Montagna / Chokroverty MD / Chokroverty Sleep Disorders Part I

1. Auflage 2012
ISBN: 978-0-444-53481-1
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 720 Seiten

Reihe: Handbook of Clinical Neurology

Sleep Disorders Part 1 offers a glimpse of developments that focus on diagnostic techniques in the field of neurobiology of sleep. This part discusses the models of the rapid eye movement (REM) sleep mechanism; issues regarding sleep states, stages, and memory consolidation; and advances in the understanding of the sleep-wake genes, gene products, the circadian clock, and the role of sleep duration. This book explains noninvasive neuroimaging studies, particularly positron emission tomographic and single photon emission computed tomographic scans. It further discusses advances in clinical science, including concepts about neurobiology of sleep, narcolepsy-cataplexy, therapy, and laboratory techniques. The significant advances in therapy have led to the addition of new drugs for the treatment of different sleeping disorders, as described in this book. Sleep is essential to humans. Awareness of its true importance leads to the development and acceptance of sleep medicines in the market. - Clinical data on groundbreaking advancements in the understanding of basic sleep science - Invaluable information on new therapies and drug protocols for sleep disorders - A state-of-the-art reference that includes the role of genetics in sleep medicine

Autoren/Hrsg.

Montagna, Pasquale

Chokroverty MD, Frcp

Chokroverty, Sudhansu

Inhaltsverzeichnis

1;Front Cover;1
2;Handbook of Clinical Neurology;3
3;Sleep Disorders;4
4;Copyright Page;5
5;Handbook of Clinical Neurology 3rd Series;6
6;Foreword;8
7;Preface;10
8;Acknowledgments;12
9;List of Contributors;14
10;Contents of Part I;18
11;Contents of Part II;22
12;Section 1: History of sleep medicine;26
12.1;Chapter 1: History of sleep medicine;28
12.1.1;Sleep in Prehistoric and Ancient Times;28
12.1.2;Sleep in the Middle Ages and the Renaissance;33
12.1.3;Sleep in the 17th and 18th Centuries;34
12.1.4;Sleep in the 19th Century;36
12.1.5;Sleep in the 20th Century;40
12.1.6;References;47
13;Section 2: Basic Science and Methods;52
13.1;Chapter 2: Normal sleep-recording and scoring techniques;54
13.1.1;Eeg and Eog Correlates of Normal Human Sleep;54
13.1.2;The Evolution of Recording Technology;63
13.1.3;References;68
13.2;Chapter 3: Assessment of daytime sleepiness;70
13.2.1;Introduction;70
13.2.2;History;70
13.2.3;Physical Examination;72
13.2.4;Subjective Testing;73
13.2.5;Nocturnal Polysomnography;74
13.2.6;Multiple Sleep Latency Test;74
13.2.7;Maintenance of Wakefulness Test;75
13.2.8;Other Testing;76
13.2.9;Practical Applications;76
13.2.10;References;77
13.3;Chapter 4: Actigraphic monitoring of sleep and circadian rhythms;80
13.3.1;Introduction;80
13.3.2;Applications;80
13.3.3;The Acceleration Signal: Movement and Artifact;81
13.3.4;Placement of the Actigraph;81
13.3.5;Estimating Sleep-Wake State and Sleep Parameters;81
13.3.6;Comparison With Polysomnography;83
13.3.7;Circadian and Diurnal Rhythms;84
13.3.8;Perspectives;85
13.3.9;References;86
13.4;Chapter 5: Video recordings and video polysomnography;90
13.4.1;Introduction;90
13.4.2;Indications;90
13.4.3;Methodology;90
13.4.4;Interpretation;93
13.4.5;Conclusions;95
13.4.6;References;95
13.5;Chapter 6: Functional neuroimaging in sleep, sleep deprivation,and sleep disorders;96
13.5.1;Introduction;96
13.5.2;Neuroimaging in Normal Humans;96
13.5.3;Neuroimaging in Sleep Disorders;100
13.5.4;Conclusions;112
13.5.5;Acknowledgments;112
13.5.6;References;113
