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This page intentionally left blank
The Parasomnias and
Other Sleep-Related
Movement Disorders
The Parasomnias and
Other Sleep-Related
Movement Disorders
Edited by
Michael J. Thorpy
Director, Sleep-Wake Disorders Center, Monteiore Medical Center and Professor of Neurology,
Albert Einstein College of Medicine, Bronx, New York, USA
Giuseppe Plazzi
Assistant Professor of Neurology, Università di Bologna and Chief of the Sleep Laboratory,
Dipartimento di Scienze Neurologiche, Università di Bologna, Bologna, Italy
CAMBRIDGE UNIVERSITY PRESS
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São Paulo, Delhi, Dubai, Tokyo

Cambridge University Press

The Edinburgh Building, Cambridge CB2 8RU, UK

Published in the United States of America by Cambridge University Press, New York

www.cambridge.org
Information on this title: www.cambridge.org/9780521111577

© Cambridge University Press 2010

This publication is in copyright. Subject to statutory exception and to the

provision of relevant collective licensing agreements, no reproduction of any part
may take place without the written permission of Cambridge University Press.
First published in print format 2010

ISBN-13 978-0-511-71264-7 eBook (NetLibrary)

ISBN-13 978-0-521-11157-7 Hardback

Cambridge University Press has no responsibility for the persistence or accuracy

of urls for external or third-party internet websites referred to in this publication,
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.
To the extent permitted by applicable law, Cambridge
University Press is not liable for direct damages or loss of any
kind resulting from the use of this product or from errors or
faults contained in it, and in every case Cambridge University
Press’s liability shall be limited to the amount actually paid by
the customer for the product.
Every effort has been made in preparing this publication to
provide accurate and up-to-date information which is in accord
with accepted standards and practice at the time of publication.
Although case histories are drawn from actual cases, every
effort has been made to disguise the identities of the individuals
involved. Nevertheless, the authors, editors and publishers can
make no warranties that the information contained herein is
totally free from error, not least because clinical standards are
constantly changing through research and regulation.The
authors, editors and publishers therefore disclaim all liability
Contents
Contributors page vii
Preface x
Credits and Acknowledgments xii
Foreword by Elio Lugaresi xiii

Section 1: Introduction Section 2: Disorders of arousal

1. Parasomnias: a short history 3 11. Confusional arousals 99
Shannon S. Sullivan and Christian Gregory Stores
Guilleminault
12. Sleepwalking 109
2. Epidemiology of parasomnias 7 Antonio Zadra and Jacques Montplaisir
Maurice M. Ohayon
13. Sleep terrors 119
3. Neuroimaging of parasomnias 13 Meredith Broderick and Christian
Eric A. Nofzinger Guilleminault
4. Clinical evaluation of parasomnias 19
Imran M. Ahmed and
Michael J. horpy
Section 3: Parasomnias usually
5. Video-polysomnography of
associated with REM sleep
parasomnias 34 14. REM sleep behavior disorder 131
Stefano Vandi Rafaele Manni and Michele Terzaghi
6. Parasomnias due to medications or 15. Recurrent isolated sleep paralysis 142
substances 42 James Allan Cheyne
Rosalind D. Cartwright
16. Nightmare disorder 153
7. Parasomnias due to medical and Michael Schredl
neurological disorders 54
Marco Zucconi and Alessandro Oldani
8. Trauma, post-traumatic stress disorder,
Section 4: Other parasomnias
and parasomnias 64 17. Sleep-related dissociative disorder 163
homas A. Mellman and Anissa M. Maroof Christina J. Calamaro and
hornton B. A. Mason
9. Sexsomnias 70
Nikola N. Trajanovic and 18. Sleep enuresis 175
Colin M. Shapiro Oliviero Bruni, Luana Novelli, Elena
Finotti and Rafaele Ferri
10. Medico-legal consequences of
parasomnias 81 19. Catathrenia (sleep-related groaning) 184
Irshaad O. Ebrahim and Roberto Vetrugno, Giuseppe Plazzi and
Colin M. Shapiro Pasquale Montagna
v
 Contents

20. Sleep-related hallucinations and 28. Sleep-related rhythmic movement

exploding head syndrome 194 disorder 270
Satish C. Rao and Michael H. Silber Timothy F. Hoban
21. Sleep-related eating disorder 202 29. Sleep panic arousals 278
John W. Winkelman Ravi Singareddy and homas W. Uhde
30. Sleep-related epilepsy 289
Section 5: Sleep-related Carl W. Bazil

movement disorders and other

variants Section 6: Therapy of parasomnias
22. Restless legs syndrome (RLS) and 31. Pharmacotherapy and parasomnias 301
periodic leg movements (PLM) 213 Rafael Pelayo and Deepti Sinha
Richard P. Allen 32. Behavioral and psychiatric treatment
23. Sleep starts 229 of parasomnias 312
Sudhansu Chokroverty and Divya Gupta Shelby F. Harris and Michael J. horpy

24. Fragmentary myoclonus 237 33. Hypnotherapy and parasomnias 323

Pasquale Montagna and Roberto Vetrugno Gina Graci

25. Sleep-related leg cramps 244

Renee Monderer and Michael J. horpy
26. Sleep-related bruxism 252 Index 330
Nelly Huynh Color plate section is between pages 210–11.
27. Propriospinal myoclonus 261
Giuseppe Plazzi and Roberto Vetrugno

vi
Contributors

Imran M. Ahmed Raffaele Ferri

Sleep-Wake Disorders Center, Monteiore Medical Sleep Research Centre, Department of Neurology,
Center, Bronx, New York, USA. Oasi Institute (IRCCS), Troina, Italy.
Richard P. Allen Elena Finotti
Neurology and Sleep Medicine, Johns Hopkins Sleep Disorders Center, Department of Neurological
University, Asthma and Allergy Bldg, Hopkins Sciences, University of Bologna, Italy.
Bayview Circle, Baltimore, Maryland, USA.
Gina Graci
Carl W. Bazil
Northwestern University, Feinberg School of
he Neurological Institute, Columbia University, New
Medicine, Robert H. Lurie Comprehensive Cancer
York, NY, USA.
Center, Chicago, Illinois, USA.
Meredith Broderick
Christian Guilleminault
Stanford University Sleep Disorders Clinic, Stanford,
California, USA. Stanford University Sleep Disorders Clinic, Stanford,
California, USA.
Oliviero Bruni
Center for Pediatric Sleep Disorders, Department of Divya Gupta
Developmental Neurology and Psychiatry, University JFK Medical Center, New Jersey Neuroscience
of Rome La Sapienza, Rome, Italy. Institute, Seton Hall University, Edison, New Jersey,
USA.
Christina J. Calamaro
Assistant Professor, University of Maryland School of Shelby F. Harris
Nursing, Department of Family and Community Sleep-Wake Disorders Center, Monteiore Medical
Health, Baltimore, Maryland, USA. Center, Bronx, New York, USA.
Rosalind D. Cartwright Timothy F. Hoban
Neuroscience Program, Graduate College, Rush he Michael S. Aldrich Sleep Disorders Center,
University Medical Center, Chicago, Illinois, USA. Department of Pediatrics, Women’s Hospital, Ann
James Allan Cheyne Arbor, Missouri, USA.
University of Waterloo, Ontario, Canada. Nelly Huynh
Sudhansu Chokroverty Sleep Diagnostic Center, Stanford University,
JFK Medical Center, New Jersey Neuroscience Stanford, California, USA.
Institute, Seton Hall University, Edison, New Jersey,
USA. Raffaele Manni
Unit of Sleep Medicine and Epilepsy, IRCCS C.
Irshaad O. Ebrahim Mondino, Institute of Neurology Foundation, Pavia,
he London Sleep Centre, London, UK. Italy.
vii
 Contributors

