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Sleep
Medicine
A Comprehensive Guide
for Transitioning Pediatric
to Adult Care
Amir Sharafkhaneh
David Gozal
Editors
123
Sleep Medicine
Amir Sharafkhaneh • David Gozal
Editors
Sleep Medicine
A Comprehensive Guide
for Transitioning Pediatric to Adult Care
Editors
Amir Sharafkhaneh David Gozal
Department of Medicine University of Missouri School of Medicine
Baylor College of Medicine Department of Child Health and the Child
Houston, TX, USA Health Research Institute
Columbia, MO, USA
ISBN 978-3-031-30009-7 ISBN 978-3-031-30010-3 (eBook)

https://doi.org/10.1007/978-3-031-30010-3
© Springer Nature Switzerland AG 2023

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
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tion, broadcasting, reproduction on microfilms or in any other physical way, and transmission or infor-
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The use of general descriptive names, registered names, trademarks, service marks, etc. in this publica-
tion does not imply, even in the absence of a specific statement, that such names are exempt from the
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The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Foreword
I am very pleased to write a foreword for this new publication on the need for seam-
less transitions from pediatric sleep medicine to adult sleep medicine especially as
I think that the area has been neglected when compared to other aspects of sleep
medicine.
When many experts are asked “why do we sleep” a common introduction to their
answer is that we still don’t know why. My own response is that we do indeed know
why, and the role of sleep in the fetus and growing infant and child gives us the most
robust and tangible high-level understanding of why. My response to the expert’s
“don’t know” answer is to ask the corollary question, “why do we wake up?” My
answer to the original question is that “we sleep so that we can wake up!”
The centrality of the brain in sleep was captured in a quote from the leading sleep
researcher, Allan Hobson [1]: “Sleep is of the brain, by the brain and for the brain,”
a quote borrowed from the famous Gettysburg Address by President Lincoln. I
would add that sleep’s role is not limited to the brain but rather it is fundamental to
the development and ongoing maintenance and entire functioning of complex
organisms evident at the cellular and molecular levels.
For me, the most compelling evidence about the why of sleep is its role during
development. The high proportion of the 24 h spent in sleep with high levels of
REM in infants and children [2] underpins the biological work needed for growth,
with REM-like phenomena occurring earlier in the fetus. To illustrate with one
example, the growing brain of the fetus drives breathing, sucking, and swallowing
in a primitive REM state. That these vital functions are driven by the fetal brain is
clear evidence of the vital role of neural activity driving development. The simplic-
ity of this example provides a starting point in understanding sleep. Breathing is not
required for gas exchange in the uterus, so why is it occurring? If prevented, the
diaphragm muscles don’t develop properly, and the requisite need for a brainstem
breathing rhythm does not occur at birth. This singular example is robust evidence
that clearly shows the reason for such basic fetal “sleep” activity and strongly sup-
ports the notion that “sleep is of the brain, by the brain, for the brain,” and I would
add “and for everything else!” There can be little doubt that similar processes are
occurring across all domains during the development of such complex biological
systems. At the other end of the age spectrum, when maintenance and repair domi-
nate the role of sleep, the now well-described process of brain washing—driven by
sleep—provides yet another robust example of the many roles of sleep in biology.
v
vi Foreword
Many examples are now being revealed at the cellular and molecular levels in the
complex interaction of sleep and circadian clocks. Synaptic growth and mitochon-
drial repair stand out as examples. The question of “why” should be replaced with
the many how’s that are yet to be discovered.
Given the high level of importance of sleep in development, I wonder why pedi-
atric sleep medicine, as a relatively new specialty, is so neglected? Perhaps this
thought reflects my own local experience; however the relative numbers of dedi-
cated pediatric sleep laboratories internationally compared to adult facilities seem
to support this impression.
While my first glimpse of sleep apnea was reading the report in Science from
Guilleminault et al. [3] “Insomnia with sleep apnea,” my career in sleep and breath-
ing began exploring potential causes of unexpected death in sleeping infants.
Prolonged apnea in sleep with upper airway obstruction was a major focus of these
unexpected deaths. Remarkably, sleep apnea was essentially unknown in the clini-
cal world. In the modern connected digital world, we can find all research publica-
tions at “light speed” using search engines like Google Scholar. However, at that
time, the few scattered early reports on sleep apnea were buried within specialist
publications and journals that could take months or even years to arrive in the
library. So it was that our small research group did not become aware of adult sleep
apnea until the arrival in our university library of the proceedings in 1975 of the
famous Rimini meeting held earlier in 1972 by Lugaresi [4]. This led to our first
all-night recording of a patient with obstructive sleep apnea and COPD with acute
on chronic respiratory failure in November 1975. This first study set in train for me
a lifetime of research into sleep and breathing and the development of the first com-
prehensive in-hospital sleep laboratory for adults at the Royal Prince Alfred
Hospital, and the beginning of clinical sleep medicine in Sydney.
However, as most of those in the clinical sleep field know, it took a great deal of
effort and negotiation to set up a clinical sleep laboratory within the hospital setting.
In his historical account of the beginning of sleep medicine in the US, Bill Dement
[5] described the first attempt at setting up a service in Palo Alto with an advertising
campaign in 1972/73 in the Bay Area of San Francisco offering help for individuals
with sleepiness. He was expecting to find patients with Narcolepsy, but the service
failed because of just a few patients. The clinical service only started again when
measures of breathing were included in sleep studies introduced by his recruit,
Christian Guilleminault, which led to the early period of the discovery of numerous
patients with sleep apnea.
Administrators, including clinical leaders, considered our work as “merely”
research, and strongly resisted the development of clinical sleep facilities, with
other priority areas taking available resources. The introduction of nasal CPAP in
1981, a nonsurgical therapy, provided us with a powerful argument as the sleep
facility was both a diagnostic and therapeutic service which was required to estab-
lish patients on CPAP. The fact that we could rescue patients with sleep apnea
induced life-threatening cardiac and respiratory failure with the application of
CPAP helped me convince the hospital managers to open a sleep laboratory as part
Foreword vii
of our in-patient respiratory service. The expanding recognition of the extent of

adult sleep apnea coupled with the dramatic improvement in these patients using
CPAP was a key part of the expansion of sleep laboratories internationally and was
a major stimulus for the growth of sleep medicine as a specialty. While all this work
was in adult sleep, I continued to work to develop services for children, which led
to the first pediatric sleep laboratories at Sydney’s two major children’s hospitals
in 1990.
Whereas adult sleep medicine went through a period of exponential growth
because of the prevalence of sleep apnea, and a practical, immediately accessible,
method of treatment, this has not occurred in pediatric sleep medicine. Yet sleep
apnea in pediatrics has a very long history in the clinic in the form of upper airway
obstruction with lymphoid tissue. The early literature had very clear descriptions of
sleep apnea even though the modern terminology was not yet used. The report by
Menashe et al. [6] is one example of early clear descriptions of upper airway
obstruction, both awake and markedly worsened in sleep, with dramatic clinical
improvements after surgical removal of the obstruction. This problem was widely
known clinically, as reported in the late 1800s (e.g., Hill [7]) and many other clinical
reports. There can be little doubt that parents and observant clinicians would have
seen the struggle to breathe with the obstructed upper airway and would have wit-
nessed the worsening in sleep in such children (as reported so clearly by Menashe).
There is no doubt that it was common clinical knowledge that surgical removal of
adenoids and tonsils relieved the child of the obstructed breathing. Perhaps this
common clinical knowledge of childhood upper airway obstruction and its therapy
is part of the reason that pediatric sleep medicine has not developed to the extent
that it deserves. Because adenotonsillectomy has such a dramatic effect in many of
these children, the need for a sleep study in such children (and a fully equipped
sleep laboratory) has never been regarded as essential. However, the sleep study—
and a sleep laboratory—has been, and remains, a key element in expanding our
knowledge of sleep in children. Moreover, I would argue that the critical role of
sleep in development demands that we strive to expand and improve sleep services
for infants and children, services that are not simply adaptations of adult sleep
laboratories.
Over the last decades, it has become apparent that diseases such as sleep apnea
that begin in childhood may last a lifetime and that care needs to be transitioned
with optimal expertise across the age boundaries commonly applied in clinical prac-
tice. This book does just that and builds upon previous similar experience with other
chronic disorders of childhood by providing examples and opportunities to get it
done well.
I congratulate the editors of the publication of this new monograph on the lifes-
pan elements of sleep dynamics, and particularly on the challenges posed by the
transition of pediatric sleep disorders into adult age. There is no doubt that expand-
ing our dialogue across the various age-based artificial partitions of the various
specialties should help in driving the growth in sleep medicine, and most impor-
tantly promote optimal outcomes for our patients.
viii Foreword
References
1. Hobson JA. Sleep is of the brain, by the brain and for the brain. Nature.
2005;437(7063):1254–6.
2. Roffwarg HP, Muzio JN, Dement WC. Ontogenetic development of the human
sleep-dream cycle: the prime role of “dreaming sleep” in early life may be in the
development of the central nervous system. Science. 1966;152(3722):604–19.
3. Guilleminault C, Eldridge FL, Dement WC. Insomnia with sleep apnea: a new
syndrome. Science. 1973;181(4102):856–8.
4. Lugaresi E, et al. Hypersomnia with periodic breathing-periodic apneas and
alveolar hypoventilation during sleep. Bull. Physio-Pathol. Respir.
1972;8(1):103–13.
5. Dement WC. The study of human sleep: a historical perspective. Thorax.
1998;53(suppl 3):S2–7.
6. Menashe VD, Farrehi C, Miller M. Hypoventilation and cor pulmonale due to
chronic upper airway obstruction. J Pediatrics. 1965;67(2):198–203
7. Hill W. On some causes of backwardness and stupidity in children. Br Med
J. 1898;2:711–2.
December 2022 Colin E. Sullivan

Faculty of Medicine and Health, University of Sydney
Camperdown, Australia
Contents
1 Brief History of Sleep Medicine in Children and Adults�� 1

A
Amir Sharafkhaneh, Max Hirshkowitz, and David Gozal
2 Neurological Aspects of Sleep Medicine, How Sleep Evolves,
and Regulation of Function�� 13
Lourdes M. DelRosso, Raffaele Ferri, and Oliviero Bruni
3 Cardiorespiratory Changes as They Relate to Sleep in Transition
from Pediatric to Adulthood �� 25
Giora Pillar
4 Sleep Assessment�� 45
Habibolah Khazaie, Amir Sharafkhaneh, Max Hirshkowitz,
Ali Zakiei, and David Gozal
5 Sleep-Disordered Breathing: Diagnosis �� 69
Daniel Álvarez, Andrea Crespo, Leila Kheirandish-Gozal,
David Gozal, and Félix del Campo
6
Transitional Care of Sleep-Disordered Breathing: Management�� 97
Thomas J. Dye and Narong Simakajornboon
7 Technology Approaches for Chronic Noninvasive Ventilatory
Support in Chronic Respiratory Conditions �� 113
Hui-Leng Tan and João Carlos Winck
8
Chronic Noninvasive Ventilatory Support in Various Chronic
Respiratory Conditions Including Protocols �� 131
Amee Revana, Shahram Moghtader, and Ritwick Agrawal
9
Insomnia Across the Life Span �� 145
Mary Rose, Sara Nowakowski, and Lisa Medalie
10
Parasomnias: Diagnosis and Management�� 159
Kevin Kaplan, Lacie Petitto, and Amee Revana
11
Movement Disorders: Diagnosis and Management�� 177
Denise Sharon and Lourdes M. DelRosso
ix
x Contents
12
Circadian Rhythm Disorders in Children and Adults�� 199
Kanta Velamuri, Supriya Singh, Ritwick Agrawal, Shahram
Moghtader, and Amir Sharafkhaneh
13
Transitional Care Aspects of the Diagnosis and Management of
Narcolepsy and Other Primary Disorders of Hypersomnia�� 211
Brian J. Murray
14 Transition of Sleep Care in Patients with Neuromuscular
and Neurodegenerative Disorders�� 225
Sonal Malhotra, Aristotle Asis, and Daniel Glaze
15 Cystic Fibrosis: A Successful Model of Transition of Care
and Lessons Learned �� 247
Taylor Baumann and Tara Lynn Barto
16
Sickle Cell Disease: Lessons Learned�� 259
Jerlym S. Porter, Cecelia Valrie, Adrienne S. Viola,
and Jelaina Shipman
Index�� 277
Contributors
Ritwick Agrawal Department of Pediatrics Pulmonary Medicine Section, Texas

Children’s Hospital, Houston, TX, USA
Pulmonary, Critical Care and Sleep Section, Department of Medicine, Michael
E. DeBakey VA Medical Centre, Houston, TX, USA
Pulmonary Critical Care and Sleep Medicine Section, Baylor College of Medicine,
Michael E. DeBakey Veteran Affairs Medical Center, Houston, TX, USA
Daniel Álvarez Biomedical Engineering Group, University of Valladolid,
Valladolid, Spain
Pneumology Department, Río Hortega University Hospital, Valladolid, Spain
Centro de Investigación Biomédica en Red – Bioingeniería, Biomateriales y
Nanomedicina (CIBER-BBN), Madrid, Spain
Aristotle Asis Department of Pulmonary Medicine, Texas Medical Center,
Houston, TX, USA
Tara Lynn Barto Department of Medicine, Baylor College of Medicine,
Houston, TX, USA
Taylor Baumann Department of Medicine, Baylor College of Medicine,
Houston, TX, USA
Oliviero Bruni Department of Social and Developmental Psychology, Sapienza
University, Rome, Italy
Félix del Campo Biomedical Engineering Group, University of Valladolid,
Valladolid, Spain
Centro de Investigación Biomédica en Red – Bioingeniería, Biomateriales y
Nanomedicina (CIBER-BBN), Madrid, Spain
Andrea Crespo Biomedical Engineering Group, University of Valladolid,
Valladolid, Spain
xi
xii Contributors
Lourdes M. DelRosso University of California San Francisco, Fresno, CA, USA

