Pain Fibryomylgia

Roberto Patarca-Montero, MD, PhD, HCLD
The Concise Encyclopedia

of Fibromyalgia
and Myofascial Pain
Pre-publication
REVIEWS,
COMMENTARIES,
EVALUATIONS . . .
“T his encyclopedia provides the

reader with a relevant and up-to-
date bibliography related to fibromyalgia
meet people with fibromyalgia. Those
engaged in patient support groups
could be interested in having this en-
and myofascial pain. This is an admirable cyclopedia at hand, as it is an easy
source for reference material for individ- way to get to the answers to the many
uals who desire increased knowledge of questions that patients with fibromy-
either of these syndromes.” algia have. Between ‘Abuse’ and
‘Zolpidem,’ there are more than 100
Kimberly Groner, MSN, RN, CANP entries. The selection of references, al-
Adult Nurse Practitioner, most 800 in all, is appropriate. The rel-
Georgetown University evant literature is well covered. Re-
search on fibromyalgia is rapidly
expanding, and I hope that the ency-
clopedia will be updated as neces-
sary.”
“W ho would need a concise ency-

clopedia of fibromyalgia and
myofascial pain? I would. And so would
Karl G. Henriksson, MD, PhD
Associate Professor
and Former Head of Neuromuscular
physicians, psychologists, social work- Unit and Pain Clinic,
ers, physiotherapists, occupational ther- University Hospital,
apists, and others who in their work Linköping, Sweden
More pre-publication
REVIEWS, COMMENTARIES, EVALUATIONS . . .
“T his book enables you to find spe-

cific information about fibromy-
algia and myofascial pain quickly and
effectively. As pathogenesis and etiol-
ogy of these diseases are still poorly
understood and as there is no highly
effective fibromyalgia therapy, this
book summarizes and presents the
available knowledge.
The extensive bibliography facili-
tates finding the relevant original work.
I recommend this book to the reader
who is interested in a wide variety of
topics and who seeks a better under-
standing of the presented disorders.”
Dieter E. Pongratz, MD
Professor of Internal Medicine
and Neurology,
Friedrich-Baur Institute,
University of Munich, Germany
The Haworth Medical Press®

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of Fibromyalgia
and Myofascial Pain
®
THE HAWORTH MEDICAL PRESS
Chronic Fatigue Syndrome, Fibromyalgia Syndrome,
and Myalgic Encephalomyelitis
Roberto Patarca-Montero, MD, PhD

Senior Editor
Concise Encyclopedia of Chronic Fatigue Syndrome by Roberto

Patarca-Montero
CFIDS, Fibromyalgia, and the Virus-Allergy Link: Hidden Viruses,
Allergies, and Uncommon Fatigue/Pain Disorders by R. Bruce
Duncan
Adolescence and Myalgic Encephalomyelitis/Chronic Fatigue
Syndrome: Journeys with the Dragon by Naida Edgar
Brotherston
Phytotherapy of Chronic Fatigue Syndrome: Evidence-Based
and Potentially Useful Botanicals in the Treatment of CFS
by Roberto Patarca-Montero
Autogenic Training: A Mind-Body Approach to the Treatment
of Fibromyalgia and Chronic Pain Syndrome by Micah R.
Sadigh
Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/
Chronic Fatigue Syndrome and Other Organ Pathologies
by John Richardson
Treatment of Chronic Fatigue Syndrome in the Antiviral Revolution
Era by Roberto Patarca-Montero
Chronic Fatigue Syndrome, Christianity, and Culture: Between
God and an Illness by James M. Rotholz
The Concise Encyclopedia of Fibromyalgia and Myofascial Pain
Chronic Fatigue Syndrome and the Body’s Immune Defense System
of Fibromyalgia
and Myofascial Pain
Roberto Patarca-Montero, MD, PhD, HCLD
The Haworth Medical Press®

An Imprint of The Haworth Press, Inc.
New York · London · Oxford
Published by
The Haworth Medical Press®, an imprint of The Haworth Press, Inc., 10 Alice Street, Binghamton,
NY 13904-1580.
© 2002 by The Haworth Press, Inc. All rights reserved. No part of this work may be reproduced or
utilized in any form or by any means, electronic or mechanical, including photocopying, microfilm,
and recording, or by any information storage and retrieval system, without permission in writing
from the publisher. Printed in the United States of America.
Medicine is an ever-changing science. As new research and clinical experience broaden our
knowledge, changes in treatment and drug therapy are required. While many suggestions for drug
usages are made herein, the book is intended for educational purposes only, and the author, editor,
and publisher do not accept liability in the event of negative consequences incurred as a result of
information presented in this book. We do not claim that this information is necessarily accurate by
the rigid, scientific standard applied for medical proof, and therefore make no warranty, expressed
or implied, with respect to the material herein contained. Therefore the patient is urged to check the
product information sheet included in the package of each drug he or she plans to administer to be
certain the protocol followed is not in conflict with the manufacturer’s inserts. When a discrepancy
arises between these inserts and information in this book the physician is encouraged to use his or
her best professional judgment.
The author has exhaustively researched all available sources to ensure the accuracy and
completeness of the information contained in this book. The publisher and author assume no
responsibility for errors, inaccuracies, omissions, or any inconsistency herein.
Cover design byAnastasia Litwak.
Library of Congress Cataloging-in-Publication Data
Patarca-Montero, Roberto.
The concise encyclopedia of fibromyalgia and myofascial pain / Roberto Patarca-Montero.
p. cm.
Includes bibliographical references and index.
ISBN 0-7890-1527-7 (hard : alk. paper)—ISBN 0-7890-1528-5 (soft : alk. paper)
1. Fibromyalgia—Encyclopedias. 2. Myofascial pain syndromes—Encyclopedias. I. Title.
[DNLM: 1. Fibromyalgia—English. 2. Myfascial Pain Syndromes—Encyclopedias—English.
WE 13 P294c 2001]
RC927.3 .P28 2001
616.7'4—dc21
2001051687
Preface
Preface
Although much has been learned over the past decade about fibro-
myalgia and myofascial pain syndromes, much remains to be discov-
ered about its causes, nosology, treatment, and overlap with a variety
of rheumatic and nonrheumatic conditions. Advances in rheuma-
tology, cardiovascular medicine, endocrinology, epidemiology, im-
munology, infectious disease, neurology, psychiatry, and psychology
have served as the basis for the formulation of new lines of research
and novel therapeutic interventions.
The purpose of this concise encyclopedia is to summarize the
knowledge gained and published mainly within the past decade. The
text has been organized in such a way that the reader can easily access
and become familiar with the highlights of the most relevant topics.
Information on particular studies involving population size and meth-
odology is summarized to provide a framework to assess the validity
and generalizability of the observations presented. The reader is en-
couraged to use the index to search for specific subtopics or terms
that are covered under more general headings.
A balanced view is presented in each category, and the lessons
learned in related disorders are also highlighted. Evidence-based
alternative medicine approaches for fibromyalgia are also included in
this text. It is the hope of the author that this compendium will inspire
more research into the field of fibromyalgia and myofascial pain syn-
dromes and that it will serve to educate and create greater awareness
among health care professionals and the general public about these
widespread problems.
v
ABOUT THE AUTHOR
Roberto Patarca-Montero, MD, PhD, HCLD, is Assistant Profes-

sor of Medicine, Microbiology, and Immunology and also serves as
Research Director of the E. M. Papper Laboratory of Clinical Immu-
nology at the University of Miami School of Medicine. Previously, he
was Assistant Professor of Pathology at the Dana-Farber Cancer In-
stitute and Harvard Medical School in Boston. Dr. Patarca serves as
Editor of Critical Reviews in Oncogenesis and the Journal of Chronic
Fatigue Syndrome. He is also the author or co-author of more than
100 articles in journals or books, as well as the Concise Encyclopedia
of Chronic Fatigue Syndrome and Chronic Fatigue Syndrome: Ad-
vances in Epidemiologic, Clinical, and Basic Science Research. He is
currently conducting research on immunotherapy of AIDS and
chronic fatigue syndrome. Dr. Patarca is a member of the Board of
Directors of the American Association for Chronic Fatigue Syn-
drome and the Acquired Non-HIV Immune Diseases Foundation.
abuse: Anderberg et al. (2000) and Anderberg (2000) doc-
umented that stressful life events in childhood/adoles-
A cence and in adulthood seem to be very common in those

who have fibromyalgia. Furthermore, these life events
were experienced as more negative than the life events ex-
perienced by healthy controls. Goldberg et al. (1999) found
that 64.7 percent of fibromyalgia patients studied—61.9
percent of those with myofascial pain and 50 percent of those with
fascial pain—had childhood traumatic events, which are significantly
related to chronic pain. Since the problem of child abuse is broad,
health and rehabilitation agencies must shift from individualized
treatment to interdisciplinary treatment of the family and patient.
Winfield (2000) pointed out that female gender, adverse experi-
ences during childhood, psychological vulnerability to stress, and a
stressful, often frightening environment and culture are important an-
tecedents of fibromyalgia. Walker et al. (1997) compared thirty-six
patients with fibromyalgia and thirty-three patients with rheumatoid
arthritis and found that those with fibromyalgia had significantly
higher lifetime prevalence rates of all forms of victimization, both
adult and childhood, as well as combinations of adult and childhood
trauma. Although childhood maltreatment was found to be a general
risk factor for fibromyalgia, particular forms of maltreatment (e.g.,
sexual abuse per se) did not have specific effects. Experiences of
physical assault in adulthood, however, showed a strong and specific
relationship with unexplained pain. Trauma severity was correlated
significantly with measures of physical disability, psychiatric dis-
tress, illness adjustment, personality, and quality of sleep in patients
with fibromyalgia but not in those with rheumatoid arthritis.
In a study of seventy-five women with fibromyalgia, 57 percent of
whom had a history of abuse, Alexander et al. (1998) reported an as-
sociation between sexual/physical abuse and increased use of out-
patient health care services and medications for pain. Abused pa-
tients also were characterized by significantly greater pain, fatigue,
functional disability, and stress, as well as by a tendency to label
dolorimeter stimuli as painful regardless of their intensities. Fine-
stone et al. (2000) also found that women with a history of childhood
sexual abuse reported more chronic pain symptoms and utilized more
health care resources than nonabused control subjects.
1
2 The Concise Encyclopedia of Fibromyalgia and Myofascial Pain
acupuncture: There are various acupuncture techniques and meth-

ods, including dry needling, electroacupuncture, acupuncture using
hypodermic needles, and injecting various solutions into the acu-
puncture sites (reviewed in Ridgway, 1999). Several review and
meta-analysis papers on clinical trials (Berman et al., 1999, 2000;
Koenig and Stevermer, 1999; Lee, 2000; Muller et al., 2000; Offen-
bacher and Stucki, 2000; Ridgway, 1999; White, 1995) as well as
NIH Consensus Conferences (Acupuncture, 1997; NIH Consensus
Conference, 1998) have found that although acupuncture as a thera-
peutic intervention is widely practiced in the United States and there
have been numerous studies regarding its potential usefulness, many
of these studies provide equivocal results because of design, sample
size, and other factors. The issue is further complicated by inherent
difficulties in the use of appropriate controls, such as placebos and
sham acupuncture groups. However, promising results have emerged,
for example, showing efficacy of acupuncture as treatment for adult
postoperative and chemotherapy nausea and vomiting and for post-
operative dental pain. There are other situations, such as addiction,
stroke rehabilitation, headache, menstrual cramps, tennis elbow, fi-
bromyalgia, myofascial pain, osteoarthritis, lower back pain, carpal
tunnel syndrome, and asthma, in which acupuncture may be useful as
an adjunct treatment or as an acceptable alternative; or it may be in-
cluded in a comprehensive management program.
Basic science research has demonstrated convincingly that, at least
in the context of acute pain, acupuncture’s effects are related to the
release of a variety of natural opioids. For instance, in a study of
twenty-nine fibromyalgia patients, Sprott et al. (1998) reported that
acupuncture treatment was associated with decreased pain levels,
fewer positive tender points, decreased serotonin concentration in
platelets, an increase of the serum levels of the pain-modulating sub-
stances serotonin and substance P, and improved microcirculation in
tender points. Ridgway (1999) also reported that acupuncture is ef-
fective for the treatment of a type of chronic back pain that is possibly
associated with a radiculopathically induced, hypersensitivity myo-
fascial syndrome that presents as a fibromyalgia-like syndrome. A
high-quality study found that real acupuncture is more effective than
sham acupuncture for relieving pain, increasing pain thresholds, im-
proving global ratings, and reducing morning stiffness of fibro-
myalgia (reviewed in Berman et al., 1999). Electroacupuncture may
Roberto Patarca-Montero 3
also be useful in the treatment of fibromyalgia (White, 1995). How-

ever, it should be noted that for some fibromyalgia patients, acupunc-
ture can exacerbate symptoms, further complicating its application
for this condition (Berman and Swyers, 1999).
affective distress and anxiety: A study in Germany by Walter et al.