Anissa M. Maroof Satish C. Rao

Department of Psychiatry, Howard University, Sleep Disorders Center, Mayo Clinic College of
Washington, DC, USA. Medicine, Rochester, Minnesota, USA.

Thornton B. A. Mason Michael Schredl

Division of Neurology, Wood Center, he Children’s Central Institute of Mental Health, Mannheim,
Hospital of Philadelphia, Philadelphia, Pennsylvania, Germany.
USA. Colin M. Shapiro
Thomas A. Mellman Sleep and Alertness Clinic, University Health
Department of Psychiatry, Howard University, Network, Toronto, Ontario, Canada.
Washington, DC, USA. Michael H. Silber
Sleep Disorders Center, Mayo Clinic College of
Renee Monderer
Medicine, Rochester, Minnesota, USA.
Sleep-Wake Disorders Center, Monteiore Medical
Center, Bronx, New York, USA. Ravi Singareddy
Department of Psychiatry (H073), Penn State College
Pasquale Montagna of Medicine, Hershey, Pennsylvania, USA.
Department of Neurological Sciences, University of
Bologna Medical School, Bologna, Italy. Deepti Sinha
Department of Pediatrics, Psychiatry, and Behavioral
Jacques Montplaisir Science, Stanford University School of Medicine,
Centre d’étude du sommeil, Hôpital du Sacré-Coeur, Stanford, California, USA.
Université de Montréal, Montréal, Québec, Canada.
Gregory Stores
Eric A. Nofzinger University of Oxford, c/o North Gate House,
Sleep Neuroimaging Research Program, University of Dorchester on hames, Oxon, UK.
Pittsburgh School of Medicine, Pittsburgh,
Shannon S. Sullivan
Pennsylvania, USA.
Stanford University Sleep Disorders Clinic, Stanford,
Luana Novelli California, USA.
Center for Pediatric Sleep Disorders, Department of Michele Terzaghi
Developmental Neurology and Psychiatry, Sapienza
Unit of Sleep Medicine and Epilepsy, IRCCS C.
University, Rome, Italy.
Mondino, Institute of Neurology Foundation, Pavia,
Maurice M. Ohayon Italy.
Stanford Sleep Epidemiology Research Center, Michael J. Thorpy
Stanford University School of Medicine, Palo Alto, Sleep-Wake Disorders Center, Monteiore Medical
California, USA. Center, and Albert Einstein College of Medicine,
Bronx, New York, USA.
Alessandro Oldani
Sleep Disorders Center, Department of Clinical Nikola N. Trajanovic
Neurosciences, H. San Rafaele Turro, Milan, Italy. Sleep and Alertness Clinic, University Health
Network, Toronto, Ontario, Canada.
Rafael Pelayo
Department of Pediatrics, Psychiatry, and Behavioral Thomas W. Uhde
Science, Stanford University School of Medicine, Department of Psychiatry (H073), Penn State College
Stanford, California, USA. of Medicine, Hershey, Pennsylvania, USA.
Giuseppe Plazzi Stefano Vandi
Department of Neurological Sciences, University of Department of Neurological Sciences, University of
viii Bologna, Bologna, Italy. Bologna, Bologna, Italy.
 Contributors

Roberto Vetrugno Antonio Zadra

Department of Neurological Sciences, University of Centre d’étude du sommeil, Hôpital du Sacré-Coeur,
Bologna, Bologna, Italy. Université de Montréal, Montréal, Québec, Canada.
John W. Winkelman Marco Zucconi
Division of Sleep Medicine, Brigham and Women’s Sleep Disorders Center, Department of Neurology,
Hospital, Harvard Medical School, Boston, Scientiic Institute and University Ospedale San
Massachusetts, USA. Rafaele, Vita-Salute University, Milan, Italy.

ix
 Preface

Intense medical and scientiic interest in an increas- afect patients’ academic and vocational performance,
ing number of topics in sleep medicine has led to as well as social and recreational activities. Accord-
the production of this volume on Parasomnias and ingly, this volume addresses issues in the etiology,
Other Sleep-Related Movement Disorders. Although pathophysiology, diagnosis, diferential diagnoses and
parasomnias are ubiquitous in childhood and occur management of parasomnias including psychosocial
across all ages, this is the irst publication to focus ramiications and efects on quality of life.
on this topic in detail. here is growing recognition In the last decade, signiicant advances in eluci-
that sleep disorders represent a major public health dating the pathophysiology of some of the parasom-
concern, and understanding the basic, translational, nias have been made. However, efective treatments are
clinical and psychosocial aspects of sleep disorders is oten lacking, and there is the need for speciic and
essential to the process of becoming a skilled clinical efective treatments for many of the disorders. A large
practitioner. number of medications have been efective in some
he earliest reported descriptions of some of the patients, even though few are FDA-approved in the
parasomnias such as sleepwalking and nightmares USA for most of the parasomnias. Behavioral inter-
have been known since antiquity; however, new para- ventions, hypnosis and psychiatric treatments can be
somnias have been described, such as REM sleep efective for some. Strategies for the management of
behavior disorder and catathrenia [1]. here have the risk for injury of both the patient or bed partner,
been numerous developments in the ield of abnormal such as securing the environment, are discussed in this
movement disorders during sleep that have led to a volume.
better understanding of the clinical features, the diag- he nature and mechanisms of parasomnias
nostic criteria and subsequently, treatments. remain largely unknown; however, the latest research
hese developments have continually deepened evidence is covered here. he parasomnias are oten
our understanding of parasomnias as pathophysiolog- misdiagnosed because similar symptoms exist and
ical conditions and have also drawn attention to the overlap with some of the movement disorders [5].
impact on the lives of those who have these conditions. hose disorders that should be considered in the
Parasomnias can be severe, chronic, debilitating and diferential diagnoses are discussed in detail with an
disabling neurological disorders, oten having early emphasis on the diferentiating features.
age of onset [2]. hey frequently involve abnormal he volume is broadly divided into six main sec-
involuntary behaviors during sleep, leading to injuries, tions: Section I: Introductory chapters; Section II: Dis-
emotional distress and even medico-legal liability [3]. orders of arousal; Section III: Parasomnias usually asso-
Despite their prominent symptoms and impact on ciated with REM sleep; Section IV: Other parasomnias;
patients’ health-related quality of life, parasomnias Section V: Sleep-related movement disorders and other
remain under-recognized and under-appreciated dis- variants, and Section VI: herapy of parasomnias.
orders, perhaps because of their predominantly night- In its irst section, the basic, translational, and clin-
time occurrence. Patients with parasomnias oten suf- ical background of parasomnias is reviewed. In this
fer from a constellation of other co-morbid medical regard, the irst three introductory chapters cover the
and/or psychiatric conditions [4]. historical, epidemiological, and neuroimaging of para-
In children and adolescents, the psychological somnias.
x and social complications of parasomnias can be In the second section of the book, the clinical
widespread and potentially severe. Parasomnias can aspects of the disorders of arousal that commonly
 Preface