14;Section 3: Basic Mechanisms of Sleep;120
14.1;Chapter 7: The phylogeny of sleep;122
14.1.1;Introduction;122
14.1.2;The Definition of Sleep;122
14.1.3;Invertebrates;124
14.1.4;Insects;124
14.1.5;Fish and Amphibians;125
14.1.6;Reptiles;127
14.1.7;Birds and Mammals;128
14.1.8;The Phylogeny of Sleep and Human Sleep Disorders;130
14.1.9;Conclusions;131
14.1.10;References;131
14.2;Chapter 8: Ontogeny of EEG sleep from neonatalthrough infancy periods;136
14.2.1;Caveats Concerning Neurophysiologic Interpretation of State;136
14.2.2;General Comments on Recording Techniques and Instrumentation for Neonates and Infants;137
14.2.3;Maturation of Electrographic Patterns in the Neonate;137
14.2.4;Maturation of Non-Eeg Physiologic Behaviors Which Define State in the Preterm Infant;141
14.2.5;Assessment of State Organization in the Full-Term Infant;143
14.2.6;Sleep Ontogenesis - State Maturation From Fetal Through Infancy Periods;144
14.2.7;Brain Adaptation to Stress As Reflected in Sleep Reorganization;146
14.2.8;Computer-Assisted Analyses of Eeg Sleep Organization in Neonates and Infants;147
14.2.9;Summary;150
14.2.10;Acknowledgment;150
14.2.11;References;150
14.3;Chapter 9: Neurobiology of waking and sleeping;156
14.3.1;Historical Background;156
14.3.2;The Reticular Activating System;158
14.3.3;Forebrain Relays of the Activating System;159
14.3.4;Diffusely Projecting Arousal Systems;160
14.3.5;Sleep-Promoting Systems;166
14.3.6;Summary;168
14.3.7;Acknowledgments;169
14.3.8;References;169
14.4;Chapter 10: Neurobiology of REM sleep;176
14.4.1;Introduction;176
14.4.2;Rem Sleep Physiology and Relevant Brain Anatomy;177
14.4.3;Rem-Suppressive Systems: Rem-off Neurons;182
14.4.4;Gabaergic Influences And Rem Sleep;186
14.4.5;A Model of Rem Sleep Generation Incorporating Gabaergic Neurons;189
14.4.6;Orexin Effects and Modeling Circadian Control of Rem Sleep;192
14.4.7;Acknowledgment;192
14.4.8;References;192
14.5;Chapter 11: Neurochemistry of sleep: an overview of animalexperimental work;198
14.5.1;Neuronal Network Responsible for Sleep Onset and Maintenance;198
14.5.2;Neuronal Network Responsible for Paradoxical (Rem) Sleep Onset and Maintenance;201
14.5.3;Conclusion: a New Network Model for Ps Onset and Maintenance (Figure 11.2);208
14.5.4;Acknowledgments;208
14.5.5;References;209
14.6;Chapter 12: Molecular neurobiology of sleep;216
14.6.1;A Cellular Function for Sleep;216
14.6.2;Gene Expression Profiling of Sleep and Wakefulness;216
14.6.3;Genetic Studies of Sleep and Wakefulness;221
14.6.4;Conclusions;224
14.6.5;Acknowledgment;225
14.6.6;References;225
14.7;Chapter 13: Manifestations and functional implicationsof sleep homeostasis;230
14.7.1;Definition;230
14.7.2;Physiological Correlates of Sleep Homeostasis;230
14.7.3;Modeling Sleep Regulation;232
14.7.4;Correlates of Sleep Homeostasis in the Waking Eeg;233
14.7.5;Use-Dependent Changes;233
14.7.6;Perspectives;235
14.7.7;References;236
14.8;Chapter 14: Thermoregulation in wakefulness and sleep in humans;240
14.8.1;Thermoregulation;240
14.8.2;Sleep Structure and Age;243
14.8.3;Sleep and Thermoregulation;243
14.8.4;Conclusions;249
14.8.5;Acknowledgments;249
14.8.6;References;249
14.9;Chapter 15: Cytokines in immune function and sleep regulation;254
14.9.1;Sleep;254
14.9.2;Humoral Regulation of Sleep;254
14.9.3;Cytokines in Sleep Regulation;254
14.9.4;Interferons and Sleep;257
14.9.5;Altered Sleep as an Acute-Phase Response: Mediators and Mechanisms;258
14.9.6;A Theory of the Brain Organization of Sleep: Cytokine Involvement in "Local" Sleep;259
14.9.7;Acknowledgments;261
14.9.8;References;261