(1998) comparing low back pain patients with and without fibro-
myalgia syndrome (15 and 120 patients, respectively) found that al-
though fibromyalgia patients showed remarkably higher levels of
pain severity and affective distress, these pronounced differences dis-
appeared after controlling for different levels of pain severity. The au-
thors concluded that affective distress is not a unique feature of
fibromyalgia but seems to be caused entirely by higher levels of pain
severity.
Wolfe and Skevington (2000) reported that fibromyalgia patients
suffered more distress in association with increased functional im-
pairment as compared to rheumatoid arthritis or osteoarthritis pa-
tients. Hallberg and Carlsson (1998) also found that fibromyalgia
patients scored significantly higher on trait anxiety and seemed to in-
terpret stressful situations as more threatening than did patients with
work-related muscular pain. Anxiety seems to be of central impor-
tance for coping with chronic pain, and anxiety-prone patients with
fibromyalgia might benefit from psychological support in the process
of coping with pain (Hallberg and Carlsson, 1998).
Celiker et al. (1997) suggest that current anxiety is not secondary
to pain but trait anxiety is possibly causally related to pain in fibro-
myalgia. Studies by Kurtze et al. (1998, 1999) of 322 fibromyalgia
patients found independent, additive effects of anxiety and depres-
sion upon levels of pain and fatigue. Whereas interaction between
anxiety and depression failed to significantly explain pain and fatigue
symptom differences among the participants, it significantly affected
quality of life, functional disability, and lifestyle and was associated
with high consumption of coffee and cigarettes. The finding that anx-
iety and depression are independently associated with severity of
pain symptoms in fibromyalgia is underscored by the study by
Fischler et al. (1997) which failed to find marked differences in ill-
ness-related features or in psychiatric morbidity between CFS pa-
tients with and without fibromyalgia.
aging and geriatrics: The prevalence of fibromyalgia increases with

age (Buckwalter and Lappin, 2000; Goldenberg, 1996). Neck pain,
joint pain, and fibromyalgia all appear to increase with age in both
genders, whereas abdominal pain and tension-type headaches de-
crease with age, and migraine headache and temporomandibular dis-
order appear to peak in the reproductive years (Meisler, 1999).
Fibromyalgia and polymyalgia rheumatica are the most common
diffuse pain syndromes in the elderly (Belilos and Carsons, 1998;
Gowin, 2000). Fibromyalgia may be a primary or a secondary phe-
nomenon of other diffuse pain syndromes associated with inflamma-
tory, endocrine, or neoplastic diseases (Gowin, 2000). The initial
manifestations of fibromyalgia and other rheumatologic disorders in
elderly patients may differ from the typical findings in younger pa-
tients. Geriatric patients may have nonspecific complaints, a decline
in physical function, or even confusion. Common soft tissue prob-
lems encountered in older adults, including fibromyalgia, selected
bursitis/tendinitis syndromes, nerve entrapment syndromes, and mis-
cellaneous manifestations such as Dupuytren’s contractures, trigger
fingers, palmar fasciitis, and reflex-sympathetic dystrophy are gener-
ally diagnosed as arthritis or normal age-related problems but need to
be distinguished clinically (Holland and Gonzalez, 1998). In the se-
lection of optimal pharmacologic and nonpharmacologic therapeutic
modalities in the geriatric population, clinicians should focus on
maintaining or improving the patient’s quality of life and level of in-
dependent function (Michet et al., 1995).
alcohol: Alcohol consumption may exacerbate symptomatology in

fibromyalgia (Eisinger, 1998).
allergy: Tuncer et al. (1997) reported a high frequency of allergy

background among thirty-two primary fibromyalgia patients when
compared with an age- and sex-matched control group. Allergic skin
tests, which could not be performed in the control group, were posi-
tive in ten of fifteen primary fibromyalgia patients. Although serum
IgE levels were found elevated in the primary fibromyalgia group, the
elevation was not statistically significant (Tuncer et al., 1997).
aloe: One study showed that freeze-dried Aloe vera gel extract or a
combination of freeze-dried Aloe vera gel extract and additional
plant-derived saccharides resulted in a remarkable reduction in initial

symptom severity among fifty patients with chronic fatigue syn-
drome and fibromyalgia, with continued improvement in the nine-
month period between initial assessment and follow-up (Dykman
et al., 1998). Aloe plants are native to eastern and southern Africa.
Gel from the inner central zone of the leaves and latex from
pericyclic cells are used for medicinal purposes. Primary active com-
ponents include anthraquinones, saccharides, prostaglandins, and
fatty acids (Hadley and Petry, 1999).
alternative and complementary medicine: Fibromyalgia is a

chronic-pain–related syndrome associated with high rates (approxi-
mately two-thirds of patients in most studies) of complementary and
alternative medicine use, usually concomitant with multiple inter-
ventions (Berman and Swyers, 1997, 1999; Dimmock et al., 1996;
Hawkins, 1998; Nicassio et al., 1997; Pioro-Boisset et al., 1996; Rao
et al., 1999). Factors associated with alternative and complementary
medicine use include high socioeconomic status, duration of fibro-
myalgia, and dissatisfaction with current hospital treatment (Dim-
mock et al., 1996). The relatively high cost of and lack of information
on complementary therapies appears to dissuade those patients who
choose not to use it (Dimmock et al., 1996). Moreover, based on a
study of eighty-two fibromyalgia patients, Fitzcharles and Esdaile
(1997) found that patients who had been treated by nonphysician
practitioners during the preceding six months reported similar pain
and functional impairment to those not receiving treatments.
Among the many alternative and complementary medicine thera-
pies frequently used by fibromyalgia patients, empirical research
data exist to support the use of only three (in order of strength of sup-
porting data): (1) mind-body techniques (e.g., biofeedback, hypno-
sis, and cognitive-behavioral therapy, particularly when utilized as
part of a multidisciplinary approach to treatment), (2) acupuncture,
and (3) manipulative therapies (e.g., chiropractic and massage) (Ber-
man and Swyers, 1999). (See BIOFEEDBACK, HYPNOSIS, COGNITIVE-
BEHAVIORAL THERAPY, ACUPUNCTURE, CHIROPRACTIC TREATMENT,
and MASSAGE for details of each). However, in one study (Pioro-
Boisset et al., 1996), patient satisfaction ratings were highest for spir-
itual interventions.
amitriptyline: Amitriptyline is a tricyclic antidepressant agent that

also has analgesic properties (Bryson and Wilde, 1996). Whether
amitriptyline’s analgesic effects are linked to its mood-altering activ-
ity or attributable to a discrete pharmacological action (or a combi-
nation of both) is unknown. Clinical trials demonstrate that oral
amitriptyline achieves at least a good or moderate response in up to
two-thirds of patients with postherpetic neuralgia and three-quarters
of patients with painful diabetic neuropathy, which are neurogenic
pain syndromes that are often unresponsive to narcotic analgesics
(Godfrey, 1996; Johnson, 1997).
Amitriptyline has also demonstrated efficacy in heterogeneous
groups of patients with chronic nonmalignant pain, such as that en-
countered in fibromyalgia. In this respect, a four-center, twelve-week
study of 130 female fibromyalgia patients not suffering from psychi-
atric disorders showed that 74 percent responded to amitriptyline
(25-37.5 mg/day) and managed best in general health, pain, sleep
quality and quantity, and fatigue (Hannonen et al., 1998). In terms of
nonresponders to amitriptyline, a study of twenty-two fibromyalgia
patients in a two-month, double-blind, crossover trial of amitriptyline
(25 mg/day) versus placebo found that an anomaly consisting of
electroencephalographic waves within the alpha frequency band dur-
ing non–rapid-eye movement sleep, which is present in only a small
proportion of patients with fibromyalgia and does not correlate with
disease severity, is not affected by treatment with amitriptyline
(Carette et al., 1995). A larger sample size will be needed to ade-
quately assess the value of this sleep anomaly in predicting the re-
sponse to amitriptyline.
Adverse events resulting from the antimuscarinic activity of ami-
triptyline (primarily dry mouth and sedation) are commonly re-
ported, even at the low dosages used for the control of pain (Lauten-
schlager, 2000). Low starting doses and careful dosage titration may
help to minimize these effects. Orthostatic hypotension and tachycar-
dia, sometimes associated with tricyclic antidepressant agents, may
also pose a problem in the elderly.
anticardiolipin antibody: Anticardiolipin antibodies occur in a wide

variety of autoimmune and nonautoimmune disorders in adults. A
study of 106 pediatric patients (36 systemic lupus erythematosus, 28
juvenile rheumatoid arthritis, 11 fibromyalgia, 7 sarcoidosis, 5 derma-
tomyositis, 3 rheumatic fever, 3 vasculitis, 2 scleroderma, and 11

miscellaneous) failed to find anticardiolipin antibodies or features of
antiphospholipid syndrome among pediatric fibromyalgia patients
(Gedalia et al., 1998).
antidepressants: O’Malley et al. (2000) performed a meta-analysis

of published English-language, randomized, placebo-controlled tri-
als (sixteen identified, thirteen of which were deemed appropriate for
data extraction) and concluded that antidepressants, regardless of
class (three assessed: tricyclics, selective serotonin reuptake inhibi-
tors, and S-adenosylmethionine), are efficacious in treating many
symptoms of fibromyalgia (sleep, fatigue, pain, and well-being, but
not trigger points). Patients were more than four times as likely to re-
port overall improvement, and reported moderate reductions in indi-
vidual symptoms, particularly pain. In the five studies where there
was adequate assessment for an effect independent of depression,
only one study found a correlation between symptom improvement
and depression scores. Whether this effect is independent of depres-
sion needs further study. A previous meta-analysis by O’Malley et al.
(1999) had arrived at similar conclusions. Arnold et al. (2000) also
reviewed twenty-one randomized, controlled clinical trials, identi-
fied sixteen involving tricyclic agents, and performed meta-analysis
with the nine of the sixteen studies that were considered suitable.
Compared with placebo, tricyclic agents were associated with effect
sizes that were substantially larger than zero for all measurements of
physician and patient overall assessment, pain, stiffness, tenderness,
fatigue, and sleep quality. The largest improvement was associated
with measures of sleep quality; the most modest improvement was
found in measures of stiffness and tenderness. Other review articles
suggest that antidepressants play an important role in the drug treat-
ment of chronic pain and fibromyalgia (Baraczka et al., 1997;
Fishbain, 2000; Godfrey, 1996; Johnson, 1997; Lautenschlager, 2000;
Maes et al., 1999; Touchon, 1995). However, moclobemide, a revers-
ible inhibitor of monoamine oxidase, seems to be ineffective and in-
ferior to amitriptyline for pain (Hannonen et al., 1998).
antiganglioside antibodies: Klein and Berg (1995) reported a de-

fined autoantibody pattern consisting of antibodies directed against
serotonin, gangliosides, and phospholipids in about 70 percent of
fibromyalgia patients and in about 55 percent of chronic fatigue syn-

drome patients. Although 71 percent of 100 fibromyalgia patients
and 43 percent of forty-two chronic fatigue syndrome patients stud-
ied had antiganglioside antibodies, antibodies directed against gan-
gliosides and phospholipids could also be detected in other disorders,
while the presence of antiserotonin antibodies seemed more closely
related to fibromyalgia and chronic fatigue syndrome. The observa-
tion that family members of fibromyalgia and chronic fatigue syn-
drome patients also had these antibodies represents an argument in
favor of a genetic predisposition (see GENETICS).
antinuclear antibodies: A study by Suarez-Almazor et al. (1998) of

711 patients showed that primary care physicians frequently re-
quested antinuclear antibodies (ANA), rheumatoid factor, and eryth-
rocyte sedimentation rate in patients referred to rheumatologists.
Most tests were negative and were often requested in patients without
connective tissue diseases, resulting in low positive predictive values
and questionable clinical utility. Suarez-Almazor et al. (1998) sug-
gest that a decrease in inappropriate use could be achieved by empha-
sizing that fatigue and diffuse musculoskeletal pain are not indicative
of connective tissue disease in the absence of other features such as
joint swelling, typical rash, or organ involvement. In fact, most pa-
tients with diffuse musculoskeletal pain and fatigue in their study had
fibromyalgia or localized soft tissue rheumatism. Based on a study
performed by fifteen international laboratories, Tan et al. (1997) rec-
ommend that laboratories performing immunofluorescent ANA tests
should report results at both the 1:40 and 1:160 dilutions and should
supply information on the percentage of normal individuals who are
positive at these dilutions, because a low-titer ANA is not necessarily
insignificant. ANA assays can be a useful discriminant in recogniz-
ing certain disease conditions, but can create misunderstanding when
the limitations are not fully appreciated (Illei and Klippel, 1999).
antiphospholipid antibodies: Berg et al. (1999) found low level co-

agulation activation from immunoglobulins, as demonstrated by anti-
B2GPI antibodies, in patients with fibromyalgia or chronic fatigue
syndrome, a finding that, according to Berg et al., would allow classi-
fication of these diseases as a type of antiphospholipid antibody syn-
drome. However, Gedalia et al. (1998) found no evidence of antiphos-
pholipid antibody syndrome among pediatric fibromyalgia patients.

Although antiphospholipid antibodies can be found in disorders other
than fibromyalgia, Klein and Berg (1995) reported an increased fre-
quency of antiphospholipid antibodies in conjunction with antigan-
gliosides or antiserotonin antibodies among fibromyalgia or chronic
fatigue syndrome patients. Heller et al. (1998) also found the latter
autoantibody pattern among patients with sudden deafness and pro-
gressive hearing loss, a significant proportion of whom also com-
plained of fatigue, myalgia, arthralgia, depression, diarrhea, and sicca
symptoms.
antipolymer antibodies: Wilson et al. (1999) found a higher sero-

prevalence of antipolymer antibodies in patients with fibromyalgia
(22/47, 47 percent) compared to patients with osteoarthritis (3/16,
19 percent) or rheumatoid arthritis (1/13, 8 percent), as well as com-
pared to banked autoimmune disease control sera from patients with
poly/dermatomyosis (2/15, 13 percent), rheumatoid arthritis (3/30,
10 percent), systemic lupus erythematosus (1/30, 3 percent), and sys-
temic sclerosis (1/30, 3 percent). The prevalence of antipolymer anti-
body seroreactivity was also significantly higher in patients with se-
vere fibromyalgia (17/28, 61 percent) compared to patients with mild
fibromyalgia (11/37, 30 percent) and controls (4/21, 19 percent). In
addition, both mean threshold and mean tolerance dolorimetry scores
were significantly lower in the antipolymer antibody seropositive pa-
tients with mild fibromyalgia compared to the seronegative patients.
Wilson et al. (1999) suggest that the antipolymer antibody assay may
be an objective marker in the diagnosis and assessment of fibro-
myalgia and may provide additional avenues of investigation into the
pathophysiological processes involved in fibromyalgia, whether pri-
mary or secondary to other disease processes, such as that associated
with silicone breast implantation (Angell, 1997; Edlavitch, 1997;
Ellis et al., 1997; Everson and Blackburn, 1997; Korn, 1997; Lamm,
1997).
antiserotonin antibodies: Klein and Berg (1995) showed the pres-

ence of a defined autoantibody pattern consisting of antiserotonin,
antiphospholipid, and antigangliosides antibodies in approximately
70 percent of fibromyalgia patients and 50 percent of chronic fatigue
syndrome patients. Antiserotonin antibodies were closely related
with fibromyalgia/chronic fatigue syndrome, while antiganglioside