occur in children, including confusional arousals, cians who evaluate and treat sleep disorders. It will
sleepwalking and sleep terrors, are discussed. also be equally interesting to psychiatry and neu-
he third section deals with the parasomnias usu- rology residents and fellows, clinical psychologists,
ally associated with REM sleep. Issues relating to the advanced graduate medical students, neuropsychol-
REM sleep behavior disorder, recurrent isolated sleep ogists, house oicers, and other mental health and
paralysis and nightmare disorder are presented. social workers who want to get an overall understand-
he fourth section deals with a group of parasom- ing of abnormal behaviors during sleep. Addition-
nias under the group heading of “other parasomnias”. ally, because of the growing medico-legal aspects of
his section addresses less commonly recognized and the parasomnias, this book has interest to the legal
less understood parasomnias such as sleep-related dis- profession.
sociative disorders, sleep-related groaning and sleep- In as much as research indings in many areas are
related eating disorder. rapidly broadening our understanding of parasom-
he ith section deals with sleep-related movement nias, it is anticipated that future editions of this volume
disorders and other variants that are oten included in of Parasomnias and Other Sleep-Related Movement
the diferential diagnosis of the parasomnias. Disorders will take these developments into account.
he sixth section discusses the pharmacologic,
behavioral and psychiatric management of the para- Michael J. horpy
somnias. Giuseppe Plazzi
he reader will ind that in addition, this volume
contains detailed discussions of important secondary
issues including the importance of medico-legal
References
1. Schenck CH, Mahowald MW. Rapid eye movement
aspects, safety, education, counselling and recognition
sleep parasomnias. Neurol Clin 2005; 23: 1107–26.
of psychiatric and cognitive comorbidities.
It has been the editors’ objective to provide a com- 2. Stores G. Aspects of parasomnias in childhood and
adolescence. Arch Dis Child 2009; 94: 63–9.
prehensive and authoritative guide for clinicians that is
presented in a manner which is both readable and eas- 3. Ebrahim IO, Fenwick P. Sleep-related automatism and
the law. Med Sci Law 2008; 48: 124–36.
ily understood. It is our hope that we have succeeded
in accomplishing this goal. 4. Lam SP, Fong SY, Ho CK, Yu MW, Wing YK.
Parasomnia among psychiatric outpatients: A clinical,
his volume is intended primarily for sleep dis-
epidemiologic, cross-sectional study. J Clin Psychiatry
orders specialists and sleep researchers. However, it 2008; 69: 1374–82.
is suitable for psychiatrists, neurologists, and any
5. Nobili L. Nocturnal frontal lobe epilepsy and
professionals and researchers interested in the inter- non-rapid eye movement sleep parasomnias:
disciplinary ield of sleep medicine. It will be of con- Diferences and similarities. Sleep Med Rev 2007; 11:
siderable interest to general practitioners, and physi- 251–4.

xi
 Credits and Acknowledgments

Parasomnias and Other Sleep-Related Movement Dis- the cutting edge of basic and applied parasomnia
orders provides scientiic and clinical information on research as well as providing the most recent infor-
abnormal movement disorders during sleep for all mation regarding how such knowledge can be used
health care workers interested in disorders of sleep. in clinical settings. heir informed opinions and
It is our pleasure to acknowledge the contributions of insights have signiicantly contributed to our scien-
those who were instrumental in the production of this tiic understanding of parasomnias and have provided
book. important interpretations regarding future research
Our sincere appreciation goes to Elio Lugaresi, directions.
Professor Emeritus, University of Bologna, Italy, who he highly talented publishing team at Cambridge
agreed to write the foreword. We wish to express our University Press made this project an especially plea-
appreciation for his contribution. surable one. heir guidance, technical expertise, and
We would like to express our deep apprecia- commitment to excellence were invaluable.
tion to all the contributors for their scholarly con- Finally, and most importantly, we want to thank
tributions that facilitated the development of this our spouses, families and colleagues for their support,
book. he expertise of contributors to Parasomnias and understanding during the development of this
and Other Sleep-Related Movement Disorders relects book.
the broad diversity and knowledge concerning para-
somnia research, which has continued to grow over Michael J. horpy
the last several decades. hese authors represent Giuseppe Plazzi

xii
Foreword

Henry Roger, a French neurologist based in Marseilles, he objective and systematic study of the parasom-
published a monograph of the lessons he gave in the nias only got underway ater Dement and Kleitman
academic years 1900–31 (H. Roger, Troubles du Som- irst described the polygraphic features of human sleep
meil. Paris: Masson et Cie editeurs, 1932). he two in 1957. In the 1960s, this was followed by the dis-
main chapters of his book concerned the insomnias covery of nocturnal myoclonus and the demonstra-
and hypersomnias, while a short chapter was devoted tion that arousal disorders are a benign condition.
to what Roger termed the parasomnias, “les petits However, landmark breakthroughs were to come in
troubles de la fonction hypnique” (unusual, but com- the 1970s–1980s when polysomnographic recordings
mon sleep events of little clinical relevance). Among performed under audiovisual control became a rou-
the parasomnias, Roger included nocturnal episodes tine means of sleep investigation. Use of this technique
known for centuries, such as sleep terror, sleepwalk- led to the discovery of RBD, nocturnal frontal lobe
ing, nightmares and enuresis, as well as disturbing seizures, and many other sleep disorders previously
dreams giving rise to agitated loud comments (reves ignored or misinterpreted.
parlès) and episodes of violent motor agitation recur- he 33 chapters of this extraordinary book docu-
ring nightly. ment the striking development of sleep medicine in
I think the dreams accompanied by somniloquy recent decades. We now know, for example, that the
correspond to what we nowadays call REM behavior term “parasomnias” does not cover all the unusual
disorder (RBD), whereas the violent nocturnal motor events arising during sleep. Some sleep-related move-
attacks resemble the epileptic nocturnal frontal lobe ment disorders and nocturnal variants of epilepsy, in
seizures described by my group in the early 1980s by fact, cannot be included among the “petits troubles de
the name of nocturnal paroxysmal dystonia. la fonction hypnique.”
he same chapter also describes the muscle jerks For these reasons, I am sure this book will be useful
arising on falling asleep. Roger noted that these move- to neurologists, psychiatrists, psychologists, child neu-
ments may occur sporadically and be of little clini- rologists and all those hoping to broaden their knowl-
cal relevance, but may also recur at very short inter- edge of these fascinating topics.
vals preventing sleep onset. Plainly, Roger’s detailed he book’s editors, Michael horpy and Giuseppe
description of myoclonias arising on falling asleep Plazzi, are to be complimented for having entrusted
refers to what we currently call hypnic jerks, noctur- each chapter to a leading expert in the ield. hey
nal myoclonus and propriospinal myoclonus. also have the merit for the diicult task of editing
his preamble serves to make my point that a neu- to bridge the stylistic gaps typical of multi-author
rologist working early in the last century and bas- works.
ing his observations on accurate history-taking alone Wishing the volume the success it deserves, I also
had described the majority of unusual events related congratulate the publisher for taking on this task at
to sleep. It was decades before the multiform semio- such a diicult time.
logical, etiopathogenetic and clinical aspects of these
events were identiied and investigated by countless Elio Lugaresi
sophisticated sleep laboratories.