University of Washington, Seattle Children’s Hospital, Settle, WA, USA
Thomas J. Dye Division of Pulmonary Medicine, Sleep Center, Cincinnati
Children’s Hospital Medical Center, Cincinnati, OH, USA
Division of Neurology, Cincinnati Children’s Hospital Medical Center,
Cincinnati, OH, USA
Department of Pediatrics, University of Cincinnati College of Medicine,
Cincinnati, OH, USA
Raffaele Ferri Sleep Research Centre, Oasi Research Institute – IRCCS,
Troina, Italy
Daniel Glaze Department of Pulmonary Medicine, Texas Medical Center,
Houston, TX, USA
David Gozal Department of Child Health and the Child Health Research Institute,
University of Missouri School of Medicine, Columbia, MO, USA
Max Hirshkowitz Michael E. DeBakey VA Medical Center, Houston, TX, USA
Baylor College of Medicine, Houston, TX, USA
Stanford University School of Medicine, Division of Public Mental Health and
Population Sciences, Stanford, CA, USA
Kevin Kaplan Pediatric Pulmonology, Children’s Sleep Center, Baylor College of
Medicine, Texas Children’s Hospital, Houston, TX, USA
Habibolah Khazaie Sleep Disorders Research Center, Kermanshah University of
Medical Sciences, Kermanshah, Iran
Leila Kheirandish-Gozal Department of Child Health and the Child Health
Research Institute, University of Missouri School of Medicine, Columbia, MO, USA
Sonal Malhotra Department of Pulmonary Medicine, Texas Medical Center,
Houston, TX, USA
Lisa Medalie Departments of Psychiatry, Medicine, Pediatrics, University of
Chicago, Chicago, IL, USA
Shahram Moghtader Department of Pediatrics Pulmonary Medicine Section,
Texas Children’s Hospital, Houston, TX, USA
Pulmonary, Critical Care and Sleep Section, Department of Medicine, Michael
E. DeBakey VA Medical Centre, Houston, TX, USA
Pulmonary Critical Care and Sleep Medicine Section, Baylor College of Medicine,
Michael E. DeBakey Veteran Affairs Medical Center, Houston, TX, USA
Brian J. Murray Neurology and Sleep Medicine, Sunnybrook Health Sciences
Centre, University of Toronto, Toronto, ON, Canada
Sara Nowakowski Baylor College of Medicine, Houston, TX, USA
Contributors xiii
Lacie Petitto Pediatric Pulmonology, Children’s Sleep Center, Baylor College of

Medicine, Texas Children’s Hospital, Houston, TX, USA
Giora Pillar Department of Pediatrics and Sleep Lab, Carmel Hospital, and
Technion Faculty of Medicine, Haifa, Israel
Jerlym S. Porter Department of Psychology and Biobehavioral Sciences, St. Jude
Children’s Research Hospital, Memphis, TN, USA
Amee Revana Department of Pediatric Pulmonology/Sleep Medicine, Texas
Pediatric Pulmonology, Children’s Sleep Center, Baylor College of Medicine, Texas
Mary Rose Baylor College of Medicine, Menninger, Sleep Department,
Houston, TX, USA
The Menninger Clinic, Houston, TX, USA
Amir Sharafkhaneh Department of Medicine, Baylor College of Medicine,
Houston, TX, USA
Denise Sharon Pomona Valley Medical Center Adult and Children Sleep Disorders
Center, Claremont, CA, USA
Jelaina Shipman Department of Psychology, Virginia Commonwealth University,
Richmond, VA, USA
Narong Simakajornboon Division of Pulmonary Medicine, Sleep Center,
Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA
Department of Pediatrics, University of Cincinnati College of Medicine,
Cincinnati, OH, USA
Supriya Singh Pulmonary, Critical Care and Sleep Section, Department of
Medicine, Michael E. DeBakey VA Medical Centre, Houston, TX, USA
Hui-Leng Tan Department of Paediatric Respiratory Medicine, Royal Brompton
Hospital, London, UK
Cecelia Valrie Department of Psychology, Virginia Commonwealth University,
Richmond, VA, USA
Kanta Velamuri Pulmonary, Critical Care and Sleep Section, Department of
Medicine, Michael E. DeBakey VA Medical Centre, Houston, TX, USA
Adrienne S. Viola Pediatrics Department, Boston Children’s Hospital,
Boston, MA, USA
João Carlos Winck Faculdade de Medicina da Universidade do Porto, Porto,
Portugal
Ali Zakiei Sleep Disorders Research Center, Kermanshah University of Medical
Sciences, Kermanshah, Iran
A Brief History of Sleep Medicine
in Children and Adults 1
Amir Sharafkhaneh, Max Hirshkowitz, and David Gozal
1.1 Introduction
Sleep and dreaming puzzle the human mind as far back as we know, and discussions
about sleep and dreams are found going back to ancient cultures and in every arche-
ological scripture. The real understanding about sleep and wakefulness however
grew as soon as better tools became available to study the central nervous system,
including recordings of electrical activity using EEG and neuroimaging including
functional MRI (fMRI). Further studies into physiology and biology of the nervous
system using various animal models allowed better understanding of how various
states of wakefulness and sleep occur. Combining the findings of almost the last two
centuries with clinical observations of astute practitioners enabled us to better
understand a long list of sleep disorders and formulate disease-specific criteria for
diagnosis and management of such conditions. Therapies aimed at either palliation
of symptoms or seeking curative approaches stemmed from the increased recogni-
tion of sleep-related ailments. Along the scientific and clinical advancements, vari-
ous associations with focus on sleep sciences and sleep disorders began to form and
along came scientifically and clinically oriented international, national, regional,
and local conferences and meetings. With increasing demand for sleep services,
A. Sharafkhaneh (*)
Department of Medicine, Baylor College of Medicine, Houston, TX, USA
e-mail: amirs@bcm.edu
M. Hirshkowitz
Michael E. DeBakey VA Medical Center, Houston, TX, USA
Stanford University School of Medicine, Division of Public Mental Health and Population
Sciences, Stanford, CA, USA
D. Gozal
Department of Child Health and the Child Health Research Institute, University of Missouri
School of Medicine, Columbia, MO, USA
e-mail: gozald@health.missouri.edu
© This is a U.S. government work and not under copyright protection in the U.S.; foreign 1
copyright protection may apply 2023
A. Sharafkhaneh, D. Gozal (eds.), Sleep Medicine,
https://doi.org/10.1007/978-3-031-30010-3_1
2 A. Sharafkhaneh et al.
sleep centers and sleep medicine training programs exponentially expanded in