and antiphospholipid antibodies could also be detected in other dis-
orders. Olin et al. (1998) confirmed the latter findings. Heller et al.
(1998) found a similar pattern of autoantibody reactivity in patients
with sudden deafness or progressive hearing loss who complained of
symptoms typical for fibromyalgia/chronic fatigue syndrome, while
Coplan et al. (1999) also found a significant prevalence of anti-
serotonin antibodies among patients with panic disorder. It remains
to be demonstrated if the peripheral autoimmunity is representative
of central nervous system serotonin neuronal alterations (Neeck et al.,
1996).
artists and musicians: Martinez-Lavin et al. (2000) reported on the

influence of fibromyalgia in Frida Kahlo’s life and art. The two great
pianists Clara Wieck Schumann (1819-1896) and Sergei Vassilievich
Rachmaninov (1873-1943) suffered from chronic pain, and a report
by Hingtgen (1999) discusses the pain syndromes that plagued these
great musicians and the effect of chronic illness on their music. It is
important for the physician to differentiate fibromyalgia from the
pain, sensory loss, and lack of coordination that may result from the
physical demands of performing on musical instruments (Potter and
Jones, 1995).
ascorbigen: In a one-month open-label trial, Bramwell et al. (2000)

gave 500 mg per day of a blend containing 100 mg ascorbigen and
400 mg broccoli powder to twelve female fibromyalgia patients. Pa-
tients showed a mean decrease in their physical impairment score and
total fibromyalgia impact scores and an increase in the mean thresh-
old pain level. However, the mean physical impairment score two
weeks posttreatment showed a significant return to near pretreatment
level, and a larger, double-blind study is needed.
attributions: Neerinckx et al. (2000) found that the majority of pa-

tients with chronic fatigue syndrome and fibromyalgia reported a
great diversity of attributions (“a chemical imbalance in my body,” “a
virus,” “stress,” and “emotional confusion”) open to a preferably per-
sonalized cognitive-behavioral approach. Neerinckx et al. (2000)
recommend paying special attention to patients with symptoms exist-
ing for more than one year and to those who had previous contact
with a self-help group because they particularly show external, sta-

ble, and global attributions that may compromise feelings of self-ef-
ficacy in dealing with the illness.
autoimmune fatigue syndrome: Itoh et al. (1997) found that among

children who chronically complain of nonspecific symptoms such as
headache, fatigue, abdominal pain, and low-grade fever, those who
were antinuclear antibody (ANA) positive (approximately 50 percent
of cases) tended to have general fatigue and low-grade fever, while
gastrointestinal problems, such as abdominal pain, diarrhea, and
orthostatic dysregulation symptoms, were commonly seen in ANA-
negative patients. Children who were unable to go to school more
than one day a week were seen significantly more among ANA-posi-
tive patients than among negative patients. Based on these observa-
tions, the authors concluded that autoimmunity may play a role in
childhood chronic nonspecific symptoms and proposed a new disease
entity: the autoimmune fatigue syndrome in children.
Itoh et al. (1999) described two patients with fibromyalgia who
had been diagnosed initially as having autoimmune fatigue syndrome
(AIFS) and proposed that ANA-positive fibromyalgia or ANA-posi-
tive chronic fatigue syndrome could be forms of AIFS. Itoh et al.
(1998) also reported that a novel autoantibody to a 62 kD protein
(anti-Sa) was found in 40 percent of ANA-positive children with
autoimmune fatigue syndrome. Similar to studies of autoimmune
diseases, Itoh et al. (2000) found that autoimmune fatigue syndrome
has an immunogenetic background: it is positively associated with
the class I antigen HLA-B61 and with the class II antigen HLA-DR9,
and negatively associated with HLA-DR2.
autonomic dysfunction: Power spectrum analyses of heart rate vari-

ability have revealed that the basal autonomic state of fibromyalgia
patients is characterized by increased sympathetic and decreased
parasympathetic tones (Cohen et al., 2000) and a deranged sympa-
thetic response to orthostatic stress (Kelemen et al., 1998; Martinez-
Lavin, 1997; Martinez-Lavin and Hermosillo, 2000). As is the case
with chronic fatigue syndrome (Wilke et al., 1998), Bou-Holaigah
et al. (1997) identified a strong association between fibromyalgia and
neurally mediated hypotension: During stage one of upright tilt,
twelve of twenty fibromyalgia patients (60 percent), but no controls,
had an abnormal drop in blood pressure; and among those with fibro-
myalgia, all eighteen who tolerated upright tilt for more than ten min-
utes reported worsening or provocation of their typical widespread fi-
bromyalgia pain during stage one, while controls were asymptomatic
(Bou-Holaigah et al., 1997). Individuals with fibromyalgia also have
diminished twenty-four-hour heart rate variability due to an in-
creased nocturnal predominance of the low-frequency band oscilla-
tions consistent with an exaggerated sympathetic modulation of the
sinus node (Martinez-Lavin et al., 1998). This abnormal chrono-
biology could explain the sleep disturbances and fatigue that occur in
this syndrome. Spectral analysis of heart rate variability may there-
fore be a useful test to identify fibromyalgia patients who have
dysautonomia.
The autonomic nervous system is a major mediator of the visceral
response to central influences such as psychological stress, and auto-
nomic dysfunction may also represent the physiological pathway ac-
counting for many of the extraintestinal symptoms seen in irritable
bowel syndrome patients and some of the frequent gastrointestinal
complaints reported by patients with disorders, such as chronic fa-
tigue and fibromyalgia (Tougas, 1999). However, sympathetic dys-
autonomia may present differentially among the latter syndromes
since denervation hypersensitivity of the pupil is not apparent in
chronic fatigue syndrome patients (Sendrowski et al., 1997).
Behcet’s syndrome: Yavuz et al. (1998) found a trend for

an increased frequency of fibromyalgia in female Behcet’s
B syndrome patients. In their study, ten (nine of whom were

women) of 108 Behcet’s syndrome patients (9.2 percent)
met the American College of Rheumatology criteria for fi-
bromyalgia, and, in contrast to those without fibromyalgia,
they had mild to moderate disease activity in which musculoskeletal
complaints were common.
benzodiazepine-induced hip fracture: Fibromyalgia patients on

long-acting benzodiazepines may be at increased risk for osteoporo-
sis and hip fracture (Robb-Nicholson, 1998).
biofeedback: Based on a study of nineteen fibromyalgia patients,

Mur et al. (1999) concluded that electromyography-based (EMG)
biofeedback training may contribute not only to a reduction of pain
and muscle tension but also to improvement of quality of life. The lat-
ter results are consistent with a previous study of eighteen patients by
Sarnoch et al. (1997), and Mur et al. recommend EMG biofeedback
as part of a multimodal pain therapy in fibromyalgia patients. In this
respect, Buckelew et al. (1998) randomized 199 fibromyalgia pa-
tients to four groups: biofeedback/relaxation, exercise, a combined
program of the latter two, and an educational/attention control pro-
gram. All three treatment interventions resulted in improved self-effi-
cacy for physical function which was best maintained by the combi-
nation group after a two-year follow-up period.
Borna disease virus: Borna disease virus is a neurotropic RNA virus

that gives rise to a characteristic pathological picture described as
meningoencephalomyelitis in horses and sheep. Epidemiological
data suggest that Borna disease virus may be closely associated with
neuropsychiatric disease (depression and schizophrenia) in humans.
Furthermore, anti-Borna disease virus antibodies and Borna disease
virus RNA was detected in a family cluster with chronic fatigue syn-
drome (Kitani et al., 1996; Nakaya et al., 1996, 1997). However, a
study of eighteen Danish patients with fibromyalgia failed to reveal
Borna disease virus in cerebrospinal fluid or serum (Wittrup et al.,
2000).
botulinum toxin: Paulson and Gill (1996) reported that, unlike the
case for migraine headaches, botulinum toxin is unsatisfactory ther-
apy for fibromyalgia.
breast implants: Although some authors in older studies have sug-

gested a link with fibromyalgia or soft tissue rheumatism (Bridges
et al., 1996; Cuellar et al., 1995; Fuchs et al., 1995; Levenson et al.,
1996; Vasey, 1997; Vasey and Aziz, 1995; Young et al., 1995), immu-
nologic and other sequelae of silicone breast implantation such as
collagen vascular diseases or fibromyalgia have not been confirmed
in large studies and reviews (Blackburn et al., 1997; Brown et al.,
1998; Friis et al., 1997; Lai et al., 2000; Levine et al., 2000; Martin,
1999; Nyren et al., 1998; Peters et al., 1997; Thomas et al., 1997;
Wolfe, 1999; Wolfe and Anderson, 1999). Several reports have dis-
cussed the possible silicone breast implant-associated induction of
autoimmunity, in particular antipolymer antibodies whose presence
has also been reported in fibromyalgia (Angell, 1997; Edlavitch,
1997; Ellis et al., 1997; Everson and Blackburn, 1997; Korn, 1997;
Lamm, 1997; Romano, 1996; Silverman et al., 1996). However,
many studies have failed to find evidence for autoimmunity or other
immunological abnormalities. For instance, Blackburn et al. (1997)
found that the levels of interleukin-6, interleukin-8, tumor necrosis
factor-alpha, soluble intercellular adhesion molecule-1, and soluble
interleukin-2 receptor were not different in silicone breast implant
disease patients from those seen in normal subjects and were signifi-
cantly less than those seen when examining chronic inflammatory
disorders such as rheumatoid arthritis or systemic lupus erythema-
tosus. Although Young et al. (1995) found a higher frequency of
HLA-DR53 among symptomatic breast implant patients and Bridges
et al. (1996) reported 5 percent positivity for antinuclear antibodies
among silicone breast implant patients, these findings have not panned
out in larger analyses. Nonetheless, some studies have found that
breast implants appear to be more common in patients with fibromy-
algia than in those without it, an observation that has led some au-
thors to postulate that there may be a common, predisposing set of
psychosocial characteristics that are shared between those who have
fibromyalgia and those who undergo silicone breast implantation
(Wolfe and Anderson, 1999).
Although uncontrolled case series have reported neurologic prob-
lems believed to be associated with silicone breast implants, one re-
view report (Rosenberg, 1996) failed to find any evidence that sili-
cone breast implants are causally related to the development of any
neurologic diseases. The latter study found that although neurologic
symptoms were frequently endorsed, including fatigue (82 percent),
memory loss and other cognitive impairment (76 percent), and gener-
alized myalgias (66 percent), most patients (66 percent) had normal
neurological examinations. Findings reported as abnormal were mild
and usually subjective, including sensory abnormalities in 23 per-
cent, mental status abnormalities in 13 percent, and reflex changes in
8 percent. No pattern of laboratory abnormalities was seen, either in
combination or in attempts to correlate them with the clinical situa-

tion. Laboratory studies appeared to be random without an attempt to
confirm or correlate with a particular diagnosis. Diagnoses by physi-
cians endorsing the concept that silicone breast implants (SBIs) cause
illness included “human adjuvant disease” in all cases, memory loss
and other cognitive impairment (“silicone encephalopathy”) and/or
“atypical neurologic disease syndrome” in 73 percent, “atypical neu-
rologic multiple sclerosis-like syndrome” in 8 percent, chronic in-
flammatory demyelinating polyneuropathy in 23 percent, and some
other type of peripheral neuropathy in 18 percent. There was no co-
herence in making these diagnoses; the presence of any symptoms in
these women was sufficient to make these diagnoses. Alternatively,
after review of the data, no neurologic diagnosis could be made in
82 percent. Neurologic symptoms could be explained in some cases
by depression (n = 16), fibromyalgia (n = 9), radiculopathy (n = 7),
anxiety disorders (n = 4), multiple sclerosis (n = 4), multifocal motor
neuropathy (n = 1), carpal tunnel syndrome (n = 1), dermatomyositis
(n = 1), and other psychiatric disorders (n = 3).
breathing: In a study of seventeen fibromyalgia patients, Sergi et al.

(1999) found that the respiratory pattern of fibromyalgia patients
showed a high occurrence of periodic breathing, a greater number of
desaturations per hour of sleep, and a lower transfer factor of the lung
for carbon monoxide despite no changes in pulmonary volumes. The
transfer factor for carbon monoxide was more impaired and the oc-
currence of periodic breathing was higher among patients complain-
ing of daytime hypersomnolence who had a higher number of tender
points, about twice as many arousals per hour and a lower sleep effi-
ciency than patients who did not report this symptom. Other studies
have shown changes in sleep respiratory patterns of fibromyalgia pa-
tients (Alvarez-Lario and Viejo Banuelos, 1997), and Ozgocmen and
Ardicoglu (1999) reported reduced chest expansion in primary fibro-
myalgia syndrome. Weiss et al. (1998) described two patients with
chronic, severe, episodic dyspnea who underwent prolonged, exten-
sive, and invasive evaluations without a diagnosis being made and
were both subsequently diagnosed with fibromyalgia. The latter au-
thors point out that fibromyalgia is rarely included in the differential
diagnosis of dyspnea, and timely diagnosis and treatment may be de-

layed.
calcitonin: In a double-blind crossover trial in which

eleven fibromyalgia patients alternatively received salmon
C calcitonin (100 IU s.c.) and isotonic saline (1 cc s.c.) for

four weeks, with a four-week washout period between
treatments, none of the eleven outcomes measures showed
a significant improvement, an observation that suggests
that subcutaneous calcitonin injection is not effective in
the treatment of fibromyalgia (Bessette et al. 1998.).
cancer chemotherapy: In a study by Warner et al. (1997), of eight

women with no previous rheumatic history, four developed poly-
arthritis (one seropositive), three fibromyalgia, and one spondylosis
after the diagnosis and during or after treatment of breast cancer. Of
fifteen women with breast cancer who had previous rheumatic symp-
toms, twelve developed worse and/or new symptoms after chemo-
therapy. In both groups, the symptoms had a significant negative im-
pact on functional status, and in some cases resolution was only
partial even after many years of follow-up. Warner et al. (1997) sug-
gest that prospective studies are needed to determine the incidence,
risk factors, and optimal management of fibromyalgia or nondestruc-
tive polyarthropathy in women who receive systemic adjuvant therapy
for breast cancer. Some chemotherapeutic agents, such as tamoxifen,
may help relieve fibromyalgia symptoms (Simonson, 1996).
carpal tunnel syndrome: An association between fibromyalgia and

carpal tunnel syndrome has been reported (Cimmino et al., 1996;
Perez-Ruiz et al., 1997) and, in a study of 100 cases, Straub (1999)
identified fibromyalgia and myofascial pain syndrome as preopera-
tive factors associated with an increased likelihood of unsatisfactory
results from endoscopic carpal tunnel release.
chemical intolerance: Several studies indicate that low level chemi-

cal intolerance (CI) is a symptom of several different chronic and
sometimes overlapping conditions in which women are over-
represented, such as fibromyalgia, chronic fatigue syndrome, multi-
ple chemical sensitivity, sick building syndrome, and Persian Gulf