xiii
Section Introduction

1
 Section 1 Introduction
Chapter

Parasomnias: a short history

1 Shannon S. Sullivan and Christian Guilleminault

If the notions of dream and nightmare are centuries inantly during slow wave sleep [4]. hese authors
old, going back to ancient Egyptian and Jewish civiliza- conirmed the clinical description of sleep terrors
tions, the distinction between nightmares and para- reported by Kanner in 1935 [5]. However, they indi-
somnias is recent. It is interesting to note that already cated that many of these phenomena occurred during
in 1932 Kouretas and Scouras [1] reported the com- NREM sleep stages 3 and 4, including enuresis. hey
plete absence of muscle tone during nightmares in one even performed cystometric recordings during sleep
of their patients, but Kleitman in his seminal mono- in children and reported that the enuretic episodes
graph places “nightmares, night terrors, somniloquy, occurred when the cystic pressure waves reached 120
bruxism and jactitation, enuresis, numbness and hyp- cm H2 O. Jacobson et al. [6] and Kales and Jacobson [7]
nalgia, and personality dissociation” under the ter- focused more on sleepwalking episodes and had sim-
minology “parasomnia” [2]. he term “parasomnia”, ilar indings to Gastaut and colleagues, indicating the
derived from the greek “para” meaning “around” and occurrence of events during NREM sleep, particularly
the latin “somnus” meaning “sleep”, had been coined stages 3 and 4. hey emphasized subjects’ “indiference
in 1932 by the French researcher Henri Roger who to environment” during episodes, and the “complete
published a monograph entitled “Les Troubles du amnesia” of the events the following morning. he
Sommeil-Hypersomnies, Insomnies, and Parasom- authors made the interesting observation that a sleep-
nies” [3]. In this monograph, Roger gave an excel- walking event could be induced by having a known
lent description of an episode of sleep terror in a somnambulistic child stand up in slow wave sleep.
child, and also described a somnambulistic episode. hese studies were presented and discussed at the
Kleitman’s review of previous literature shows that the 15th European Meeting on Electro-encephalography
diference between nightmares and sleep terrors was held in 1967 in Bologna, Italy, a meeting organized
not well perceived before Roger; rather, many syn- by Lugaresi and Gastaut and attended by European
dromes now understood to be within the rubric “para- and North American researchers. hereater, in
somnia” had been investigated independently. 1968 Broughton questioned the pathophysiological
As parasomnias became distinguishable from mechanisms underlying sleepwalking, sleep terrors,
nightmares, a possible link between such episodic and head-banging [8]. He dissociated them formally
nocturnal phenomena and seizure disorders was pro- from nocturnal epilepsy, emphasizing the well-
posed. Henri Gastaut in Marseille, France, wanted to demonstrated presence of sleep disturbance and
understand whether a relationship existed between occurrence in NREM sleep – and more particularly
the common parasomnias and seizures. To resolve stage 4 sleep; he termed such events “disorders of
this question, the Marseille team monitored individ- arousal”. He also diferentiated nocturnal enuresis
uals with abnormal nocturnal behavior and normal from the other phenomena.
matched controls during nocturnal sleep. In 1965, During the same period several authors empha-
Gastaut and Broughton reported some of their ind- sized the familial nature of the disorders. Kales and
ings and hypothesized that most “episodic phenom- Jacobson [7] indicated that sleepwalking was found in
ena,” as they called events, were non-epileptic in families; in 1980, Kales et al. suggested a two-threshold
nature and occurred out of NREM sleep, predom- multifactorial mode of inheritance [9]. Bakwin (1970)

he Parasomnias and Other Sleep-Related Movement Disorders, ed. M. J. horpy and G. Plazzi. Published by 3
Cambridge University Press.