capacity all over the world. Additionally, with recognition of the potentially adverse
effects of sleep disorders and sleep deprivation on safety, various regulations were
developed to provide safer environment and operation. As would be expected, legal
cases have been brought to courts to further investigate effects of sleep deprivation
on professional performance and as part of the determinants leading to accidents or
disasters. Although different aspects of sleep science and medicine started at differ-
ent points in time, in their emerging beginnings that all have grown in parallel. This
chapter is a brief review of the history of sleep medicine. There are several detailed
reviews written by authors who have firsthand knowledge of the field. We refer the
readers to these in depth [1–4].
1.2 Sleep Medicine in Ancient Cultures
Sleep and dreaming are topics that have been discussed frequently in various cul-
tures going back several millennia. There is no doubt that humans are fascinated
with sleep in general and more particularly with dreams. In the context of the lack
of understanding of brain function by previous civilizations, it is a fascinating
opportunity to witness a process in which we and almost any other living organism
enter a coma-like state that may resemble death and return from this adventure
refreshed while unavoidably repeating it daily. Not surprisingly then that the topic
of sleep has been discussed to various degrees in ancient cultures. The current avail-
able literature points to discussions in Indian, Egyptian, Greek and Romans,
Chinese, and other ancient cultures. Many of these ancient cultures viewed sleep
and death similarly, sleep as temporary death, and the other as a permanent event.
Literature discovered from ancient Egypt elaborates on health and disease with
some focus on sleep. In particular, dreams and their interpretation were given major
importance. For example, then and now, in the Middle East and North Africa, dream
of death of an individual is interpreted as the life of that person being prolonged.
The story of the dream of pharaoh interpreted by Joseph is a typical example of how
ancient Egyptians took their dreams seriously. Egyptian physicians used poppy
seed, alcohol, and nightshade (scopolamine) in addition of purging and enemas for
treatment of insomnia [4, 5].
Chinese ancient culture and to some degree the current traditional Chinese medi-
cine believe in two forces of positive (yang) and negative (yin) that in balance create
health or disease. Chinese believed in the humoral system that regulated various
bodily functions including sleep. They used different methods including acupunc-
ture, massage, breathing exercises, and various herbal medicines (ephedra and gin-
seng) to treat ailments including insomnia [5].
Indus Valley civilization goes back for thousands of years. The traditional Indian
medicine is called Ayurveda. According to Ayurveda principles, three basic types of
energy exist in each individual. These include Vata (the energy of movement), Pitta
(energy of digestion/metabolism), and Kapha (energy of lubrication and structure).
Accordingly, hypersomnia is considered to be the disturbance of Kapha and
1 A Brief History of Sleep Medicine in Children and Adults 3
insomnia is due to the disturbance in Vata. Sleep was divided into being physiologic
or pathological (due to a disease). Proper sleep also was linked to happiness,
strength, knowledge, and even longevity [6].
Greeks both through their literature and through their scientific dialogues are
among the earlier civilizations that discussed and documented sleep-related topics
in their writings. Alcmaeon (about 500 BC) proposed that sleep is produced by
withdrawal of blood from the body surface to larger central vessels. Hippocrates
and later Aristotle discussed sleep in more depth in their writings. Among medica-
tions, narcotics from opium poppy were used to induce sleep-like states [5].
In contrast to other cultures, physicians from Rome theorized that sleep is caused
by partial or complete splitting of atoms. Interestingly, neural theory of sleep as loss
of central control of peripheral muscles also was discussed in ancient writings from
Rome [4].
1.3 Sleep in the Scriptures
Jewish, Christian, and Islamic scriptures all have repeatedly discussed sleep and in
particular dreams. Sleep is seen as an essential physiologic function given by the
Creator. The scriptures consider sleep similar to death except that sleep is tempo-
rary, while death is final loss of consciousness. In the scriptures, the value of good
sleep, especially the one that is at night, is mentioned and recommended, with 8 h
sleep per day being advocated as desirable [7]. Scriptures view the dreams as a
method of prophecy. The most famous of them are the dreams of Joseph, the son of
Jacob. In the scriptures, various dreams experienced by Joseph while he was with
his father and subsequently Joseph’s role as a trusted interpreter of the dreams of the
pharaoh are emphasized and attest to the unique importance of the underworld acti-
vated by sleep to control the events and future reality of wakefulness. The dreams
may have been considered as a method of communication and of conveying com-
mands by the Creator. An example in the Bible is the dream of Joseph to take Mary
as his wife. As a matter of fact, interpretation of the dreams is considered a very
important and a scary task that can only be assumed by a few selected ones who
possess singular clairvoyance. Many elements of sleep hygiene, restorative effects
of sleep, circadian rhythms of sleep, and discussions about treatment of insomnia
and excessive daytime sleepiness are discussed in the religious texts including the
Bible, Talmud, and Quran [4, 5, 8, 9] and the related texts of these holy books as
drafted by religious scholars. In general, scriptures consider sleep an essential func-
tion and dreams were a way of the Creator commanding and prophesizing.
Interpretation of scriptures affected the communities of the followers. Further, the
interpretations of the scriptures are influenced by the cultures and the advancement
of sleep science. Interestingly, the religious establishment significantly influenced
practice of medicine in the earlier part of the Middle Ages (AD 476 to AD 1453).
Establishment of medical schools during the latter part of the Middle Ages allowed
for a transition to more observation-based medical diagnosis and treatment rather
than mysticism for all ailments including sleep disorders [4].
1.4 Scientific History of Sleep Medicine
Theories about sleep and dreaming were and remain abundant and have originated
from philosophers, clinicians, and scientists. Many of these theories were generated
by observations of individuals during sleep. The theories includes the vascular theo-
ries related to increased (congestion) or decreased blood (anemia) supply to the
brain, the neural theories (reduced neural activities), chemical theories (accumula-
tion of substances or neurotoxins), and behavioral theories [4, 10]. Interestingly,
most of these theories either in their entirety or partially have been refuted by the
recent advances of the last 80 years. However, it was not until scientific tools to
study the nervous system became available that our understanding of sleep became
better defined.
The electroencephalogram (EEG) was developed as a noninvasive tool to study
the brain during sleep and answer the fundamental question of whether the brain in
sleep is active or inactive. To this end, Nathaniel Kleitman stated that “It is perhaps
not sleep that needs to be explained, but wakefulness” [11]. This tool gradually
moved from the research laboratory to clinical practice and tremendously helped to
diagnose and treat many sleep disorders. Understanding of sleep would not have
been possible until the discovery that neurons are connected through synapses and
knowing that the cells communicate with each other through electrical signals and
neurotransmitters. Luigi Galvani (eighteenth century) elucidated the electrical
activity of nervous system, Richard Caton (1875) discovered the electrical activity
of the brain, and Hans Berger (1929) recorded the electrical activity of the brain
(electroencephalogram) during wake and sleep [5, 10]. He identified alpha rhythm
(also was called Berger’s wave) in addition to recognizing that when a person fell
asleep, the alpha rhythm disappeared.
Subsequently, studies in early decades of the twentieth century by groups from
Harvard University and the University of Chicago showed that in fact sleep has its
own characteristic electrical activities [12]. The discoveries showed different stages
of sleep including calm wakefulness with dominance of alpha, periods of synchro-
nized slow activities, and periods of sleep with increased activity.
The next important stage in understanding sleep physiology comes with the
ability to study eye movements using electro-oculogram which helped scientists
to discover rapid eye movements (REMs) and associate these movements with
dreaming. Indeed, when patients were awakened during REM sleep periods, they
could describe vivid dreams while they were not able to do so when they would
be aroused from a quiet sleep. Additionally, the increases in heart rate and breath-
ing rate that were seen during the rapid eye movements contrasted with the slow-
ing of respiration and cardiac frequency during non-REM sleep [13, 14]. The next
important piece of information about sleep came after studying subjects’ sleep in
the entirety of the night and discovering the alternating pattern of non-REM and
REM sleep [15]. Subsequently, REM sleep muscle atonia was discovered, and
consequently REM sleep was defined as sleep with rapid eye movements, dreams,
and active brain EEG similar to wakefulness but in the presence of diffuse muscle
atonia [10].
After defining the various stages of sleep, further studies investigated the neuro-
physiological mechanisms involved in transitioning from one state to another.
Discovering the link between hypothalamic pathology and hypersomnia and the
link between lesions of preoptic area and anterior hypothalamic region to insomnia
were major breakthroughs in connecting the anatomy to sleep-related symptoms
[16]. Further studies in the early 1900s showed that stimulation of central thalamus
results in sleep [5]. One of the earlier discoveries on this topic was understanding
that reticular activating system may be feeding the cortex and thus maintaining
wakefulness [17]. Later, Michel Jouvet in Lyon, France, demonstrated that stimula-
tion of the caudal mesencephalic region and pontine tegmentum leads to a REM-
like state and coined the term “sommeil paradoxal” (paradoxical sleep) to REM
sleep [18]. The discovery of two peptides (1998) in the hypothalamic area, by two
independent groups, with effects on wakefulness and appetite (and hence named
hypocretin/orexin) significantly increased our understanding of neurophysiological
mechanisms of sleep, REM sleep, and narcolepsy [3].
Another aspect of sleep science focuses on circadian rhythms that exist in all liv-
ing beings. The anterior hypothalamus was identified as the main region governing
the biological clock by Curt Richter (1965) and more specifically the suprachias-
matic nucleus [19]. Further studies in the 1960s and 1970s clarified the circadian
variations in endocrine function and thermoregulation and ultimately extended the
concept of circadian rhythms to all cells denoting the presence of a major central
clock and a myriad of peripheral clocks regulated by the central one [5]. As recently
as 2017, the fundamental discoveries of molecular mechanisms controlling the cir-
cadian rhythm led to the attribution of the Nobel Prize in Physiology or Medicine to
Jeffrey C. Hall, Michael Rosbash, and Michael W. Young.
1.5 History of Polysomnography in Sleep Medicine
Polysomnography, i.e., the objective scientific method used for studying sleep,
developed in the second quarter of the twentieth century. The polysomnogram, born
out of electroencephalography, originated in psychophysiology, matured with clini-
cal science, and ultimately became employed by sleep medicine. Owing its roots to
electroencephalography and other electrophysiological recording techniques, poly-
somnography rapidly evolved from its role for scientific inquiry to clinical applica-
tions [20]. A major issue with EEG at the beginning was the inability to record for
long periods of time. Gibbs and Garceau were able to construct a one-channel EEG
machine by adapting the Weston Union Morse Code ink-writing undulator, while
Albert Grass who was working on earthquake seismographs created a three-channel
EEG machine. After 1938, EEG rapidly gained popularity as both a research and a
clinical tool. Polygraphic recording devices (e.g., the Grass Model 1) became then
commercially available [20].
As use of polysomnography became widespread, the lack of standardization in
scoring became apparent. In a very interesting study, Monroe compared 28 raters
from 14 sleep centers who scored the same 398 min of a sleep study. The study
showed that the interrater reliability was low and recommended standardization of
sleep stages [21]. In 1967, a committee of experts, led by Allan Rechtschaffen and
Anthony Kales, took on the task of developing standard rules for scoring sleep
stages. The result of this work was published as “A manual of standardized termi-
nology, techniques and scoring system for sleep stages of human subjects” and is
known of R&K scoring rules [22]. In 1971, “A Manual for Standardized Techniques
and Criteria for Scoring of States of Sleep and Wakefulness in Newborn infants”
was published [23]. The R&K guidelines were developed for normal sleep and had
major limitations when used in clinical settings. Thus, the American Academy of
Sleep Medicine developed an improved and expanded scoring manual named
“AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology,
and Technical Specifications” in 2007. Subsequently, the board of Directors of the
AASM mandated that the scoring manual be updated regularly and be published
online. The Version 2.0 is the first scoring manual transitioned to a true digital for-
mat [24]. The latest update to the scoring manual, Version 2.6, was published in
2020. The AASM updated the visual scoring of sleep in infants 0–2 months of age
in 2016 [25]. Additionally, international groups formed to develop standards for
recording and scoring clinical polysomnographic information. Notable among these
groups is the team that published an atlas for cyclic alternating pattern scoring and
the World Association of Sleep Medicine (WASM) in collaboration with the
International Restless Legs Syndrome Study Group (IRLSSG) who updated the
guidelines for periodic leg movement assessment (which ultimately was adopted
virtually unchanged by the AASM) [26, 27].
Another major advancement in the field of sleep disorders was the creation of a
system for sleep disorder classification that could be used for clinical diagnosis and
coding of all known sleep disorders. This task was commissioned by the Association
of Sleep Disorders Centers (ASDC) and the first publication appeared in the SLEEP
journal in 1979 [28]. Subsequently, the International Classification of Sleep
Disorders: Diagnostic and Coding Manual (ICSD) was developed [3]. Since then,
the American Academy of Sleep Medicine updated the manual under ICSD-2 in
2005 and later ICSD-3 in 2014 [29].
The emergence of sleep apnea as a highly prevalent disorder was the engine driv-
ing the huge expansion of the use of clinical PSG. Currently, 80–90% of all clinical
PSGs conducted attempt to rule in or rule out sleep-disordered breathing. For 40
years, attended polysomnography dominated as the preferred technique for evaluat-
ing sleep apnea and/or titrating positive airway pressure therapy. The widespread
recognition of sleep apnea as a significant medical condition affecting nearly one
billion people around the world was paired with a PSG’s billable CPT code and
produced a meteoric rise in sleep medicine. However, economics drove the market
toward finding a less expensive alternative; thus, the cardiopulmonary recording
arise, also known as home-sleep testing (HST) or out-of-center sleep testing
(OCST). HST involves making overnight recordings of airflow, respiratory effort,
oxyhemoglobin saturation level, heart rate, and sometimes snoring sounds and
EEG. Its only validated use is to verify the presence of sleep apnea [30]. Other HST
devices use non-flow-based evaluation of respiration and cardiac functions during
sleep, and with current microelectronics and sophisticated digital processing analyt-
ics, this field is developing extremely rapidly and creating many different instru-
ments enabling diagnostic approaches for sleep apnea and other sleep disorders.
1.6 History of Sleep Medicine as a Medical Field
The field of sleep medicine grew out of the advancement in understanding of sleep,
development of reliable tools, and recognition of various sleep disorders by patients
and clinicians. Research in the field of sleep medicine continues increasingly and thus
expands the clinical field of sleep. Out of this growth is better understanding of physi-
ology of sleep and improved classification of the sleep disorders to better diagnose
and manage these ailments and discovery of novel molecular targets for developing
therapeutic agents. Of course, the field of sleep medicine would not have grown as
much if it was not for the societies related to sleep, various related scientific meetings,
establishment of various sleep clinics, and sleep medicine training programs.
The progress of a medical field depends not only on how science moves forward
on the field but also on how the related experts and scientists organize and form
scientific and professional societies. The first professional society related to sleep
and their related meeting in the USA, with international representation of sleep
scientists, was the Association for the Psychophysiological Study of Sleep (APSS)
organized by Dr. Dement in 1961. This initial organization also created a yearly
meeting to present scientific data. The meeting proceedings were originally pub-
lished in the Psychophysiology (the journal for the Society for Psychophysiological
Research) which showed the image of a polysomnographic tracing on its cover. For
the first time in 1971, the APSS meeting went outside the USA to Bruges in Belgium
and published a meeting book titled The Sleeping Brain. Along with the growth of
APSS, the European Sleep Research Society (ESRS) was formed in 1972 with the
leadership of Dr. Koella [31]. As APSS and clinical sleep services grew, the
Association of Sleep Disorder Centers (ASDC) with initially only five member cen-
ters started to function in early 1976 with Dr. Dement as its president and Dr.
Weitzman as vice president [3]. Out of ASDC came development of a specialty
board exam for sleep medicine. Along the APSS and ASDC, the Japanese Sleep
Society was formed and later led to the Asian Sleep Society. Additional outcome of
APSS, ASDC, and ESRS was the journal SLEEP with its first issue in 1977. The
ESRS later in 1992 developed its own publication named Journal of Sleep Research.
As field of sleep grew, other major sleep-related societies including the Australian
Sleep Association (1988) and the Chinese Sleep Research Society (1994) were
formed. In the meanwhile, in the USA, the Association of Polysomnographic
Technologists (APT) was formed in 1978, and a board of polysomnographic tech-
nologist registry (BRPT) administered its first examination in 1979. These groups
ultimately formed a confederation in 1986 called the Association of Professional
Sleep Societies (reusing the initials APSS), and ASDC was renamed the American
Sleep Disorders Association (ASDA) the following year (eventually becoming the
American Academy of Sleep Medicine [AASM] in 1999) [20].
The World Federation of Sleep Research Societies (WFSRS) was formed in

