasal pressure signal also can signals. The inductance of each coil varies with changes in the
detect snoring if the frequency range of the amplifier is ade- area enclosed by the bands. In general, RIP belts are more accu-
quate. The only significant disadvantage of nasal pressure mon- rate in estimating the amount of chest/abdominal movement
itoring is that mouth breathing often may not be adequately than piezoelectric belts. The sum of the two signals [RIPsum =
detected (10% to 15% of patients). This can be easily handled (a RC) + (b AB)] can be calibrated by choosing appropri-
by monitoring with both nasal pressure and a nasal-oral therm- ate constants: a and b. Changes in the RIPsum are estimates of
istor. An alternative approach to measuring flow is to use respi- changes in tidal volume (28). During upper-airway narrowing
ratory inductance plethysmography. The changes in the sum of or total occlusion, the chest and abdominal bands may move
the rib cage and abdomen band signals (RIPsum) can be used paradoxically. Of note, a change in body position may alter the
to estimate changes in tidal volume (26, 27). During positive- ability of either piezoelectric belts or RIP bands to detect chest/
pressure titration, an airflow signal from the flow-generating abdominal movement. Changes in body position may require
device is often recorded instead of using thermistors or nasal adjusting band placement or amplifier sensitivity. In addition,
pressure. This flow signal originates from a pneumotachograph very obese patients may show little chest/abdominal wall move-
or other flow-measuring device inside the flow generator. ment despite considerable inspiratory effort. Thus, one must be
In pediatric polysomnography, exhaled CO2 is often mon- cautious about making the diagnosis of central apnea solely on
itored. Apnea usually causes an absence of fluctuations in the basis of surface detection of inspiratory effort.
this signal although small expiratory puffs rich in CO2 can Arterial oxygen saturation (SaO2) is measured during sleep
sometimes be misleading (6, 21). The end-tidal PCO2 (value studies using pulse oximetry (finger or ear probes). This is often
at the end of exhalation) is an estimate of arterial PCO2. denoted as SpO2 to specify the method of SaO2 determination.
A desaturation is defined as a decrease in SaO2 of 4% or more usually not possible. In clinical practice, one usually identifies
from baseline. Note that the nadir in SaO2 commonly follows an obstructive hypopnea by the presence of airflow vibration
apnea (hypopnea) termination by approximately 6 to 8 sec- (snoring), chest-abdominal paradox (increased load), or evi-
onds (longer in severe desaturations). This delay is secondary dence of airflow flattening (airflow limitation) in the nasal
to circulation time and instrumental delay (the oximeter aver- pressure signal. In both examples, the nasal pressure shows a
ages over several cycles before producing a reading). Various flattened profile not seen in the thermistor. In the second exam-
measures have been applied to assess the severity of desatu- ple, there is chest-abdominal paradox during the event. Note the
ration, including computing the number of desaturations, the sudden transition from a flattened nasal pressure profile to a
average minimum SaO2 of desaturations, the time below 80%, more rounded profile at event termination. A central hypopnea
85%, and 90%, as well as the mean SaO2 and the minimum is associated with an absence of snoring, a round airflow pro-
saturation during NREM and REM sleep. Oximeters may vary file (nasal pressure), and absence of chest-abdominal paradox.
considerably in the number of desaturations they detect and However, in the absence of esophageal pressure monitoring,
their ability to discard movement artifact. Using long averaging a central hypopnea cannot always be classified with certainty.
times may dramatically impair the detection of desaturations. In addition, obstructive hypopnea may not always be associ-
ated with chest-abdominal paradox. Because of the limitations
in exactly determining the type of hypopnea, most sleep cen-
ADULT RESPIRATORY DEFINITIONS ters usually report only the total number and frequency of
hypopneas.
In adults, apnea is defined as absence of airflow at the mouth for The new requirements for an event to be classified as a
10 seconds or longer (20, 21). If one measures airflow with a very hypopnea are as follows. A hypopnea should be scored only if
sensitive device, such as a pneumotachograph, small expiratory all of the following criteria are present.
puffs can sometimes be detected during an apparent apnea. In
The nasal pressure signal excursions (or those of the alterna-
this case, there is inspiratory apnea. Many sleep centers regard a
tive hypopnea sensor) drop by more than 30% of baseline
severe decrease in airflow (to <10% of baseline) to be an apnea.
The event duration is at least 10 seconds
An obstructive apnea is cessation of airflow with persistent
There is more than 4% oxygen desaturation from pre-event
inspiratory effort. The cause of apnea is an obstruction in the
baseline
upper airway. In central apnea, there is an absence of inspira-
At least 90% of the events duration must meet the amplitude
tory effort. A mixed apnea is defined as an apnea with an initial
reduction of criteria for hypopnea
central portion followed by an obstructive portion. A hypopnea
is a reduction in airflow for 10 seconds or longer (20). The Alternatively, a hypopnea can also be scored if all of these cri-
apnea + hypopnea index (AHI) is the total number of apneas teria are present.
and hypopneas per hour of sleep. In adults, an AHI of less than
The nasal pressure signal excursions (or those of the alterna-
5 is considered normal.
tive hypopnea sensor) drop by more than 50% of baseline
Hypopneas can be further classified as obstructive, central,
The duration of the event is at least 10 seconds
or mixed. If the upper airway narrows significantly, airflow can
There is more than 3% oxygen desaturation from pre-event
fall (obstructive hypopnea). Alternatively, airflow can fall from a
baseline or the event is associated with arousal
decrease in respiratory effort (central hypopnea). Finally, a com-
At least 90% of the events duration must meet the amplitude
bination is possible (mixed hypopnea) with both a decrease in
reduction of criteria for hypopnea
respiratory effort and an increase in upper-airway resistance.
However, unless accurate measures of airflow and esophageal Respiratory events that do not meet criteria for either apnea or
or supraglottic pressure are obtained, such differentiation is hypopnea can induce arousal from sleep. Such events have been
called upper-airway resistance events (UARE), after the UARS 20 seconds of normal respiration. Periodic breathing is seen
(10). An AASM task force recommended that such events be called primarily in premature infants and mainly during active sleep
respiratory effort-related arousals (RERAs). The recommended (30). Although controversial, some feel that the presence of
criteria for a RERA is a respiratory event of 10 seconds or longer periodic breathing for more than 5% of TST or during quiet
followed by an arousal that does not meet criteria for an apnea sleep in term infants is abnormal. Central apnea in infants is
or hypopnea, but is associated with a crescendo of inspiratory thought to be abnormal if the event is greater than 20 seconds
effort (esophageal monitoring) or a flattened waveform on nasal in duration or associated with arterial oxygen desaturation or
pressure monitoring (27). Typically, following arousal, there is a significant bradycardia (3033).
sudden drop in esophageal pressure deflections. The exact defi- In children, a cessation of airflow of any duration (usu-
nition of hypopnea that one uses will often determine whether ally two or more respiratory cycles) is considered an apnea
a given event is classified as a hypopnea or a RERA. when the event is obstructive (3033), i.e., the 10-second
One can also detect flow-limitation arousals (FLA) using an rule for adults does not apply. Of note, the respiratory rate
accurate measure of airflow, such as nasal pressure. Such events in children (20 to 30 per minute) is greater than in adults
are characterized by flow limitation (flattening) over several (12 to 15 per minute). In fact, 10 seconds in an adult is usu-
breaths followed by an arousal and sudden, but often tempo- ally the time required for two to three respiratory cycles.
rary, restoration of a normal-round airflow profile. One study Obstructive apnea is very uncommon in normal children.
suggested that the number of FLA per hour corresponded closely Therefore, an obstructive AHI greater than 1 is considered
to the RERA index identified by esophageal pressure monitoring abnormal. In children with OSA, the predominant event
(29). Some centers compute a RAI, determined as the arousals during NREM sleep is obstructive hypoventilation rather
per hour associated with apnea, hypopnea, or RERA/FLA events. than a discrete apnea or hypopnea. Obstructive hypoventila-
The AHI and respiratory disturbance index (RDI) are often used tion is characterized by a long period of upper-airway nar-
as equivalent terms. However, in some sleep centers the RDI rowing with a stable reduction in airflow and an increase in
= AHI + RERA index, where the RERA index is the number of the end-tidal PCO2. There is usually a mild decrease in the
RERAs per hour of sleep, and RERAs are arousals associated with arterial oxygen desaturation. The rib cage is not completely
respiratory events not meeting criteria for apnea or hypopnea. calcified in infants and young children. Therefore, some
One can use the AHI to grade the severity of sleep apnea. Stan- paradoxical breathing is not necessarily abnormal. However,
dard levels include normal (<5), mild (5 to <15), moderate (15 to worsening paradox during an event would still suggest a par-
29), and severe (>30) per hour. Many sleep centers also give sepa- tial airway obstruction. Nasal pressure monitoring is being
rate AHI values for NREM and REM sleep and various body posi- used more frequently in children and periods of hypoventi-
tions. Some patients have a much higher AHI during REM sleep lation are more easily detected (reduced airflow with a flat-
or in the supine position (REM-related or postural sleep apnea). tened profile). Normative values have been published for the
Because the AHI does not always express the severity of oxygen end-tidal PCO2. One paper suggested that a peak end-tidal
desaturation, one might also grade the severity of desaturation. PCO2 greater than 53 mm Hg or end-tidal PCO2 greater than
For example, it is possible for the overall AHI to be mild, but for 45 mm Hg for more than 60% of TST should be considered
the patient to have quite severe desaturation during REM sleep. abnormal (31).
Central apnea in infants was discussed above. The signifi-
cance of central apnea in older children is less certain. Most do
PEDIATRIC RESPIRATORY DEFINITIONS not consider central apneas following sighs (big breaths) to be
abnormal. Some central apnea is probably normal in children,
Periodic breathing is defined as three or more respiratory especially during REM sleep. In one study, up to 30% of normal
pauses of at least 3 seconds in duration separated by less than children had some central apnea. Central apneas, when longer
than 20 seconds, or those of any length associated with SaO2 or following (within 1 to 2 seconds) a PLM. The PLM arousal
below 90%, are often considered abnormal, although a few index is the number of PLM arousals per hour of sleep.
such events have been noted in normal children (34). There- A PLM arousal index of more than 25 per hour is considered
fore, most would recommend observation alone unless the severe. LMs that occur during wake or after an arousal are
events are frequent. either not counted or tabulated separately. For example, the
PLMW (PLMwake) index is the number of PLMs per hour of
wake. Of note, frequent LMs during wake, especially at sleep
LEG MOVEMENT MONITORING onset, may suggest the presence of the restless legs syndrome.