C Cambridge University Press 2010.
 Section 1: Introduction

found that monozygotic twins were concordant for alternating pattern (CAP) scoring system, indicated
sleepwalking considerably more than dizygotic twins that various parasomnias were associated with an
(p = 0.06) [10]. In 1972, Hallstrom suggested an auto- abnormally elevated CAP rate [20]. his inding was
somal dominant pattern of heredity for sleep terrors conirmed by Guilleminault et al. both in children and
[11]. None of these studies fully explained observed in young adult sleepwalkers [21,22].
patterns of inheritance, despite the fact that familial Another type of investigation of the sleep EEG
patterns were seen in parasomnias. In 1971, Klacken- was performed by Gaudreau et al. [23] and Guillem-
berg, in his classic longitudinal study which followed inault et al. [24] using quantiied EEG. Both of these
about 200 children from birth in 1955 until age 16 groups showed that subjects with chronic parasom-
in Stockholm [12], made an interesting observation: nias had a signiicant decrease in delta power dur-
children who would become somnambulistic later in ing the irst NREM–REM sleep cycle, and lower than
life had much more restless sleep at the age of 4–5 expected delta power in the second cycle. Guillem-
years. Another important inding of this longitudinal inault et al. compared quantiied EEG and CAP analy-
study was that somnambulism and sleep terrors could ses and showed that the results were concordant when
be very rare or chronic. In the “chronic” or “habitual” these two analyses were applied to the same subjects
sleepwalkers, enuresis occurred from 5 until 16 years [21]. he conclusions drawn by these authors were that
of age and represented 2.5% of the sample. his num- sleep EEG analyses indicated an “instability of NREM
ber is of interest, as another epidemiologic study found sleep.” he investigations of Guilleminault et al. of
similar results. Ohayon et al., based on a representative children and adults [25] with chronic parasomnias
sample of the adult population, found that sleepwalk- showed that: (1) the individuals with chronic para-
ing afects 2.5% of the population [13]. Hublin et al., somnia presented such an instability of NREM sleep
on the other hand, indicated that 25% of children with every night, with or without the presence of the para-
a history of sleepwalking will sleepwalk as adults [14]. somnia; (2) the subjects presented with another sleep
he following 20 years focused on pharmacological disorder (most commonly SDB) which was responsi-
treatment of parasomnias with emphasis on the use of ble for the instability of NREM sleep; (3) the presence
benzodiazepines, with variable results. A short report of an additional factor (e.g. stress, alcohol, fever, sleep
by an English orthodontist was completely ignored. deprivation) was needed to provoke the parasomnia
Timms, who performed rapid maxillary expansion episode; and (4) treatment of the underlying sleep dis-
on children with a narrow hard palate, but who did order (including rapid maxillary distraction as noted
not routinely perform sleep studies, described clini- by Timms) alleviated the instability of NREM sleep
cal amelioration of symptoms that today would sug- and eliminated or improved the parasomnia.
gest the presence of sleep-disordered breathing [15]. Recent work on bruxism suggests that teeth-
He also described the elimination of chronic sleep- grinding may be an attempt to protect against the
walking events following rapid maxillary expansion. occurrence of sleep apnea, which raises the question
In 1999, Ohayon et al. in their epidemiologi- of whether this symptom should be placed in the same
cal studies on sleepwalking and sleep terrors found category as the others, despite the fact that it is also
that obstructive sleep apnea syndrome was the most associated with NREM sleep instability. Understand-
common sleep disorder associated with parasomnias ing of parasomnias has evolved over time and will con-
between the ages of 15 and 24 years [13]. In 2002, Espa tinue to evolve. As suggested by Guilleminault et al.,
et al. reported a similar association in a small number to the extent that parasomnias are triggered by unsta-
of subjects focusing on sleepwalking, as did Guillem- ble NREM sleep caused by SDB, the heritability of
inault et al., investigating sexual violence and confu- parasomnias may be related to the underlying familial
sional arousal [16,17]. Around the same time, Ohayon facial traits involved in the development of SDB [26].
et al. reported an important relationship between Epileptic disorders were shown to be rarely
bruxism and the presence of sleep-disordered breath- involved in abnormal behavior during NREM sleep,
ing (SDB) [18]. Goodwin et al., in the pediatric Tus- but when sleep-related seizure disorders are present,
con sleep cohort, also identiied a frequent association speciic seizure entities are implicated. In sleep-
between SDB and sleepwalking in 2004 [19]. related seizure disorder, polysomnographic studies
4 Investigations of sleep EEG in parasomnias became have demonstrated that a frontal lobe locus is most
more focused. In 1995, Zucconi et al., using a cyclic common, and less frequently the mesiotemporal
 Chapter 1: Parasomnias: a short history

region is involved. Pedley and Guilleminault [27] tried showed that subjects with RBD but without any
to chronicle distinguishing characteristics between other neurologic disorder already had the presence of
NREM parasomnias and sleep-related seizures, but Lewy bodies in the medulla. Progressively, the notion
such diferences are based on statistical analyses and emerged that RBD is commonly related to Lewy bod-
may not be true for every event. he stereotypy of the ies [36] and that a progressive rostral invasion of neu-
abnormal behavior of a seizure disorder is the most rons occurs over time, leading to the development of
constant inding. Seizures are also more likely to occur associated neurological syndromes. RBD is oten con-
out of stage 2 NREM and during the second half of the sidered to be a synucleinopathy with risk of developing
night. Studies from the 1970s and 1980s have demon- another neurological syndrome in the years to come.
strated that nocturnal seizures represent a bit less than Questions still have to be answered. Are all RBD
1% of the abnormal behavior during sleep. related to a synucleinopathy? Probably not; but the
Finally, nocturnal polysomnography has allowed percentage of RBD that is associated with synu-
the dissociation of NREM from REM sleep abnor- cleinopathy is unknown, despite preliminary data
mal behavior. he initial description of what is now which indicate that this association is common. Are
known as “REM sleep behavior disorder” (RBD) came other neurodegenerative diseases involved in RBD?
from Japanese researchers. It was related to the disap- Alzheimer’s Disease has been reported in associa-
pearance of the normal atonia of REM sleep reported tion with RBD, but this seems rare to exceptional;
during delirium secondary to alcohol intoxication other neurodegenerative diseases are involved more
[28]; it was again described by Japanese researchers frequently. Whether idiopathic RBD truly exists is still
in psychiatric patients [29]. In 1986, Quera-Salva an unanswered question.
and Guilleminault presented cases of olivo-ponto-
cerebellar degeneration and REM without atonia asso- References
ciated with the acting out of dreams [30]. 1. Kouretas D, Scouras P. Sur un trouble particulier du
In the same year, Schenk et al. reported the pres- sommeil: le cauchemar. Encephale 1932, 7: 622–7.
ence of other neurological syndromes, particularly 2. Kleitman N. Sleep and Wakefulness. Chicago:
parkinsonianism, and called it a “new category of para- University of Chicago Press, 1939; 280–9.
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pathic cases and named the syndrome “REM sleep Cie, 1932; 275–83.
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Further investigation indicated that many patients studies. Science 1965; 148: 975–7.
with Parkinson’s Disease and multisystem atrophy 7. Kales A, Jacobson A. Clinical and electrophysiological
manifested this disorder, and that it could also studies of somnambulism. In Gastaut H, Lugaresi E,
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8. Broughton RJ. Sleep disorders: disorders of arousal?
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11. Hallstrom T. Night terror in adults through 24. Guilleminault C, Poyares D, Abat F, Palombini
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Chan A. Sleepwalking, a disorder of NREM sleep older men initially diagnosed with idiopathic rapid eye
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6
 Section 1 Introduction
Chapter