1987 to facilitate international collaboration among professional sleep societies.
WFSRS ceased to exist after it merged with the World Association of Sleep Medicine
(WASM) to form the World Sleep Society (WSS). While WFSRS focused on sleep
research, clinical researchers and practitioners felt the need to create an interna-
tional society to exchange sleep medicine information. Consequently, WASM was
founded in June 2003 with the main mission to advance sleep health worldwide by
promoting sleep medicine education, research, and patient care with more focus on
the areas of the world where sleep medicine is less developed [32]. Sleep Medicine
is the official journal of WASM. In 2011, WASM and WFSRS started discussing
and developing a path to create a unified organization to cover sleep internationally.
Out of this effort came the World Sleep Society (WSS) in 2016. The WSS has a
similar mission to WASM. With formation of WSS, WASM ceased to exist on 31
December 2017. With the expansion of sleep, currently WSS has more than 40
associate society members from all over the world [33]. Additional societies have
emerged along with their journals. For instance, the Society of Behavioral Sleep
Medicine has emerged as a very promising organization and venue aiming to imple-
ment psychology- and psychiatry-related methods to sleep disorders and improve
the understanding of sleep regulation and interactions with personality, physiology,
mood, and emotions. Similarly, the National Sleep Foundation was founded in 1990
with the specific mission of unraveling activities that link sleep and health through
theory, research, and practice. NSF’s mission is to improve health and well-being
through sleep education and advocacy. As the global voice of sleep health, NSF has
assembled experts in sleep to develop and publish evidence-based consensus guide-
lines and recommendations in crucial areas such as sleep duration, sleep quality,
sleep satisfaction, and drowsy driving, among others. NSF is known internationally
for its annual Sleep Awareness Week® and Drowsy Driving Prevention Week® advo-
cacy campaigns. NSF conducts research programs including the annual Sleep in
America® poll and quarterly Sleep Health Index® which are designed to explore
sleep health topics of interest and report on the status of sleep health in large and
small population groups. In 2015, NSF launched its journal Sleep Health to provide
a multidisciplinary peer-reviewed platform for sleep’s role in population health.
NSF’s journal and public health textbook Foundations of Sleep Health complement
its work translating rigorous science and scholarship into practical guidance so any-
one and everyone can be their Best Slept Self® [34].
The first clinic for sleep disorders was established by the late Dr. Dement as
Stanford University Narcolepsy Clinic, later morphing into a comprehensive Sleep
Disorders Clinic [2]. As clinical PSG gained ground, sleep disorder centers began to
open. Some notable early programs included the ones in Baptist Memorial
(Memphis), Baylor College of Medicine (Houston), Western Psychiatric (Pittsburgh),
Presbyterian (Oklahoma City), Ohio State (Columbus), Montefiore (New York),
Henry Ford (Detroit), Mount Sinai (Miami), Stanford University (Palo Alto, CA),
University of California (Irvine, CA), and Holy Cross (Mission Hills). This core
group collaborated on a variety of projects and their leaders were instrumental in
developing PSG applications for sleep medicine [20]. These sleep disorder centers
created a nucleus from which the Association of Sleep Disorders Centers (ASDC)
grew. The main focus of these sleep centers was to conduct clinical PSG procedures.
AASM accredited for the first time a sleep center in 1977. As of 2022, there are
2582 AASM-accredited sleep disorder centers (personal communication
with AASM).
1.7 Education and Training History of Sleep Medicine
As the field of sleep medicine grew and needs for sleep clinical services became
apparent, so came the need to provide training and certification in the field of sleep
medicine. ASDC formed an education committee in charge of developing a curricu-
lum for sleep medicine. As training programs started, a plan for certification for the
purpose of competency was envisioned. Dr. Helmut Schmidt led the ASDC sub-
committee in charge of certification. Many of the materials came from the record-
ings performed at Stanford and Cincinnati. The first exam was administered by
Thomas Roth, Helmut Schmidt, and Christian Guilleminault at Stanford and later
was moved to Columbus Ohio. ASDC administered the sleep medicine competency
evaluation from 1978 to 1990. Subsequently, the American Board of Sleep Medicine
as an independent certification body administered the exam from 1991 to 2006 and
issued the certificate abbreviated as Diplomat-ABSM to 3445 diplomats [35].
Initially, the candidates responded to written true-false questions and oral questions.
However, starting in 1980, the exam was taken in a two-part format administered on
separate days. Sleep medicine was recognized as an independent subspecialty by
the Accreditation Council for Graduate Medical Education (ACGME) in 2003
which paved the way for developing a subspecialty exam by the American Board of
Medical Specialties (ABMS). Since 2007, ABMS has been administering the certi-
fication examination in sleep medicine. Initially, the exam was administered bian-
nually, but currently, the applicants can take the certification exam annually [36].
Since 2011, the only pathway for ABMS Sleep Medicine certification is through
Accreditation Council for Graduate Medical Education (ACGME)-accredited
1-year sleep medicine fellowship training [35].
Another milestone in the field of sleep medicine was the publication of Principles
and Practice of Sleep Medicine by Kryger, Roth, and Dement in 1989 with 739
pages. The latest (7th) edition of this book was published as a two-volume set in
2021 with 213 chapters in 2240 pages. The Principles and Practice of Pediatric
Sleep Medicine came out in 2001 and with the second edition in 2012 expanded the
field. A third edition of this book is expected soon.
In summary, sleep and dreams have perplexed human beings since the dawn of
humanity. However, it is really the major advances that occurred during last 100
years or so that have immensely increased our knowledge and understanding of
sleep and sleep disorders and their treatment. History of sleep is clearly in the mak-
ing, and we are all part of it.
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Neurological Aspects of Sleep Medicine,
How Sleep Evolves, and Regulation 2
of Function
Lourdes M. DelRosso, Raffaele Ferri, and Oliviero Bruni
2.1 Introduction
The brain undergoes dynamic structural and functional changes across the life span.
Some of these changes are more evident in the transition from adolescence to adult-
hood. The various structures, regions, and neural networks undergo maturation and
development of their distinct trajectories and connections. In the past century, the
discoveries and advances in diagnostic technology methods have contributed to our
understanding of the neural networks involved in sleep; in particular, electroen-
cephalography (EEG) and magnetic resonance imaging (MRI) have shed light on
the identification of specific brain areas/structures involved in the physiology of
sleep and wakefulness. These and other techniques have allowed the identification
of sleep stages and the changes of sleep stages and EEG activity across the life span.
For instance, markers of sleep such as K-complexes, sleep spindles, and slow wave
activity (SWA) have been studied in relation to changes across various age
groups [1, 2].
Healthy sleep is necessary for normal growth, development, cognition, and over-
all good physical health [3]. For instance, the finding that short sleep duration in the
first 3 years of life is associated with hyperactivity/impulsivity and lower cognitive
performance on neurodevelopmental tests at 6 years of age is very important and is
L. M. DelRosso
University of California San Francisco, Fresno, CA, USA
R. Ferri
Sleep Research Centre, Oasi Research Institute – IRCCS, Troina, Italy
e-mail: rferri@oasi.en.it
O. Bruni (*)
Department of Social and Developmental Psychology, Sapienza University, Rome, Italy
e-mail: oliviero.bruni@uniroma1.it
© Springer Nature Switzerland AG 2023 13

https://doi.org/10.1007/978-3-031-30010-3_2
14 L. M. DelRosso et al.
consistent with previous evidence for short-term effects of sleep loss. Furthermore,
it has been reported that specific cognitive deficits and high hyperactivity scores at
6 years of age are most strongly associated with a pattern of short sleep duration at
2.5 years of age suggesting that insufficient sleep during the first few years of life
may have long-standing consequences [4].
The Millennium Cohort Study on 11,000 children showed that nonregular bed-
time at the age of 3 years is independently associated, in girls and boys, with lower
reading, math, and spatial scores. Girls who never had regular bedtimes at the ages
of 3, 5, and 7 years had significantly lower reading, math, and spatial scores, while
for boys this was the case for those having nonregular bedtimes at any two ages (3,
5, or 7 years) [5].
However, sleep is not a static but rather is a dynamic state, involving variations
in cerebral blood flow, neurotransmitters, immune response, and metabolic changes
[6]. The understanding of the changes across the life span can help the sleep physi-
cian understand processes that occur in sleep and wakefulness while helping adoles-
cents in their transition into adulthood.
In this chapter, we will further explore the neurological aspects that can influence
sleep and wakefulness in the adolescent patient during transitioning into adulthood.
We hope that this understanding will add to our set of tools to evaluate and treat
patients with sleep disorders.
2.2 Brain Changes Across the Life Span
Recent advances in neuroimaging techniques have demonstrated important changes

in brain structure, function, and metabolism across the life span. In 1990, Van Der
Knaap et al. [7] demonstrated changes in the brain metabolism of children aged
3–16 years, using magnetic resonance spectroscopy. The transition from childhood
to adulthood has also been shown to be accompanied by increased levels of
γ-aminobutyric acid (GABA) in the frontal cortex, while, in the subcortical region,
the levels of glutamate were found to be decreased. Glutamine increases during the
first years of childhood and then decreases from childhood to adulthood and contin-
ues decreasing until elderly. This glutamate reduction was postulated to represent a
maturational change in the function or the density of glial cells [8].
Structural Brain Changes
Brain volume peaks at the age of 10.5 years in females and 14.5 years in males, fol-
lowing a decline (inverse U-shaped trajectory) with aging (Box 2.1) [9]. The cere-
bellum follows a similar inverse U shape, with a peak volume a little bit later at 11.3
years in girls and 15.6 years in boys, but the cerebellar vermis does not show changes
across the life span [10]. The gray matter also shows an inverted U-shaped trajec-
tory, and the white matter volume increases through adolescence, probably second-
ary to the increase in myelin [9]. These trajectories, shape, and changes in volume
2 Neurological Aspects of Sleep Medicine, How Sleep Evolves, and Regulation… 15
may help to clarify functional phenotypes and changes in sleep disorders. An exam-
ple is seen in the changes in periodic leg movements across the life span described
by Ferri et al. [11] who found peculiar changes only in the periodic leg movements
mirroring changes in dopaminergic networks, not shared by the other leg movement
indices. These changes also include maturation and changes in brain connectivity
networks. Synaptic density, for example, is low at birth, increases significantly over
the first years of life to a maximum during mid-childhood, and then declines across
adolescence, so that synaptic density at 10 years is approximately the double of that
found at the age of 20 years [12]. The maximum synapse density varies in a way that
is specific to each brain region and reaches a maximum at different ages, for exam-
ple, the highest synapse density for the auditory cortex occurs at 3 months of age.
Tests of brain glucose utilization have been used as markers of nerve cell functional
activity. Regional cerebral blood flow increases during infancy until school age and
then decreases to adult levels at around the age of 16–18 years [13].
Box 2.1 Summary of Brain Changes from Adolescence to Adulthood

1. Brain volume peaks at the age of 10.5 years in females and 14.5 years
in males.
2. White matter increases through adolescence.
3. Synaptic density is maximum during childhood and decreases in
adolescence.
4. Regional brain flow increases during childhood but decreases to adult lev-
els at age 16–18.
Functional Changes in Neurotransmitters
The maturation and development of the human brain also involves the maturation
and development of the neurotransmitter systems. Unfortunately, research on the
difference between the individual changes in neurotransmitters remains sparse. A
deeper understanding of these changes is of utmost importance, particularly in the
area of psychopharmacology and treatment of sleep disorders with medications
approved and studied in adults but with unknown effects in adolescents.
Studies have shown a U-shaped progression of norepinephrine levels (Box 2.2)
in plasma with an initial sharp drop starting at 5 years and reaching the lowest levels
at the onset of puberty, after which they tend to increase until the age of 40–60 years
[14]. Adrenergic receptors in the brain of animal models have shown an increase in
the first years of life, followed by a plateau and subsequent decline during the young
adult years [15]. There are also important functional differences in the upregulation
of noradrenergic receptors. While in adults higher norepinephrine levels in the brain
cause downregulation of receptors, in the developing brain, higher norepinephrine
levels cause upregulation of alpha-2 receptors. One must think of the psychophar-
macological applicability of this finding, in particular using medications that are
proven to be effective in adults and extrapolating their use in adolescents. An exam-

ple is the use of tricyclic antidepressants which may not be effective in children (or
adolescents) but are effective in adult depression [16].
Dopamine is essential for movement, arousal, and reward, among other impor-
tant functions. Dysfunction in dopaminergic networks has been implicated in rest-
less legs syndrome and periodic leg movement disorder, among other sleep
disorders. Dopamine levels peak in various brain regions during adolescence.
Animal models have also shown a prepubertal peak in D1 and D2 receptors in the
brain, with a subsequent plateau and decline during adulthood [17].
Serotonin is also involved in sleep and arousal, among other functions. Positron
emission tomography studies have demonstrated that serotonin synthesis capacity
increases in the first years of life, decreasing to adult levels by the age 14 [18]. Brain
area-specific and receptor-specific changes are seen in childhood and adolescence
but with an overall peak in serotonergic activity in the child brain [15]. The clinical
implication of these findings is related to side effects of selective serotonin reuptake
inhibitors.
Box 2.2 Trough and Peak Levels of Neurotransmitters in Childhood and