14.10;Chapter 16: Endocrine and metabolic changes during sleep;266
14.10.1;Introduction;266
14.10.2;Hypothalamo-Pituitary-Somatotrophic System;266
14.10.3;Hypothalamo-Pituitary-Adrenocortical System;269
14.10.4;Hypothalamo-Pituitary-Thyroid (Hpt) System;271
14.10.5;Leptin and Ghrelin;272
14.10.6;Insulin;272
14.10.7;Prolactin;273
14.10.8;Other Neuropeptides;273
14.10.9;Melatonin;274
14.10.10;Gonadal Hormones;274
14.10.11;Neuroactive Steroids;275
14.10.12;Conclusions;275
14.10.13;Acknowledgment;276
14.10.14;References;276
14.11;Chapter 17: Sleep, memory, and molecular neurobiology ;284
14.11.1;New Experimental Paradigms and Technological Advances;284
14.11.2;Types of Memory;285
14.11.3;Rem Sleep and Memory;286
14.11.4;Nrem Sleep and Memory;289
14.11.5;Biochemical and Genetic Factors;293
14.11.6;Implications;294
15;Section 4: Clinical Aspects of Sleep Disorders;298
15.1;Chapter 18: Epidemiology of sleep disorders;300
15.1.1;Epidemiological Methods In Sleep Medicine;300
15.1.2;Epidemiology of Sleep Disorders;307
15.1.3;Sleep Length: Natural Short And Long Sleepers;310
15.1.4;Daytime Sleepiness;311
15.1.5;Narcolepsy;314
15.1.6;Snoring and Sleep Apnea;314
15.1.7;Parasomnias;325
15.1.8;Restless-Legs Syndrome;325
15.1.9;Sleep-Related Isolated Symptoms;328
15.1.10;References;328
15.2;Chapter 19: Cardiovascular and cerebrovascular physiology in sleep;340
15.2.1;Cardiovascular Physiology During Sleep;340
15.2.2;Cardiovascular Effects of Arousal;341
15.2.3;Circadian Variation in Cardiovascular and Cerebrovascular Events;341
15.2.4;Cerebrovascular Physiology During Sleep;342
15.2.5;Obstructive Sleep Apnea;344
15.2.6;Central Sleep Apnea;346
15.2.7;Conclusions;347
15.2.8;References;348
15.3;Chapter 20: Cardiovascular diseases and sleep apnea;352
15.3.1;Introduction;352
15.3.2;Definitions;352
15.3.3;Polysomnography;354
15.3.4;Obstructive Sleep Apnea;354
15.3.5;Manifestations of Obstructive Sleep Apnea;354
15.3.6;Obstructive Sleep Apnea is an Inflammatory Disorder Resulting in Cardiocerebrovascular Disorders;355
15.3.7;Cardiovascular Complications Of Obstructive Sleep Apnea;356
15.3.8;Osa as a Cause of Mortality;359
15.3.9;Treatment of Osa;360
15.3.10;Sleep Apnea in Patients With Established Congestive Heart Failure;361
15.3.11;References;367
15.4;Chapter 21: Alterations in gastrointestinal functioning during sleep;372
15.4.1;Upper Gi Functioning During Sleep;372
15.4.2;Conclusions;378
15.4.3;References;378
15.5;Chapter 22: Sleep and genitourinary systems: physiology and disorders;380
15.5.1;Introduction;380
15.5.2;Sleep and the Genitourinary System;380
15.5.3;References;385
15.6;Chapter 23: Sleep enuresis;388
15.6.1;Definitions and Epidemiology;388
15.6.2;Etiology and Pathogenesis;388
15.6.3;Treatment, Theoretic Considerations;390
15.6.4;Practical Management;391
15.6.5;References;393
15.7;Chapter 24: Respiratory physiology in sleep and wakefulness;396
15.7.1;Introduction;396
15.7.2;Central Neuronal Control Of Breathing;396
15.7.3;Feedback Regulation Of Respiration;400
15.7.4;Airway Resistance and Respiratory Muscle Tone;402
15.7.5;Arousal Thresholds;403
15.7.6;References;404
15.8;Chapter 25: Obstructive sleep apnea: diagnosis, risk factors,and pathophysiology;408
15.8.1;Obstructive Sleep Apnea: A Brief History;408
15.8.2;Epidemiology;409
15.8.3;Diagnosis;409
15.8.4;Risk Factors;411
15.8.5;Pathophysiology;414
15.8.6;Summary;418
15.8.7;References;418
15.9;Chapter 26: Upper-airway resistance syndrome;426
15.9.1;Introduction;426
15.9.2;Epidemiology;427
15.9.3;Clinical Symptoms;427
15.9.4;Physical Examination;427
15.9.5;Pathophysiology;429
15.9.6;Treatment;432
15.9.7;References;432