War syndrome (Bell, Baldwin, Russek, et al., 1998; Bell, Baldwin,
and Schwartz, 1998; Bell et al., 1999; Csef, 1998; Fiedler et al., 1996;
Gibson et al., 1998; Lohmann et al., 1996; “Multiple Chemical Sensi-
tivity: A 1999 Consensus,” 1999; Slotkoff et al., 1997; Weiss, 1998).
Severe CI is a characteristic of 20 to 47 percent of individuals with
apparent fibromyalgia and/or chronic fatigue syndrome, all patients
with multiple chemical sensitivity syndrome, and approximately 4 to
6 percent of the general population (Bell, Baldwin, Russek, et al.,
1998; Bell, Baldwin, and Schwartz, 1998; Bell et al., 1999; Slotkoff
et al., 1997). In the general population, 15 to 30 percent report at least
minor problems with CI.
Agents whose exposures are associated with symptoms and sus-
pected of causing onset of chemical intolerance with chronic illness
include gasoline, kerosene, natural gas, pesticides (especially chlor-
dane and chlorpyrifos), solvents, new carpet and other renovation
materials, adhesives/glues, fiberglass, carbonless copy paper, fabric
softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl
sulfate) and other cleaning agents, isocyanates, combustion products
(poorly vented gas heaters, overheated batteries), and medications
(dinitrochlorobenzene for warts, intranasally packed neosynephrine,
prolonged antibiotics, and general anesthesia with petrochemicals).
Disorders commonly seen in chemical intolerance patients are mainly
nonspecific and include headache (often migraine), chronic fatigue,
musculoskeletal aching, chronic respiratory inflammation (rhinitis,
sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (in
affected younger children). Less common disorders include tremor,
seizures, and mitral valve prolapse (Ziem and McTamney, 1997).
Although the levels of chemicals reported to trigger CI would nor-
mally be considered nontoxic or subtoxic, host factors may contrib-
ute to generating a disabling intensity to the resultant multisystem
dysfunctions in CI (Bell, Baldwin, Russek, et al., 1998; Bell, Baldwin,
and Schwartz, 1998; Bell et al., 1999; Rowat, 1999). Explanatory
mechanisms of chemical intolerance include psychiatric diagnoses
such as somatization (CI had strong positive correlations between
serum neopterin levels and all of the scales measuring somatization)
(Bell, Patarca, et al., 1998), behavioral mechanisms, such as condi-
tioning and generalization, neuropharmacological mechanisms, such
as kindling and time-dependent sensitization (including an olfactory-
limbic and/or mesolimbic neural sensitization model for intolerance
to low-level chemicals in the environment) (Bell, Baldwin, Russek,

et al., 1998; Bell, Baldwin, and Schwartz, 1998; Bell et al., 1999), im-
paired porphyrin metabolism (multiple organs), and psychoneuro-
immunological mechanisms, such as neurogenic inflammation (re-
spiratory, gastrointestinal, genitourinary) and those involving the
hypothalamic-pituitary-adrenal axis (Ziem and McTamney, 1997).
Laboratory animal experimentation and controlled clinical trials, es-
pecially with inhaled material, provide the means for exploring the
proffered explanations. In a study of cell-mediated sensitivity to en-
vironmental chemicals in thirty-nine fibromyalgia patients, Shanklin
et al. (2000) found significantly higher lymphocyte proliferation in-
dexes in response to aluminum, lead, and platinum and borderline
higher to cadmium and silicon. However, fibromyalgia patients
showed sporadic responses to the specific substances tested, with no
high-frequency result. Miller (1999) proposed that fibromyalgia and
other related conditions may be secondary to “toxicant-induced loss
of tolerance,” a two-step disease process in which (1) certain chemi-
cal exposures, e.g., indoor air contaminants, chemical spills, or pesti-
cide applications, cause certain susceptible persons to lose their prior
natural tolerance for common chemicals, foods, and drugs (initia-
tion); (2) subsequently, previously tolerated exposures trigger symp-
toms.
Chiari malformation: Muller et al. (1998) point out that distur-

bances of posture of the vertebral column are frequently found in fi-
bromyalgia as well as in low back pain patients. Also, reduction in the
mobility of the whole spine and localized movement impairments are
present in both conditions. It is likely that the disturbances are re-
sponsible for the first manifestations of fibromyalgia in a single lo-
calization, especially in lumbar and cervical regions. A particular de-
fect in the vertebral column at the cervical level which causes partial
compression of the spinal cord, the Chiari malformation, has been
proposed to play an etiologic role in fibromyalgia, but compelling ev-
idence remains elusive (Bradley and Alarcon, 1999). The latter con-
dition is diagnosed radiologically and treated surgically.
chiropractic treatment: In a preliminary study, Hains and Hains

(2000) found that nine of fifteen female fibromyalgia patients re-
sponded to a regimen of thirty chiropractic treatments that effectively
combine ischemic compression and spinal manipulation. Reductions
in pain intensity, sleep disturbance, and fatigue associated with fibro-

myalgia were apparent. A trend, determined as statistically insignifi-
cant, suggests that older subjects with severe and more chronic pain
and a greater number of tender points responded more poorly to treat-
ment. Other preliminary studies have suggested the efficacy of chiro-
practic management in the treatment of fibromyalgia (Blunt et al.,
1997; Harper and Liu, 1998; Schneider, 1998).
chlamydia: Although it has been proposed that infection with

chlamydia may be an etiologic factor for chronic fatigue syndrome
and fibromyalgia, this contention needs epidemiogical and serologic
substantiation because evidence of infection appears to be nonspecific
(Machtey, 1997).
Chlorella pyrenoidosa: The results of a pilot study of eighteen fibro-

myalgia patients suggest that adding daily for two months nutritional
supplements derived from the unicellular green alga, Chlorella pyre-
noidosa (10 g of “Sun Chlorella” tablets and 100 mL of liquid
“Wakasa Gold”), results in a statistically significant improvement in
average tender point index (Merchant et al., 2000). Seven patients felt
that the dietary supplement had improved their fibromyalgia symp-
toms, while six thought they had experienced no change, and five be-
lieved the symptoms had worsened over the time of the trial. A larger,
more comprehensive, double-blind, placebo-controlled clinical trial
is needed.
chronic fatigue syndrome: Despite remarkably different diagnostic

criteria, fibromyalgia and chronic fatigue syndrome have many de-
mographic and clinical similarities (Bazelmans et al., 1999; Buch-
wald, 1996; Buchwald, Umali, et al., 1996; Clauw and Chrousos,
1997; Demitrack, 1998; Hoffmann et al., 1996; Kenner, 1998; Lloyd,
1998; White et al., 2000; Ziem and Donnay, 1995). More specifically,
few differences exist in the domains of symptoms, examination find-
ings, laboratory tests, functional status, psychosocial features, and
psychiatric disorders. Among the differences between the two syn-
dromes, Evengard et al. (1998) found that although substance P lev-
els were normal in the cerebrospinal fluid of fifteen patients with
chronic fatigue syndrome, the majority of fibromyalgia patients stud-
ied had increased cerebrospinal fluid levels of substance P. Further
clarification of the similarities and differences between chronic fa-

tigue syndrome and fibromyalgia may be useful in studies of progno-
sis and may help define subsets of patients who might benefit from
specific therapeutic interventions.
Chronic fatigue syndrome (CFS) is a disease entity of so far un-
known etiopathogenesis, without specific markers, that presents with
a complex array of symptoms in patients with diverse health histories
(see all references cited under this heading in the Bibliography). Fa-
tigue is one of the most prominent features of CFS and one of the
most common medical complaints in general. Patients with un-
explained chronic pain and/or fatigue have been described for centu-
ries in the medical literature, although the terms used to describe
these symptom complexes have changed frequently. Neurasthenia
dominated medical thinking at the turn of the century; the term
“myalgic encephalomyelitis” was introduced in the United Kingdom
in 1957, and, in the mid-1980s, the term “chronic Epstein-Barr virus
syndrome” emerged and was then converted to chronic fatigue syn-
drome and, by some, to “chronic fatigue immune dysfunction syn-
drome.” The currently preferred term, albeit a misnomer, is chronic
fatigue syndrome, a name that describes the prominent clinical fea-
tures of the illness without any attempt to identify the cause but that
has the endorsement of the United States Centers for Disease Control
and Prevention (CDC) and several professional organizations. Re-
lated diseases include fibromyalgia, sick building syndrome, Gulf
War syndrome, and multiple chemical sensitivity syndrome. Opin-
ions on CFS range from nondisease via psychiatric disorder to so-
matic disturbance. Nevertheless, CFS has emerged as a public health
concern over the past decade in many countries, and some court rul-
ings have legitimized the diagnosis of CFS in certain societal set-
tings.
The diagnosis of CFS is based on clinical criteria, and it is largely
dependent upon ruling out other organic and psychologic causes of
fatigue. CFS is defined by primary and secondary criteria, which are,
however, largely subjective. CFS includes cases of long-standing (six
months or longer) fatigue that are not explained by an existing medi-
cal or psychiatric diagnosis and which cause considerable disabilities
in professional, social, and/or personal functioning (at least 50 per-
cent reduction in baseline level). Other CFS criteria include: fever,
painful adenopathy, muscle weakness, myalgia, headache, migratory
arthralgia, neuropsychologic symptoms, and sleep disorder. Although
several studies have validated these criteria, much controversy per-

sists and an attempt at formulating new criteria based on laboratory
parameters is being attempted. The working case definition of CFS in
1988 was an attempt to establish a uniform basis for the previously
heterogeneous approaches to research of this severe and inexplicable
state of fatigue. At the same time, researchers wished to narrow down
a pathogenetically founded disease entity a priori by specifying pre-
cise disease criteria. The case definition has also been used to estab-
lish prevalence estimates using physician-based surveillance and
random dial telephone surveys. Although the original 1988 definition
was revised in 1994, the empirical data gathered in accordance with
the CFS definition have failed to confirm the assumption that the dis-
ease entity is pathogenetically uniform.
The onset of CFS may be associated with preceding stressful
events and multiple other precipitants. A study that divided CFS pa-
tients into two groups based on whether onset was sudden or gradual
found that the rate of concurrent psychiatric disease was significantly
greater in the CFS-gradual group relative to the CFS-sudden group.
Although both CFS groups showed a significant reduction in infor-
mation processing ability relative to controls, impairment in memory
was more severe in the CFS-sudden group. Some authors also make a
distinction between an acute phase (up to one month after the first
consultation), a subacute phase (until six months after the onset of the
complaints and disabilities), and a chronic phase (from six months af-
ter the onset of the complaints and disabilities) of the disease. CFS
evolves toward chronicity in an important number of cases.
Somatic pathogenetic hypotheses for CFS include persisting in-
fections, intoxications, metabolic or immunologic disturbances, ner-
vous system diseases, endocrine pathology, and psychosomatic influ-
ences. An infectious illness is not uniformly present at the onset and
no single infectious agent has been found. Various components of the
central nervous system appear to be involved in CFS, including the
hypothalamic pituitary axes, pain-processing pathways, sleep-wake
cycle, and autonomic nervous system. Many studies have provided
evidence for abnormalities in immunological markers among individ-
uals diagnosed with CFS. Nonetheless, a clear picture has not been
achieved in any area of research because of the noticeable variability
in the nature and magnitude of the findings reported by different
groups. Moreover, little support has been garnered for an association
between the laboratory abnormalities and the diverse physical and
health status changes in the CFS population. For instance, some au-
thors think that although a subset of CFS patients with immune sys-
tem activation can be identified, serum markers of inflammation and
immune activation are of limited diagnostic usefulness in the evalua-
tion of patients with CFS and chronic fatigue because changes in
their values may reflect an intercurrent, transient, common condition,
such as an upper respiratory infection, or may be the result of an on-
going illness-associated process. On the other hand, other authors
have found that CFS patients can be categorized based on immuno-
logical findings or that when patients are classified according to
whether the disease started suddenly or gradually, immunological
changes are apparent. It is also worth noting that although the degree
of overlap between distributions of soluble immune mediators in
CFS and controls has fueled criticism on the validity or clinical sig-
nificance of immune abnormalities in CFS, the latter degree of over-
lap is not unique to CFS and is also present, for instance, in sepsis
syndrome and HIV-1-associated disease, clinical entities where stud-
ies of immune abnormalities are providing insight into pathophys-
iology. The latter statement also applies to nonimmunological pa-
rameters in CFS.
Based on the discrepancies described above, some authors argue
that the conceptual model of CFS needs to be changed from one de-
termined by a single cause/agent to one in which dysfunction is the
end stage of a multifactorial process. A study of author bias in litera-
ture citation in CFS reviews revealed that citation of literature is in-
fluenced by the authors’ disciplines and nationalities, a finding which
is compatible with the lack of consensus and integrated efforts among
professionals from different disciplines who are working on CFS.
Cogan I syndrome: Cogan I syndrome is a rare, inflammatory, sys-

temic disease that is typically characterized by severe audiovestibular
dysfunction and various inflammatory eye changes (uveitis, scleritis,
keratitis, and episcleritis). In a study of ten patients with Cogan I syn-
drome, Zierhut et al. (2000) reported other manifestations of this
syndrome, including pericarditis associated with arthritis and poly-
serositis in one patient and fibromyalgia in two patients.
cognitive-behavioral therapy: Cognitive-behavioral approaches ap-