The latter is a clinical diagnosis made on the basis of patient
The EMG of the anterior tibial muscle (anterior lateral aspect symptoms.
of the calf) of both legs is monitored to detect leg movements
(LMs) (35). Two electrodes are placed on the belly of the upper
portion of the muscle of each leg about 2 to 4 cm apart. A elec-
trode loop is taped in place to provide strain relief. Usually, POLYSOMNOGRAPHY, BIOCALIBRATIONS,
each leg is displayed on a separate channel. However, if the AND TECHNICAL ISSUES
number of recording channels is limited, one can link an elec-
trode on each leg and display both leg EMGs on a single trac- In addition to the standard physiological parameters moni-
ing. Recording from both legs is required to accurately assess tored in polysomnography, body position (using low-light
the number of movements. During biocalibration, the patient video monitoring) and treatment level (CPAP, bilevel pres-
is asked to dorsiflex and plantarflex the great toe of the right sure) are usually added in comments by the technologists. In
and then the left leg to determine the adequacy of the elec- most centers, a video recording is also made on traditional
trodes and amplifier settings. The amplitude should be 1 cm video tape or digitally as part of the digital recording. It is
(paper recording) or at least one half of the channel width on standard practice to perform amplifier calibrations at the
digital recording. start of recording. In traditional paper recording, a calibra-
An LM is defined as an increase in the EMG signal of a tion voltage signal (square wave voltage) was applied and the
least one fourth the amplitude exhibited during biocalibra- resulting pen deflections, along with the sensitivity, polarity,
tion that is one-half to 10 seconds in duration (35). Periodic and filter settings on each channel, were documented on the
LMs (PLMs) should be differentiated from bursts of spikelike paper. Similarly, in digital recording, a voltage is applied,
phasic activity that occur during REM sleep. To be considered although it is often a sine-wave voltage. The impedance of the
a PLM, the movement must occur in a group of four or more head electrodes is also checked prior to recording. An ideal
movements, each separated by more than 5 seconds and less impedance is less than 5,000 W although 10,000 W or less
than 90 seconds (measured onset to onset). To be scored as is acceptable. Electrodes with higher impedances should be
a periodic leg movement in sleep, an LM must be preceded changed.
by at least 10 seconds of sleep. In most sleep centers, LMs A biocalibration procedure is performed (Table 1-7)
associated with termination of respiratory events are not while signals are acquired with the patient connected to the
counted as PLMs. Some may score and tabulate this type of monitoring equipment (4,5). This procedure permits check-
LM separately. The PLM index is the number of periodic LMs ing of amplifier settings and integrity of monitoring leads/
divided by the hours of sleep (TST in hours). Rough guide- transducers. It also provides a record of the patients EEG and
lines for the PLM index are more than 5 to less than 25 mild, eye movements during wakefulness with eyes closed and open.
25 to less than 50 moderate, and 50 per hour severe (36). A summary of typical commands and their utility is listed in
A PLM arousal is an arousal that occurs simultaneously with Table 1-7.
23. Berry RB. Nasal and esophageal pressure monitoring. In: Lee-Chiong 30. American Thoracic Society. Standards and indication for cardio-
TL, Sateia MJ, Caraskadon MA. eds. Sleep Medicine. Philadelphia, PA: pulmonary sleep studies in children. Am J Respir Crit Care Med
Hanley and Belfus, 2002:661671. 1996;153:866878.
24. Monserrat JP, Farr R, Ballester E, et al. Evaluation of nasal prongs for 31. Marcus CL, Omlin KJ, Basinki J, et al. Normal polysomnographic
estimating nasal flow. Am J Respir Crit Care Med 1997;155:211215. values for children and adolescents. Am Rev Respir Dis 1992;146:
25. Farr R, Rigau J, Montserrat JM, et al. Relevance of linearizing nasal 12351239.
prongs for assessing hypopneas and flow limitation during sleep. Am 32. American Thoracic Society. Cardiorespiratory studies in children:
J Respir Crit Care Med 2001;163:494497. Establishment of normative data and polysomnographic predictors
26. Tobin M, Cohn MA, Sackner MA. Breathing abnormalities during of morbidity. Am J Resp Crit Care Med 1999;160:13811387.
sleep. Arch Intern Med 1983;143:12211228. 33. Marcus CL. Sleep-disordered breathing in childrenState of the art.
27. Iber C, Ancoli-Israel S, Chesson A, and Quan SF for the American Am J Resp Crit Care Med 2001;164:1630.
Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep 34. Weese-Mayer DE, Morrow AS, Conway LP, et al. Assessing clinical
and Associated Events: Rules, Terminology and Technical Specifications. significance of apnea exceeding fifteen seconds with event record-
1st Ed. Westchester, IL: American Academy of Sleep Medicine, 2007. ing. J Pediatr 1990;117:568574.
28. Chada TS, Watson H, Birch S, et al. Validation of respiratory inductance 35. ASDA Task Force. Recording and scoring leg movements. Sleep
plethysmography using different calibration procedures. Am Rev Respir 1993;16:749759.
Dis 1982;125:644649. 36. Diagnostic and Classification Steering Committee. In: Thorpy MJ,
29. Ayappa I, Norman RG, Krieger AC, et al. Non-invasive detection of Chairman. International Classification of Sleep Disorders: Diagnostic and
respiratory effort related arousals (RERAs) by a nasal cannula/pressure Coding Manual. Rochester, MN: American Sleep Disorders Association,
transducer system. Sleep 2000;23:763771. 1990:6571.
2 Staging
James D. Geyer, MD
Troy A. Payne, MD
Paul R. Carney, MD
17
FIGURE 2-1 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 55-year-old man.
Staging: Stage wake. Biocalibration of eye movements. The patient is instructed to look up and down, left
and right, and to open and close the eyes. The representations of these eye movements insure that the eye
movement is properly recorded and provide a reference for identification of rapid eye movements during
REM sleep and wakefulness.
FIGURE 2-2 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 55-year-old man.
Staging: Stage wake. Biocalibration of breathing and leg movements. The representations of these activi-
ties insure that they are recorded properly and assist in the identification of breathing and leg move-
ment abnormalities during sleep.
* ^
FIGURE 2-3 Polysomnogram: Standard montage; 30-second page.
Clinical: 47-year-old woman.
Staging: Stage wake. Eyes are open. There is a well-modulated posteriorly dominant 9-Hz alpha rhythm
which is attenuated when eyes are open (*) and becomes more prominent with eye closure ().
FIGURE 2-6 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 29-year-old man.
Staging: Stage wake. Slow eye movements with continued alpha activity indicate that the subject is
drowsy and approaching the transition to stage N1 sleep.
* *
FIGURE 2-7 Polysomnogram: Standard montage; 30-second page.
Clinical: 39-year-old woman.
Staging: Stage wake. Although alpha activity is present during the majority of the epoch, intermittent
prominent theta activity (*) is consistent with brief episodes of sleep (microsleep).
FIGURE 2-8 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 34-year-old man.
Staging: Stage N1 sleep. Transition from wakefulness to stage N1 sleep with slow eye movements.
The alpha rhythm is present during the first 6 seconds, becomes intermittent for the next 11 seconds,
and is fully replaced by theta activity during the final 13 seconds.
*
FIGURE 2-11 Polysomnogram: Standard montage; 30-second page.
Clinical: 29-year-old man.
Staging: Stage N1 sleep with an arousal (*) followed by movement artifact. Several seconds of stage N1
sleep are followed by an awakening. The respiratory and EEG channels are obscured by artifact for sev-
eral seconds. Alpha activity characteristic of wakefulness is present during the final third of the epoch.
* ^
FIGURE 2-12 Polysomnogram: Standard montage; 30-second page.
Clinical: 5-year-old girl.
Staging: Stage N1 sleep.
EEG: Rhythmic moderate to high amplitude 4- to 5-Hz activity, referred to as hypnagogic hypersyn-
chrony (*), is a prominent feature of drowsy wakefulness and stage N1 sleep between the ages of
6 months and 6 years. It becomes less prominent during late childhood and adolescence. Near the
end of the epoch, a K complex () indicates the transition to stage N2 sleep.
* * ^
FIGURE 2-13 Polysomnogram: Standard montage; 30-second page.
Clinical: 55-year-old man.
Staging: Stage N1 sleep. There are positive occipital sharp transients (POSTs) (*) and vertex waves ().
These transients are seen in most persons during stage N1 sleep and occasionally during stage N2 sleep.
* * *
FIGURE 2-14 Polysomnogram: Standard montage; 7.5-second page.
Clinical: 55-year-old man.
Staging: Stage N1 sleep with several POSTs (*).
* ^
FIGURE 2-15 Polysomnogram: Standard montage; 30-second page.
Clinical: 62-year-old man.
Staging: Stage N2 sleep with a K complex (*) and repetitive POSTs ().
*
FIGURE 2-16 Polysomnogram: Standard montage; 30-second page.
Clinical: 34-year-old man.
Staging: Stage N2 sleep with sleep spindles (*).
^ * ^
FIGURE 2-17 Polysomnogram: CPAP montage; 30-second page.
Clinical: 38-year-old woman.
Staging: Stage N2 sleep with K complexes (*) and sleep spindles ().
* ^
FIGURE 2-18 Polysomnogram: Standard montage; 30-second page.
Clinical: 44-year-old woman.
Staging: Stage N2 sleep with a K complex (*). A vertex wave () is also evident; although they are most
prominent in stage N1 sleep, they can be seen occasionally in stage N2 sleep.
^ ** * ^
FIGURE 2-19 Polysomnogram: Standard montage; 60-second page.
Clinical: 57-year-old man.
Staging: Stage N2 sleep with a K complex (*) and vertex waves (). A transient with features intermedi-
ate between a K complex and a vertex wave is evident (**).
* ^ ^
FIGURE 2-20 Polysomnogram: Standard montage; 60-second page.
Clinical: 44-year-old woman.
Staging: Stage N2 sleep with K complexes (*) and sleep spindles (). The individual waves of the sleep
spindles cannot be distinguished with the 60-second display.
* ^
FIGURE 2-21 Polysomnogram: Expanded EEG montage; 30-second page.
Clinical: 24-year-old man.
Staging: Stage N2 sleep with sleep spindles (*) and a vertex wave (). The expanded EEG montage
demonstrates the frontocentral topography of the sleep spindle and the parasagittal topography of
the vertex wave.
* ^ * * *
FIGURE 2-22 Polysomnogram: Expanded EEG montage; 30-second page.
Clinical: 24-year-old man.
Staging: Stage N2 sleep with frequent sleep spindles (*) and K complexes ().
*
FIGURE 2-23 Polysomnogram: EEG channels only; 30-second page.
Clinical: 24-year-old man.
Staging: Stage N2 sleep with sleep spindles and vertex waves. The asymmetric topography of the initial
spindle (*), with greater amplitude in the right temporal derivations than in the left temporal deriva-
tions, is within normal limits.
*
FIGURE 2-24 Polysomnogram: EEG channels only; 30-second page.
Clinical: 24-year-old man.
Staging: Stage N2 sleep with sleep spindles and K complexes. Some spindles (*) are better represented in
temporal derivations than in other derivations.
*
FIGURE 2-25 Polysomnogram: CPAP montage; 30-second page.
Clinical: 67-year-old man.
Staging: Stage N2 sleep with K complexes and sleep spindles. The presence of delta waves (*)
presages the transition to stage N3 sleep.
* ^
FIGURE 2-26 Polysomnogram: Expanded EEG montage with CO2 monitoring; 30-second page.
Clinical: 68-year-old man with excessive daytime sleepiness and chronic obstructive pulmonary
disease (COPD).
Staging: Stage N2 sleep.
Respiratory: Normal respirations.
EEG: Asymmetric sleep spindles occurring first on the right (*) and then on the left (). Other features of
stage N2 sleep are present including K complexes and POSTs.
*
FIGURE 2-27 EEG channels from an expanded EEG montage polysomnogram; 10-second page.
Clinical: 68-year-old man with excessive daytime sleepiness and COPD.
Staging: Stage N2 sleep.
EEG: Asymmetric sleep spindles (*) most prominent over the left hemisphere especially channels Fp1-F3
and F3-C3. POSTs are prominent in the occipital derivations.