Epidemiology of parasomnias
2 Maurice M. Ohayon

Introduction sleep to wakefulness. he sleeper appears awake but

behavior may be very inappropriate, marked by mem-
Parasomnias are sleep disorders characterized by
ory deicits, disorientation in time and space and slow
abnormal behavioral or physiological events occur-
mentation and speech. An episode can be triggered
ring at diferent sleep stages. hese disorders have sel-
by a forced awakening. Complex behaviors may occur,
dom been investigated in the adult general population
resulting in potentially dangerous situations for the
although, as we will see, they are very frequent. Many
sleeper and others.
of these parasomnias are accompanied with behaviors
Confusional arousals have received little attention
that can be potentially dangerous to the sleeper or to
in epidemiological studies. In children, Laberge et al.
others, leading sometimes to dramatic consequences,
[2] have estimated that about 17% of children between
such as self-mutilation, murder or suicide.
3 and 13 years are experiencing occasional or frequent
Parasomnias presented in this chapter are those
episodes of confusional arousals. In our study, we have
included in the latest International Classiication of
estimated their frequency in the general population to
Sleep Disorders (ICSD-2) [1]. hey are divided into
be 4.2%; decreasing from 6.1% in the 15–24 age group
three main categories: disorders of arousal, parasom-
to 3.3% in the 25–34 and stabilizing around 2% ater
nias associated with REM sleep, and other parasom-
35 years old [3]. No other igure exists for compara-
nias. here are 15 possible diagnoses of parasomnias.
tive purposes. Although confusional arousals are sus-
For many of them, information about their prevalence
pected to have a genetic component, genetic epidemi-
and incidence is limited or inexistent.
ological prevalence is yet to be determined.
he phenomenon, however, has generated much
Disorders of arousal more interest from a forensic standpoint. he irst
Arousal parasomnias occur mainly during NREM review of the literature devoted to assaults committed
sleep. his group consists of confusional arousals, in a state of confusional arousal was completed in
sleepwalking and sleep terrors. hese parasomnias 1905 by Gudden [4]. It included 18 cases among
occur primarily in childhood and normally cease by which 10 resulted in homicides. In 1943, a similar
adolescence. A same individual may experience more review by Schmidt [5] covered 35 cases (15 homi-
than one type of arousal parasomnias. However, epi- cides and 20 bodily injuries). hirty later years,
demiological igures for these co-occurrences are yet A. Bonkalo [6] reviewed cases of murder com-
to be determined. mitted during confusional arousals that occurred
from 1791 to 1974. He identiied approximately 20
cases, mostly perpetrated by men. More recently,
Confusional arousals B. Raschka [7] has brought the case of a man of
Confusional arousals, or sleep drunkenness, cor- 54 years that, for no apparent reason, had assaulted two
respond to a mental confusion occurring upon police oicers shortly ater they had awakened him
wakening, be it at night or in the morning. Physiologi- in his car. Polysomnographic indings indicated
cally speaking, cerebral reactivation to external stim- that the man sufered from obstructive sleep apnea
uli is altered in the transitional period from NREM syndrome. It was concluded that the combination

he Parasomnias and Other Sleep-Related Movement Disorders, ed. M. J. horpy and G. Plazzi. Published by 7
Cambridge University Press.

C Cambridge University Press 2010.
 Section 1: Introduction

of this disorder with alcohol intake and sudden fell 20 feet into some bushes, lacerating his head
arousal had prompted the violent behavior. and fracturing his tenth thoracic vertebra. he other
Several studies and case reports [7–10] have under- involved a 20-year-old man who smashed through
scored the association between sleep apnea and vio- a glass door, resulting in a severe laceration of his
lent behavior. One of these found that cerebral hypoxia right wrist. Several cases of murder while sleepwalk-
provoked by recurrent breathing pauses during sleep ing have also been documented. Studying 100 patients
could, over the long term, cause excessive daytime who claimed amnesia for their crime at the time
sleepiness, road accidents, impulsive behaviors at of hospitalization, Hopwood and Shell identiied one
awakening, and even cerebral damage [10]. Being sud- case of somnambulistic homicide: a ireman who bat-
denly awakened when in a relative state of cerebral tered his wife to death with a shovel during a sleep-
anoxia can produce a confusional state that can trans- walking episode [21]. More recently, Broughton et al.
late into violent behavior [7]. described the extraordinary case of a man who, dur-
Precipitant factors of confusional arousals include ing a sleepwalking episode, drove his car several kilo-
sleep deprivation, consumption of alcohol, hypnotics meters to the home of his wife’s parents before killing
or tranquilizers prior to bedtime, or a sudden awaken- them [22].
ing from sleep [3,11,12].

Sleep terrors
Sleepwalking Sleep terrors, too, are parasomnias that occur in
Sleepwalking is a parasomnia that occurs in NREM NREM sleep stages 3 and 4. Typically, these episodes
sleep stages 3 and 4, usually in the irst third of the begin with an abrupt awakening from sleep accompa-
principal sleep episode. his disorder is characterized nied by a panicky scream. he individual is generally
by automatic behavior during which the sleepwalker inconsolable during an episode. At awakening, there is
is usually unaware of his surroundings and almost complete or partial amnesia of the frightening dream.
entirely unresponsive to external stimuli. Sleepwalkers Like sleepwalking, sleep terrors occur more com-
may leave their bed, walk around their bedrooms and monly in childhood, but less frequently than sleep-
perform semi-purposeful acts. hey may also carry walking. Between 1 and 6.5% of children are alicted
out complex motor automatisms, such as driving a car. by sleep terrors [23,24], and as many prepubertal chil-
here is always complete amnesia for the episode at dren have recurrent episodes [25]. Occurrence of a few
awakening. episodes of sleep terrors in childhood is estimated to
Sleepwalking is more common in childhood, with occur in 20–30% [26]. In the adult general population,
a prevalence ranging from 5 to 30% for occasional or the prevalence of sleep terrors has been estimated to be
frequent episodes of somnambulism [13,14]. he dis- about 1% for weekly episodes [27] and around 2% for
order, however, can also appear for the irst time less frequent episodes [18,27].
in adulthood [10,15]. he prevalence of sleepwalk- One of the earliest reports of murder during a sleep
ing oscillates between 2 and 5% in the adult gen- terror episode is the case of Esther Griggs, who in 1858
eral population according to some authors [14,16–18]. threw her baby out of a window. She was apparently
As for confusional arousals, prevalence signiicantly dreaming her house was on ire at the time and was
decreases with age from 4.9% in the 15–24-year age actually attempting to save her baby. We can ind in
group to 0.5% in the ≥65-year age group [18]. A strong the literature several cases of sleepwalking/sleep ter-
familial occurrence has oten been reported in sleep- ror episodes that resulted in murder or serious injury
walking; for example, in a prospective study, Abe et al. [28–30]. he individual typically has no or only frag-
reported a sleepwalking occurrence of 14% in children mentary memory of the dream being acted out. From
aged between 8 and 10 years who had one of their par- the accounts of those who remember their dreams in
ents with a sleepwalking history and 2% of sleepwalk- part, certain recurring themes emerge. hese include
ing in children with non-sleepwalking parents [19]. defending oneself against attacks from others or beasts,
It is not uncommon for sleepwalkers to inlict trying to escape a danger, or trying to protect a loved
injury to themselves or others during an episode. one against potential danger.
8 Rauch and Stern described two cases of self-inlicted Sleepwalking and sleep terrors can be triggered
injury [20]. One involved a 34-year-old man who by stress, sleep deprivation, alcohol ingestion, and
 Chapter 2: Epidemiology