pear to offer a viable alternative for the management of fibromyalgia
and arthritis pain (Bradley and Alberts, 1999; Callahan and Blalock,
1997; Keefe and Caldwell, 1997). In a pilot study of twenty fibromy-
algia patients, Singh et al. (1998) showed that a mind-body approach
(cognitive-behavioral therapy: eight weekly sessions, two and a half
hours each, with three components: an educational component focus-
ing on the mind-body connection, a portion focusing on relaxation re-
sponse mechanisms, primarily mindfulness meditation techniques,
and a qigong movement therapy session) resulted in a significant re-
duction in pain, fatigue, and sleeplessness; as well as improved func-
tion, mood state, and general health. A study by Nicassio et al. (1997)
also underscored the value of a ten-week psychoeducational inter-
vention in decreasing the psychological and behavioral effect of fi-
bromyalgia by reducing dysfunctional coping and helplessness. How-
ever, in randomized clinical trial comparisons of educational only
versus educational-cognitive interventions in 131 fibromyalgia pa-
tients, Goossens et al. (1996) and Vlaeyen et al. (1996) found that the
addition of a cognitive component to the educational intervention led
to significantly higher health care costs (Goossens et al., 2000;
Maetzel et al., 1998; Ruof et al., 1999) and no additional improve-
ment in quality of life compared to the educational intervention
alone. Some authors suggest the use of mind-body approaches in
combination with other interventions (see ALTERNATIVE AND COM-
PLEMENTARY MEDICINE).
cognitive function: A study by Grace et al. (1999) on cognitive func-

tion reported that thirty fibromyalgia patients studied performed more
poorly on tests of immediate and delayed recall and sustained audi-
tory concentration, and their ratings of both their memory abilities
and sleep quality were lower than those of the thirty controls. Fur-
thermore, perceived memory deficits of the fibromyalgia subjects
were disproportionately greater than their objective deficits. There
were also significant correlations between performance on memory
and concentration measures and scores on questionnaires of pain se-
verity and trait anxiety. Landro et al. (1997) also reported that, com-
pared to eighteen healthy controls, both twenty-five fibromyalgia
patients and twenty-two patients with major depression were signifi-
cantly impaired on long-term memory tasks requiring effortful pro-
cessing. However, when the depressive status of the fibromyalgia pa-
tients was accounted for, only the subsample with a lifetime major
depressive disorder showed memory impairment as compared with

the healthy controls.
collagen: In a study of thirty-nine fibromyalgia patients, Sprott et al.

(1998) found evidence for abnormal collagen metabolism by analyz-
ing urine and serum samples to determine levels of pyridinoline
(Pyd) and deoxypyridinoline (Dpyd), which represent products of
lysyl oxidase-mediated cross-linking in collagen and are indicators
of connective tissue and bone degradation, respectively, and of hy-
droxypyroline (Hyp), a collagen turnover marker. Based on the find-
ings of significantly decreased urine and serum Pyd/Dpyd ratios and
urine Hyp levels in fibromyalgia patients as compared to healthy con-
trols, Sprott et al. (1998) concluded that decreased levels of collagen
cross-linking may both contribute to remodeling of the extracellular
matrix and collagen deposition around the nerve fibers in fibromyal-
gia, and underlie the lower pain threshold at the tender points (Malle-
son, 1998; Sprott and Muller, 1998). The latter results are consistent
with the electron microscopic findings of highly ordered cuffs of col-
lagen around the terminal nerve fibers in biopsy tissue from all eight
fibromyalgia patients but none of the control skin samples examined
by Sprott et al. (1997) in a previous study (see also EHLERS-DANLOS
SYNDROME).
coping: Savelkoul et al. (2000) reported that coping by awaiting/

avoidance in fibromyalgia patients led to less social support and that
this decrease in social support negatively influenced subjective well-
being. Akkasilpa et al. (2000) found that systemic lupus erythe-
matosus patients with fibromyalgic tender points are less likely to be
good “copers,” i.e., they display less hardiness. Patient readiness to
adopt new beliefs and coping responses to pain may predict response
to multidisciplinary or cognitive-behavioral pain treatments that em-
phasize changes in beliefs and coping behaviors (Jensen et al., 2000).
Hellstrom et al. (1999) found that the meaning structures revealed in
the patients’ ways of describing their experiences of living with fibro-
myalgia seemed to be partially constituted by their efforts to stand
forth as afflicted with a disease, which could be a way to help them to
manage the demands that they place upon themselves.
Based on their finding of a relationship between coping strategies
and functional disability in fibromyalgia, Martin et al. (1996) suggest
that investigators should attempt to identify coping attempts strate-

gies that best reduce patients’ psychological distress in the laboratory
and then teach patients to use these strategies to reduce distress in
their home and work environments. In this regard, Kelley and Clif-
ford (1997) suggest that narrative ethnographic approaches help
fibromyalgia patients find both their own strengths and means of
coping and their own identities other than as patients. Higher levels
of self-efficacy are associated with better outcome (tender point in-
dex, disease severity, and pain) and may mediate the effectiveness of
rehabilitation-based treatment programs for fibromyalgia in adults
and children (Buckelew et al., 1996; Schanberg et al., 1996). In a
study of twenty-nine patients, Schanberg et al. (1998) found that
family environment and parental pain history may be related to how
children cope with fibromyalgia. Behavioral interventions targeting
the family may improve the long-term functional status of children
with fibromyalgia.
copper: A double-blind, with two parallel groups, versus placebo

study of forty-eight fibromyalgia patients showed that the use of a
pure copper wire bedsheet reduces painful symptomatology at the
tender point level and improves sleep quality, with a positive effect on
the patients’ cenesthesia at awakening (Biasi et al., 1999).
cortisol: Hypocortisolism has been reported not only in patients with

fibromyalgia but also in those with chronic fatigue syndrome, rheu-
matoid arthritis, asthma, and post-traumatic stress disorder (Heim
et al., 2000). The nature of the underlying mechanisms and the hom-
ology of these mechanisms within and across clinical groups remain
speculative. Potential mechanisms include dysregulations on several
levels of the hypothalamic-pituitary-adrenal axis, genetic vulnerabil-
ity, previous stress experience, and coping and personality styles (see
also NEUROENDOCRINOLOGY).
cryotherapy: A study by Metzger et al. (2000) of 120 patients, 40.7

percent of whom suffered from primary fibromyalgia, 3.6 percent
from secondary fibromyalgia, and the rest from rheumatoid arthritis
(17.3 percent), chronic low back pain (16.4 percent), ankylosing
spondylitis (10.9 percent), osteoarthritis (9.1 percent), and other auto-
immune diseases (1.8 percent) (mean duration of symptoms: four

years), concluded that whole-body cold therapy (average 2.5-minute
applications, –105°C) generates important short-term effects (de-
creased pain level for about ninety minutes) and somewhat weaker
effects over a four-week treatment period as a whole. Short-term pain
reduction facilitates intensive application of physiotherapy and occu-
pational therapy.
debrisoquine/sparteine polymorphism: The scientific

literature suggests an association between impaired detox-
D ification and certain diseases, including cancer, Parkin-

son’s disease, fibromyalgia, and chronic fatigue and im-
mune dysfunction syndrome (Liska, 1998). Based on a
study of thirty-five fibromyalgia patients, Skeith et al.
(1997) found that adverse drug reactions in fibromyalgia
patients do not correlate with the poor metabolizer phenotype of the
P450IID6 oxidative enzyme. Skeith et al. (1997) also concluded that
it is unlikely that altered xenobiotic detoxification attributable to the
P450IID6 poor metabolizer phenotype would have a significant role
in the development of fibromyalgia.
dehydroepiandrosterone sulphate: Dessein et al. (1999) docu-

mented hyposecretion of adrenal androgens (dehydroepiandrosterone
sulphate, free testosterone) in fifty-seven female fibromyalgia patients.
Low serum androgen levels correlated with poor health status, and the
decrease in serum androgen levels was more pronounced in obese pa-
tients. Longitudinal studies are needed to elucidate whether these are
cause and/or effect relationships (see also NEUROENDOCRINOLOGY).
dentistry: Although mercury exposure from dental amalgam fillings

has been proposed as a cause of fibromyalgia and chronic fatigue
syndrome, several studies have failed to substantiate this hypothesis
(Kotter et al., 1995; Langworth and Stromberg, 1996; Malt et al.,
1997). Patients suffering from fibromyalgia can also demonstrate the
same clinical features as temporomandibular disorders or myofascial
pain. Avon (1996) admonishes that dentists should be aware that cer-
tain dental treatments will not be effective in patients suffering from
temporal and masseter pain if fibromyalgia has been diagnosed.
depression: Wacker (2000) reported comorbidity of depressive dis-

orders and fibromyalgia, and Okifuji et al. (2000) found that although
concurrent depressive disorders are prevalent in fibromyalgia (56 per-
cent in a sample of sixty-nine patients) and may be independent of the
cardinal features of fibromyalgia, namely, pain severity and hyper-
sensitivity to pressure pain, depressive disorders are related to the
cognitive appraisals of the effects of symptoms on daily life and func-
tional activities. Morriss et al. (1999) arrived at a similar conclusion
in chronic fatigue syndrome patients in a study where they found that
depression is not associated with the reporting of pain, psycho-
physiological syndromes, and medically unexplained symptoms.
Offenbaecher et al. (1998) reported that of the 27 percent of 304
fibromyalgia patients with depression, 23 percent had a familial his-
tory of depression, 46 percent a familial history of fibromyalgia, and
46 percent had been diagnosed with depression in the past. In terms
of comorbidity with other psychiatric diagnoses, Kurtze et al. (1998,
1999) found significant effects of anxiety and depression on quality
of life, functional disability, and lifestyle among 322 fibromyalgia
patients. Anxiety and depression interacted to yield relatively high
consumption of coffee and cigarettes among the anxious and de-
pressed subgroup. Meyer-Lindenberg and Gallhofer (1998) recom-
mend that clinical indicators, such as a family history of depressive
disorders, circadian disturbances, pronounced loss of appetite or li-
bido, and chronic psychosocial stressors should be assessed and, if
present, prompt the initiation of psychiatric evaluation and treatment,
including pharmaco- and psychotherapeutic modalities in fibromyal-
gia patients.
disability and functional impairment: Arthritis and other rheu-
matic conditions (e.g., osteoarthritis, rheumatoid arthritis, gout, fibro-
myalgia, and other diseases of the joints) are leading causes of dis-
ability and are among the most prevalent chronic conditions in the
United States, affecting approximately 40 million persons in 1995
and a projected 60 million persons in 2020.
Personal and occupational disability is a serious concern in fibro-
myalgia (Beger, 1997; Bennett, 1996; Bombardier and Buchwald,
1996; Cohen and Quintner, 1998; Duro, 1997; “Fibromyalgia Syn-
drome: Feeling More Pain,” 1999; Jason et al., 2000; Kaplan et al.,
2000; Krapac et al., 1997; Littlejohn, 1998; Pellegrino and Waylonis,
1997; Rocca, 1999; Smith, 1997; Turk et al., 1996; White et al., 1995,
1999; Wolfe, 1996; Wolfe et al., 1997a,b). Gordon (1999) stresses

that, despite the presence of disability risk factors, most patients with
fibromyalgia maintain a good range of normal daily activities and
continue working. Based on a survey of 176 fibromyalgia female pa-
tients (50 percent employed, 15 percent full-time, 23 percent not
working because of fibromyalgia), Henriksson and Liedberg (2000)
recommended early intervention in the work situation by incorporat-
ing individual adjustments that allow patients to find a level match-
ing their ability and to continue to work (Henriksson and Burckhardt,
1996). Crook et al. (1998) also recommend that the employer’s pro-
vision of a “modified job” is important in the prevention of continued
disability for workers with musculoskeletal problems.
Several instruments and methods, including the Functional Impact
Questionnaire, the Multidimensional Health Questionnaire, the Mod-
ified Stanford Health Assessment Questionnaire, the Arthritis Impact
Measurement Scales, the Arthritis Self-Efficacy Scales, the Quality
of Life Scale, the Medical Outcomes Study Short-Form General
Health Survey (SF-36), the Western Ontario MacMaster (WOMAC),
the six-minute walk, the Evaluation of Daily Activity Questionnaire
(EDAQ), and Multidimensional Pain Inventory, to assess disability
and functional limitation in fibromyalgia patients have been tested
and are available for different ethnic and linguistic groups (Bakker
et al., 1995; Bellamy et al., 1999; Blackmore et al., 1995; Buchwald
et al., 1996; Burckhardt and Bjelle, 1996; Buskila and Neumann,
1996; Escalante et al., 1996; Friedman, 1997; Goldenberg et al.,
1995; Goossens et al., 1999; Huston, 2000; Kaplan et al., 2000; King
et al., 1999; Lousberg et al., 1999; Mannerkorpi and Ekdahl, 1997;
Mannerkorpi et al., 1999; Neumann et al., 1999; Neumann, Berzak,
et al., 2000; Neumann, Press, et al., 2000; Nordenskiold, 1997;
Offenbaecher et al., 2000; Ortiz et al., 1999; Pincus et al., 1999;
Wigers, 1996; Wolfe, 1999; Wolfe and Hawtley, 1999; Wolfe and
Kong, 1999; Wolfe, 2000; Wolfe et al., 2000).
Despite the availability of the previously mentioned assessment
instruments, several authors stress that fibromyalgia is unduly cited
as a cause of disability and that it is hard to assess disability in this
condition (Keitel, 1999; Kovarsky, 1997; Malterud, 1999; Wolfe and
Potter, 1996; Worz, 1999). For instance, Wolfe et al. (1997a,b) found
that although most fibromyalgia patients (64 percent of 1,604 sur-
veyed) reported being able to work, there were high rates of self-
reported work disability awards. Huber (2000) considers fibromyal-