FIGURE 2-37 Polysomnogram: Expanded EEG montage; 30-second page with 1-second lines.
Clinical: 29-year-old man.
Staging: Stage N3 sleep with delta activity. The delta waves are diffusely distributed with greater ampli-
tude in anterior derivations.
FIGURE 2-43 Polysomnogram: CPAP montage with CO2 monitoring; 30-second page.
Clinical: 57-year-old man.
Staging: Stage N3 sleep with alpha activity during delta sleep. The alpha activity is nearly continuous
during the second half of the epoch.
*
FIGURE 2-44 Polysomnogram: CPAP montage; 30-second page.
Clinical: 35-year-old woman.
Staging: Stage R sleep. Sawtooth waves (*) characteristic of REM sleep are evident. Epochs of REM
sleep, such as this one, that do not contain rapid eye movements are sometimes referred to as tonic
REM sleep.
*
FIGURE 2-45 Polysomnogram: CPAP montage; 60-second page.
Clinical: 35-year-old woman.
Staging: Stage R sleep with sawtooth waves (*).
*
FIGURE 2-48 Polysomnogram: CPAP montage; 7.5-second page.
Clinical: 64-year-old man.
Staging: Stage R sleep with sawtooth waves (*).
^ *
FIGURE 2-49 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 39-year-old woman.
Staging: Stage R sleep with sawtooth waves (*). Although a single K complex () is present, rapid eye movements
were present in preceding and succeeding epochs, indicating that this epoch should be scored as REM sleep.
*
FIGURE 2-50 Polysomnogram: CPAP montage; 30-second page.
Clinical: 41-year-old man.
Staging: Stage R sleep with alpha activity (*). The amount of posterior dominant alpha activity during
REM sleep varies widely among individuals.
FIGURE 2-53 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 24-year-old man.
Staging: Transition from NREM sleep to REM sleep. During the transition into REM sleep, the EMG tone
decreases to complete muscle atonia about midway through the epoch, followed by the appearance
of rapid eye movements.
*
FIGURE 2-54 Polysomnogram: Standard montage; 30-second page.
Clinical: 49-year-old man.
Staging: Stage R sleep with sawtooth waves (*).
* ^
FIGURE 2-59 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 28-year-old man.
Staging: Transition from NREM sleep to REM sleep. There are elements of REM sleep including sawtooth
waves (*) and decreased muscle tone. There are also several sleep spindles (). Features of REM and
NREM sleep are often intermixed for a few seconds or minutes before and after a period of REM sleep.
FIGURE 2-61 Polysomnogram: CPAP montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 22-year-old woman treated with fluoxetine.
Staging: Stage N3 sleep with alpha activity (alpha-delta sleep).
EOG: Slow eye movements. Slow eye movements are usually confined to drowsy wakefulness and stage
N1 sleep. However, fluoxetine and other antidepressants may cause such eye movements to occur in
all stages of sleep.
Patient:
Account Number:
Medical Records:
Study Number:
Date of Study:
Date of Birth:
Requesting Physician:
Referring Physician:
Indications for Study: Sleep disturbance with hypersomnolence (780.54).
Study Description: Polysomnogram
Equipment: Central, frontal, and occipital EEG, EOG, EKG, submentalis EMG, intercostal EMG, airflow, thoracic motion, abdominal
motion, snore sensor, anterior tibialis EMG, and pulse oximetry were recorded throughout the study. The tracing was recorded in
30-second epochs.
Sleep Study Summary Report:
Record Time: 485.5 minutes; Sleep Time: 423.5 minutes
Analysissee detailed analysis tables
EEG/Sleep Stage
Stage N1 sleep: 15.7% (4%8%) Sleep latency: 43 minutes
Stage N2 sleep: 65.1% (45%63%) R latency: 130.5 minutes
Stage N3 sleep: 0% (4%20%) Sleep efficiency: 87.2%
Stage R sleep: 19.2% (23%31%)
Respiratory
AHI: 1 NR AHI: 0.8 R AHI: 2 Supine AHI: 0.9
RERA Index: 1.3 (9 RERA)
Total Respiratory Events: 7 (7 obstructive)
Arousal Index: 15.2
Minimum Oxygen Saturation: 93%
Snoring: moderate.
EKG: unRarkable.
Limb Movement
PLM Index: 46.5
PLM Arousal Index: 11.5
Impression: Sleep disturbance with hypersomnolence (780.54). Periodic limb movements (327.51).
There is no evidence of a sleep-related breathing disorder. A normal polysomnogram does not exclude the possibility of obstructive
sleep apnea or other sleep disorders. The findings indicate periodic limb movements with associated arousals. Clinical correlation is
advised.
Recommendations: The patient will be scheduled for a follow-up visit.
______________ , MD
The physician reviewed the record in its entirety, including sleep staging, EMG activity, EKG, EEG, respiration, oxygen saturation, body
position, and behavior unless otherwise noted. The interpretation is based on this information in addition to the available clinical history
and physical examination. This is a summary report. Please see the additional tabular report from this study for more detailed analysis.
TR:
DD:
DT:
89
*
FIGURE 3-4 Multiple Sleep Latency Test: 30-second page.
Clinical: 24-year-old woman with excessive daytime sleepiness.
Staging: Stage N1 sleep with slow eye movements and attenuation of the alpha rhythm.
Theta activity (*) is evident in C3-A2 and C4-A1 derivations.
^
*
FIGURE 3-6 Multiple Sleep Latency Test: 30-second page.
Clinical: 27-year-old man with excessive daytime sleepiness.
Staging: Stage N2 sleep with a K complex (*) and sleep spindles ().
4 Breathing Disorders
James D. Geyer, MD
Troy A. Payne, MD
Paul R. Carney, MD
101
FIGURE 4-3 Strip chart: Pulse oximetry, position, and CPAP settings.
Pulse oximetry: Severe obstructive sleep apnea. The initial half of the night (labeled CPAP setting 1.0) is
the baseline portion of the recording with no CPAP. CPAP is applied at four different settings, ranging
from 5 cm of water (setting 2.0) to 11 cm of water (setting 5.0). Continued moderate obstructive sleep
apnea is present with CPAP at levels 2.0 and 3.0. Further improvement of the obstructive sleep apnea is
evident at CPAP levels 4.0 and 5.0.
FIGURE 4-4 Strip chart: Pulse oximetry, position, and CPAP settings.
Pulse oximetry: Severe obstructive sleep apnea. The initial half of the night (labeled CPAP setting 1.0) is
the baseline portion of the recording with no CPAP. CPAP is applied at three different settings, ranging
from 5 cm of water (setting 2.0) to 9 cm of water (setting 4.0). Continued moderate obstructive sleep
apnea is present with CPAP at levels 2.0 and 3.0. Further improvement of the obstructive sleep apnea is
evident at CPAP level 4.0.
*
FIGURE 4-11 Polysomnogram: Standard montage; 60-second page.
Clinical: 42-year-old man with a low-lying soft palate and suspected obstructive sleep apnea.
Staging: Stage N2 sleep with transition into REM sleep. Although the epoch does not meet scoring
criteria for REM sleep due to the absence of rapid eye movements, the reduction in chin EMG activity
and the occurrence of sawtooth waves (*) are consistent with REM sleep.
Respiratory: Obstructive apnea with decreased but in-phase respiratory effort followed by an arousal
and an oxygen desaturation.
*
FIGURE 4-12 Polysomnogram: Standard montage; 60-second page.
Clinical: 42-year-old man with a low-lying soft palate and suspected obstructive sleep apnea.
Staging: Stage R sleep with rapid eye movements and arousals.
Respiratory: Obstructive apnea with increasing respiratory effort followed by an arousal.
EEG: Sawtooth waves (*) in REM sleep.
*
FIGURE 4-15 Polysomnogram: Standard montage; 120-second page.
Clinical: 12-year-old with large tonsils and suspected obstructive sleep apnea.
Staging: Stage R sleep with rapid eye movements.
Respiratory: Prolonged obstructive apnea with decreased but in-phase respiratory effort followed by an
arousal and an oxygen desaturation. There is also a brief post-arousal central apnea (*). The oxygen desatu-
ration at the beginning of this page was caused by an apnea from the preceding page of the record.
FIGURE 4-20 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 44-year-old woman with snoring and excessive daytime sleepiness.
Staging: Stage N1 sleep with arousals.
Respiratory: Mixed apnea with an initial portion without respiratory effort followed by two obstructed
breaths. Respiratory effort, as measured by the esophageal pressure monitor (Pes), increases with the
second obstructed breath and then decreases after the arousal and resumption of breathing. There is
minimal oxygen desaturation from 94% to 91%.
* ^
FIGURE 4-21 Polysomnogram: Standard montage; 60-second page.
Clinical: 77-year-old thin man with severe polyneuropathy and excessive daytime sleepiness.
Staging: Stage N2 sleep with an arousal.
Respiratory: Hypopnea (onset at *) with decreased airflow and respiratory effort followed by an arousal ().
*
FIGURE 4-22 Polysomnogram: Standard montage; 60-second page.
Clinical: 64-year-old obese woman with cognitive impairment.
Staging: Stage R sleep with rapid eye movements.
Respiratory: Hypopnea with minimal airflow and decreased respiratory motion followed by an arousal
and an oxygen desaturation. The oxygen desaturation at the beginning of this page was caused by an
apnea from the preceding page of the record.
EEG: Sawtooth waves (*) and alpha activity during REM sleep.
FIGURE 4-26 Polysomnogram: Standard montage with intrathoracic pressure (Pes) monitoring; 60-second page.
Clinical: 37-year-old man with fatigue.
Staging: Stage N3 sleep with an arousal.
Respiratory: Increasing respiratory effort best appreciated in the Pes channel, is apparent in several
breaths preceding the arousal. There is only minimal oxygen desaturation associated with this event.
FIGURE 4-27 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 29-year-old woman with excessive daytime sleepiness.
Staging: Stage N2 sleep with alpha intrusion.
Respiratory: Hypopnea with an associated oxygen desaturation from 94% to 88%. The change in the
respiratory effort is most clearly seen with the intrathoracic pressure (Pes) monitor.
FIGURE 4-28 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 29-year-old woman with excessive daytime sleepiness.
Staging: Stage N3 sleep with an arousal.
Respiratory: Hypopnea followed by an arousal then a post-arousal central apnea. Intrathoracic pres-
sure monitoring shows increasing effort during the hypopnea and no effort during the post-arousal
central apnea.
FIGURE 4-29 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 36-year-old man with suspected upper-airway resistance syndrome.
Staging: Stage N3 sleep.
Respiratory: Decreased airflow with a high baseline intrathoracic pressure and a gradual increase in
intrathoracic pressure. There is no arousal or oxygen desaturation with this event.
* ^
FIGURE 4-31 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 26-year-old man with excessive daytime sleepiness and several motor vehicle accidents.
Staging: Stage N2 sleep with an arousal.
Respiratory: There is a high baseline negative intrathoracic pressure with a progressive increase in intratho-
racic pressure from 20 (*) to 29 () cm of water.
FIGURE 4-32 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 31-year-old woman with excessive fatigue and chronic headaches.
Staging: Stage N2 sleep.
Respiratory: Snoring with a persistently elevated negative intrathoracic pressure at 22 cm of water.
There is no associated hypopnea, arousal, or oxygen desaturation.
* ^
FIGURE 4-33 Polysomnogram: Standard montage with intrathoracic pressure (Pes) monitoring; 60-second page.