Adulthood
Neurotransmitter Age at trough level Age at peak level

Norepinephrine Adolescence Adulthood
Dopamine Older adult Adolescence
Serotonin Adolescence Childhood
2.3 EEG and Sleep Changes
It has been shown that distinct patterns of EEG activity become associated with dif-
ferent behavioral states when the cortex becomes able to generate its own oscilla-
tory rhythms, independent of sensory stimulation. One could speculate that the goal
of neural activity during the development is to refine cortical circuits, by pruning
and synaptic potentiation, and this process seems to occur at all times, during wake-
fulness or sleep [19]. In normal healthy infants, sleep cycles typically last a mean of
50–60 min (range: 30–70 min). Wakefulness represents only 8–10% of a 24-h day
in infants up to 8 weeks post-term. Until approximately 44 weeks of conceptional
age, sleep cycles repeat in a polyphasic pattern across the 24 h, interrupted approxi-
mately every 3–4 h by an awakening for care and feeding. Within a given sleep
cycle, REM sleep lasts 10–45 (mean 25) min, NREM near to 20 min, and transi-
tional sleep about 10 min. NREM and REM sleep are typically evenly distributed
during the night.
The most conspicuous changes in sleep architecture during infancy and early
childhood are (1) decrease in total sleep time, (2) gradual consolidation of periods
of sleep at night or wakefulness during the day, (3) decrease in the intensity of (EEG
power) of NREM sleep stage 3 slow-wave activity (SWA), and (4) a steady decline
in the percentage of sleep time spent in REM sleep [20]. We will proceed to discuss
these changes in more detail.
Scholle et al. [21] published normative values for one-night PSG in children
aged 1–18 years using the American Academy of Sleep Medicine (AASM) sleep
scoring to standard criteria [22]. They found that sleep architecture showed signifi-
cant changes with increasing age. REM latency, awakening index, sleep efficiency,
mean sleep cycle duration, and number of sleep stage shifts increased with age.
Total sleep time, wakefulness after sleep onset, movement time, number of sleep
cycles, NREM sleep stage 3, and REM sleep decreased. Sleep parameters which
showed a dependency on Tanner staging, as well as corresponding age, were total
sleep time, awakening index, REM latency, NREM sleep stages 2 and 3, number of
sleep cycles, and mean sleep cycle duration. No gender dependencies were found.
The delta power of NREM sleep stage 3 EEG activity decreases by more than 60%
between the ages of 10 and 20 years. SWA also declines across recurring periods of
NREM sleep within a night. Longitudinal studies have shown that the delta power
of the sleep EEG begins to decrease at around 11.5 years and is reduced by 60% at
16 years. The fall in delta power begins earlier in girls than in boys (consistent with
age-related changes in gray matter volume) but with time the overall rate decline
becomes similar between girls and boys at 16 years of age (Box 2.3).
The main characteristics of the normal adolescent EEG are indistinguishable
from the adult EEG. In fact, the AASM allows to score sleep recordings of patients
aged 13 years and older based on adult criteria. During wakefulness, the EEG is
characterized by beta waves and gamma waves with low voltage (5–10 μV) and
high frequency (30–120 Hz) [23]. During relaxed wakefulness, alpha rhythm
appears in the EEG with a frequency of 8–13 Hz. During sleep, REM, NREM, and
its sub-stages (N1, N2, and N3) can be identified by their unique EEG, electroocu-
lography (EOG), and electromyography (EMG) findings.
Sleep stage N1 is characterized by low-amplitude, mixed frequency activity (4–7
Hz) for more than 50% of an epoch. Vertex sharp waves can be observed in sleep
stages N1 and N2 with a maximum duration of 0.5 s. The EOG can show slow eye
movements (SEM) during N1. Stage N2 is characterized by the K-complexes and
sleep spindles. K-complexes have a negative followed by positive deflection and last
at least 0.5 s. K-complexes decrease with age both in frequency and amplitude [24].
This change is thought to be secondary to age-related changes of the thalamocorti-
cal regulatory mechanisms. Sleep spindles have a frequency of 11–16 Hz and last at
least 0.5 s. Two types of sleep spindles have been reported in the literature: slow
(11–12 Hz), which is found over the frontal regions, and fast (14 Hz), which is
found over the central and parietal regions. Each type of spindle shows a different
maturation course. Centroparietal spindles appear to gradually increase with age,
while frontal spindles decrease from early childhood to adolescence and become
stable at 13 years of age [25]. Stage N3 slow waves have a frequency of 0.5–2 Hz
with a minimal amplitude of 75 μV. One of the most dramatic changes in sleep
architecture during adolescence is the significant decline in slow wave sleep (60%
between 11 and 16 years) [26]. Delta power begins to decline at 11 years and shows
a steep decline until about the age of 17 years during which this decline begins to
slow down. It has been suggested that this decline in slow wave sleep is associated
with maturation of networks in the frontal cortex.
Synaptic pruning during adolescence is accompanied by a reorganization of neu-
ronal connections, whereby mistargeted axons and unused synapses are eliminated
and connectivity becomes more specific. The decrease of synaptic density during
adolescence, which is reflected by changes in gray matter, proceeds asynchronously
in different brain areas, in line with the maturation of specific cognitive functions.
Changes in synaptic density are paralleled by changes in slow-wave amplitude [12,
26] and brain metabolism, presumably due to the increased energy requirements
associated with increased synaptic activity [27].
During development, none of the classical frequency bands change as dramati-
cally as the slow wave activity (SWA) band. The change of the amplitude of slow
waves parallels the number of synapses, that is, reduced synaptic density following
pruning is reflected by a decline in amplitude, and the location over which maximal
SWA can be measured undergoes a shift from the posterior to the anterior regions of
the scalp across childhood and adolescence, matching the time course of cortical
maturation, as tracked by MRI and behavioral studies [28], most likely reflecting
cortical plasticity during development. SWA is highest over the posterior regions
during early childhood and then shifts over the central derivations to the frontal
cortex in late adolescence. This trajectory of SWA topography matches the course
of the cortical gray matter maturation. Interestingly, synaptic density and slow-wave
amplitude are highest shortly before puberty and decline thereafter during adoles-
cence, reaching overall stable levels during adulthood. SWA is not merely reflecting
cortical changes but plays an active role in brain maturation [29]. Thus, sleep SWA
might be considered as a reliable indicator of net changes in average synaptic den-
sity/strength, both in the course of the night (sleep homeostasis) and in the course of
development. Investigation of sleep SWA topography during childhood and adoles-
cence confirmed this assumption by showing that the location on the scalp exhibit-
ing maximal SWA changed during development, shifting from the posterior to the
anterior scalp regions with time [28]. The changes in SWA topography probably
reflect synaptic changes accompanying the pruning process during cortical matura-
tion. Another link between cortical maturation and slow waves arises from a study
that compared the SWA decrease during adolescence with alterations in gray matter
volume [2, 30].
A study recently highlighted the connection between sleep restriction and neural
growth in school-age children revealing a local sleep homeostatic response follow-
ing acute sleep restriction, as indicated by the increase in SWA, over the parieto-
occipital areas and the negative relationship between the homeostatic SWA increase
in adjacent, parieto-temporal areas and local myelin content in the optic radiation.
These data suggest high plasticity in the parietal-occipital areas in children, which
is consistent with anatomical, neuroimaging, and behavioral data. The SWA rebound
after sleep restriction in children is strongest at the beginning of the night and levels
off with time in about 60 min, which is consistent with existing knowledge of the
homeostatic time course of sleep regulation. The parieto-occipital region is impli-

cated in processing visual signals (occipital lobe) and sensory information (parietal
lobe), thus affecting planned movements, spatial reasoning, and attention; based on
the study, these regions may be more vulnerable to a lack of sleep [2].
The main characteristics of REM sleep are the rapid eye movements seen in the
EOG with an initial deflection lasting less than 0.5 s and the simultaneous loss of
muscle tone characterized by the absent chin tone on EMG. The loss of muscle tone
is called REM sleep atonia. Quantitative EMG analysis has demonstrated that ado-
lescence is the stage with the most evident REM sleep atonia which decreases dur-
ing adulthood [31].
Box 2.3 Summary of EEG Changes During Sleep from Childhood into Adulthood
NREM REM
Slow wave sleep decreases during adolescence Latency increases with age
K-complexes decrease with age both in frequency and Amount decreases with age
amplitude
Centroparietal spindles gradually increase with age, Atonia peaks during
while frontal spindles decrease from early childhood to adolescence and then
adolescence and become stable at 13 years of age decreases with aging
2.4 Circadian and Homeostatic Changes
Process C (circadian regulation) and process S (homeostatic regulation) are part of

the two-process model of sleep regulation proposed in 1982 by Alexander Borbely;
these biological processes regulate the timing and length of sleep [32]. Process C
represents the 24-hour sleep-wake cycle regulated by the suprachiasmatic nucleus
(SCN) of the hypothalamus and has the core body temperature and melatonin levels
as the main markers [33, 34]. Process S, or the homeostatic process, refers to the
propensity to fall asleep, based on the previous amount of wakefulness [35] and has
as main markers NREM sleep and slow wave activity [36]. Sleep occurs when pro-
cess S approaches the upper threshold of process C, and wakefulness occurs when
process S approaches the lower threshold of process C [32].
Circadian Changes from Adolescence to Adulthood
Growing evidence supports that endogenous circadian period is altered during

puberty and explains the development of delayed sleep phase in adolescents.
Pediatric sleep doctors commonly see and evaluate teenagers who are often thought
to have insomnia due to the inability to fall asleep earlier than 11 pm or midnight,
yet, when allowed to go to sleep at these times, sleep latency is brief and sleep is
continuous until spontaneous awakening 9 h later. This is the hallmark of a delayed
circadian cycle. The disorder ensues when school demands a wakeup time at 6 or 7
am allowing only for 6 or 7 h of sleep. The adolescent then presents with symptoms
of daytime sleepiness, fatigue, and poor school performance. There is consensus
that sleep requirements are about 9 h of sleep at night for adolescents and do not
change significantly across puberty. Delayed bedtime and early school wakeup time
contribute to sleep insufficiency during school days and are the causes of catching
up sleep in the morning during weekends and of common complaints of excessive
daytime sleepiness in adolescents.
Research has shown a significant association between this circadian delay in
adolescents and puberty. Females start showing a delay in sleep time approximately
1 year earlier than males, paralleling the onset of puberty. The maximum delay in
sleep time also occurs earlier in females than in males (19.5 vs. 20.9 years). Global
research has also demonstrated that this delay in sleep onset occurs in adolescents
irrespective of cultural or geographical differences. This delay in sleep correlates
with the pubertal development of secondary sexual characteristics and persists for
weeks after sleep schedule is adjusted [37] (Box 2.4).
Few mechanisms have been postulated to explain the association between circa-
dian delay and puberty. The first and more obvious, due to the relationship with
puberty, involves the potential role of gonadal hormones in the regulation of the
circadian rhythm. Gonadectomy and/or administration of estrogen, testosterone, or
progesterone in rodents has shown an immediate effect on the circadian cycle [38].
The effect of gonadal hormones on circadian rhythms can be attributed to their
modulation of the suprachiasmatic nucleus either by producing anatomical changes,
entrainment, or rhythm generation [39]. Another mechanism proposed for changes
in circadian rhythm during adolescence and early adulthood suggests that age-
related sleep changes are associated with intrinsic changes in the circadian process,
such as age-related variation in the patterns of clock gene expression [40] or changes
in neuronal synchronization at the level of the suprachiasmatic nucleus. This may be
particularly applicable to changes seen in circadian rhythms of the core body tem-
perature and melatonin production in the elderly [41].
Homeostatic Changes from Adolescence to Adulthood
The decline in N3 during adolescence parallels a decline in homeostatic sleep pres-

sure. Jenni et al. [42] demonstrated that older mature adolescents (tanner 5) exhib-
ited slower buildup of homeostatic sleep pressure when compared to prepubertal or
early pubertal children; EEG after sleep deprivation, however, showed similar
changes in adolescents and adults [42]. These findings have important implications
as adolescents are often seen in sleep clinics for concerns of delayed sleep onset.
Typical recommendations to increase sleep pressure by prescription of sleep depri-
vation may not work due to their reduced homeostatic drive (Box 2.4).
In conclusion, changes in both circadian and homeostatic processes are
responsible for the sleep-onset delay seen during adolescence. Since both pro-
cesses change simultaneously [43], the delay during this age period is quite
evident. After adolescence, the return to earlier sleep time is not completely
understood but may continue to be associated with a balance between process C
and process S.
Box 2.4 Summary of Circadian and Homeostatic Changes
Circadian delay occurs during adolescence.

Decrease in homeostatic pressure accompanies the decline in slow-wave sleep.
2.5 Clinical Implications
In order to provide effective clinical sleep recommendations to our patients, we

need to have a better understanding of the physiological and structural neurological
changes that occur across the life span and, for this particular textbook, the changes
that occur during the transition from adolescence into adulthood which can translate
into changes in sleep time and duration.
Changes in brain maturation and growth have shown increased peaks of activity
or concentration of various neurotransmitters involved in sleep and wakefulness.
The peak in activity may be associated with significant side effects to medications
commonly used to treat sleep disorders in adults or children (i.e., dopaminergics),
and caution must be established when using these treatments off label with particu-
lar attention to activating side effects, or exacerbation of symptoms.
Circadian and homeostatic control of sleep simultaneously change during ado-
lescence explaining the delay in sleep onset that occurs in this age group. The
understanding of this physiological change will help sleep physicians with strate-
gies to improve sleep and daytime functioning in their patients. Such strategies
include policy changing advocating for late school times, counseling to families
about sleep requirements, and choosing activities that start at times that match the
natural brain sleep schedule.
2.6 Summary
Changes in sleep time and duration occur during childhood and adolescence and
may or may not persist into adulthood. The changes during adolescence have been
studied in relation to the two-process model of sleep regulation and in terms of the
contribution of hormonal changes and social demands during this period. Although
changes in brain development, neuronal connectivity, and neurotransmitter modula-
tion are known during this period, their contribution to sleep and sleep disorders still
need to be elucidated. Importantly, the understanding of sleep neuropharmacology
requires a complete understanding of these changes during adolescence and early
adulthood.
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Cardiorespiratory Changes as They
Relate to Sleep in Transition 3
from Pediatric to Adulthood
Giora Pillar
Abbreviation
CPAP Continuous positive airway pressure

ED Endothelial dysfunction
OSA Obstructive sleep apnea
SDB Sleep-disordered breathing
UAW Upper airway
3.1 Introduction
The cardiorespiratory system plays a major role in sleep, with a bidirectional rela-
tionships. It both affects sleep and is affected by sleep. Sleep deprivation or reduced
sleep quality or sleep-disordered breathing (SDB) is associated with a wide range of
diseases and adverse health outcomes, both physical and mental, and specifically in
children may also affect maturation (physical, mental, emotional). Some specific
factors may result in individuals vulnerability to SDB. The interrelationship between
the cardiorespiratory system and sleep may be affected by age and may change dur-
ing development. They are influenced by a variety of complex internal and external
factors. The current chapter describes various anatomical and physiological changes
in cardiovascular characteristics and their effects on sleep, during the transition
from childhood into adulthood. It focuses on characteristics that are likely to affect
or be affected by sleep such as upper airway (UAW) anatomy/physiology, cortical/
autonomic arousal thresholds, and vascular endothelial function.
G. Pillar (*)
Department of Pediatrics and Sleep Lab, Carmel Hospital, and Technion Faculty of Medicine,
Haifa, Israel
e-mail: gpillar@technion.ac.il; giorapi@clalit.org.il
© Springer Nature Switzerland AG 2023 25