gia a psychosomatic disease and points out that a significant propor-
tion of early retirees (at least 30 percent), because of occupational
disability, are psychosomatically ill and that an additional large num-
ber of retirees suffer from untreatable pain and may have a chronic
somatoform pain disorder. Wolfe and Hawley (1999) found that fibro-
myalgia patients report more medical conditions and report that these
conditions are more important to them than do patients with rheuma-
toid arthritis or osteoarthritis. Van Linthoudt et al. (2000) pointed out
that 8 percent of 413 cases seeking insurance compensation in Swit-
zerland were ascribed to fibromyalgia, and admonish that practitio-
ners can contribute to chronicity of rheumatological complaints by
perpetuating work interruption for nonmedical reasons. Fibromyal-
gia also became a major reason for disability pension in Norway. In
1989, more than 7 percent of the new cases had this diagnosis. The
parliament (Stortinget) passed controversial amendments to the Na-
tional Insurance Acts in 1991 and 1995 which restricted the criteria
for obtaining a disability pension (Gjesdal and Kristiansen, 1997).
Other authors warn that patients should be made aware that chronic
rheumatological complaints do not necessarily result in insurance
compensations. A case reported by Mailis et al. (2000) on a family of
six all diagnosed with fibromyalgia and who brought the case to court
after ten years of significant medical expenses exemplified that com-
pensations are usually used up by legal fees. Moreover, lawyer Karen
Capen (1995) and researcher Wolfe (2000) say physicians who pro-
vide expert opinion in court should be aware that there are specific re-
quirements regarding their qualifications. In an Alberta, Canada,
court case, a judge discounted evidence provided by a rheumatologist
who ran a clinic that treated fibromyalgia patients because of his
“personal and perhaps financial interest in perpetuating the existence
of this condition” (Capen, 1995, p. 207). The judge ruled that “this
particular disorder is often found in individuals who will not or can-
not cope with everyday stresses of life and convert this inability into
acceptable physical symptoms to avoid dealing with reality.”
In contrast to the reports mentioned in the previous paragraph,
Helfenstein and Feldman (2000) describe their experience with
103 patients referred to a health reference center for workers for the
management of repetitive strain injury and work-related arm pain.
They found that the patients’ illness is far more global than the work-
related arm pain that such labeling implies. From the total group, sev-
enty-three fulfilled the American College of Rheumatology criteria
for the classification of fibromyalgia syndrome. This means that they
were suffering pain above and below the diaphragm, far from the arm
pain for which they were referred. These seventy-three patients were
clinically and psychologically indistinguishable from 165 patients
followed in Helfenstein and Feldman’s clinic at the Federal Univer-
sity of Sao Paulo, Rheumatology Division, who also fulfilled these
criteria but did not consider their illness to be work related. Some
governmental institutions have taken action, and, for instance, the
Department of Veterans Affairs of the United States has adopted a
rule to add a diagnostic code and evaluation criteria for fibromyalgia
to their Schedule for Rating Disabilities (Department of Veterans Af-
fairs, 1999). The intended effect of this rule is to insure that veterans
diagnosed with this condition meet uniform criteria and receive con-
sistent evaluations.
A study by Soderberg et al. (1999) highlights the importance of
treating people suffering with illness with respect for their human
dignity. The findings of the latter study show that being a woman with
fibromyalgia means living a life greatly influenced by the illness in
various ways: loss of freedom, threat to integrity, and a struggle to
achieve relief and understanding. Soderberg et al. (1999) recommend
that the care of women with fibromyalgia must empower the women
to bring to bear their own resources so that they can manage to live
with the illness. Martin et al. (1996) also recommends assessing and
improving the patients’ coping strategies.
Wolfe et al. (1997a,b) reported that half of 538 fibromyalgia pa-
tients studied were dissatisfied with their health, and 59 percent rated
their health as fair or poor. In terms of the relevance of fibromyalgia
symptomatology, Long et al. (2000) found that although patient satis-
faction with health appears to be relatively independent of traditional
clinical measures of physical functioning, pain, and disease status
among patients with psoriatic arthritis, it was associated with func-
tional class and number of fibromyalgia tender points.
dizziness: A study by Rusy et al. (1999) suggests that central (brain-

stem) and peripheral vestibular (inner ear) mechanisms do not ac-
count for the complaints of dizziness in the pediatric patient with
fibromyalgia. The common musculoskeletal abnormalities of fibro-
myalgia may affect their proprioceptive orientation, therefore giving

them a sense of imbalance.
effort: Norregaard et al. (1997) found a low degree of ef-

fort but near normal physical capacity in a study of 181 fe-
E male fibromyalgia patients. Fibromyalgia patients exhib-

ited a significant reduction in voluntary muscle strength of
the knee and elbow, and flexors and extensors in the order
of 20 to 30 percent. However, the coefficient of variation
was higher among patients, thus indicating lower effort. Moreover,
unlike work status, degree of effort or physical capacity did not corre-
late to psychometric scores.
Ehlers-Danlos syndrome: Fibromalgia may be concurrent with

Ehlers-Danlos syndrome (Miller et al., 1997), a disease characterized
by a genetic defect in collagen synthesis (see COLLAGEN).
eosinophilia-myalgia syndrome: The eosinophilia-myalgia syn-

drome (EMS), caused by intake of contaminated L-tryptophan, re-
sembles fibromyalgia in its clinical presentation (Barth et al., 1999;
Hudson et al., 1996). In one study, the similar incidence (81 percent)
of myalgia and arthralgia and the presence of antibodies directed
against serotonin, gangliosides, and phospholipids in both chronic
EMS and fibromyalgia patients, as well as the predominant produc-
tion of type 2 cytokines in vitro after stimulation with different L-
tryptophan preparations of peripheral blood mononuclear cells from
fibromyalgia patients, led Barth et al. (1999) to postulate that EMS
may have developed in patients suffering primarily from fibromyal-
gia as an allergic reaction toward a more immunogenic L-tryptophan
preparation. Nonetheless, Taylor et al. (1996) point out that four vari-
ables, namely extremity edema, leukocyte count greater than 12.5 ×
109/L, dyspnea, and absence of arthralgias, differentiate EMS from
other common myalgia syndromes (sensitivity of 95.6 percent, a
specificity of 96.9 percent, and positive and negative predictive val-
ues of 93.5 and 97.9 percent, respectively).
epidemiology: In 1995, an estimated 15 percent (40 million) of

Americans had some form of musculoskeletal pain disorder, includ-
ing fibromyalgia, and, by the year 2020, an estimated 18.2 percent

(59.4 million) will be affected (Lawrence et al., 1998). Pain syn-
dromes can be divided anatomically into those that cause generalized
pain, such as fibromyalgia syndrome and myofascial pain syndromes,
and those that are confined to one regional anatomical area. The latter
group comprise those of the neck, shoulder, elbow, wrist/hand, hip,
knee, and ankle/foot (Linaker et al., 1999). Fibromyalgia can also be
secondary to other rheumatologic disorders (Karaaslan et al., 1999).
It is estimated that fibromyalgia affects up to 6 million patients
worldwide (Gordon and Morrison, 1998; Smith, 1998). The preva-
lence of fibromyalgia in the United States general population was
found to be 2 percent, and increases with age (Goldenberg, 1996).
Extrapolation of a survey of 4,027 general practitioners by Bazel-
mans et al. (1997) indicates that in 1997 there were at least 24,000
primary fibromyalgia patients in the Netherlands. A population sur-
vey of 2,498 females living in South Norway yielded a calculated an-
nual incidence of fibromyalgia of 583 per 100,000 (Forseth, 1997;
Forseth et al., 1997). Major problems associated with interpreting and
comparing epidemiologic studies on pain syndromes in adults and
children include the diversity of classification criteria and selection
bias (Gare, 1996). The prevalence of fibromyalgia in a study of 548
schoolchildren by Clark et al. (1998) was 1.2 percent, a figure that is
fivefold lower than previously reported. This variance may be due
to: (1) racial and sociocultural differences between populations; and
(2) differences in methodological approach. However, Sardini et al.
(1996) found the same incidence of fibromyalgia of 1.2 percent in
students of the schools of Castiglione delle Stiviere (Mantova, Italy).
Case definitions and overlap between different syndromes affect
the results of the different epidemiological studies. For example, of
32 individuals with chronic fatigue syndrome identified in a random
sample of 18,675 Chicago residents, 40.6 percent met criteria for
multiple chemical sensitivity and 15.6 percent met criteria for fibro-
myalgia (Jason et al., 2000). Referral practices and primary care phy-
sicians’ perceptions of fibromyalgia (Bellamy et al., 1998) also affect
epidemiological estimates. For instance, Gran and Nordvag (2000)
found that the annual incidence of referrals of new patients to a
rheumatology clinic was 423 per 100,000. The main cause of referral
was diagnosis, and more than half of the diagnoses suggested were
changed at the visit. Few of the referred patients had severe disease.
In a study of 100 confirmed fibromyalgia cases, 76 widespread pain

controls, and 135 general controls in a random community survey of
3,395 noninstitutionalized adults living in London, Ontario, White,
Harth, et al., (1999), and White et al., (1999a-c) found that adults who
meet the American College of Rheumatology definition of fibromy-
algia appear to have four distinct features compared to those with
chronic widespread pain who do not meet criteria, namely pain sever-
ity, severe fatigue lasting twenty-four hours after minimal activity,
weakness, and self-reported swelling of neck glands. In a different re-
port from the same study, White et al. (1999c) reported that being fe-
male, middle-aged, of less education, lower household income, being
divorced, and being disabled are associated with increased odds of
having fibromyalgia. White et al. (1999b) also determined that fibro-
myalgia has a major effect on direct health care costs. The latter is
particularly relevant because fibromyalgia is prevalent among lower
income people. In a study of 1,997 Pakistani adults distributed evenly
between poor rural and poor urban communities and relatively afflu-
ent urban people, Farooqi and Gibson (1998) found that there was
significantly more soft tissue rheumatism and back pain in the rural
population compared with those in the city. Fibromyalgia was almost
completely absent from the urban affluent, but osteoarthritis of the
knee was significantly more common in this community, perhaps due
to relative obesity. In contrast with the latter results, no chronic wide-
spread pain was identified in a survey of Pima Indians, a finding that
suggests that this population has different pain perception or different
patterns of risk factors for these disorders (Jacobsson et al., 1996).
Epstein-Barr virus: Rheumatologic complications of infections with

herpes viruses, such as the Epstein-Barr virus, need to be included in
the differential for the diagnosis of fibromyalgia (McCarty and Csuka,
1998).
Erb gene: Lowe et al. (1997) have proposed the hypothesis that in
euthyroid fibromyalgia a mutant c-erbA beta 1 gene (or alternately,
the c-erbA alpha 1 gene) results in low-affinity thyroid hormone re-
ceptors that prevent normal thyroid hormone regulation of transcrip-
tion. As in hypothyroidism, this would cause a shift toward alpha-
adrenergic dominance and increases in both cyclic adenosine 3'-5'-
phosphate phosphodiesterase and inhibitory G proteins. The result
would be tissue-specific hypothyroid-like symptoms despite normal

circulating thyroid hormone levels.
ergonomics: Working daily for a long time with a standard micro-
scope causes back pain, soft tissue rheumatism or fibromyalgia, or
tension headache in up to 80 percent of microscopists. These com-
plaints may be prevented by an ergonomic design of the microscope
workstation, leading to a beneficial and significant reduction of
electromyographical activity in the most strained muscle groups, as
shown by surface electromyographic recordings (Kreczy et al., 1999;
Van Houdenhove and Neerinckx, 1999).
erythrocyte sedimentation rate: In a study of 711 patients referred
to rheumatology clinics, Suarez-Almazor et al. (1998) found that pri-
mary care physicians frequently requested erythrocyte sedimentation
rate (ESR) (29 percent) in patients with fatigue and diffuse musculo-
skeletal pain. The majority of test results were negative, which
caused low predictive values for positive ESR tests (35 percent for
connective tissue disease, 17 percent for rheumatoid arthritis, and
3 percent for systemic lupus erythematosus). Suarez-Almazor et al.
(1998) admonished that a decrease in inappropriate ESR test ordering
could be achieved by emphasizing that fatigue and diffuse musculo-
skeletal pain are not indicative of connective tissue disease in the ab-
sence of other features such as joint swelling, typical rash, or organ
involvement.
exercise: Exercise programs alone or in combination with other in-
terventions have proven useful in the treatment of fibromyalgia
(Buckelew et al., 1998; Deuster, 1996; Dominick et al., 1999; Wigers
et al., 1996). The type, duration, and intensity of the exercise program
deserves special consideration. Training has shown little benefit as
regards pain but has improved the physical fitness of the patients.
Since pain may be exacerbated by physical activity, many patients
become physically inactive, with possible development of reduced
physical fitness. In the long run, fibromyalgia patients who exercise
report fewer symptoms than sedentary patients do. Thus, exercise
should be aimed at preventing physical inactivity and improving the
patients’ physical fitness (Mengshoel, 1996).
A study of fifty-eight fibromyalgia patients by Mannerkorpi et al.
(2000) concluded that six months of exercises in a temperate pool
combined with a six-session education program improve physical

function, grip strength, pain severity, social functioning, psychologi-
cal distress, and quality of life. Gowans et al. (1999) found similar ef-
ficacy for a six-week exercise and educational program tested on
forty-one subjects. Meiworm et al. (2000) reported a positive effect
for twelve weeks of aerobic endurance exercise (jogging, walking,
cycling, or swimming) on pain parameters, cardiovascular status, fit-
ness, and well-being of twenty-seven fibromyalgia patients com-
pared to sedentary patient controls. Ramsay et al. (2000) found that
although there was no improvement in pain in a study of seventy-four
fibromyalgia patients following either a supervised twelve-week aer-
obic exercise class or unsupervised home aerobic exercises, there
was some significant benefit in psychological well-being in the exer-
cise class group and perhaps a slowing of functional deterioration.
Based on a limited study, Meyer and Lemley (2000) suggest that in-
dividuals with fibromyalgia can adhere to low-intensity walking pro-
grams two to three times per week, possibly reducing fibromyalgia
impact on daily activities. Self-help programs that include stretching
exercises are also beneficial (Han, 1998).
A study of thirty-eight fibromyalgia patients by Martin et al.
(1996) showed that an exercise program that included aerobic, flexi-
bility, and strengthening elements had no adverse effects and was ef-
fective in the short term. Normal muscle metabolism during exercise
and no muscle damage after physical activity have been reported in
fibromyalgia patients (Mengshoel et al., 1995; Mengshoel, 1996).
However, no rise in blood noradrenaline concentration during exer-
cise was found in fibromyalgia patients.
fatigue: A study of 1,488 patients by Wolfe et al. (1996)