Clinical: 49-year-old man with suspected upper-airway resistance syndrome.
Staging: Stage N2 sleep with an arousal.
Respiratory: Negative intrathoracic pressure increases gradually over several breaths from 12 (*) to 19
() cm of water. There is a subsequent arousal but no oxygen desaturation. These events, sometimes
referred to as upper-airway resistance events, are characteristic of the upper-airway resistance syndrome.
* ^
FIGURE 4-34 Polysomnogram: Standard montage with intrathoracic pressure (Pes) monitoring; 120-second page.
Clinical: 49-year-old man with upper-airway resistance syndrome.
Staging: Stage N2 sleep with an arousal.
Respiratory: Negative intrathoracic pressure increases gradually from 12 (*) to 19 () cm of water.
There is a subsequent arousal but no oxygen desaturation.
FIGURE 4-35 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 60-second page.
Clinical: 17-year-old woman with mild retrognathia, excessive daytime sleepiness associated with
recent weight gain.
Staging: Stage N3 sleep with alpha intrusion and an arousal.
Respiratory: Negative intrathoracic pressure increases gradually over several breaths followed by an
arousal but no oxygen desaturation. Snoring is minimal. The increased respiratory effort preceding
the arousal would be more difficult to appreciate without the Pes monitoring.
*
FIGURE 4-36 Polysomnogram: Standard montage; 60-second page.
Clinical: 39-year-old man with snoring, unrefreshing sleep, and headaches.
Staging: Stage N2 sleep with an arousal.
Respiratory: Snoring increases in amplitude for several breaths and then is followed by an arousal (*). The
increase in snoring is inferential evidence of increased respiratory effort, which is difficult to detect in
the thoracic and abdominal channels.
FIGURE 4-43 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 54-year-old man with excessive daytime sleepiness and congestive heart failure.
Staging: Stage N2 sleep with an arousal.
Respiratory: Central apnea with no effort on intrathoracic pressure monitoring followed by a snort
and an arousal. These central apneas resolved with CPAP treatment.
*
FIGURE 4-44 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 33-year-old man with witnessed episodes of apnea.
Staging: Stage N2 sleep with an arousal (*).
Respiratory: Central apnea with no effort on intrathoracic pressure monitoring.
FIGURE 4-47 Polysomnogram: Expanded EEG montage with CO2 monitoring; 30-second page.
Clinical: 39-year-old man with hypertension and several motor vehicle accidents which related to
sleepiness.
Staging: Stage R sleep.
Respiratory: Central apnea followed by an oxygen desaturation and tachycardia.
FIGURE 4-50 Polysomnogram: Standard montage with CO2 monitoring; 60-second page.
Clinical: 52-year-old obese man with witnessed apneas.
Staging: Stage N2 sleep with arousals.
Respiratory: Central apnea. The capnogram indicates that CO2 is highest with the first breath following
the apnea and then rapidly returns to normal (60 to 41 torr).
* ^
FIGURE 4-53 Polysomnogram: CPAP montage; 60-second page.
Clinical: 59-year-old man with congestive heart failure and excessive daytime sleepiness.
Staging: Stage N2 sleep with an arousal.
Respiratory: Central apnea and Cheyne-Stokes respirations with an EEG arousal (*) occurring at the
onset of breathing and movement () occurring at the apex of the respiratory cycle.
*
FIGURE 4-54 Polysomnogram: Standard montage; 120-second page.
Clinical: 67-year-old man with frequent witnessed apneas.
Staging: Stage N2 sleep with an arousal.
Respiratory: Central apnea and Cheyne-Stokes respirations with an EEG arousal (*) and movement occur-
ring at the apex of the respirations. This pattern in which the arousal does not accompany resumption of
breathing, but instead, occurs at the apex of the respiratory cycle, differs from the pattern usually seen
with obstructive apnea in which the arousal coincides with the resumption of breathing.
FIGURE 4-60 Polysomnogram: CPAP montage with CO2 monitoring; 30-second page.
Clinical: 48-year-old obese man with witnessed apneas.
Staging: Stage N3 sleep.
Respiratory: Normal respirations.
*
FIGURE 4-65 Polysomnogram: CPAP montage; 60-second page.
Clinical: 28-year-old man with obstructive sleep apnea.
Staging: Stage R sleep with an arousal.
Respiratory: Hypopnea followed by an arousal and movement. The beginning of the hypopnea is
marked (*).
* ^
FIGURE 4-67 Polysomnogram: CPAP montage; 120-second page.
Clinical: 49-year-old morbidly obese man with obstructive sleep apnea and poorly controlled
hypertension.
Staging: Stage R sleep.
Respiratory: Prolonged obstructive apnea (*) followed by an arousal, a snort, right leg movement, and
a brief post-arousal central apnea ().
FIGURE 4-70 Strip chart: Pulse oximetry, CPAP settings, position, and sleep staging.
Six CPAP settings were used during the study. The first three settings (5 cm, 7 cm, 9 cm) were inad-
equate and apneas continued to occur (*). At the fourth CPAP setting (11 cm), apneas became much
less frequent and there was marked REM sleep rebound (increased amounts of REM sleep).
FIGURE 4-74 Strip chart: Pulse oximetry, CPAP settings, and position.
Obstructive sleep apnea with severe oxygen desaturations during REM sleep. The initial half of the
night (labeled CPAP setting 1.0) is the baseline portion of the recording with no CPAP. When
CPAP is applied, at six different settings, ranging from 5 cm of water (setting 2.0) to 15 cm of
water (setting 7.0), apneas and associated hypoxemia were almost completely eliminated.
*
FIGURE 4-75 Strip chart: Pulse oximetry, CPAP settings, position, and sleep staging.
Prolonged oxygen desaturation during REM sleep (*) in a patient with obesity hypoventilation
syndrome. There are also frequent oxygen desaturations caused by obstructive sleep apnea.
FIGURE 4-76 Strip chart: Pulse oximetry, PAP settings, position, and sleep staging.
PAP titration in a patient with obstructive sleep apnea.
FIGURE 4-77 Strip chart: Pulse oximetry, PAP settings, position, and sleep staging.
PAP titration in a patient with obstructive sleep apnea.
FIGURE 4-78 Strip chart: Pulse oximetry, PAP settings, position, and sleep staging.
PAP titration in a patient with obstructive sleep apnea with marked
improvement in sleep depth and respirations.
LOC
ROC
Chin
F3
F4
C3
C4
O1
O2
EKG
LAT
RAT
Snorer
Nasal Pressure
Airflow
Chest
Abd
Intercostal EMG
SaO2
Patient:
Account Number:
Medical Records:
Study Number:
Date of Study:
Date of Birth:
Requesting Physician:
Referring Physician:
Indications for Study: Sleep disturbance with hypersomnolence (780.54).
Study Description: Polysomnogram
Equipment: Central, frontal, and occipital EEG, EOG, EKG, submentalis EMG, intercostal EMG, airflow, thoracic motion, abdominal
motion, snore sensor, anterior tibialis EMG, and pulse oximetry were recorded throughout the study. The tracing was recorded in
30-second epochs.
Sleep Study Summary Report:
Record time: 485.5 minutes; sleep time: 423.5 minutes
Analysissee detailed analysis tables
EEG/Sleep stage
Stage N1 sleep: 15.7% (4%8%) Sleep latency: 43 minutes
Stage N2 sleep: 65.1% (45%63%) REM latency: 130.5 minutes
Stage N3 sleep: 0% (4%20%) Sleep efficiency: 87.2%
Stage R sleep: 19.2% (23%31%)
Respiratory
AHI: 9.1 NREM AHI: 4.6 REM AHI: 28 Supine AHI: 9.1
RERA index: 9.8 (69 RERA)
Total respiratory events: 64 (63 obstructive)
Arousal index: 19.7
Minimum oxygen saturation: 90%
Snoring: loud.
EKG: PVCs.
Limb movement
PLM index: 0
PLM arousal index: 0.8
Impression: Obstructive sleep apnea (327.23).
The findings indicate obstructive sleep apnea consisting apneas and hypopneas with associated arousals and oxygen desaturations which was
most prominent during REM sleep. Obstructive sleep apnea may be related to other medical conditions. Clinical correlation is advised.
Recommendations: The patient will be scheduled for a follow-up visit along with a CPAP titration.
______________________ , M.D.
The physician reviewed the record in its entirety, including sleep staging, EMG activity, EKG, EEG, respiration, oxygen saturation, body
position, and behavior unless otherwise noted. The interpretation is based on this information in addition to the available clinical history
and physical examination. This is a summary report. Please see the additional tabular report from this study for more detailed analysis.
TR:
DD:
DT:
Patient:
Account Number:
Medical Records:
Study Number:
Date of Study:
Date of Birth:
Requesting Physician:
Referring Physician:
Indications for Study: Sleep disturbance with hypersomnolence (780.54) and witnessed apneas.
Study Description: Polysomnogram
Equipment: Central, frontal, and occipital EEG, EOG, EKG, submentalis EMG, intercostal EMG, airflow, thoracic motion, abdominal
motion, snore sensor, anterior tibialis EMG, and pulse oximetry were recorded throughout the study. The tracing was recorded in
30-second epochs.
Sleep Study Summary Report:
Record time: 393.5 minutes; sleep time: 355.5 minutes
Analysissee detailed analysis tables
EEG/Sleep stage
Stage N1 sleep: 11% (2%9%) Sleep latency: 25 minutes
Stage N2 sleep: 78.9% (50%64%) REM latency: 264.5 minutes
Stage N3 sleep: 0% (7%18%) Sleep efficiency: 90.3%
Stage R sleep: 10.1% (20%27%)
Respiratory
AHI: 35.6 NREM AHI: 32.1 REM AHI: 66.7 Supine AHI: 35.6
RERA index: 0 (0 RERA)
Total respiratory events: 211 (211 obstructive)
Arousal index: 35.3
Minimum oxygen saturation: 80%
Snoring: moderate.
EKG: unremarkable.
Limb movement
PLM index: 0.7
PLM arousal index: 0.8
Impression: Obstructive sleep apnea (327.23).
The findings indicate severe obstructive sleep apnea consisting of apneas and hypopneas with associated arousals and oxygen
desaturations. Obstructive sleep apnea may be related to other medical conditions. Clinical correlation is advised.
Recommendations: The patient will be scheduled for a follow-up visit along with a CPAP titration.
____________________ , M.D.
The physician reviewed the record in its entirety, including sleep staging, EMG activity, EKG, EEG, respiration, oxygen saturation, body
position, and behavior unless otherwise noted. The interpretation is based on this information in addition to the available clinical history
and physical examination. This is a summary report. Please see the additional tabular report from this study for more detailed analysis.
TR:
DD:
DT:
Oximetry Histogram
SaO2 Histogram
30
%
20
T
i
m 10
e
0
50 60 70 80 90 100
% O2
Average Maximum
(seconds) (seconds)
Apnea (NREM): 15.2 21.5
Hypopnea (NREM): 17.7 31.9
RERA (NREM): 0 0
Apnea (REM): 13.0 20.6
Hypopnea (REM): 14.4 28.0
RERA (REM): 0 0
NREM REM
Non-supine Supine Non-supine Supine TOTAL
Obstructive Apnea: 0 33 0 21 54
Mixed Apnea: 0 0 0 0 0
Central Apnea: 0 0 0 0 0
All Apneas: 0 33 0 21 54
Hypopneas: 0 138 0 19 157
Apneas + Hypopneas: 0 171 0 40 211
RERA: 0 0 0 0 0
A/H INDEX: 0 32.1 0 66.7 35.6
RDI: 0 32.1 0 66.7 35.6
Positional RDI
Left: 0
Right: 0
Prone: 0
Supine: 35.6
Yes No
Cheyne Stokes:
Hypoventilation:
Number Indexa
LM Arousals: 5 0.8
Isolated Limb Movements: 2 0.3
Periodic Limb Movements: 4 0.7
TOTAL Limb Movements: 6 1.0
a
Index is number per hour of sleep.