almost all sedative medications (hypnotics, tranquiliz- REM sleep behavior disorders
ers, antihistamines, stimulants).
REM sleep behavior disorders (RBD) were irst
described in the late 1970s by Japanese researchers and
Parasomnias associated with labeled as such by Schenck et al. [43]. his sleep dis-
order is characterized by a loss of generalized skeletal
REM sleep muscle REM-related atonia and the presence of physi-
his group of parasomnias is composed of three cal dream enactment. he individual has no conscious-
disorders occurring essentially during REM sleep. ness of acting out a dream, but is generally able to
hese disorders are nightmare disorder, recurrent iso- recount the dream upon awakening. his syndrome
lated sleep paralysis and REM sleep behavior disorder oten results in behavior dangerous to oneself or others
(RBD). [40–42]. heir initial sample [40] included four men
and one woman, all aged 60 years or over. Four of
them had neurological disorders. Most of these cases
Nightmare disorder had excessive slow-wave sleep for their age. his is not,
Nightmares are frightening dreams occurring gener- however, a sine qua non condition. Indeed, Tachibana
ally during REM sleep and oten resulting in awaken- et al. [43] reported seven cases of RBD without neuro-
ing the dreamer. his disorder is frequent in children. logical or psychiatric disorder that had a normal quan-
It afects boys and girls equally. Nightmares occur tity of slow-wave sleep. In all studies, this disorder is
always or oten in 2–11% of children and now and then observed almost exclusively in men.
in 15–31% [31]. About a third of adults with recurrent According to Schenck and Mahowald [44], prodro-
nightmares have onset of the symptom during child- mal symptoms of RBD appeared 10–40 years before
hood [16]. Nightmares have been reported to occur the full manifestation of the disorder in 25% of the
at least once a week in 5% of the adult population studied cases. his prodrome is characterized by sleep
[32] and always or oten in 1–5% [26]. Women are 2– talking, yelling, or limb-jerking during sleep.
4 times more frequently afected than men. here are he mechanism underlying this disorder is not
persistent genetic efects on the disposition to night- yet fully understood. Polysomnographic recordings
mares in about 45% of childhood and 37% of adult of individuals with RBD showed a reduction of the
nightmares [33]. tonic phenomena of REM sleep and the activation of
the phasic phenomena. Destruction of the brainstem
Recurrent isolated sleep paralysis regions responsible for the REM sleep atonia has been
hypothesized as responsible of such phenomena.
Sleep paralysis is one of the main symptoms associ-
he prevalence of RBD in the general population
ated with narcolepsy, but it can also occur individu-
is little-documented. Ohayon et al. [45] estimated it at
ally (i.e. isolated sleep paralysis). Téllez-Lòpez et al.
0.5% in the general population using minimal criteria
[34] found that 11.3% of their general population sam-
proposed by the International Classiication of Sleep
ple had sleep paralysis episodes at least sometimes.
Disorder (ICSD). However, as many as 2% of the gen-
Where more narrowly deined populations are con-
eral population reported experiencing violent behav-
cerned, Goode [35] and Everett [36] observed rates of
iors during sleep, with a male predominance [45].
4.7% and 15.4%, respectively, for self-reported sleep
paralysis in medical students, and Bell et al. [37] noted
a prevalence of 41% in Black Americans. In a study of Other parasomnias
adults living on the northeast coast of Newfoundland, his group of parasomnias comprises sleep-related
Ness [38] reported a rate of 62% for “old hag” attacks, dissociative disorders, sleep enuresis, catathrenia,
as sleep paralysis is popularly known in that part of exploding head syndrome, sleep-related hallucina-
Canada. An epidemiological study performed with tions, sleep-related eating disorder, unspeciied para-
8085 subjects between 15 and 99 years of age found somnia, parasomnia due to a drug or substance and
that 6.2% had at least one episode of sleep paralysis parasomnia due to a medical condition.
in their lifetime; 0.8% experienced severe sleep paraly- Epidemiological data on this group of parasom-
sis (at least one episode per week); and 1.4% moderate nias are scarce. Prevalence in the general population 9
sleep paralysis (at least one episode per month) [39]. is unknown for most of the parasomnias. Catathrenia,
 Section 1: Introduction

or sleep-related groaning, is a newly described para- Information about the associated factors and trig-
somnia occurring in both REM and NREM sleep [46]. gers of an episode is also limited. As shown, parasom-
nias are frequent in the general population; more than
30% of individuals experiences at least one type of
Sleep enuresis parasomnia. he consequences on daytime function-
Sleep enuresis, also called nocturnal bedwetting, is ing and the emotional distress experienced following
characterized by recurrent involuntary voiding during a parasomnia episode are undocumented at the epi-
the night. It is considered primary when the individual demiological level. herefore, it is diicult to ascertain
never experienced a dry period for at least six consec- what proportion of these individuals are in need of
utive months. treatment.
Sleep enuresis is relatively common in childhood At the genetic level, there is growing evidence that
(≥5 years old) and progressively decreases with age. many parasomnias have a genetic component. here-
At 4–5 years of age, the prevalence of sleep enuresis fore, epidemiological genetic links need to be studied.
is estimated to be between 20 and 30%. At 7 years, Ethnicity also could play a role in some parasomnias.
it decreases to about 10%, and further decreases to However, with the exception of sleep paralysis, the role
around 3% in 12-year-olds. he prevalence during of race has not been investigated.
adolescence and adulthood is around 2% [31,47,48].
Sleep enuresis in prepubertal children is twice as fre-
quent among boys than girls. In adulthood, the preva-
lence is comparable in both sexes. However, in the
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polysomnographically documented case of adult
Our knowledge about the prevalence and incidence of somnambulism with long-distance automobile driving
parasomnias is still limited compared to dyssomnias. and frequent nocturnal violence: parasomnia with
10 Most of the available data are based on the main symp- continuing danger as a noninsane automatism? Sleep
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219–24. Neurology 2002; 58: 1826–33.