15.10;Chapter 27: Central sleep apnea;436
15.10.1;Definition;436
15.10.2;Hypercapnic Central Sleep Apnea and Sleep Hypoventilation Syndrome;436
15.10.3;Hypocapnic Central Apnea;437
15.10.4;Complex Sleep Apnea;442
15.10.5;Conclusion;442
15.10.6;References;442
15.11;Chapter 28: Positive-pressure treatment of obstructive sleepapnea syndrome;446
15.11.1;Introduction;446
15.11.2;Continuous Positive Airway Pressure;447
15.11.3;Practical Aspects of Treatment;447
15.11.4;Autotitrating Continuous Positive Airway Pressure;451
15.11.5;Problems and Side-Effects;453
15.11.6;Comparison With Other Treatments;455
15.11.7;Compliance;455
15.11.8;Management of Cpap Failure;457
15.11.9;Health Outcomes and Nasal Continuous Positive Airway Pressure;457
15.11.10;Cpap and Cardiovascular Outcomes;458
15.11.11;Cpap and Cardiac Failure;458
15.11.12;Summary;459
15.11.13;Acknowledgments;459
15.11.14;References;459
15.12;Chapter 29: Medical and surgical treatment of obstructive sleepapnea syndrome, including dental appliances;466
15.12.1;Introduction;466
15.12.2;Lifestyle Modification;467
15.12.3;Pharmacotherapy;469
15.12.4;Oxygen;470
15.12.5;Miscellaneous Devices;470
15.12.6;Dental Appliances;470
15.12.7;Upper-Airway Surgery;473
15.12.8;References;476
15.13;Chapter 30: Noninvasive positive ventilation in the treatmentof sleep-related breathing disorders;484
15.13.1;Introduction;484
15.13.2;Nippv Methods and Uses;484
15.13.3;Criteria for Use of Nippv;485
15.13.4;Nippv Survival in Different Diseases;486
15.13.5;Indications for Nippv;487
15.13.6;Management of Nippv;488
15.13.7;Management of Complications;489
15.13.8;Nippv Effects (Other than Survival) and Related Mechanisms;490
15.13.9;Conclusion;490
15.13.10;References;490
15.14;Chapter 31: Sleep and pulmonary diseases;496
15.14.1;Historical Perspective of Sleep and Pulmonary Diseases;496
15.14.2;Introduction;496
15.14.3;Specific Etiologies;498
15.14.4;Whom to Study;501
15.14.5;How to Treat;502
15.14.6;Final Remarks;505
15.14.7;Summary;505
15.14.8;Conclusions;507
15.14.9;References;508
15.15;Chapter 32: Sleep-associated respiratory disorders and theirpsychobehavioral consequences in children;514
15.15.1;Sleep Disturbances in Children;514
15.15.2;Behavioral Consequences Of Sleep Disturbance;515
15.15.3;Psychobehavioral Consequences of Sleep Disruption in Sdb;518
15.15.4;Acknowledgments;521
15.15.5;References;521
15.16;Chapter 33: Sudden death in infants during sleep;526
15.16.1;Definitions;526
15.16.2;Pathologic Examinations;527
15.16.3;Incidence;527
15.16.4;Risk and Protective Factors;527
15.16.5;Model for Sids;531
15.16.6;Mechanisms Implicated in Sids Deaths;533
15.16.7;Physiopathology;535
15.16.8;Conclusion;536
15.16.9;References;537
15.17;Chapter 34: Neurobiology and the neurological basis of dreaming;544
15.17.1;Background;544
15.17.2;Clinicoanatomical Findings;544
15.17.3;Functional Neuroimaging Findings;556
15.17.4;Neurochemical and Psychopharmacological Findings;558
15.17.5;Theoretical Considerations;564
15.17.6;References;565
15.18;Chapter 35: Abnormal dreams and nightmare disorders;570
15.18.1;Introduction;570
15.18.2;Clinical Disorders and Abnormalities of Dreaming;572
15.18.3;Abnormalities of Dreaming That May Not Present as Clinical Complaints;577
15.18.4;An Unusual Variant of Normal Dreaming;578
15.18.5;References;579
15.19;Chapter 36: Sleep and psychiatric diseases;582
15.19.1;Introduction;582
15.19.2;Depression;582
15.19.3;Mania;590
15.19.4;Anxiety;591
15.19.5;Obsessive-Compulsive Disorders (Ocd);591
15.19.6;Posttraumatic Stress Disorder (Ptsd);591
15.19.7;Schizophrenia;594
15.19.8;References;596
15.20;Chapter 37: Sleep-related eating disorder ;602