Cardiac Events:
Highest heart rate: 91 bpm, during wake time. Lowest heart rate: 55 bpm. No pauses observed.
197
6 Parasomnias
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*
FIGURE 6-3 Polysomnogram: Standard montage; 30-second page.
Clinical: 47-year-old woman with excessive daytime sleepiness.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
Behavior: Movements of the left leg (*) occur rhythmically at a rate of about 1/second, characteristic of
rhythmic movement disorder. Movement artifact is evident in the thoracic and abdominal channels.
* * * *
FIGURE 6-4 Polysomnogram: Standard montage; 120-second page.
Clinical: 47-year-old woman with excessive daytime sleepiness.
Staging: Stage wake.
Respiratory: Normal respirations.
Behavior: Movements of the left leg (*) occur rhythmically at a rate of about 1/second, with a brief
period of quiescence between the runs of movement. This pattern is characteristic of rhythmic
movement disorder. Movement artifact is evident in the thoracic and abdominal channels.
*
FIGURE 6-5 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 7-year-old boy with nocturnal episodes of inconsolable fear.
Staging: Stage N3 sleep with an arousal.
Respiratory: Normal respirations.
EEG: Arousal (*) with delta activity associated with screaming and inconsolable fear, characteristic of
sleep terrors. The EEG following the arousal consists of a mixture of delta and faster frequencies. This
EEG pattern commonly accompanies arousals from slow-wave sleep in children with arousal disorders.
*
FIGURE 6-6 Polysomnogram: Expanded EEG montage; 30-second page.
Clinical: 38-year-old woman with sleep talking.
Staging: Stage N3 sleep.
Respiratory: Normal respirations.
EEG: Spontaneous arousal (*) from stage N3 sleep associated with sleep talking. The EEG following the
arousal consists of a mixture of theta and delta frequencies.
*
FIGURE 6-7 Polysomnogram: Expanded EEG montage; 30-second page.
Clinical: 51-year-old man with frequent nocturnal arousals.
Staging: Stage N2 sleep.
Respiratory: Normal respirations.
EEG: An arousal (*) is followed a few seconds later by a full awakening and sleep talking. Sleep talking
can occur with arousals from any stage of sleep.
*
FIGURE 6-8 Polysomnogram: Expanded EEG montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 53-year-old man with confusional arousals.
Staging: Stage N3 sleep.
Respiratory: Normal respirations.
EEG: Following the arousal (*), the EEG shows continued delta activity intermixed with faster frequen-
cies, associated with moving and crying. The observed behavior was typical of a confusional arousal.
In the 5 to 6 seconds preceding the arousal, the EEG shows delta activity that is more rhythmic and
synchronous than the delta activity that usually occurs in slow-wave sleep. Rhythmic, synchronous
delta activity sometimes precedes or accompanies arousals from slow-wave sleep in patients with
arousal disorders.
225
*
FIGURE 7-1 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 29-year-old woman with complex partial seizures, snoring, and excessive daytime sleepiness.
Staging: Stage N2 sleep.
Respiratory: Snoring with normal respirations.
EEG: Subtle right hemispheric sharp waves (*) during stage N2 sleep with sleep spindles, K complexes,
and POSTs.
*
FIGURE 7-2 Polysomnogram: Standard montage; 30-second page.
Clinical: 44-year-old man with a right frontal glioma, epilepsy, and excessive daytime sleepiness.
Staging: Stage R sleep.
Respiratory: Normal respirations.
EEG: Right hemispheric sharp and slow waves most prominent in the C4 electrode (*). The sharp wave
can also be seen in the O2-avg derivation.
*
FIGURE 7-4 Polysomnogram: Standard montage; 120-second page.
Clinical: 44-year-old man with a right frontal glioma, epilepsy, and excessive daytime sleepiness.
Staging: Stage R sleep.
Respiratory: Normal respirations.
EEG: Right hemispheric (electrode C4) sharp and slow waves (*). When compared to the previous two
figures, the abnormality is almost impossible to identify because of time compression.
*
FIGURE 7-5 Polysomnogram: Expanded montage; 30-second page.
Clinical: 4-year-old with symptomatic generalized epilepsy and witnessed apneas.
Staging: Stage N2 sleep.
Respiratory: Normal respirations.
EEG: Right frontal sharp and slow waves maximal at electrodes F4 and C4 (*). The expanded EEG mon-
tage permits localization of the discharge.
*
FIGURE 7-6 Polysomnogram: Expanded EEG montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 28-year-old with frontal epilepsy and episodes of apnea and snoring.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
EEG: A left frontal spike and wave is maximal at electrode Fp1 (*). It is not seen in the standard sleep staging
channels (C3-A2, C4-A1, O1-A2, O2-A1) but has a subtle representation in the LOC (left eye) channel.
*
FIGURE 7-7 Polysomnogram: Expanded EEG montage; 60-second page.
Clinical: 18-month-old boy with seizures and apnea.
Staging: Stage N2 sleep. This page is difficult to stage because of seizure activity.
Respiratory: Increased respiratory effort at the onset of seizure activity.
EEG: Onset (*) of a focal seizure with medium amplitude rhythmic sharp waves maximal in channels
F7-T3 and C3-P3. As commonly occurs with focal seizures, the frequency of the ictal activity gradually
decreases and the amplitude gradually increases.
*
FIGURE 7-8 Polysomnogram: Expanded EEG montage; 120-second page.
Clinical: 18-month-old boy with seizures and apnea.
Staging: Stage N2 sleep. This page is difficult to stage because of seizure activity.
Respiratory: Increased respiratory effort at the onset of seizure activity.
EEG: Onset (*) of a focal seizure with medium amplitude rhythmic sharp waves maximal in channels
F7-T3 and C3-P3. The evolution of ictal activity is readily apparent with the compressed time base.
FIGURE 7-9 Polysomnogram: Expanded EEG montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 18-year-old patient with primary generalized epilepsy and excessive daytime sleepiness.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
EEG: Generalized, high amplitude spike, and wave discharges are recorded in all EEG channels and in the
EOG channels. The very high amplitudes are cut off in the display.
FIGURE 7-10 Polysomnogram: Standard montage with CO2 monitoring; 30-second page.
Clinical: 7-year-old boy with symptomatic generalized epilepsy and episodes of apnea.
Staging: Stage N3 sleep. Staging is difficult with such severe EEG abnormalities.
Respiratory: Normal respirations.
EEG: Multifocal independent spike and wave discharges and generalized spike and wave discharges.
*
FIGURE 7-11 Polysomnogram: CPAP montage; 30-second page.
Clinical: 17-year-old man with epilepsy and obstructive sleep apnea.
Staging: Unable to accurately stage because of generalized spike and wave discharges during this
generalized tonic-clonic seizure and subsequent postictal slowing.
Respiratory: Ictal and postictal obstructive apnea associated with an arousal and an oxygen desaturation.
EEG: Generalized spike and wave discharges. At the end of the seizure (*), there is generalized delta
activity during the postictal phase.
Artifact: The tidal volume channel has artifact caused by the mask being pulled from the patients face
during postictal confusion.
8 Artifacts
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251
*
FIGURE 8-1 Polysomnogram: Standard montage; 60-second page.
Clinical: 47-year-old man with witnessed apneas.
Staging: Stage N1 sleep with an arousal.
Respiratory: Mixed apnea followed by an arousal. The oxygen desaturation on this page is a result of the
apnea on the preceding page of the record.
Artifact: Cardioballistic artifact in the abdominal effort channel (*).
FIGURE 8-2 Polysomnogram: CPAP montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 43-year-old woman with upper-airway resistance syndrome.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
Artifact: Cardioballistic artifact in the intrathoracic pressure channel (*).
FIGURE 8-4 Polysomnogram: Standard montage with intrathoracic pressure monitoring; 30-second page.
Clinical: 33-year-old woman with snoring and excessive daytime sleepiness.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
Artifact: Swallow artifact in the intrathoracic pressure monitor.
FIGURE 8-5 Polysomnogram: Standard montage with expanded EEG and CO2 monitoring; 60-second page.
Clinical: 4-month-old patient with apneic episodes.
Staging: Difficult to stage because of artifact.
Artifact: Apparent diffuse rhythmic delta activity caused by patting the babys chest. The rhythmic
activity is also evident in the thoracic channel.
FIGURE 8-6 Polysomnogram: Standard montage with expanded EEG; 60-second page.
Clinical: 57-year-old man with excessive daytime sleepiness.
Staging: Difficult to stage because of severe 60 Hz artifact.
Artifact: Severe 60 Hz artifact caused by a laptop computer.
* ^
FIGURE 8-8 Polysomnogram: Standard montage; 30-second page.
Clinical: 47-year-old obese man with loud snoring and witnessed apneas.
Staging: Stage wake.
Respiratory: Normal respirations.
Artifact: Sweat artifact resulting in a wandering baseline with blocking in the O1-avg (*) and EOG
() channels.
9 Electrocardiography
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*
FIGURE 9-1 Polysomnogram: CPAP montage; 30-second page.
Clinical: 56-year-old man with snoring and excessive daytime sleepiness.
Staging: Stage N2 sleep.
Respiratory: Intermittent snoring.
EKG: Frequent premature ventricular complexes (PVCs) with couplets (*).
* *
FIGURE 9-2 Polysomnogram: Standard montage; 30-second page.
Clinical: 48-year-old woman with intermittent snoring and witnessed apneas.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
EKG: Narrow premature complexes (*) without definite P waves.
*
FIGURE 9-3 Polysomnogram: Standard montage; 10-second page.
Clinical: 48-year-old woman with intermittent snoring and witnessed apneas.
Staging: Stage N1 sleep.
Respiratory: Normal respirations.
EKG: Narrow premature complexes (*) without definite P waves.
*
FIGURE 9-10 Polysomnogram: Standard montage; 60-second page.
Clinical: 50-year-old man with obstructive sleep apnea and hypertension.
Staging: Stage R sleep with arousals.
Respiratory: Mixed apneas followed by arousals.
EKG: Wide complex tachycardia with a rate of more than 160 beats/minute accompanies the second arousal (*).
*
FIGURE 9-11 Polysomnogram: Standard montage; 30-second page.
Clinical: 50-year-old man with obstructive sleep apnea and hypertension.
Staging: Stage R sleep with an arousal.
Respiratory: Mixed apnea followed by an arousal.
EKG: Wide complex tachycardia with a rate of more than 160 beats/minute accompanies the arousal (*).
10 Calibrations
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11 Actigraphy
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12 Technical Background
James D. Geyer, MD
Troy A. Payne, MD
Paul R. Carney, MD
If input 2 is positive compared to input 1, an upward signal attenuated, all EEG activity in that range is also attenuated.
is displayed. Given these and other problems associated with the use of
the 60 Hz notch filter, it should be used only when absolutely
necessary.