12
 Section 1 Introduction
Chapter

Neuroimaging of parasomnias
3 Eric A. Nofzinger

Introduction mus. his suggests that the thalamocortical circuits

that play an important role in NREM sleep function
In the past few decades, structural and functional neu-
are those involving regions that support waking, con-
roimaging methods have emerged as a way to assess
scious, goal-directed behavior. Preclinical work shows
brain function in health and in pathology. hese meth-
that REM sleep is associated with an electrophysiolo-
ods allow for the quantiication of a variety of aspects
gically active cortex, with selective activation of cholin-
of brain structure and function including regional
ergic networks that originate in the brainstem and
brain volumes, metabolism, blood low, white matter
basal forebrain and that densely innervate the limbic
tract integrity, brain iron concentrations and receptor
and paralimbic cortex. Consistent with this, in rela-
binding. Given that sleep is regulated by the brain and
tion to waking and NREM sleep, REM sleep is asso-
may ultimately serve brain function, these tools may
ciated with increased relative activity in the pontine
provide important information regarding abnormal
reticular formation, as well as limbic (e.g. amygdala
brain function in sleep disorder patients such as those
and hypothalamus) and paralimbic cortex (e.g. ventral
with parasomnias. If so, such assessments may serve an
striatum, anterior cingulate and medial prefrontal cor-
important function in the evaluation and management
tex). his suggests that REM sleep may play an impor-
of parasomnia patients and in the development of new
tant role in emotional behavior, given the important
pharmacologic agents to treat parasomnias. his chap-
involvement of these structures in the regulation of
ter will briely review the use of structural and func-
afect and in motivated behavior.
tional neuroimaging in the assessment and manage-
ment of parasomnias.
Restless legs syndrome (RLS)/periodic limb
Neuroimaging studies of healthy movement disorders of sleep (PLMD)
human sleep he majority of the work in the area of neuroimaging
Neuroimaging studies have revealed reliable broad and parasomnias and sleep-related movment disor-
changes in cerebral activity across the sleep wake ders has been in the area of RLS and PLMD. he scope
cycle. Globally, brain activity decreases from waking of the work performed to date has been both driven
to NREM sleep, then increases to waking levels again by, and constrained by, clinical manifestations of the
during REM sleep [1–17]. Preclinical studies support disorder and by the measurements currently available
a deaferentation of the cortex at the level of the tha- using neuroimaging tools.
lamus and the occurrence of intrinsic thalamocortical he most extensive work has been performed
electrical oscillations in NREM sleep. Studies across in the area of central dopaminergic dysfunction in
several laboratories and using various imaging meth- these disorders. A series of studies measured cen-
ods have demonstrated that from waking to NREM tral dopamine D2-receptor occupancy with [123I]-
sleep there are relative regional reductions in activity labeled (S)-2-hydroxy-3-iodo-6-methoxy-([1-ethyl-2-
in the heteromodal association cortex in the frontal, pyrrolidinyl]methyl) benzamide (IBZM) and SPECT
parietal and temporal lobes as well as in the thala- in patients with PLMD [18–20]. hey found lower

he Parasomnias and Other Sleep-Related Movement Disorders, ed. M. J. horpy and G. Plazzi. Published by 13
Cambridge University Press.

C Cambridge University Press 2010.
 Section 1: Introduction

striatal [123I]IBZM binding in patients with PLMD involvement of the dopamine system in both striatal
and higher binding following dopaminergic therapy. and extrastriatal brain regions in the pathophysiology
Michaud et al. report the results of pre- and post- of RLS. Increased D2-receptor availability in RLS may
synaptic dopaminergic status using [123I]beta-CIT correspond to higher receptor densities or lower levels
and [123I]IBZM SPECT, respectively, in ten patients of endogenous dopamine, either of which would sup-
with both RLS and PLMD [21]. hey found no port the hypothesis of hypoactive dopaminergic neu-
diferences in DA transporter binding, but lower rotransmission in RLS.
striatal D2-receptor binding in patients (p = .006). Restless legs syndrome has been associated with
hey suggest that this indicates a decreased number of iron depletion and serum ferritin levels have been
D2-receptors or a decreased ainity of D2-receptors shown to be decreased by 13% per allele of a common
for IBZM. his supports a central striatal D2 receptor variant in an intron of BTBD9 on chromosome 6p21.2
abnormality in the pathophysiology of RSL/PLMD. found to be associated with RLS. Neuroimaging meth-
Tribl et al. [22] assessed patients with idiopathic RLS ods allow for the regional quantiication of brain iron
(iRLS) and periodic limb movements in sleep (PLMS) content, prompting sleep neuroimaging researchers to
who had exhibited a good response to dopaminergic assess brain iron content in patients with RLS. Allen
and non-dopaminergic treatment, and ten healthy et al. studied brain iron insuiciency in RLS [24].
sex- and age-matched controls using 123I-IBZM and Using a special MRI measurement (R2′ ), the authors
SPECT. he patients showed no signiicant diferences assessed regional brain iron concentrations in 10 sub-
in striatal to frontal IBZM binding to D2 receptors jects (5 with RLS, 5 controls). R2′ was signiicantly
compared to controls. hese indings show the normal decreased in the substantia nigra, and somewhat less
function of striatal D2 receptors in successfully treated signiicantly in the putamen, both in proportion to
patients with iRLS and PLMS. Eisensehr [23] studied RLS severity. he results show the potential utility of
14 drug-naive and 11 levodopa-treated patients this MRI measurement, and also indicate that brain
with idiopathic restless legs syndrome (RLS), and iron insuiciency may occur in patients with RLS in
10 controls age-matched to each RLS group with some brain regions. A replication and extension study
polysomnography (PSG), [(123)I]-(N)-(3-iodopro- by the same group in 22 early-onset and 19 late-onset
pen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophen- RLS subjects showed a reduced mean iron index from
yl) tropane ((123)I-IPT) SPECT, and [(123)I]-(S)- the substantia nigra in early-onset, but not late-onset
2-hydroxy-3-iodo-6-methoxy-[(1-ethyl-2-pyrrolidin- RLS patients [14]. hese data support a role of low
yl)methyl] benzamide ((123)I-IBZM) SPECT. Drug- brain iron in the SN in at least those RLS patients with
naive and levodopa-treated patients with RLS and early-onset. A small study by Godau et al. also demon-
controls showed similar striatal dopamine transporter strated brain iron deiciency in RLS patients using
and dopamine D(2)-receptor binding, the latter MRI T2 relaxometry and sonographically assessed
declining with age. he authors conclude that striatal echogenicity in multiple brain regions, suggesting the
dopamine transporter and receptor density is normal possible involvement of other brain regions in addi-
in drug-naive and levodopa-treated patients with RLS. tion to the substantia nigra [14]. In a larger study of
Cervenka et al. assessed 16 RLS patients naive late-onset RLS patients, Astrakas et al. also found low
to dopaminergic drugs and 16 matched control sub- substantia nigra iron content in the substantia nigra
jects with PET [13]. [11C]Raclopride and [11C]FLB using MRI T2 relaxometry. Low brain iron content,
457 were used to estimate D2-receptor availability therefore, especially in the basal ganglia, appears to
in the striatum and extrastriatal regions, respectively. be a replicable neuroimaging inding in patients with
Examinations were performed both in the morning RLS [1].
(starting between 10:00 and 12:00 h) and evening Neuroimaging methods allow for the determina-
(starting at 18:00 h). In the striatum, patients had tion of brain volumetric changes in patient samples to
signiicantly higher [11C]raclopride binding poten- see if structural cerebral abnormalities may play a role
tial (BP) values than controls. In extrastriatal regions, in the disorder. Etgen et al. assessed 51 RLS patients
[11C]FLB 457 BP was higher in patients than con- and 51 age- and sex-matched controls using high-
trols, and in the regional analysis the diference was resolution T1-weighted magnetic resonance imaging,
14 statistically signiicant in subregions of the thalamus and analyzed diferences between patient and con-
and the anterior cingulate cortex. he study supports trol groups using voxel-based morphometry [16]. hey
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