https://doi.org/10.1007/978-3-031-30010-3_3
26 G. Pillar
3.2 UAW Anatomy
Anatomical abnormalities in the upper airway (UAW) play a major role in the
pathophysiology of obstructive sleep apnea (OSA) in all ages. In children, it is very
common to find hypertrophy of adenoids and/or tonsils, while in adults, anatomical
abnormalities may consist of fat deposits within the UAW making them narrow,
crowded posterior pharyngeal space (with or without enlarged tonsils), long UAW,
or change in the antero-posterior to lateral dimensions of the UAW. In some specific
pediatric syndromes, airway anatomy can be compromised. These include children
with Apert, Crouzon, or Pfeiffer syndrome, who develop obstructive sleep apnea
(OSA) mainly due to midface hypoplasia. Midface advancement is often the treat-
ment of choice, which results in moderate success [1]. It has recently been shown
that in children with craniosynostosis syndromes the cross-sectional retropalatal
area is predictive of OSA [2]. Children with Pierre Robin (PR) sequence [3] or
Treacher Collins syndrome [4] commonly suffer from OSA due to retromicrogna-
thia or mandibular hypoplasia [5]. There are several common imaging techniques
utilized to demonstrate these, such as CT, MRI, or video nasopharyngoscopy (VNP)
[6]. Mandibular distraction with mandible advancement which increases the airway
lumen is an effective treatment in such children [7]. Several such children who suf-
fered from severe OSA who required tracheostomy were completely cured follow-
ing this procedure [8]. Additional disorders which may be associated with inadequate
airway anatomy include cleft lip and palate [9], Chiari malformation [10], Schwartz-
Jampel syndrome [11], and achondroplasia [12, 13]. Down syndrome is an addi-
tional well-established disorder associated with high prevalence of OSA. It affects
both the anatomy and the physiology of the UAW, making them vulnerable for
collapse. Children with Down syndrome commonly have lymphoid hyperplasia,
macroglossia, and narrow nasopharynx [14–16], along with hypotony of the upper
airway dilatory muscles. Additional anatomical features of Down syndrome include
pharyngeal and maxillary hypoplasia and sometimes constricted maxillary arch
with nasal obstruction. Maxillary expansion has been suggested to relieve airway
obstruction in these children [17]. In adults, the most recognized anatomical risk
factor for OSA is obesity, especially the male-type obesity which can be observed
by increased neck circumference. Retrognathia, a small, crowded posterior pharyn-
geal space (with or without enlarged tonsils), and/or nasal obstruction can also
result in susceptibility for airway obstruction. The current chapter focuses on two
major anatomical changes which occur in the transition from childhood to adult-
hood: changes in tonsillar and adenoidal sizes and changes in upper airway length.
3.3 Tonsils and Adenoids
Adenotonsillar hypertrophy is the most common cause of OSAS in children, but not
in adults. Understanding the natural history of adenoids and tonsils and the factors
responsible for their growth and regression during development is of great impor-
tance especially for planning the treatment of OSA. While in children both adenoids
3 Cardiorespiratory Changes as They Relate to Sleep in Transition from Pediatric… 27
and tonsils generally have a major effect on the UAW, obesity when present may
have a major effect as well [18]. The impact of adenotonsillar size on childhood
OSA may be altered by both age and obesity [19, 20]. Tagaya et al. [19] emphasized
that the correlation between adenoid size and OSA is more prominent in preschool
children than in school-aged children. In quite many other studies, the correlation
between adenotonsillar size and severity of OSA was relatively small. Although
generally in most children with OSA the majority of the studies indicate that there
is increased tonsillar and adenoidal size [19, 21–25], it cannot well predict the
severity of the OSA. However, adenotonsillectomy has been shown as the most
effective treatment for children with OSA [26–31]. Since adenoid and tonsil hyper-
trophy is similar between genders, it may explain the similar prevalence of OSA in
prepubertal boys and girls (as opposed to the well-established substantial male pre-
dominance in adults with OSA). The adenoids are midline structures of lymphoepi-
thelial tissue located in the superior aspect and the roof of the nasopharynx. They
are part of the Waldeyer ring, whose components include the adenoids, the palatine
tonsils, and the lingual tonsils. They are composed of lymphoid tissues which are
considered (along with other lymphatic tissue in the nasopharynx) as the first line of
defense against ingested or inhaled pathogens. They are part of the lymphoid system
and are involved in the development of both B and T cells. Within the adenoidal
tissues, the immune system battles against infections. Activation of B cells within
the adenoids leads to their proliferation and hypertrophy. Recent studies have pro-
vided some evidence that adenoids produce T lymphocytes as well [32–34]. They
can be identified in utero (usually as early as the seventh month of gestation) and
typically grow until ages 4–7 when they reach their peak size. Commonly, their
hypertrophy is in parallel to upper respiratory tract infections, but their hypertrophy
can also be seen without chronic infections. They then tend to diminish in size until
they are almost unseen at puberty and adolescence in most individuals [32, 33, 35].
Early studies reported that in general adenoids and tonsils reach approximately
200% growth by late childhood and then involute during adulthood [36]. Other
studies also showed that adenoids decrease in size with age, typically atrophying
completely by the teenage years [37]. In a recent Japanese study, it was reported that
adenoidal and tonsillar size gradually decreased when compared between lower
primary school stage (ages 3–6) and young adult stage (ages 18–20 years). However,
they showed that sometimes adenoids, and even more often tonsils, do not com-
pletely vanish and in some individuals they may persist into adulthood [38]. Chuang
et al. [39] on the other hand reported that increased neck circumference and tonsillar
hypertrophy were the most influential factors for younger children, whereas adenoi-
dal hypertrophy became more important at an older age [39]. It should be high-
lighted that even when the lymphoid tissues of the adenoids and/or tonsils do not
decrease with age, their impact on the upper airway diminishes since the upper air-
way grows substantially and thus the ratio of lymphoid size within the lumen tend
to decrease even then [38]. Persistence of adenoid tissue into adulthood is an uncom-
mon clinical finding and when seen should raise suspicion of immunocompromised
patients, in whom this finding may be caused by regressed adenoid tissue reprolif-
erating in response to infections [19, 32–35].
28 G. Pillar
Similarly to adenoids, tonsils tend to grow during childhood, reach the maximal
relative size around age 5.1–8 years [40], and then regress. In some adults, tonsils
may remain enlarged into adulthood. There are several methods for assessing tonsil-
lar size such as by subjective score during physical examination, imaging tech-
niques such as MRI or transcervical ultrasonography, endoscopy, digital
morphometrics based on a laser ruler, and more. This chapter does not focus on the
way of assessing tonsillar size but rather on their change from childhood to adult-
hood and on their impact in terms of sleep-disordered breathing. In children without
sleep-disordered breathing, using MRI, Arens et al. [41] reported that soft tissues,
including tonsils and adenoid, grow proportionally to the skeletal structures during
the development from age 1 to 11 years [41]. Cohen et al. [40] on the other hand
reported that the bony nasopharynx and the pharyngeal tonsil tissue both grow dur-
ing childhood. Different growth rates result in the narrowest airway in the age group
of 5.1–8 years [40]. While the transition from childhood to adulthood is associated
with reduced tonsillar size, it is usually also associated with increased weight, which
questions the relative contribution of each to OSA. In a study by Dayyat et al. [20],
412 children with OSA, with or without obesity, were assessed for tonsils and ade-
noid sizes and Mallampati class scores. They reported that the magnitude of adeno-
tonsillar hypertrophy required for any given magnitude of obstructive
apnea-hypopnea index (AHI) is more likely to be smaller in obese children com-
pared to nonobese children. Increased Mallampati scores in obese children sug-
gested that soft-tissue changes and potentially fat deposition in the upper airway
may play a significant role in the global differences in tonsillar and adenoidal size
among obese and nonobese children with OSA [20]. Interestingly, in obese adoles-
cents aged 12–16 years, Schwab et al. [42] found that increased size of the pharyn-
geal lymphoid tissue, rather than enlargement of the upper airway soft tissue
structures, is the primary anatomic risk factor for OSA. Thus, they suggested that
adenotonsillectomy (and not only weight reduction) should be considered as the
initial treatment for OSA in obese adolescents [42].
When tonsils remain enlarged into adulthood, they definitely have an effect and
may contribute to OSA. Tonsillectomy in adults with OSA and tonsillar hypertro-
phy revealed positive therapeutic results in many studies [43–45]. Furthermore, ton-
sillar hypertrophy may have an effect on other therapies. Tschopp has recently
shown that tonsil grade and volume both showed a significant correlation with pre-
operative AHI [43]. They have performed uvulopalatopharyngoplasty (UPPP) to
their patients and found that the AHI reduction after surgery increased significantly
with larger volume and higher tonsil grade [43]. They concluded that large tonsils
are responsible for higher preoperative AHI values, and their removal leads to
greater reduction of initial AHI. Interestingly, in contrast to previous studies, Jara
and Weaver reported that subjective tonsillar grade was more strongly associated
with AHI than objectively measured tonsillar volume [46]. They therefore con-
cluded that the space that the tonsils occupy within the oropharyngeal airway, rather
than their actual measured volume, is more predictive of OSA severity [46].
To summarize this part, pharyngeal lymphoid tissues (tonsils and adenoids) tend
to grow during childhood initially more than the upper airway, resulting in a peak
3 Cardiorespiratory Changes as They Relate to Sleep in Transition from Pediatric… 29
relative size during early childhood. These tissues tend to shrink during adolescence
into adulthood, but not in all. When these tissues remain enlarged in adults, they do
play a role in the pathophysiology of OSA and their removal results in alleviation of
sleep-disordered breathing.
3.4 UAW Length
The length of the pharyngeal airway (from the hard palate to the epiglottis) is also
of great importance while dealing with UAW anatomical changes from childhood to
adulthood. It is a physical characteristic of a collapsible tube to increase collaps-
ibility as the tube is longer. In adults, it was previously reported that UAW length
was higher in normal males compared to females, even after correction for body
height [47]. It was therefore concluded that UAW length may play a role in the male
predisposition to pharyngeal collapse [47]. Furthermore, a major impact of UAW
length on pharyngeal mechanics and collapsibility have been demonstrated utilizing
computational modeling [47]. In adolescents, however, it has been found that the
UAW length in pre-pubertal children is equal between genders, while following
puberty, males were found to have longer upper airways than females (corrected for
height). This study of 69 healthy adolescents who had undergone CT scans of the
neck may therefore partially potentially explain the relatively strong male predomi-
nance in adults but not in children with OSA [48]. The transition from childhood to
adolescence was not associated with general lengthening of the corrected UAW
length (UAW length divided by height) but rather with gender effects [48], i.e., the
ratio of UAW length to body height becomes higher in males vs females. Thus,
gender-related differences in upper airway length may explain to some extent the
male predisposition to airway collapse that occurs in post-pubertals and adults.
Moreover, data show that UAW length is greater in patients with OSA than in con-
trols, with a positive significant correlation between the UAW length and the sever-
ity of OSA [49]. This was the case in both adults [49] and children [50]. Fifty
children aged 10.3 ± 0.6 years with syndromic craniosynostoses (50% boys, 48%
with OSA) underwent both UAW imaging and sleep studies. Those with OSA had
significantly higher UAW length (P = 0.016) [50]. Interestingly, weight gain and
obesity may play a role in this regard as well. It was recently reported that weight
gain leads to significant fat infiltration in the tongue, causing the hyoid to move
downward and lengthen the airway in patients with OSA [51]. The apnea-hypopnea
index (AHI) strongly correlated to airway length and tongue size [51]. Furthermore,
24 weeks of weight reduction program in patients with OSA resulted in UAW length
shortening, although the exact mechanisms remained unclear [52]. Thus, UAW
length is an important anatomical feature of the airway which should be taken into
consideration when assessing tendency to collapse and potential explanation of
OSA in both children and adults. It seems that the most relevant change that occurs
from childhood to adulthood is the greater corrected UAW length in males vs
females. The higher UAW length seen in OSA vs non-OSA patients seems similar
in children and adults.
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CHAPTER X.
BATTLE OF MECHANICSVILLE.
Two days later Gen. Stoneman pushed forward with cavalry and
artillery, on a bold reconnoissance toward the rebel capital. Gen.
Davidson’s Brigade followed, as a support, the rest of the Division
remaining behind. About four o’clock in the afternoon, the General
fell in with the enemy—“Howell Cobb’s Brigade”—who retreated after
a few shots had been exchanged. Stoneman again moved forward,
halting for the night just east of Beaver Dam Creek, and the Brigade,
crossing over, took up position on an elevated spot, and slept on
their arms. This creek is a narrow, muddy stream, emptying into the
Chickahominy.
A part of the Thirty-third were employed on picket duty until the
next morning, being stationed in close proximity to the rebels. At
daybreak the infantry pushed on towards Mechanicsville; General
Stoneman with the cavalry proceeding further to the right. Three
companies of the Thirty-third acted as the advance guard, and were
deployed as skirmishers. When within two hundred yards of
Mechanicsville, the rebels, who had fallen back during the night,
were discovered drawn up in the principal street, and in a
neighboring grove. The skirmishers immediately opened upon them,
when taking refuge in buildings and behind walls, they returned the
fire.
The whole Brigade now moved up on both sides of the road, and
two sections of Wheeler’s battery were got into position, and
commenced tossing shell into the village. This placed the
skirmishers between two fires, and for a time, they were nearly as
much exposed to our own as the rebels. One had his canteen
perforated by a piece of shell thrown from the Union battery, another
had a part of his shoe taken away. The firing of the rebel cannoniers,
at first slow, became very rapid and accurate as the battle
progressed. One solid shot passed between Major Platner and
Captain Guion, as they stood conversing together. A second whizzed
close by the head of Colonel Taylor’s horse, and a third striking the
roll of blankets strapped on behind a horseman, threw them high into
the air. Every one held their breath for a moment, supposing that it
was the rider himself, but he escaped unharmed.
The guns were afterwards removed to the right of the skirmishers,
and a section of flying artillery posted on the left. A heavy fire was
now concentrated on the buildings in which the confederates had
concealed themselves, soon causing an exodus on their part, and
the whole force commenced falling back in the direction of
Richmond. Seeing this, Gen. Davidson ordered a charge, when the
Thirty-third and Seventy-seventh gallantly charged down upon the
place, driving everything before them.
MECHANICSVILLE, VA.
Large numbers of knapsacks and blankets which the rebels had
thrown away in their flight were picked up in the streets. They were
most of them marked “Rome (Ga.) Light Guards.” Guns, equipments,
blankets, and other materials of war, were likewise found in large
quantities. Nearly all the houses were more or less pockmarked with
shot and shell. The Mayor’s residence, an elegant mansion, had
been struck seventeen different times. Those of the inhabitants who
had not fled, were found packed away like sardines, in cellars and
other places of refuge. They were very much frightened, and not until
repeatedly assured that we would not harm them, could they be
prevailed upon to come out.
After taking possession of the village, a line of skirmishers was
thrown out half a mile on the Richmond road. Detachments of the
Thirty-third, Seventh Maine, and five companies of cavalry were left
in charge of the town. They were relieved upon the following day,
and rejoined their regiments on the Beaver Dam, to which the
Brigade had returned after the engagement. Some members of
Company E discovered a grist mill here, and spent most of the night
in grinding corn, and making hoe-cake.
Gen. Stoneman had in the meantime proceeded several miles to
the right, and accomplished the object of the expedition by
destroying the Richmond and Fredericksburg railroad bridge over the
Chickahominy.
With one exception this was the nearest point attained to
Richmond during the entire Peninsular campaign. Gen. Hooker, after
the battle of Fair Oaks, followed the fleeing enemy to within less than
four miles of their capital.
That it could then have been taken had General Davidson’s
brigade been reinforced and permitted to proceed, is a truth which
admits of no denial. There were no rebel forces between
Mechanicsville and the city, with the exception of those driven from
the former place, they being concentrated on the left of our lines.
There were no fortifications of any extent on that side of the capital,
as the attack was expected to be made from the other direction. The
approaches were all left open, and the appearance of this single
brigade of “Yankees” struck terror to the rebels, who inferred that all
was lost.
CHAPTER XI.
“Gaines’ Farm.”—Liberty Hall.—Battle of Seven Pines.—Fair Oaks.—Rapid rise
of the Chickahominy.—The Gaines Estate.—An aged Negro.—Golden’s
Farm.—Camp Lincoln.—Letter from an Officer.
Davidson’s brigade again moved from Beaver Dam Creek, on the