Filters
Phase shift: Shift of a waveform either earlier or later in time
Filters allow the technologist and polysomnographer an caused by filtering.
opportunity to attenuate artifacts. The low frequency filter may cause a significant phase shift.
Low frequency filter: Ideally, the low frequency filter attenu- Increasing the low frequency filter attenuates the signal and
ates all frequencies below the cutoff frequency of the filter shifts it to the left or earlier in time. This may have a signifi-
and allows all frequencies above the cutoff frequency to pass cant effect on the interpretation of epileptiform discharges in
unchanged. In reality, the cutoff does not occur at a distinct expanded EEG studies.
single frequency but over a range of frequencies with a vari- The phase shift secondary to the high frequency filter and the
able attenuation. For EEG, the cutoff frequency is defined as 60 Hz notch filter has a minimal effect on the signals recorded
the frequency at which the output is reduced by 30%. In digital during polysomnography. The phase shift caused by decreasing
recording, little filtering is performed prior to digitization. Sub- the high frequency filter is to the right or later in time.
sequent digital filtering can be performed as needed.
High frequency filter: Ideally, the high frequency filter atten-
uates all frequencies above the cutoff frequency of the filter SLEEP MONTAGES
and allows all frequencies below the cutoff frequency to pass
unchanged. In reality, the cutoff does not occur at a distinct Abbreviations used:
single frequency but over a range of frequencies with a vari- EKG = electrocardiogram
able attenuation. For EEG, the cutoff frequency is defined as hff = high frequency filter in Hz
the frequency at which the output is reduced by 30%. In digital LAT and RAT = left and right anterior tibialis surface EMG
recording, little filtering is performed prior to digitization. Sub- LEOG and REOG = left and right electrooculogram
sequent digital filtering can be performed as needed. lff = low frequency filter in Hz
60 Hz notch filter: Ideally, the 60 Hz notch frequency filter N/O airflow = nasal/oral airflow
removes 60 Hz noise from electrical sources without affect- Pes = intrathoracic (esophageal) pressure monitor
ing other frequencies. In reality, the 60 Hz filter attenuates SaO2 = pulse oximetry
a range of frequencies around 60 Hz. When 60 Hz noise is sens = sensitivity in microvolts/millimeter
ARTIFACTS IN POLYSOMNOGRAPHY The artifact in the EEG channels should be time locked to the
RECORDINGS EKG.
Method for reducing or eliminating the artifact: Re-reference
Loose Electrode the EEG channels to A1 + A2.
309
Method for reducing or eliminating the artifact: Reprep and belt is no longer tight enough or in the appropriate location to
repaste the electrode to decrease the impedance. accurately reflect movement.
Method for reducing or eliminating the artifact: Tighten the
loose belt.
Cardioballistic Artifact
Description: A pulse wave may be seen in the chest belt or
abdominal belt that has only a slight delay behind the EKG Swallow Artifact
channel. A representation of the pulse wave may be seen in Description: The glossokinetic potential occurs because the tip
airflow channels, nasal pressure monitors, and in esophageal of the tongue is more electrically negative than the base of the
pressure-monitoring channels. tongue. Movement of the tongue may result in a slow wave,
Method for reducing or eliminating the artifact: This artifact is predominantly in the temporal regions. One can see the swal-
very difficult to reduce but should be recognized as a normal low occurring during the arousals.
physiologic occurrence. Method for reducing or eliminating the artifact: This artifact is
very difficult to reduce but should be recognized as a normal
Blink Artifact physiologic occurrence.
Method for reducing or eliminating the artifact: This artifact is Nasal congestionincrease heated humidity, nasal spine
very difficult to reduce but should be recognized as a normal saline spray, nasal steroid spray, and when occurring on an
physiologic occurrence. infrequent basis, over-the-counter nasal decongestant sprays.
Poor seal/mask leaktighten headgear, refit mask, try a new
style of mask.
Sixty-Hertz Artifact Sore noseloosen headgear, if no improvement try a new
Description: Lighting, electrical wiring, and machinery can pro- mask style, topical antibiotic ointment.
duce electrical artifact, which occurs at approximately 60 Hz. Nasal drynessincrease heated humidification, nasal saline
This may be superimposed on baseline EEG, EKG, EOG, and spray.
EMG waveforms. Nosebleedsincrease heated humidification, nasal saline
Method for reducing or eliminating the artifact: Reprep or reat- spray.
tach electrodes. Check ground lines. Turn off lighting and any Allergy to mask materialchange to a hypoallergenic mask.
unnecessary electrical equipment. Patient reports that pressure is too high, but study shows that
setting is correctchange to C-flex produced by Respironics.
Difficulty exhalinguse lowest possible CPAP setting, change
to a bilevel pressure system, change to C-flex by Respironics.
CONTINUOUS POSITIVE AIR PRESSURE Claustrophobiaeducate patients on the possibility of
COMPLICATIONS AND POTENTIAL claustrophobia and that it will likely improve over time,
RESPONSES select mask for patient comfort, meditation, CPAP adjust-
ment periods during wakefulness, sedative medications, or
anxiolytic medications at bedtime if necessary.
Nasal drainagetreat with nasal saline spray, nasal steroid Air swallowing (aerophagia) and gaschin strap, bilevel pres-
spray, or over-the-counter nasal decongestant sprays. sure, educate patients on the possibility that this may occur.
1.1. All material should be assembled on a tray and positioned 1.2.6. Calculate 10% of the distance between the two
for easy access during hookup. preauricular points and make a mark 10% above
1.2. The patients head is measured and electrode placement the left preauricular point. Then locate the 30%
sites are plotted according to the International 10/20 mark by measuring half the distance between the
system of electrode placement. The nasion is the inden- 10% mark above the preauricular points and the
tation above the bridge of the nose, below the forehead. center mark at the top of the head (Cz). Repeat
The inion is the small bony protrusion at the back of the the same procedure on the opposite side of the
head. The preauricular points are the small indentations head.
in the front of the ears. 1.2.7. At this time, you should have a 10% mark above
1.2.1. The first measurement is made by applying the the nasion, a 10% mark above the inion, and 10%
tape measure across the top of the head measur- marks above each preauricular point. Holding the
ing the distance from the nasion to the inion. tape through these four landmarks, measure the
A mark is made of the top of the head. circumference of the patients head.
1.2.2. Calculate 10% of the distance between the nasion and 1.2.8. Calculate 5% of the head circumference and make
the inion and make a mark 10% above the nasion. a mark 5% to the left and 5% to the right of the
1.2.3. Look down the bridge of the patients nose and FPz on the patients forehead. These locations
center the 10% mark in line with the nose. This are designated Fp1 and Fp2. This spacing should
location is called FPz. be 10% of the total head circumference.
1.2.4. Make a mark 10% above the inion. 1.2.9. Center the 10% mark above the inion by calculat-
1.2.5. Measure the patients head across from left to right ing one-half the head circumference and vertically
preauricular points, holding the measuring tape intersecting that 10% mark. This location is called
directly through the center mark at the top of the Oz. Then measure 5% over to the left and 5% over
head. The midpoint between the two preauricular to the right. These locations are designated O1
points is identified as Cz. and O2.
313
1.2.10. To locate C3, measure the distance between Fp1 1.7. Respiratory sensors include nasal/oral thermocouple
and O1 holding the tape through the 30% mark and piezocrystal respiratory effort bands. The leads from
above the left preauricular point. Calculating half of these devices are plugged directly into the electrode jack
that distance, intersect the 30% mark. This intersect box. The thermocouple should be placed directly in the
site is the placement for electrode C3. path of the patients oral and nasal outflow tracts. They
1.2.11. To locate electrodes site C4, repeat the same pro- should be secured in place with tape.
cedure on the right side of the head, measuring 1.8. The pressure transducer should be applied in a fashion
from Fp2 to O2, holding the tape through the similar to nasal cannula oxygen in order to monitor nasal
30% mark above the right preauricular point. pressure. Exact sensor location should be obtained from
1.3. Gloves should be worn. the transducer package instructions.
1.4. Examine the condition of the electrodes. 1.9. Leg EMG electrodes are placed in close proximity of the
1.4.1. Check for frayed or loose connections. ridge of the anterior tibialis muscle. The leads are taped
1.5. Electrode application to the patients leg and routed through the patients bed-
1.5.1. The electrodes cups are filled with conductive gel clothes. They are then plugged into the jack box.
which serves as an interface between the patient 1.10. Oximetry is used for measuring and recording blood oxy-
and the electrode providing a pathway for the gen saturation levels. A probe is attached to the patients
electrical signals. finger. It is then plugged into the appropriate socket.
1.5.2. Surface electrodes are applied by using electrode 1.11. Intercostal EMG electrodes (if used) are placed in the
paste. Electrode paste is a thick substance which area over the respiratory muscles. They should be placed
holds electrodes in place and is easily removed in close proximity to each other.
after the study. The paste should be squeezed from 1.12. The snoring sensor should be placed to the side of the
the tube onto the gauze pad for each electrode. larynx.
Press the electrode into the paste to obtain a cap 1.13. Electrode leads should be plugged into the electrode jack
full leaving the remainder on the gauze to cover box in the appropriate pen sockets. The jack box should
the entire electrode. Press this on the patients be placed in the jack box holder.
scalp with the gauze over the electrode. Too much 1.14. Impedances should be checked. If unable to achieve read-
paste can cause the electrode to shift during the ings below 30 kW without overscrubbing the electrode
study. sites, try to balance the impedances between the two loca-
1.6. Facial electrodes are applied using infant pellet tions. This will help minimize artifact caused by voltage
electrodes. imbalances between two similar electrode locations.
1. Patient calibrations are performed before the start of each 1.6. Ask the patient to smile, or grit his or her teeth, or make
test to verify that all the channels being recorded are work- a chewing motion.
ing properly. The patient should be instructed to do these 1.7. Ask the patient to point the toes on his or her left foot
simple exercises. As these are done, the commands should only, toward the end of the bed.
be clearly documented on the recording. If a piece of equip- 1.8. Ask the patient to point the toes on his or her right foot
ment is malfunctioning, it should be repaired prior to the only, toward the end of the bed.
start of the test. Occasionally, a patient may be so sleepy 1.9. Ask the patient breathe through his or her nose only for
that he or she is unable to stay awake during the pretrials; 30 seconds.
when these situations occur, the technician should docu- 1.10. Ask the patient to breathe through his or her mouth
ment that the patient is unable to complete the pretrials and only for 30 seconds.
use better judgment as to what pieces of equipment need to 1.11. Ask the patient to hold his or her breath for 10 seconds.
be repaired. 1.12. If a snore sensor is being used, ask the patient to make
1.1. Ask the patient to relax with his or her eyes open and three snoring noises.
stare straight ahead for 30 seconds. 1.13. Abbreviations
1.2. With eyes open, move your eyes to the L, R, L, R, U, D, 1.13.1. L = left
U, D. 1.13.2. R = right
1.3. Ask the patient to close his or her eyes for 30 seconds. 1.13.3. U = up
1.4. With eyes closed, move your eyes to the L, R, L, R, U, D, 1.13.4. D = down
U, D.
1.5. Ask the patient to open his or her eyes and then to blink
three times.
315
1.1. The MSLT should be conducted at the sleep laboratory amphetamine-based medications, should be withdrawn
following the polysomnogram or CPAP retitration. 2 weeks prior to the study if possible.