documented that fatigue is common across all rheumatic
F diseases, is associated with all measures of distress, and is

a predictor of work dysfunction and overall health status.
The correlates of fatigue (pain, sleep disturbances, and dis-
ability) are generally similar across fibromyalgia, rheuma-
toid arthritis, and osteoarthritis. However, in a review of 425 medical
charts, Ward et al. (1996) found that the workup for chronic fatigue is
often incomplete or lacks documentation. This oversight is likely due
to the problem that focus is not being directed at the chronic fatigue
complaints. Also complicating the evaluation process are the multiple
associated disorders, the prevalence of the complaint, and cost/benefit

issues facing the primary care physician (Groopman, 1998; Llewelyn,
1996; Ream and Richardson, 1996; Shapiro, 1998; Tiesinga et al.,
1996; White, 1997). Fatigue is a complex, multicausal, multidimen-
sional, nonspecific, and subjective phenomenon for which no single
definition is widely accepted. The condition of fatigue requires ade-
quate assessment, innovative planning and interventions, and patient-
centered evaluations by health care professionals. Fatigue, whether
acute or chronic, needs to be recognized as a true and valid condition
for treatment to be successful. Chronic fatigue and acute fatigue can
be quite different conditions, requiring different approaches. Miller
et al. (1996) reported that neither poor motivation, reflex pain inhibi-
tion, nor muscle contractile failure are important in the pathogenesis
of fatigue in fibromyalgia patients. However, the subjective response
to exercise is commonly excessive.
fibromyalgia: Fibromyalgia is a form of nonarticular, or soft tissue,

rheumatism characterized by spontaneous widespread musculo-
skeletal aching, tenderness on palpation with multiple tender points
(at least eleven out of eighteen in defined locations) (hyperalgesia),
decreased pain threshold (allodynia), fatigue, poor sleep, mood dis-
turbances, and other systemic symptoms (Ang and Wilke, 1999;
Bennett, 1998; Briggs, 1997; Celiker et al., 1997; Clauw, 1995;
Coward, 1999; “Fibromyalgia,” 2000; “Fibromyalgia Syndrome,”
1997; Fordyce, 2000; Gerster, 1999; Gordon and Morrison, 1998;
Hadler, 1996a,b; Healey, 1996; Krsnich-Shriwise, 1997; Leslie, 1999;
Lilleaas, 1997; Littlejohn, 1996; MacFarlane et al., 1996; Mailis,
1996; Nishikai, 1999; Parziale and Chen, 1996; Pasero, 1998; Pro-
ceedings of the International Fibromyalgia Conference, 1998; Rankin,
1999; Raspe and Croft, 1995; Reiffenberger and Amundson, 1996;
Reveille, 1997; Reynolds, 1996; Romano, 1996; Siegmeth, 1999;
Simms, 1996; Slavkin, 1997; Tabeeva et al., 2000; Unger, 1996; Van
Santen-Hoeufft, 1996; Wallace, 1999; Wallace et al., 1999; Winfield,
1997; Wootton, 2000; Xie and Ye, 1997). The concept and diagnosis
of fibromyalgia became popular, especially in North America, in the
1970s. It is noticeable that there does not appear to be an early case
report, as there is, for instance, for gout, rheumatoid arthritis, or cer-
tain vasculitides. Operational definitions and classification criteria
were given in 1990, with the endorsement of the American College of

Rheumatology and are now the most widely used.
Although nearly all rheumatologists now accept fibromyalgia as a
distinct diagnostic entity, and it is also recognized by the World
Health Organization, the validity of fibromyalgia as a distinct clinical
entity has been challenged for several reasons: the subjective nature
of chronic pain; the subjectivity of the tender point examination; the
failure to agree on the importance and biological nature of tenderness
itself; the lack of a gold standard laboratory test; the absence of a
clear pathogenic mechanism; the use of a syndromic description
without a unifying concept; the relative nature of the pain-distress re-
lationship in the rheumatology clinic; the apparently continuous rela-
tionship between tender points and somatic distress across a variety
of clinical disorders; the failure to distinguish a clinical feature from
a disease process; legal defenses of insurance carriers motivated by
economic concerns; psychiatric dogma; uninformed posturing; sus-
picion of malingering; ignorance of nociceptive physiology; and, oc-
casionally, honest misunderstanding (Buskila et al., 1997; Cathebras
et al., 1998; Cathebras, 2000; Cohen, 1999; Finestone, 1997; Fitz-
charles, 1999; Gamaz-Nava et al., 1998; Goldenberg, 1999; Gordon,
1997; Hadler, 1996a,b, 1997a,b; Hamilton, 1998; Handler, 1998;
Hantzschel and Boche, 1999; Helliwell, 1995; Hellstrom, 1995;
Hilden, 1996; Holoweiko, 1996; Hudson, 1998; Hunt et al., 1998;
Hyams, 1998; Jones, 1996; Kaden and Bubenzer, 1999; Katz et al.,
1997; Kissel and Mahnig, 1998; Laser, 1998; Leonhardt, 2000;
Lindberg and Lindberg, 2000; Makela, 1999; Marlowe, 1998; Mat-
sumoto, 1999; Neeck, 1998; Neerinckx et al., 2000; Peloso, 1998;
Quintner and Cohen, 1997, 1999; Raspe, 1996; Rau and Russell,
2000; Rekola et al., 1997; Romano, 1998; Russell, 1999; Safran,
1998; Shojania, 2000; Smith MD, 1998; Smith WA, 1998; Solomon
and Liang, 1997; Thorson, 1998; Wessely and Hotopf, 1999; White
and Harth, 1998; Wigley, 1999; Wilke, 1996a,b; Wolfe, 1997; Wolfe
et al., 1997). In the United States, fibromyalgia is the third or fourth
most common reason for rheumatology referral (Celiker et al., 1997;
Gamez-Nava et al., 1998; Wallace, 1997) and several Web sites are
dedicated to this condition (Armstrong, 2000; Jahn and Klenke,
1999). Fibromyalgia is predominant in middle-aged women but has
also been reported in men, elderly individuals, and in the pediatric
population (Borenstein, 1996; Buskila, 1999; Cathebras et al., 1998;
Holland and Gonzalez, 1998).
According to the American College of Rheumatology, the diagno-

sis of fibromyalgia is based on criteria consisting entirely of clinical
signs and symptoms (Alarcon, 1997; Barth, 1997; Bassetti, 1996;
Brown, 1997; Garfin, 1995; Hart, 1998; Jacobsen, 2000; Kavanaugh,
1996; Kjaergaard, 1998; Maier, 1998; Pongratz and Sievers, 2000;
Reinhold-Keller, 1997; “Unraveling a Mysterious Cause of Pain,”
1998; Weber, 1998; Xie and Ye, 1997; Zborovskii and Babaeva,
1998). The American College of Rheumatology criteria, established
in 1990, provide the primary care provider with definitive subjective
and objective findings that have shown to be 88 percent accurate in
their ability to diagnose patients with the syndrome (Smith MD,
1998; Smith WA, 1998). In the majority of fibromyalgia patients gen-
eralized pain is preceded by localized or regional pain, usually in the
musculoskeletal system. In many fibromyalgia patients there are
findings compatible with tissue injury pain, with pain mechanisms
involving both the primary afferent neuron and the nociceptive sys-
tem in the central nervous system (Henriksson, 1999; Olin and
Lidbeck, 1996). The distinction between fibromyalgia (tender points)
and myofascial pain syndrome (trigger points) is essential (Klineberg
et al., 1998; Uppgaard, 2000) (see TENDER POINT PATHOPHYSIOL-
OGY; see also TRIGGER POINTS). Also, macrophagic myofasciitis, a
recently identified inflammatory myopathy that can be detected by
deltoid muscle biopsy and is manifested mainly in the lower limbs,
can be differentiated from fibromyalgia and sarcoidosis by gallium-
67 scintigraphy (Cherin et al., 2000). Fitzcharles and Esdaile (1997)
reported that eleven women with spondyloarthritis had been incor-
rectly diagnosed as having fibromyalgia. Internal and neurological
disorders as a primary cause of fibromyalgia have to be excluded
(Olin and Lidbeck, 1996).
The etiology and pathogenesis of fibromyalgia still remain uncer-
tain, and some reports suggest a genetic component (Bennett, 1998;
Gelfand, 1998; Kelly, 1997; Kenner, 1998; Monroe, 1998; Shelkov-
nikov and Krivoruchko, 1997). Fibromyalgia symptoms last, on aver-
age, at least fifteen years after illness onset (de Jesus, 2000; Kennedy
and Felson, 1996). However, most patients experience some im-
provement in symptoms before that time (Kennedy and Felson,
1996). Patients with fibromyalgia report greater difficulty in per-
forming activities of daily living as well as increased pain, fatigue,
and weakness compared with healthy controls (Bennett, 1998; Celiker
et al., 1997; Hadler, 1996a,b; Kennedy and Felson, 1996;

MacFarlane et al., 1996; Slavkin, 1997). Associated disorders are
restless leg syndrome, irritable bowel syndrome, irritable bladder
syndrome, interstitial cystitis, headaches, ocular and vestibular com-
plaints, cognitive dysfunction, cold intolerance, multiple sensitivi-
ties, and dizziness (Asencio-Marchante and Terriza-Garcia, 1998;
Bennett, 1998; Maurizio and Rogers, 1997; Siegmeth, 1999). Some
muscle abnormalities have been reported (Park et al., 1998); the
myopathological patterns in fibromyalgia are nonspecific: type II fi-
ber atrophy, an increase of lipid droplets, a slight proliferation of mi-
tochondria, and a slightly elevated incidence of ragged red fibers
(Pongratz and Sievers, 2000). However, most studies agree on an ab-
sence of inflammatory or structural musculoskeletal abnormalities
(Matsumoto, 1999), and, therefore, the original term “fibrositis” was
replaced with fibromyalgia (Simms, 1998).
There is clinical, and in many cases demographic, overlap between
fibromyalgia, chronic fatigue syndrome, Persian Gulf War syndrome,
silicone implant-associated syndrome, sick building syndrome, mul-
tiple chemical sensitivity, and syndromes including neurally medi-
ated hypotension, abnormalities of the growth hormone-insulin-like
growth factor-1 axis, chemical intolerance, altered functioning of
the stress-response system, and the presence of autoantibodies
(Baschetti, 1999; Bazelmans et al., 1997; Bennett, 1998; Buchwald,
1996; Buskila, 1999, 2000; Chambers, 1997; Csef, 1999; Gold-
enberg, 1997; Granzow, 1999; Hoffmann et al., 1996; Kelly, 1997;
Kenner, 1998; Klimas, 1998; Pocinki, 1997; Robertson, 1999; Sabal,
1997; Slavkin, 1997; Vree, 1997; Wallace, 1997; Wessely and Hotopf,
1999). However, there are differences among the latter syndromes
(Matsumoto, 1999). Fibromyalgia may also be affected by psycho-
social, cultural, psychological, and environmental factors (Affleck et
al., 1998; Ben-Zion et al., 1996; Cathebras, 1997; Hadler, 1996a,b;
Hausotter, 1998; Kissel and Mahnig, 1998; Kuhn, 2000; Kurtze et al.,
1998; Reid et al., 1997; Schaefer, 1997; Schuck et al., 1997; Turk
et al., 1996). On the other hand, fibromyalgia may complicate other
syndromes (Kelemen and Muller, 1998; Potter, 1997), as is the case
in some patients with hyperlaxity syndromes, such as benign joint
hypermobility syndrome (Grahame, 2000).
Fibromyalgia patients journey along a continuum from experienc-
ing symptoms, through seeking a diagnosis, to coping with the ill-
ness. Experiencing symptoms usually entails pain, a precipitating

event, associated symptoms, and modulating factors. Seeking a diag-
nosis is associated with frustration and social isolation. Confirmation
of diagnosis brings relief but anxiety about the future. After diagno-
sis, several steps lead to creation of adaptive coping strategies (Manne-
korpi et al., 1999; Raymond and Brown, 2000; Thorson, 1999).
Treatment of patients with fibromyalgia and CFS continues to be of
limited success, although the role of multidisciplinary group interven-
tion appears promising (Bennett, 1998; Celiker et al., 1997;
Goldenberg, 1996, 1997; Hadler, 1996a,b; MacFarlane et al., 1996;
Slavkin, 1997) and several strategies have proven useful (Keitel,
1997; Maidannik, 1996; Moldofsky et al., 1996; Reiffenberger and
Amundson, 1996; Scharf et al., 1998; Stoll, 2000; Wilke, 1996a,b).
The conventional medical model fails to address the complex experi-
ence of fibromyalgia, and adopting a patient-centered approach is im-
portant for helping patients cope with this disease (Cunningham,
1996; Fitzcharles, 1999; Hellstrom et al., 1998; Leslie, 1999; Ray-
mond and Brown, 2000; Romano, 1999; Smith MD, 1998; Smith
WA, 1998).
fitness: Although regular physical activity is associated with impor-

tant physical and mental health benefits, an estimated 53 million U.S.
adults are inactive during their leisure time—the period most amena-
ble to efforts to increase physical activity. The presence of chronic
conditions, especially those associated with disabilities, may reduce
levels of leisure time physical activity, and a government report docu-
mented a decreased leisure-time physical activity prevalence among
persons with arthritis and other rheumatic conditions, such as fibro-
myalgia (“Prevalence of Leisure-Time Physical Activity,” 1997).
Nielens et al. (2000) found that cardiorespiratory fitness, as ex-
pressed by a submaximal work capacity index, seems normal, despite
increased perceived exertion scores, in thirty female fibromyalgia pa-
tients compared with sixty-seven age- and sex-matched healthy in-
dividuals. However, Natvig et al. (1998) reported that fibromyalgia
patients had higher physical leisure activity levels, but lower physical
fitness than the control women in a population survey. The difference
in physical leisure activity persisted even after controlling for a series
of possible confounders, including employment status and workload.
Fitness should therefore be objectively assessed before recommend-
ing interventions involving physical activity in fibromyalgia pa-