26th of May, down the left bank of the Chickahominy (the enemy
throwing a few shells at them as they marched), and encamped on
“Gaines’ Farm,” where they remained until the 5th of June,
performing picket duty and building corduroy roads. Not far from
here was “Liberty Hall,” where Patrick Henry was born, May 29,
1736. The building, which his father had used as a grammar school,
was now appropriated for a National Hospital, and the little farm on
which Patrick had commenced life in company with his young wife,
the daughter of a neighboring farmer, occupied by our troops.
General Keyes’ corps, followed by that of General Heintzelman,
had now crossed the Chickahominy, the remainder of the army still
resting on the left bank. General Casey’s division held the extreme
advance; his pickets being within five miles of Richmond. Relying
upon the sudden and rapid rise of the river preventing our crossing
over more troops, Gen’l Johnston, then commander of the rebel
forces, hurled his whole army upon these two corps on the morning
of the 31st, with the expectation of annihilating them. Casey’s
Division, which bore the brunt of the attack, was forced back from
their rifle-pits and second line of battle, after fighting for several
hours and losing 1,443 men.
Liberty Hall, Birth-place of Patrick Henry.
The courageous Sumner, who, notwithstanding the freshet, had

crossed his corps, now drove fiercely at the enemy, and saved the
left wing from destruction. Yet the whole force was obliged to fall
back nearly two miles, owing to the overwhelming numbers and
impetuous onslaught of the rebels. Here they maintained their
ground, refusing to yield an inch more, and the fighting ended for the
day. This was known as the battle of Seven Pines.
The enemy renewed the conflict on the morrow, attacking General
Sumner at “Fair Oaks,” from which the second day’s struggle derives
its name. They were everywhere repulsed, and compelled to retreat
back to their stronghold, followed by our victorious troops to within
four miles of the capital, when, for a second time, it was given up for
lost. “The enemy,” wrote General McClellan to the Secretary of War,
after the close of the contest, “attacked in force, and with great spirit,
yesterday morning, but are everywhere most signally repulsed with
great loss. Our troops charged frequently on both days, and
uniformly broke the enemy. The result is, that our left is within four
miles of Richmond. I only wait for the river to fall to cross with the
rest of the force and make a general attack. Should I find them
holding firm in a very strong position, I may wait for what troops I can
bring up from Fort Monroe. But the morale of my troops is now such
that I can venture much. I do not fear for odds against me. The
victory is complete, and all credit is due to the gallantry of our
officers and men.”
The Thirty-third, at the commencement of the conflict, was doing
picket duty near one of the bridges which were being constructed
over the Chickahominy. So sudden was the rise in the river, that the
force which proceeded at two o’clock Sunday morning to relieve the
pickets stationed near the bridge three hours previous, found them
nearly surrounded with water. Some were standing up to their arm-
pits in the now new channel, and others, having lost their footing,
were clinging to trees, for dear life. Boats were obtained, and they
were rescued from their perilous position. At 3 o’clock, General
Brooks came down to the river with his Brigade, the second in
Smith’s Division—Davidson’s being the third, and Hancock’s the first,
—to cross over and render what assistance he could on the opposite
side. By this time the bridge was most of it swept away, and the
General, instead of attempting to cross, set his men to repairing it. At
sunrise the river had overflowed to the width of half a mile, and he
experienced much difficulty in getting his troops back to dry land
again. All day Sunday the heavy roar of artillery and sharp firing of
musketry could be heard. Just at night, General McClellan,
accompanied by General Hancock, rode down to the right of the
Thirty-third, where they remained until dark, watching the progress of
the battle.
Dr. Gaines, the owner of the farm on which the Regiment was now
encamped, possessed one of the finest estates in Virginia. One
wheat field alone comprised four hundred and fifty acres. In the rear
of his dwelling, furnished in the most costly manner, was a
picturesque grove, which furnished a cool retreat for the officers
during the intense heat of the mid-day. In front was an extensive
garden, abounding in flowers and shrubs of native and foreign with
all its beautiful surroundings, was overrun by the “invader.”
Camp Lincoln.
Attack of the 7th and 8th Georgia.
The Regiment remained here until the 5th of June, when the
Division was ordered to cross the Chickahominy and encamp on
“Golden’s Farm,” nearly opposite. The Third Brigade took the
advance. Owing to the high stage of the water, it was obliged to
proceed down the river to “Dispatch Station,” before effecting a
crossing. When marching up on the opposite bank, the men fell in
with a gray-haired, toothless negro, 102 years of age, who
entertained them with a recital of many incidents which had
transpired during his long period of slave life. After having marched
over fifteen miles to reach a point only three miles opposite the old
encampment, the Thirty-third arrived at Golden’s Farm, where
Baxter’s Fire Zouaves, of Philadelphia, were found briskly
skirmishing with the enemy.
Our artillery, which immediately opened upon them, put the rebels
to flight, and the picket line was moved forward, for some distance.
Col. Taylor halted his command in a beautiful corn-field, and on the
following day occupied a more advanced position, less than one
thousand yards from the enemy’s lines. There it remained until the
28th of June, the spot being christened “Camp Lincoln.”
An officer of the Regiment, in a communication from here, dated
June 8th, wrote:
“We are now six miles from Richmond, behind entrenchments,
waiting for something to turn up. The pickets are very close together,
and many prisoners are coming in every day. A Sergeant and five
men just came through the lines, and reported to Colonel Taylor,
Field Officer of the day. The Sergeant is from Ulster County, N. Y.
Doubtless a great number would desert, if it were possible to do so
without incurring danger. Yesterday much amusement was created
by the operation of a new and original line of telegraph between our
forces and the enemy. It seems a number of dogs have been
wandering around in front for some days. One of them yesterday
came in with a letter tied around his neck. It was read by our men,
the Thirty-third being on picket duty at the time, and an answer sent
back the same way; another note was likewise written, and
answered. The import of the first letter was, that they were much
‘obliged for the tender of cannon they took from us the other day,
and anything more of the same sort sent them, they would cheerfully
receive.’ No doubt of it. The second was rough in its language, and
full of empty boastings. The battle-field of last Saturday week is
close by us, and bears evidence of the murderous conflict, when
tens of thousands bore down upon barely a Division, and
unsuccessfully tried to cut them off, or thrust or crush them into the
river.
The difficulties attendant upon transporting troops and various
munitions of war, has retarded us some, but now we are ready. This
morning (the Sabbath) there was some sharp firing in front, but it
was quickly subdued by a battery of our 20-pounders. A new
Regiment has been added to our Brigade—Col. Max Weber’s
Regiment—the 20th N. Y. Vols. We have a fine Brigade now, and our
General thinks an effective one. Our picket line has been advanced
twice, the enemy retiring each time. The regular receipt of the mails
has been interrupted again, and of course is a source of regret to us.
Sitting on the ramparts of our rifle-pits this morning, writing this letter,
the view looking up the river, reminds one of Big Flats, at Geneseo,
flooded by heavy rains. The stream here is unusually high. An old
negro, 102 years old, who has always lived in this section, says that
he never knew such an immense quantity of rain to fall before in the
same space of time, at this season of the year. Gen. Prim and Staff,
with our Division Staff, just passed through our camp on a
reconnoissance to the front.”
CHAPTER XII.
Proximity to the Rebels.—Colonel Taylor fired at by a Sharpshooter.—Picket
Skirmishing.—Building a Bridge.—Position of Affairs.—General McClellan
Reconnoitring.—He writes to the President.—Lee’s Plans.—Second Battle of
Mechanicsville.—Shelling the Thirty-third’s Camp.—Battle of Gaines’ Farm.
—A Retreat to the James decided upon.
Soon after reaching “Camp Lincoln,” the Thirty-third was set to

work on a formidable redoubt, since known as “Fort Davidson,” and
likewise constructed numerous rifle-pits. The enemy daily threw shot
and shell at our encampments, apparently for mere pastime, many of
them striking among the tents. On one occasion a round shot,
passing entirely over the officers’ quarters, killed Dr. Spencer’s
Orderly in the rear. Not long after another came whizzing through the
air, and carried away the shoulder blade of a reckless cavalryman,
who was laughing as he rode along at the manœuvres of the men,
declaring that he would not “dodge for their guns.” A member of the
Seventy-seventh was killed in hospital close by.
Fort Davidson—Chickahominy Swamps.
The rebels also had a very disagreeable habit of climbing up in the