1.2. The night postsleep questionnaire, immediately following 1.10. Sleep logs may be obtained for the one week before the
the patients arising in the morning, should be completed. MSLT to assess the patients recent sleep-wake schedule.
1.3. The patients arising time should be noted on the night 1.11. After arising in the morning, the patient should toilet,
summary sheet, which is completed by the night tech- dress in street clothes, and eat breakfast.
nologist near the end of the overnight polysomnogram 1.12. The MSLT procedure is explained to the patient.
or CPAP retitration. 1.13. Between naps the patient should be out of bed and con-
1.4. After completion of the polysomnogram, airflow, respi- tinuously monitored visually by technicians to insure
ratory monitoring devices, chest respiration belts, oxime- that no napping occurs.
ter probe, and limb EMG electrodes should be removed 1.14. The first nap begins 1.5 to 3 hours after the ending of the
as well as any loose scalp or facial electrodes. patients nighttime sleep study and every 2 hours afterward.
1.5. The technologist conducting the MSLT is responsible 1.15. Perform five nap opportunities at 2-hour intervals.
for replacing necessary electrodes as well as measuring A shorter four nap test may be performed if at least two
impedances on those left attached. sleep onset REM periods have occurred.
1.6. The daytime technologist conducting the MSLT upon 1.16. Patients are not allowed to remain in bed or sleep
arriving should introduce his/her self, explain the days between naps. They are not allowed to consume caffeine
itinerary and other necessary information, and answer during the day.
any appropriate questions the patient may have. 1.17. MSLT Montage
1.7. Patients may freshen up and attend to minimum daily 1.17.1. LEOG-A2
personal routines. 1.17.2. REOG-Al
1.8. A urine drug screen should be obtained. 1.17.3. Submental EMG
1.9. REM suppressant medications and stimulant medi- 1.17.4. C3-A2
cations, including Provigil/Nuvigil and traditional 1.17.5. C4-Al
317
1.17.6. Ol-A2 from the first page of scorable REM). The maximum
1.17.7. O2-Al nap time in this scenario could be as long as 40 minutes.
1.17.8. EKG 1.25. Sleep onset is defined as
1.18. Perform machine and patient calibrations prior to 1.25.1. the first page of the first epoch of sleep (whether
nap #1. stage N1 or a combination of sleep stages).
1.19. A quiet and dark room, conducive to sleep and with 1.26. The absence of sleep on a nap opportunity is recorded as
minimal interruptions, should be used. Any noise inter- a sleep latency of 20 minutes.
ruptions especially those producing arousals or delayed 1.27. In order to assess the occurrence of REM sleep, the test
sleep should be documented. continues for 15 minutes after the first recorded epoch
1.20. No caffeine should be ingested on the day of the test. of sleep. The duration of 15 minutes is determined by
1.21. MSLT Instruction Summary clock time and is not determined by a sleep time of
1.21.1. Prior to testing: 15 minutes. REM latency is the time of the first epoch
1.21.2. Time procedure of sleep to the beginning of the first epoch of REM
1.21.3. 30 minutes: Suspend tobacco smoking sleep regardless of the intervening stages of sleep or
1.21.4. 15 minutes: Subdue physical activity wakefulness.
1.21.5. 10 minutes: Patient prepares for bed and gets 1.28. Patient calibration is conducted in the same way as the
into bed nighttime polysomnogram, with the exception of leg
1.21.6. 6 minutes: Presleep questionnaire, asking the movement and respiratory documentation.
patient for his subjective opinion of his sleepiness 1.28.1. A 50-mV standard calibration is performed for all
1.21.7. 4 minutes: Patient hooked up recording channels.
1.21.8. 2 minutes: Patient calibration, instructing the 1.28.2. The electrodes are visually inspected for good
patient to get into a comfortable position for adherence and any loose electrodes are replaced.
falling asleep, to lie still with eyes closed, and to 1.28.3. An impedance check is performed and any elec-
try to fall asleep (relax and please lie still, keep trodes more than 10,000W are replaced and
your eyes closed, and let yourself fall asleep). If rechecked.
the patient uses CPAP, the patient should use the 1.28.4. Patient is placed in bed at naptime and equip-
CPAP during the naps. ment plugged in.
1.21.9. 30 seconds: 60 cycle check and good-night phrase 1.28.5. Technologist starts polygraph or computer and
1.21.10. 0 second: Lights out and begin test makes adjustments in tracing. When tracing is
1.22. Duration of nap acceptable, technologist performs the following
1.23. End nap after: Condition patient biocalibrations:
1.23.1. 20 minutes: No scorable epochs of sleep 1.28.5.1. Eyes open for 30 seconds
1.23.2. 15 minutes: First scorable epoch of sleep (even if 1.28.5.2. Eyes closed for 30 seconds
not until the second epoch of 19th minute) 1.28.5.3. Moving eyes only, look right
1.23.3. 20 minutes after first epoch of sleep if first REM 1.28.5.4. Moving eyes only, look left
epoch occurs in second epoch of last anticipated 1.28.5.5. Moving eyes only, look up
minute before end of nap. 1.28.5.6. Moving eyes only, look down
1.24. If the patient has not had a scorable epoch of REM until 1.28.5.7. Blink several times
the last 4.5 minutes of the nap, the test should be run 1.28.5.8. Swallow
another 5 minutes (in other words, add at least 5 minutes 1.28.5.9. Grit teeth
1.29. Knock and enter the patients room, disconnect jack box 1.32.4. If CPAP and/or oxygen equipment was used,
from head of bed, and get patient out of bed. Inform remove and empty humidifier, connecting tubing,
them that they must stay out of bed and awake until the nasal cannula, and any other equipment and
start of the next nap at approximate (time). place in designated dirty equipment area for
1.30. End of study: cleaning and disinfecting.
1.30.1. At the end of the last nap, do post test machine 1.32.5. Discard disposable equipment such as the nasal
calibrations and turn off polygraph or exit com- cannula or disposable oximeter probe.
puter. 1.32.6. Remove any lint from CPAP equipment filter.
1.30.2. Gently remove all sensors from patient. Take care 1.32.7. Leave patient suites in clean and orderly
to avoid irritation of patients skin. condition.
1.30.3. Carefully soak each electrode site with warm 1.33. Scoring:
water until the electrode lifts away from the 1.33.1. Sleep stage scoring should be based on the AASM
patients skin. scoring guidelines. The sleep latency is deter-
1.30.4. Assure that all paste residue has been removed mined from lights out to the first scored epoch
by using a wet washcloth on the skin and a fine- of any stage of sleep. REM latency is scored from
toothed comb after all electrodes have been sleep onset to the first epoch of REM. MSLT laten-
removed. cies are based on Guidelines for the multiple
1.30.5. When patient is ready to leave, ask him or her if he sleep latency test (MSLT): a standard measure of
or she has a follow-up appointment. If not, take sleepiness, (1986) by Carskadon et al.
him or her to the front desk to schedule a follow-up 1.34. Amplifier calibration is done at the beginning of the MSLT
and then discharge him or her from the lab. and at the end of the day. An all-channel calibration is
1.31. After the polysomnogram: done and also an individual amplifier calibration.
1.31.1. Carefully sort wires and group them together by 1.35. MSLT Report
lengths and application sites. 1.35.1. Should include the start and end times of each
1.31.2. Remove any remaining tape and wash elec- nap or nap opportunity.
trodes with soap and water, rinse and allow to 1.35.2. Latency from lights out to the first epoch of
soak in disinfectant solution for a minimum sleep.
of 10 minutes. Rinse well and allow to dry. 1.35.3. Mean sleep latency (arithmetic mean of all naps
Inspect wires at this time to insure their integ- or nap opportunities).
rity. Return any equipment and all cleaned 1.35.4. Number of sleep-onset REM periods (defined
and disinfected wires to their storage area for as greater than 15 seconds of REM sleep in a
future use. 30-second epoch).
1.32. General cleanup checklist: 1.36. Reference
1.32.1. Discard all used tape, collars, gauze, etc.
1.32.2. Return patient preparation box to appropriate Standards of Practice Committee of the AASM. Practice param-
area. eters for clinical use of the multiple sleep latency test and the
1.32.3. Stock patient preparation box as needed. maintenance of wakefulness test. Sleep 28(1):2005.
1.1. The MWT may be conducted at the sleep laboratory fol- 1.9. Stimulant medications, including modafanil and tradi-
lowing the polysomnogram or CPAP retitration (based tional stimulant based medications, may be withdrawn
on the clinical considerations as decided by the sleep 2 weeks prior to the study if possible unless the study is
specialist). If the patient does have a sleep study on the being performed to assess the effectiveness of treatment.
night before the MWT please see 1.21.4. 1.10. MWT Montage
1.2. The night postsleep questionnaire, immediately following 1.10.1. LEOG-A2
the patients arising in the morning, may be completed. 1.10.2. REOG-Al
1.3. The patients arising time may be noted on the night 1.10.3. Submental EMG
summary sheet, which is completed by the night tech- 1.10.4. C3-A2
nologist near the end of the overnight polysomnogram 1.10.5. C4-Al
or CPAP retitration. 1.10.6. Ol-A2
1.4. Respiratory monitoring devices and tibialis electrodes 1.10.7. O2-Al
may be removed from the patient as well as any loose 1.10.8. EKG
scalp or facial electrodes. 1.11. Perform machine and patient calibrations prior to nap
1.5. The technologist conducting the MWT is responsible #1.
for replacing necessary electrodes as well as measuring 1.12. A quiet and dark room, conducive to sleep and with min-
impedances on those left attached. imal interruptions, may be used. Any noise interruptions
1.6. The daytime technologist conducting the MWT upon especially those producing arousals or delayed sleep may
arriving may introduce his/her self, explain the days be documented.
itinerary and other necessary information, and answer 1.13. No caffeine may be ingested on the day of the test.
any appropriate questions the patient may have. 1.14. The use of medications and tobacco may be decided on
1.7. Patients may freshen up and attend to minimum daily an individual basis by the sleep specialist.
personal routines. 1.15. The first trial may begin 1.5 to 3 hours after the patients
1.8. A urine drug screen may be obtained. usual wake-up time.
321
1.16. Four 40-minute trials may be run. 1.21. Sleep onset is defined as
1.17. Trials may be run every 2 hours. 1.21.1. the first page of the first epoch of sleep (whether
1.18. The room may be dark with a light source positioned stage N1 or a combination of sleep stages). Sleep
slightly behind the patients head, just out of vision. The is defined as greater than 15 seconds of cumula-
light source may deliver an illumination of 0.10 to 0.13 tive sleep in a 30-second epoch.
lux at the corneal level (a 7.5 watt night light can be used, 1.22. Patient calibration is conducted in the same way as the
placed one foot off the floor and 3 feet laterally removed night time polysomnogram with the exception of leg
from the patients head). movement and respiratory documentation.
1.19. MWT instruction summary 1.23. Amplifier calibration is done at the beginning of the
1.19.1. Prior to testing: MWT and at the end of the day. An all channel calibration
1.19.2. Time Procedure is done and also an individual amplifier calibration.
1.19.3. 30 minutes: Suspend tobacco smoking 1.24. Clinicians might recommend that patients with a mean
1.19.4. 15 minutes: Subdue physical activity sleep latency on MWT avoid driving or engaging in other
1.19.5. 10 minutes: Patient prepares for the test (includ- potentially dangerous activities.
ing going to the restroom if needed) 1.25. MWT Report
1.19.6. 6 minutes: Presleep questionnaire, asking the 1.25.1. The following data may be noted
patient for his subjective opinion of his sleepi- 1.25.1.1. Start and stop times for each trial.
ness 1.25.1.2. Sleep latency.