15.20.1;History of Night Eating as A Clinical Condition;602
15.20.2;Characteristics of Sred;603
15.20.3;Differential Diagnosis Of Sred and Nes;604
15.20.4;Prevalence;605
15.20.5;Consequences;605
15.20.6;Associations With Other Disorders;606
15.20.7;Physiology of Sred;606
15.20.8;Treatment;607
15.20.9;Summary;608
15.20.10;References;608
15.21;Chapter 38: Alcohol, toxins, and medications as a causeof sleep dysfunction;612
15.21.1;Introduction;612
15.21.2;Drugs of Abuse;612
15.21.3;Prescribed Medications;618
15.21.4;Heavy Metals;628
15.21.5;References;629
15.22;Chapter 39: Sleep, pain, fibromyalgia, and chronic fatigue syndrome;638
15.22.1;Introduction: the Problem of Sleep Disturbance and Pain;638
15.22.2;Sleep and Pain Interaction;639
15.22.3;Fibromyalgia and Chronic Fatigue Syndrome;646
15.22.4;Diagnosis of Fm and Cfs;653
15.22.5;Summary and Recommendations;655
15.22.6;Acknowledgment;656
15.22.7;References;656
15.23;Chapter 40: Women and sleep;664
15.23.1;Objective Differences in Females' Sleep;664
15.23.2;Subjective Differences in Women's Sleep;667
15.23.3;Hormonal Factors;667
15.23.4;Physiologic Changes Over the Lifespan;668
15.23.5;Differences in Female Psychosocial Issues and the Impact on Sleep;671
15.23.6;Conclusions;673
15.23.7;References;673
15.24;Chapter 41: Normal and abnormal sleep in the elderly;678
15.24.1;Introduction;678
15.24.2;Sleep and Aging;678
15.24.3;Insomnia;678
15.24.4;Circadian Rhythm Disturbances;681
15.24.5;Primary Sleep Disorders;682
15.24.6;Sleep in Dementia;686
15.24.7;Summary;687
15.24.8;Acknowledgements;687
15.24.9;References;687
16;Subject Index;692

Leseproben

Handbook of Clinical Neurology, Vol. 98, No. Suppl C, 2011 ISSN: 0072-9752 doi: 10.1016/B978-0-444-52006-7.00001-0 Chapter 1History of sleep medicine Michael J. Thorpy? Sleep–Wake Disorders Center, Montefiore Medical Center, and Albert Einstein College of Medicine, New York, NY, USA ?Correspondence to: Michael J. Thorpy, M.D., Sleep–Wake Disorders Center, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467, USA. Tel: [phone], Fax: [phone], E-mail address: [e-mail] Sleep; King of all the gods and of all mortals, hearken now, prithee, to my word; and if ever before thou didst listen, obey me now, and I will ever be grateful to thee all my days (Homer, 14th book of the Iliad:Mueller, 1984). Only a few physiological conditions have received as much attention from poets, novelists, scholars, and scientists as sleep. Writers from Aristotle and Ovid to Shakespeare and Dante have been fascinated by sleep and its impact upon our emotions, behavior, and health. Causes and reasons for sleep have been pondered by some of the world's greatest minds. Regardless of what the reason is, it is likely that sleep and dreams developed in animals because they were of some evolutionary benefit. Not only has sleep evolved through the ages but the environment for sleep has also undergone a change. From communal sleeping rooms with beds of twigs, straw, or skins, the bedroom has changed in the 21st century into a private place with electronic equipment, including remote-controlled television, DVD players, internet access, and even exercise equipment. The size of bedrooms has enlarged over the years. A rudimentary understanding of insomnia and sleepiness was known in ancient times, but specific sleep disorders, such as narcolepsy, began to be recognized only in the late 19th century. Differentiation between causes of sleepiness and insomnia has reached a peak within the last 50 years since the development of sophisticated technology for the investigation of