forest trees and firing at us, some times even when sitting in the
camp doors. One afternoon, as Colonel Taylor was reclining upon a
lounge in the Lieutenant Colonel’s tent, a sharp-shooter deliberately
fired at him from a neighboring tree, the ball passing through the
lounge and out at the back side of the tent. He immediately ordered
out several of his best shots to pick off the impudent rebel.
Not content with constantly annoying us during the daytime, they
frequently got up night demonstrations, compelling our “troops” to
turn out at very unseasonable hours. The Thirty-third were aroused
from their slumbers one night by the bursting of a shell directly over
the centre of the encampment. Gorman’s Brigade frequently
engaged in these night skirmishes. Colonel Taylor’s command rarely
indulged in picket firing, as many of the Regiments did, unless it was
provoked by the enemy. This custom, so prevalent at the
commencement of the war, has almost wholly ceased, and now,
instead of “blazing away” on the slightest pretext, the pickets patrol
their beats month after month within speaking distance, without
molesting one another.
As the month advanced, the troops were kept busily employed in
throwing up breastworks and constructing a new bridge over the
Chickahominy, below the point where the lowest of the three
previously carried away by the freshet was built. Frequently they
were compelled to stand waist deep in the water, while cutting
timbers, which were carried to the river on handspikes, many of them
requiring sixteen or more men to transport them. This bridge, when
completed, was an imposing structure, and afterwards saved the
right wing of the army, by furnishing a passage to the opposite side
of the river, when the rebel legions were hurled against it with such
rapidity and violence.
Nearly three months had now elapsed since the Army of the
Potomac landed at Fortress Monroe, and began the Peninsular
Campaign. Yorktown had been evacuated, the bloody battles of
“Williamsburg,” “West Point,” “Fair Oaks” and “Seven Pines,” besides
several lesser engagements, fought, the troops arrived before and
around Richmond, and our labors were apparently about to be
crowned with success by its capture.
One evening, about the 20th of the month, Gen. McClellan,
accompanied by Gens. Smith, Gorman and Porter, rode down to the
picket line where Captain Warford, with his Company, was stationed.
After removing their coats, in order to conceal their rank, and fording
a small creek, they ascended to a tree-top to reconnoitre the
enemy’s position. Their pickets were only about twenty rods distant,
on the opposite side of a wheat field. Descending, the Commander-
in-Chief remarked to Gen. Smith, with a smile on his face, “I have got
them now,” accompanying the remark with a significant doubling up
of his right fist. His army then numbered one hundred and fifteen
thousand men fit for duty.
A few brief hours served to dispel the visions of success and glory
which had brightened up his countenance. On the evening of the
25th, Gen. McClellan telegraphed to the President: “I incline to think
that Jackson will attack my right and rear. The rebel force is stated at
two hundred thousand, including Jackson and Beauregard. I shall
have to contend against vastly superior odds, if these reports be
true, but this army will do all in the power of man to hold their
position, and repulse an attack. I regret my inferiority in numbers, but
feel that I am in no way responsible for it, as I have not failed to
represent repeatedly the necessity of reinforcements; that this was
the decisive point, and that all should be concentrated here. I will do
all that a General can do, with the splendid army I have the honor to
command, and if it is destroyed by overwhelming numbers, can at
least die with it and share its fate.... I shall probably be attacked to-
morrow, and now go to the other side of the Chickahominy to
arrange for the defence on that side.”
The reader will understand that our army was then arranged in the
form of a semi-circle, extending across the Chickahominy, the left
resting upon Savage’s Station, and the right upon Mechanicsville. In
the rear of the right wing was “White House,” on the Pamunkey
River, used as a base of supplies for the army, which were brought
by way of York River. The plan of Gen. Lee, who had now
succeeded Gen. Johnston, was to concentrate his whole force on
our right wing, destroy it before the troops on the other side of the
river could be brought against him, gain possession of White House,
thereby cutting off our supplies as well as way of retreat, and capture
the entire army. He had no sooner however, taken the initiatory step
in this programme, by calling Jackson to his assistance, than Gen.
McClellan, as appears from the above letter to the President, divined
his whole strategy.
On the afternoon of Thursday, June 26th, the enemy fell upon
Gen. McCall’s Division at Mechanicsville. Reynolds’ and Seymour’s
Brigades bore the brunt of the attack. The battle continued until
sundown, when the rebels were handsomely repulsed. At midnight
the force fell back, in accordance with orders, to “Gaines’ Farm,”
where was fought the bloody engagement of Friday, June 27th,
resulting in a Federal loss of 9,000 killed, wounded and missing.
Smith’s Division, it will be remembered, was now located nearly
opposite from Gaines’ Farm, or Mill.
While the battle was progressing, on Thursday, at Mechanicsville,
the enemy stationed on the opposite side of the river opened a
furious cannonade on Gen. Smith, to divert attention. The tents of
the Thirty-third were considerably damaged with shot and shell, and
the horses of the Major and Quartermaster killed, in addition to
several other animals. Very fortunately the men had just completed a
formidable breastwork directly in front of the encampment, and
taking refuge behind this, none of them were killed.
The contrabands, of whom a considerable number now
accompanied the Regiment, were terribly frightened, and scampered
away rapidly. Two of them sought refuge behind a pile of cracker-
boxes, but they had hardly gained this shelter before a bursting shell
scattered the boxes and contents in all directions, much to the horror
of the fleeing negroes and amusement of the soldiers, who were
ensconced away behind the earthworks. Several of them received
such a fright that they were never seen afterwards. Of this number
was one of the negroes who communicated the information before
Yorktown of its evacuation.
On the following day, the 27th, a portion of Gen. Franklin’s Corps
was sent back across the river to aid Gen. Porter in holding his
position at Gaines’ Farm. Several of our batteries were likewise
wheeled about and brought to bear upon the enemy. But these and
other reinforcements were not sufficient to turn the tide of battle. The
overwhelming numbers of the enemy, estimated by Gen. McClellan
at full eighty thousand, precluded any hope of successfully resisting
them and maintaining the position. All the troops on the east bank of
the river accordingly crossed that night to the opposite side,
destroying the bridge after them.
Gen. McClellan immediately summoned several of his Generals,
and informed them that there was only one of two things to be done,
either to mass all of his troops at that point, near “Golden’s Farm,”
and risk a sanguinary battle, or to retire immediately and rapidly to
the James River. In the former case, defeat would ensure the
destruction of the army, whereas by abandoning the siege of
Richmond for the time being, he could retreat in safety to the James,
saving most of his men and material. The result of the interview was
a determination on the part of the Commanding General to “change
his base,” and, under cover of night, preparations were made for the
retreat.
CHAPTER XIII.
BATTLE OF GOLDEN’S FARM.
During the following morning, Saturday, June 28th, Col. Taylor, in

accordance with orders from Gen. Smith, moved with a portion of his
command to relieve and support the picket line, then within two
hundred yards of the enemy, leaving the remainder in camp, under
command of acting Adjutant Tyler, to strike tents, secure baggage,
&c., preparatory to retreating. The men had hardly reached the
picket line before the confederates opened a heavy artillery fire from
twenty pieces, which was mainly concentrated upon the camp.
Shot and shell flew in every direction, crashing through the trees,
ploughing up the ground, completely riddling the tents, firing the
baggage and commissary stores, and rendering every foot of the
camp enclosure untenable. The camp guard, prisoners, sick,
convalescents and, others, seizing their arms, immediately sought
refuge behind the earthworks, consisting of ditches and the
breastwork in front, which had afforded such good protection on the
Thursday previous.
Several of the enemy’s missiles struck the breastworks and rolled
over, occasioning not a little confusion. One shell dropped down into
the ditch beneath the parapet among the men, but was quickly
tossed out by J. W. Hendricks, Co. A, and again taken up by Peter
Roach, of the same Company, and thrown down the hill, where it
exploded, doing no injury. This heroic deed of these brave fellows
undoubtedly saved the lives of several of their comrades at the
imminent peril of their own.
Not being replied to by our guns, nearly all of which had been
taken to the rear to form in the line of retreat, their artillery firing
ceased at the end of an hour, leading our officers to infer that the
rebels had withdrawn to some other point. The mistake was soon
discovered, however, when the picket line (embracing, in addition to
a part of the Thirty-third, two companies of the Forty-ninth
Pennsylvania), which had firmly maintained its position, in spite of
the artillery fire, was fiercely attacked by two full regiments of
infantry.
The men stood their ground manfully at first, but were at length
forced back to the earthworks, wheeling and firing steadily as they
retreated. The defences gained, and the co-operation of the
remainder of the Regiment secured, a most gallant stand was made.
Colonel Taylor had hardly stationed the men in their places before
the rebels, flushed with their first success, and confident of easily
storming the defences and capturing the defenders, came charging
furiously down upon them.
All became hushed along the line as the men nerved themselves
for the encounter. The orders to “reserve fire,” “fire low,” &c., were
given in a quiet undertone, and the soldiers, bringing their firelocks to
their shoulders and resting them over the top of the parapet, calmly
waited the approach of the enemy. On they came, yelling and
shouting like demons, till within a few yards of the breastwork when
there instantly shot forth from behind it a sheet of flame, followed by
another and another, until, staggered by the galling fire, the rebels
wavered, broke and fled in great disorder from the field.
When the smoke cleared away the number of killed and wounded
that appeared scattered upon the ground testified to the accuracy of
our aim. Nearly every one had brought down his man. They
continued firing upon the retreating enemy until out of range. Not
satisfied with the reception which they had received, the
confederates, re-forming, again advanced, though more cautiously
than at first. But they were again met by a murderous fire and
compelled to fall back, leaving many of their number on the field.
Maddened by the defeat and carnage which had taken place
around him, Colonel Lamar, of the Eighth Ga., who commanded the
enemy, now sprang forward in front of his men, and, waving his
sword and hat in the air, incited them to a renewal of the charge.
Over a hundred rifles were instantly levelled at him, and he fell,
dangerously wounded, to the ground. At the same time a section of
Mott’s battery, which had come up, opened an enfilading fire upon
them from the left, and the victory was complete, the enemy fleeing
in all directions.
Huzza after huzza followed from our men, who could be restrained
only with the greatest difficulty from leaping over the parapet and
pursuing them. This it would not have been prudent to do, owing to
the great disparity in numbers. A small party was, however, sent
forward to secure several prisoners who had voluntarily surrendered,
and also our wounded.
This attempt, on the part of the Seventh and Eighth Ga.
Regiments, to capture the Thirty-third, resulted to them in a loss of
91 killed and left upon the field, a large number of wounded, 50
prisoners, including the wounded Col. Lamar of the Eighth and Lieut.
Colonel Tower of the Seventh Ga., and two hundred stand of arms.
We lost several, in killed and wounded, during the first part of the
engagement, when forced back to the entrenchments. A number
were also taken prisoners, including Captain Hamilton, of Company
G, who was exchanged, and returned to the Regiment at Harrison’s
Landing. The enemy’s balls mostly passed several feet over, or
lodged in the earthworks, doing but little injury.
First Lieutenant Moses Church, of Company E, fearless to a fault,
seized a musket and, going out from behind the protection of the
works, fired repeatedly, with deliberate aim, at the advancing rebels,
until he dropped dead, pierced through the head with a minie-ball.
He was a brave and beloved officer, and was buried close to the spot
where he so nobly died. Private Hildreth, of the same Company, also
exposed himself in a similar manner, and was shot dead, the ball
penetrating his eye.
Immediately after the final discomfiture of the rebels, Major Platner
was sent by Colonel Taylor to establish a new picket line, and both
parties buried their dead, under a flag of truce. One of the prisoners,
belonging to the Eighth Ga., on seeing the mangled remains of his
brother, wept bitterly and for a time refused to leave them. The same
soldier afterwards conversed with members of the Thirty-third at the
first battle of Fredericksburg, and reverted to the circumstance, and
also to the fact that his Regiment had encountered the Thirty-third for
the fourth time in battle.
While the engagement was going on, the Seventy-seventh N. Y.,
to the command of which Lieut.-Colonel Corning had been
temporarily assigned, was drawn up in line of battle further to the left,
to prevent a flank movement.
The following is Colonel Taylor’s report of the engagement:
Head-Quarters Thirty-third Regiment, N. Y. S. V.,

Virginia, July 10, 1862.
To the A. A. Gen’l, Third Brigade:
... On June 28th, the entire Regiment, with the exception of
the camp guard, cooks, and a few convalescent sick, was
ordered out on picket. Soon after, they became engaged with
the enemy, and according to instructions they fell back,
contesting every inch, into the rifle pits in front of their camp.
During this time Lieutenant Lucius C. Mix and Lieutenant Ed.
J. Tyler, of Company A, succeeded, under a galling fire, in
collecting and placing in good order, the former his camp
guard, and the latter all others in camp—some fifty men. Both
of these officers were conspicuous in their endeavors to stop
those who had become panic stricken, of which there were a
few, and arranging them to good effect in the rifle pit—many
of whom fought nobly. I can also mention the name of
Quartermaster Sergeant John J. Carter, now Lieutenant of
Company B, in connection with this affair, who not only did
good service in quieting the men, but conduced to keeping up
a continual fire on the enemy. Much praise is due to Captain
Warford and Lieutenant Church, of Company E, also to
Lieutenant Corning, of Company B, and Lieutenant Gale, of
Company G, for their coolness in drawing in the men, and
establishing order under such circumstances, at one time
being nearly surrounded. Captain Hamilton, of Company G,
was taken prisoner while actively engaged in rallying his men,

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December 2022 Colin E. Sullivan

1  Brief History of Sleep Medicine in Children and Adults�������������������� 1

Ritwick Agrawal Department of Pediatrics Pulmonary Medicine Section, Texas

Lourdes M. DelRosso University of California San Francisco, Fresno, CA, USA

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sleep centers and sleep medicine training programs exponentially expanded in

1.2 Sleep Medicine in Ancient Cultures

1.3 Sleep in the Scriptures

1.4 Scientific History of Sleep Medicine

1.5 History of Polysomnography in Sleep Medicine

1.6 History of Sleep Medicine as a Medical Field

The World Federation of Sleep Research Societies (WFSRS) was formed in

1.7 Education and Training History of Sleep Medicine

Lourdes M. DelRosso, Raffaele Ferri, and Oliviero Bruni

© Springer Nature Switzerland AG 2023 13

2.2 Brain Changes Across the Life Span

Recent advances in neuroimaging techniques have demonstrated important changes

Structural Brain Changes

Box 2.1 Summary of Brain Changes from Adolescence to Adulthood

Functional Changes in Neurotransmitters

proven to be effective in adults and extrapolating their use in adolescents. An exam-

Box 2.2 Trough and Peak Levels of Neurotransmitters in Childhood and

Neurotransmitter Age at trough level Age at peak level

2.3 EEG and Sleep Changes

homeostatic time course of sleep regulation. The parieto-occipital region is impli-

2.4 Circadian and Homeostatic Changes

Process C (circadian regulation) and process S (homeostatic regulation) are part of

Circadian Changes from Adolescence to Adulthood

Growing evidence supports that endogenous circadian period is altered during

Homeostatic Changes from Adolescence to Adulthood

The decline in N3 during adolescence parallels a decline in homeostatic sleep pres-

Box 2.4 Summary of Circadian and Homeostatic Changes

Circadian delay occurs during adolescence.

2.5 Clinical Implications

In order to provide effective clinical sleep recommendations to our patients, we

CPAP Continuous positive airway pressure

© Springer Nature Switzerland AG 2023 25

3.2 UAW Anatomy

3.3 Tonsils and Adenoids

3.4 UAW Length

Davidson’s brigade again moved from Beaver Dam Creek, on the

The courageous Sumner, who, notwithstanding the freshet, had

Attack of the 7th and 8th Georgia.

Soon after reaching “Camp Lincoln,” the Thirty-third was set to

The rebels also had a very disagreeable habit of climbing up in the

1 Brief History of Sleep Medicine in Children and Adults�� 1

1.2 Sleep Medicine in Ancient Cultures

1.3 Sleep in the Scriptures

1.4 Scientific History of Sleep Medicine

1.5 History of Polysomnography in Sleep Medicine

1.6 History of Sleep Medicine as a Medical Field

1.7 Education and Training History of Sleep Medicine

2.2 Brain Changes Across the Life Span

Structural Brain Changes

Functional Changes in Neurotransmitters

2.3 EEG and Sleep Changes

2.4 Circadian and Homeostatic Changes

Circadian Changes from Adolescence to Adulthood

Homeostatic Changes from Adolescence to Adulthood

2.5 Clinical Implications

3.2 UAW Anatomy

3.3 Tonsils and Adenoids

3.4 UAW Length