1.19.7. 4 minutes: Patient hooked up 1.25.1.3. Total sleep time.
1.19.8. 2 minutes: Patient calibration, instructing the 1.25.1.4. Stages of sleep achieved for each trial.
patient to sit in a comfortable chair with the 1.25.1.5. Mean sleep latency (the arithmetic
head supported such that the neck is not uncom- mean of the four trials).
fortably flexed or extended and to stay awake as 1.26. Reference
long as possible (relax and please sit still, and
Standards of Practice Committee of the AASM. Practice param-
stay awake as long as possible looking straight
eters for clinical use of the multiple sleep latency test and the
ahead but not at the light).
maintenance of wakefulness test. Sleep 28(1):2005.
1.19.9. 30 seconds: 60 cycle check and start phrase
1.19.10. 0 second: Begin test
1.20. End a trial after 40 minutes if no sleep is recorded, after
unequivocal sleep (three consecutive epochs of stage N1
sleep), or one epoch of any other stage of sleep.
1.20.1. 40 minutes: No scorable epochs of sleep
323
I M N
Ictal activity, 232233, 236 Maintenance of wakefulness test (MWT) Nasal and oral airflow, 8
Infant (see also Neonate) calibration test, 9091 Negative intrathoracic pressure, 132136
chest patting, 256 protocol, 321322 Neonate (see also Infant)
NREM sleep, 85 rapid eye movements, 92 myoclonic encephalopathy, 244
periodic breathing, 12 wakefulness to stage 1 transition in, REM sleep, 84
sleep staging, 8, 9t 94, 100 seizures, 249
Infantile spasms, 237, 246 Mask leak, CPAP, 172174 Nocturnal seizures, 160, 242
Intrathoracic pressure (Pes) monitoring, Mixed apnea Non-rapid eye movement (NREM) sleep
127, 132 arousal, 158 alpha activity, 8
central apnea, 144145 arousals and minimal oxygen characteristics, 6
epilepsy, 234 desaturation, 119 Cheyne-Stokes respirations, 156
filters, 305t306t in-phase respiratory effort, 118 chin EMG, 4
hypopnea, 128129 oxygen desaturation, 117 desaturation, 11
montages, 305t306t paradoxical respiration, 120 infants and children, 8
negative intrathoracic pressure, respiratory effort, 121 intrathoracic pressure monitoring,
132136 Montages 70, 76
non-rapid eye movement (NREM) sleep, for CPAP trial, 304t305t movement arousals, 7
70, 76 for intrathoracic pressure monitoring, periodic breathing, 12
oxygen desaturation, 130, 136 305t306t symmetric sleep spindles and
rapid eye movement (REM) sleep, 18, 70, for multiple sleep latency test, 304t vertex waves, 85
76 for parasomnias, 306t307t trace discontinuity, 8183
respiratory effort, 127, 136 for REM sleep behavior disorder, types, 1
snoring, 133 307t308t
upper-airway resistance syndrome, 130, for seizures, 306t307t O
134135 for standard polysomnogram, 303t Obesity hypoventilation syndrome, 176
Movement time (MT), 1 Obstructive sleep apnea (OSA), 186
K Multiple sleep latency test (MSLT) arousals and oxygen desaturations, 108
K complexes, 34, 6 (see also Sleep protocol, 317319 chest wall motion, 109
spindles) stage N1 sleep CPAP montage
children, 8 slow eye movements, 93 oxygen desaturation, 175
stage N2 sleep wakefulness to stage 1 transition in, postictal confusion, 236
CPAP montage, 34, 42 94, 100 pulse oximetry, 104105
expanded EEG montage, 3941, 43 stage N2 sleep, 95 stage N1 sleep, 163164, 173174
standard montage, 37, 200, 226 stage N3 sleep, 96, 9697 stage N2 sleep, 165, 172, 201, 203,
stage R sleep, 9899 266268
L wakefulness stage R sleep, 166170, 276
Laptop computer, artifact, 257 calibration test, 9091 hypoventilation, 103
Left frontal spike and wave, 231 rapid eye movements, 92 in-phase respiratory effort, 111116
Limb movement disorders, 198207 Muscle movements oxygen desaturation, 110
Limb movements, 195t monitoring (see Electromyography paradoxical respiration, 106107
periodic (see Periodic limb movement) (EMG)) respiratory effort and airflow, 167
Lip quiver, CPAP mask leak, 173, 174 REM sleep, 4 RIP recording, 181182
Low frequency filter, 302 Myoclonus, fragmentary, 201 sample report, 189190
Respiratory effort (Continued) architecture, 12, 2t, 191t multiple sleep latency test (MSLT)
intrathoracic pressure (Pes) monitoring, cycles, 1 slow eye movements, 93
127, 136 respiratory monitoring wakefulness to stage 1 transition in,
loud snoring and nocturnal reflux, 185 airflow, 8, 10 94, 100
mixed apnea, 118, 121 arterial oxygen saturation (SaO2), obstructive apnea, 163, 173
monitoring, 810 1011 parasomnias
myocardial infarction, 156 respiratory effort, 10 bruxism, 210211
obstructive apnea, 111116, 167 staging, 1 rhythmic movement disorder, 212
phasic REM sleep, 126, 280 arousal, 67 snoring, 138
seizure activity, 232233 atypical patterns, 78 staging, 2531, 78
snoring, 137138 children, 8 theta waves, 6, 25, 27, 9394
unrefreshing sleep, 131 infants, 8, 9t wakefulness, 6, 25, 28
Restless legs syndrome, 13, 119, 199, 207 stage awake, 5 Stage N2 sleep
Rhythmic movement disorder, 212, 213 stage N1, 56 alpha waves, 124, 128
Right frontal sharp and slow waves, 230 stage N2, 6 central apnea, 144145, 151155, 159, 187
Right hemispheric sharp waves, 226229 stage N3, 6 delta waves, 6, 42
stage R, 6 hypopnea, 122, 124, 128, 184185
S Sleep apnea, obstructive (see Obstructive k complexes, 34, 37, 3943, 200, 226
Sawtooth waves, REM sleep sleep apnea (OSA)) limb movement disorders, 200206
frequency range, 4 Sleep montages (see Montages) mixed apnea, 117
stage R sleep Sleep onset central apnea, 146 multiple sleep latency test (MSLT), 95
CPAP montage, 6163, 65 Sleep spindles myocardial infarction, 181
standard montage, 66, 71, 113114, 123 characteristics, 3 negative intrathoracic pressure, 132
Seizures (see also Epilepsy) children, 8 nocturnal seizures, 160
complex partial, EEG, 226 infants, 8, 85 obstructive sleep apnea, 107109, 111112,
focal seizure, EEG, 232, 233 NREM sleep, 76, 85 170, 172, 174
Lennox-Gastaut syndrome, 248 REM sleep, 76 parasomnias, 216
montage for, 306t307t stage N2 sleep, 6, 3334, 3744, snoring, 133, 137, 139140, 165
myoclonic seizure, 243 95, 226 staging, 3244, 80
neonate, 249 Sleep talking, 215, 216 upper-airway resistance syndrome,
nocturnal, 160 Sleep terrors, 214 134135
Sharp waves Slow waves Stage N3 sleep
medium amplitude, 232, 233 stage N2 sleep, 230 alpha waves, 5860, 9697
right frontal, 230 stage N3 NREM sleep, 6 arousal, 127, 129
right hemispheric, 226 stage R sleep, 227229 delta waves, 6, 45, 5460, 96, 217
Signal processing Snoring, 137143 limb movement disorders, 199
common mode rejection ratio (CMRR), CPAP level, 165 mixed apnea, 118
301 hypopnea, 162 multiple sleep latency test (MSLT), 96,
differential amplifier, 301 tachycardia, 281282 9697
filters, 302 Stage N1 sleep parasomnias, 214215, 217
polarity, 301302 central apnea, 146, 157 snoring, 141143
Sinus arrhythmia, 277279 hypopnea, 162, 163, 183 staging, 4560, 80
Sleep limb movement disorders, 198 theta waves, 215
actigraphy, 298299 mixed apnea, 119121 upper-airway resistance syndrome, 130
Staging U Waves
awake state, 1824, 79, 86 Upper-airway resistance syndrome alpha
continuous mixed frequency background arousal, 7 alpha-delta sleep, 58, 78
activity, 84 stage N1 sleep, 253 arousals, 7
delta brushes, 8183 stage N2 sleep, 134135 frequency range, 2
stage N1 sleep, 2531, 78 stage N3 sleep, 130 hypopnea, 143
stage N2 sleep, 3244, 80 NREM sleep, 8
stage N3 sleep, 4560, 80 V stage N1, 56, 25, 28, 9394
stage R sleep, 6177, 80 Ventricular bigeminy, 265 stage N2 sleep, 124, 128
symmetric sleep spindles and vertex Ventricular quintigeminy, 267 stage N3 sleep, 5860, 9697
waves, 85 Ventricular tachycardia stage R sleep, 6, 6768, 9899
Swallow artifact, 255 central apnea, 284 stage wake, 5, 2024
Sweat artifact, 259 hypopnea, 286 delta
mixed apnea, 273 arousals, 7, 214215
T nasal pressure waveform, 283 chest patting, 256
Tachycardia Ventricular trigeminy, 266 frequency range, 2
central apnea, 148, 283 Vertex waves infants and children, 8
hypopnea, 285286 infant, 85 seizure, 236
mixed apnea, 271273 stage N1 sleep, 6 slow-wave activity, 3
nasal pressure waveform, 283 stage N2 sleep, 3536, 38, 40 stage N1, 238, 239
obstructive sleep apnea, 275276 staging, 3031 stage N2 sleep, 6, 42
periodic leg movements, 204206 stage N3 sleep, 6, 45, 5460, 96, 217
snoring, 281282 W sweat artifact, 310
Teeth grinding, 290, 315 Wakefulness (see also Maintenance of trac alternant pattern, 83
Theta waves wakefulness test (MWT) ) trace discontinuity, 8182
frequency range, 2 alpha activity, 2 sawtooth
movement arousals, 7 alpha-delta sleep, 58 frequency, 4
REM sleep, 4 arousals, 67 REM sleep, 76, 112
seizure activity, 245 biocalibration, 13, 18 stage R sleep, 6, 6162, 6466, 71,
stage N1 sleep, 6, 25, 27, 9394 calibration test, 90 113114, 123
stage N3 sleep, 215 central apnea, 146, 156 theta
stage wake, 23 Cheyne-Stokes respirations, 156 frequency range, 2
trac alternant pattern, 83 claustrophobia, 311 movement arousals, 7
Third-degree atrioventricular block, 274 electromyographic recording, 4 REM sleep, 4
Tonic REM sleep, 61 infants and children, 8 seizure activity, 245
Trac alternant pattern open eyes and rapid eye stage N1 sleep, 6, 25, 27, 9394
delta and theta activity, 83 movements, 21 stage N3 sleep, 215
infants, 8 rapid eye movements, 92 stage wake, 23
Tumors, brain, EEG abnormalities, 227229, restless legs syndrome, 207 trac alternant pattern, 83
238239 slow eye movements, 78 Wide complex tachycardia,
Turner syndrome, 237 stage N1 sleep, 6, 25, 28 271272