sleep. Although most sleep disorders have probably been present since humans evolved, modern society has inadvertently produced several new disorders. The electric light bulb, developed by Thomas Edison, has allowed the light of day to be extended into night so that shift work can now occur around the clock, but at the expense of circadian rhythm disruption and sleep disturbance. Similarly, international jet travel has enabled the rapid crossing of time zones, which also can lead to a disruption of circadian rhythms and to sleep disturbance. Scientific investigation has produced more information on the physiology and pathophysiology of sleep in recent years than ever before. This rapid advance in sleep research and the development of sleep disorders medicine are producing answers to questions that date from antiquity. Sleep in Prehistoric and Ancient Times
Sleep's the only medicine that gives ease (Sophocles, Philoctetes: Lloyd Jones, 1994). The sleep patterns and sleep disorders of prehistoric humans are unknown, and therefore we must speculate from the comparative physiology of animals and from evidence of other behaviors and illnesses. Theories on the phylogenetic development of sleep stages in mammals have been developed from information available on the mammal-like reptiles. The earliest form of life developed about 600 million years ago in the pre-Cambrian period, and mammal-like reptiles evolved approximately 250 million years ago. The monotremes (egg-laying mammals) evolved as a separate line from the therian (live-bearing) mammals about 180 million years ago. It is about this time when it is believed that slow-wave sleep appeared; rapid eye movement (REM) sleep (paradoxical sleep) appeared about 50 million years later. Recent sleep research on one of the three surviving monotremes, the Australian short-nosed echidna and platypus, has provided some of the evidence for the evolution of sleep stages. The monotremes have high-voltage REM sleep, which suggests that REM sleep may have had its origin in reptilian ancestors (Karmanova, 1982; Siegel et al., 1998). The pattern of sleep and waking behavior in prehistoric humans can be deduced from studies of animal groups phylogenetically closest to humans, namely nonhuman primates, such as apes and Old World monkeys. Sleep–wake patterns in nonhuman primates consist mainly of polyphasic episodes of rest and activity with frequent (up to 12) cycles of wakeful activity throughout the 24-hour day. Humans have the most developed monophasic pattern, with one episode of consolidated sleep and one main episode of wakefulness. Some animals, e.g., the chimpanzee, have a biphasic sleep–wake pattern, with a nap taken during the daytime. The chimpanzee has a rather prolonged sleep episode from dusk to dawn of approximately 10 hours; however, during this time there are frequent, brief awakenings. The daytime is characterized by two long episodes of wakefulness and an approximately 5-hour midday nap, which also includes frequent, brief wakefulness episodes. This type of sleep pattern may have the advantage of providing some security from predators. Extrapolating from nonhuman primate studies, it seems likely that a similar polyphasic sleep pattern was likely to have been present in earliest humans (prior to the Neolithic period), particularly if they also attempted to sleep between dusk and dawn. There would have been frequent awakenings during the major sleep episode, as a single sleep episode of more than 10 hours appears unlikely. The monophasic sleep–wake pattern probably began in the latter part of the Neolithic period (since 10   000 BC). Neanderthal humans (70   000–40   000 BC) may well have been in a transitional stage between a polyphasic sleep pattern and the monophasic pattern seen today. Prehistoric humans may have attempted to treat sleep disturbances, but how early they would have done this is unknown. Therapy probably resembled that utilized by sick animals, such as the removal of infective agents, eating various plants to induce emesis, and possibly even bloodletting. Bloodletting became an increasingly frequent therapeutic means for treating disease, including sleep disorders, in more advanced ancient civilizations. Primitive societies, even today, consider many illnesses and diseases to be caused by gods, magic, and spirits, and therefore various forms of divination, such as the casting of bones, moving of beads, charms, fetishes, chanting or the use of elaborate ceremonies, are invoked for therapeutic reasons. For disturbances of sleep and wakefulness, prehistoric humans probably applied similar forms of treatment. Ancient Egypt
Most of our current knowledge of ancient Egyptian medicine derives from the ancient medical papyruses of Egypt (Ebbell, 1937). The Chester Beatty papyrus, which was written around 1350 BC, contains information on the interpretation of dreams. Dreams were regarded as being contrary predictions; for example, a dream of death meant a long life. However, an extensive text on a variety of medical subjects, including treatment, the Georg Ebers papyrus (1600 BC), has not been reported to contain any information on sleep disturbances. Ancient Egyptian medical practice consisted largely of praying to the gods and invoking the help of these divine healers. Thoth, who was a physician to the gods, and Imhotep were both important gods of healing at that time. The ancient Egyptians were known for their attention to hygiene and cleanliness, and it is likely that such attention was also paid to sleeping habits. Medical opinion at the time held that the body was made up of a system of channels (Metu), which conveyed air to all parts of the body. Because they believed that bodily fluids could enter this system of channels, the ancient Egyptians were particularly concerned about feces entering the Metu. Hence, purging and enemas were the treatment modalities of many illnesses of that time, which included infective illnesses, such as malaria, parasitic infections, smallpox, and leprosy. Wine and other mildly alcoholic drinks (as compared to distilled alcoholic products) were consumed in large amounts and were probably the earliest treatments for insomnia but also may have been important in its development. Medicinal plants were utilized, particularly the product of the opium poppy (Papaver somniferum), and hyoscyamine and scopolamine, derived from belladonna and nightshade (Gunther, 1959). The word “opium” is derived from the Greek word for “juice,” as the drug is derived from the juice of the poppy. Papaver somniferum was coined at a much later date; somniferum was derived from the Latin word Somnus (the Roman god of sleep). In subsequent periods in history opium (laudanum) was widely used as a treatment for insomnia, and it is likely that it was used as far back as the Sumerian age. Accordingly, opium may have been the first hypnotic medication used. Another common treatment performed by the ancient Egyptians for a variety of ailments and illnesses was bloodletting. This was likely to have been used for sleep disorders, particularly for those disorders that produced excessive sleepiness or stupor. Medical treatment by physicians was...