tients.
functional somatic syndromes: Barsky and Borus (1999), among

other authors (Ford, 1997; Masi, 1998; Robbins et al., 1997; Walker
et al., 1997), have applied the term functional somatic syndromes to
several related syndromes characterized more by symptoms, suffer-
ing, and disability than by consistently demonstrable tissue abnor-
mality. These syndromes include multiple chemical sensitivity, sick
building syndrome, repetition stress injury, the side effects of silicone
breast implants, Gulf War syndrome, chronic whiplash, chronic fa-
tigue syndrome, irritable bowel syndrome, and fibromyalgia. Barsky
and Borus (1999) purport that although discrete pathophysiologic
causes may ultimately be found in some patients with functional so-
matic syndromes, the suffering of these patients is exacerbated by a
self-perpetuating, self-validating cycle in which common, endemic,
somatic symptoms are incorrectly attributed to serious abnormality,
reinforcing the patient’s belief that he or she has a serious disease.
Ford (1997) considers these syndromes a “fashionable” way to hide
the diagnosis of hysteria.
G Gamma-hydroxybutyrate: A preliminary study found

that gamma-hydroxybutyrate administered in divided doses
at night in eleven fibromyalgia patients resulted in signifi-
cant improvement in both fatigue and pain, with an increase in slow-
wave sleep and a decrease in the severity of the alpha anomaly (Rus-
sell, 1999; Scharf et al., 1998).
gender: The heterogeneous group of diseases that causes chronic

arthralgia and arthritis is the most common cause of activity limita-
tion and disability among middle aged and older women (Holtedahl,
1999; Stormorken and Brosstad, 1999). For reasons that remain
poorly understood, this group of diseases affects women substan-
tially more frequently than men (Belilos and Carsons, 1998; Forseth
et al., 1999; Meisler, 1999). In particular, the prevalence rates of the
most common causes of arthralgia and arthritis, osteoarthritis and
rheumatoid arthritis, and the prevalence rates of less common dis-
eases that cause arthralgia, including systemic lupus erythematosus,
systemic sclerosis, and fibromyalgia, are between two and ten times
higher in women (Buckwalter and Lappin, 2000; Burckhardt and
Bjelle, 1996). Forseth et al. (1997) estimated an annual incidence of
fibromyalgia in women of 583 per 100,000. Because many women
with these conditions seek medical care from orthopaedists, ortho-
paedic residency education and continuing medical education should
place emphasis on early diagnosis and nonoperative treatment of pa-
tients with arthralgia and arthritis and, when appropriate, early refer-
ral to rheumatologists (Schaefer, 1997).
A study by Buskila et al. (2000), comparing forty men and forty
women with fibromyalgia, concluded that although fibromyalgia is
uncommon in men, its health outcome is worse than in women (more
severe symptoms, decreased physical function, and lower quality of
life in men despite similar mean tender point counts). In contrast to
the latter study, Yunus et al. (2000), in a comparative study of sixty-
seven men and 469 women with fibromyalgia, found that male
fibromyalgia patients had fewer symptoms and fewer tender points,
and less common “hurt all over” complaints, fatigue, morning fa-
tigue, and irritable bowel syndrome, compared with female patients.
Further studies of gender comparisons are needed.
genetics: A familial inheritance of fibromyalgia is suggested by the

report by Buskila and Neumann (1997), who found that relatives of
fibromyalgia patients have a higher prevalence (26 percent: 14 per-
cent in male relatives and 41 percent in female relatives) of fibromy-
algia and suffer more nonarticular point tenderness than the general
population. Moreover, Buskila et al. (1996) also reported a high prev-
alence (28 percent) of fibromyalgia among offspring of fibromyalgic
mothers. Because psychological and familial factors were not differ-
ent in children with and without fibromyalgia, the high familial oc-
currence of this syndrome may be attributable to genetic factors. In
terms of possible genes involved, the serotonin transporter promoter
gene seems to be associated with neurotic anxiety and fibromyalgia
(Ackenheil, 1998) (see also SEROTONIN RECEPTOR GENE). Several
studies by Yunus (1998) and Yunus et al. (1999) have suggested the
existence of a possible gene for fibromyalgia that is linked with the
human leukocyte antigen (HLA) region (Buskila, 2000). In contrast
to the latter findings in fibromyalgia, myofascial temporomandibular
disorder does not run in families (Buskila, 2000). Klein and Berg
(1995) also found a higher frequency of an autoantibody pattern,

characteristically found among fibromyalgia patients and consisting
of antiganglioside, antiphospholipid, and antiserotonin antibodies,
among relatives of fibromyalgia patients.
glucocorticoid: Ernberg et al. (1997) reported that patients with

fibromyalgia and those with localized myalgia of the masseter mus-
cle show a similar positive response (decreased pain to palpation) to
local glucocorticoid treatment, an observation that points to a possi-
ble common pathophysiology in both disorders.
growth hormone: The various components of the growth hormone

(GH)-insulin-like growth factor (IGF-I) axis and their binding pro-
teins have many peripheral effects, mainly on bone, growth, activation
of main cellular functions, energy metabolism, and protein anabolism.
They contribute to adapting an individual to circumstances of life and
illness (Schlienger and Goichot, 1998). It has been suggested that
growth hormone deficiency may be a pathogenic factor in fibromyal-
gia, and decreased serum levels of IGF-I, a surrogate marker for low
growth hormone secretion, are common in fibromyalgia patients
(Bennett, 1998; Berwaerts et al., 1998; Leal-Cerro et al., 1999).
Growth hormone deficiency is characterized by diminished energy,
dysphoria, impaired cognition, poor general health, reduced exercise
capacity, muscle weakness, and cold intolerance. However, Dinser et
al. (2000) found that in only one of fifty-six subjects tested did growth
hormone levels remain below 3 ng/mL after hypoglycemia and addi-
tional arginine stimulation, an observation that satisfies the criteria
for adult growth hormone deficiency. Dinser et al. (2000) and Bennett
(1998) also observed an impaired reactivity of the somatotropic axis
in one-third of fibromyalgia patients, in keeping with other studies
that have found a functional alteration of the hypothalamus. For in-
stance, Leal-Cerro et al. (1999) found that fibromyalgia patients ex-
hibit a marked decrease in spontaneous growth hormone secretion,
but normal pituitary responsiveness to exogenously administered
growth hormone releasing hormone. Defective growth hormone se-
cretion in fibromyalgia patients appears to be due to increased somat-
ostatin tone in the hypothalamus, which in turn may be secondary to
upregulation of beta-adrenergic receptors in the hypothalamus (Ben-
nett, 1998; Bennett et al., 1998). Although some preliminary studies
have shown that treatment of growth hormone-deficient fibromyal-

gia patients with recombinant growth hormone (daily for nine
months) improves several clinical features, including the tender point
count, large double-blind, placebo-controlled clinical trials are needed
(Bagge et al., 1998; Bennett, 1998; Bennett et al., 1998; Schlienger
and Goichot, 1998).
gynecology: A strong association between musculoskeletal disor-

ders and gynecological disease was found by Wadsworth et al. (1995)
and Ostensen and Schei (1997). In the latter study, differences be-
tween healthy women and women reporting pelvic joint syndrome,
fibromyalgia, whiplash, or arthritis were significant in terms of bleed-
ing disorders, chronic pelvic pain, and inflammatory pelvic disease.
ter Borg et al. (1999) have also reported a high frequency of hysterec-
tomies among fibromyalgia patients.
H hair electrolytes: Some patients with fibromyalgia were

observed to have high hair calcium and magnesium levels
compared with healthy subjects; in these patients supple-
menting calcium with magnesium reduces the number of
tender points detected by digital palpation (Ng, 1999).
headache: According to a model presented based on the data from

Bendtsen (2000), the main problem in chronic tension-type head-
aches, myofascial pain syndromes, and fibromyalgia is central sensi-
tization at the level of the spinal dorsal horn/trigeminal nucleus due to
prolonged nociceptive inputs from pericranial myofascial tissues.
The increased nociceptive input to supraspinal structures may in turn
result in supraspinal sensitization. The central neuroplastic changes
may affect the regulation of peripheral mechanisms and thereby lead
to, for example, increased pericranial muscle activity or release of
neurotransmitters in the myofascial tissues. By such mechanisms, the
central sensitization may be maintained even after the initial eliciting
factors have been normalized, resulting in the conversion of episodic
into chronic tension-type headaches, or of episodic pain into the
chronic pain of fibromyalgia (Bendtsen, 2000). Okifuji et al. (1999)
reported that extensive dysregulation in pain modulation is important
for a substantial minority of recurrent headache patients (twenty-
eight out of seventy studied), who seem to be quite similar to fibro-

myalgia patients (presence of widespread tender point pain suggest-
ing generalized hyperalgesia). Defects in serotonergic analgesia and
hyperalgesic states are proposed as features common to headache and
fibromyalgia (Nicolodi and Sicuteri, 1996; Nicolodi et al., 1998).
The benefit to both migraine and fibromyalgia from inhibiting iono-
tropic N-methyl-D-aspartate receptor activity implies that redundant
hyperalgesia-related neuroplastic changes are crucial for severe or
chronic migraine and primary fibromyalgia. In fact, there is a high
prevalence of migraine in the population of fibromyalgia sufferers,
and migraine may represent a risk factor for fibromyalgia (Nicolodi
and Sicuteri, 1996; Nicolodi et al., 1998).
Because of the similarities mentioned, chronic tension-type head-
ache, premenstrual headache, and migraines are in the differential
of the fibromyalgia diagnosis. Fox and Davis (1998) documented
chronobiological features that may assist in the differential diagnosis
of migraine: Migraine attacks start more frequently between 4 a.m.
and 9 a.m. and within the first few days after onset of menses; this mi-
graine periodicity is strongest among women not using oral contra-
ceptives. Seasonal periodicity, if any, is clearly weaker than circadian
or menstrual. Paiva et al. (1995) documented that polysomnography
was useful in the diagnosis of patients presenting with morning and
nocturnal headaches: thirteen out of fifteen patients had their diagno-
sis changed from one of the headache entities (cluster, chronic parox-
ysmal hemicrania, migraine, tension, combined headache, and chronic
substance abuse headache) to periodic movements of sleep, fibromy-
algia syndrome, and obstructive sleep apnea. In terms of differential
response to treatment, Stone and Wharton (1997) reported that the
application of a unique physical therapy device combining trans-
cutaneous electrical nerve stimulation, traction, massage, vibration,
and acupressure applied to the forehead, posterior cervical spine, and
scapula yielded improvement for neck pain and headache patients,
but fibromyalgia trigger points were unaffected. In contrast to pa-
tients with chronic tension-type headaches, Schepelmann et al. (1998)
found no changes of the second suppressive period of the extero-
ceptive suppression of the temporalis muscle activity in fibromyalgia
patients.
hearing: Although central nervous system dysfunction frequently

occurs in fibromyalgia patients, proprioceptive disturbances might
also explain some of the abnormalities observed. Rosenhall et al.
(1996) reported that 72 percent of 168 fibromyalgia patients studied
suffered from vertigo/dizziness, 15 percent were afflicted with sensor-
ineural hearing loss, 30 percent had evidence of brainstem dysfunc-
tion, 28 percent had abnormal saccades and 58 percent had pathologi-
cal smooth pursuit eye movements in oculomotor studies, and 45
percent had a pathological electronystagmography. On the other
hand, Heller et al. (1998) reported that twenty-eight of eighty patients
with sudden deafness and progressive hearing losses (approximately
half of whom had phospholipid antibodies that can cause venous
or arterial vasculopathies, or serotonin and ganglioside antibodies)
displayed symptoms typical for fibromyalgia and chronic fatigue dis-
orders, including fatigue, myalgia, arthralgia, depressions, sicca
symptoms, and diarrhea. Klein and Berg (1995) described a higher
frequency of the latter autoantibody pattern among relatives of fibro-
myalgia patients. Heller et al. (1998) recommend questioning pa-
tients suffering from inner ear disorders for symptoms typical for
fibromyalgia or chronic fatigue, since these diseases are often closely
related to inner ear disorders. If symptoms are present, antibodies
should be tested against phospholipids, serotonin, and gangliosides.
Dohrenbusch et al. (1997) found reduced unpleasantness thresh-
olds for all audiometric frequencies and an asymptomatic hearing
loss for higher frequencies among thirty fibromyalgia patients com-
pared to thirty-six matched controls. The hearing loss correlated sig-
nificantly with experience of noise at the place of work, which was
also elevated in the fibromyalgia group. Generalized pain had a high
impact on the interaction between threshold of unpleasantness and
daily noise experience. Dohrenbusch et al. (1997) interpreted the dif-
ferences in thresholds of hearing and of unpleasantness in patients
with fibromyalgia as a form of either preconscious or conscious acts
to protect against disturbing stimulation. The latter results support
the notion of a generalized disturbance of perceptual thresholds in
patients with fibromyalgia not restricted to the perception of pain
(Kroner-Herwig, 1997).
hepatitis C: Hepatitis C virus (HCV) is both a hepatotropic and a

lymphotropic virus; because of this latter biological peculiarity, HCV
may trigger a constellation of autoimmune-lymphoproliferative dis-

orders. Rheumatologic complications of HCV infection are common
and include mixed cryoglobulinemia, vasculitis, sicca symptoms,
myalgia, arthritis, carpal tunnel syndrome, tenosynovitis, and fibro-
myalgia (Barkhuizen and Bennett, 1997; Buskila, 2000; Ferri and
Zignego, 2000; Jendro et al., 1997; Killenberg, 2000; Lovy et al.,
1996; Rivera et al., 1997). However, rheumatic complications are not
associated with liver disease severity, subjects’ gender, presence of
autoantibodies (cryoglobulins, rheumatoid factor, antinuclear anti-
bodies, antismooth muscle antibodies, antiphospholipid antibodies,
and antithyroid antibodies) or response to treatment with interferon-
alpha (Buskila et al., 1998; Buskila, 2000; Jendro et al., 1997; Rivera
et al., 1997). The identification of HCV infection in rheumatic pa-
tients is important to minimize the risk of aggravating hepatitis by
prescription of hepatotoxic drugs and because of the availability of
alpha-interferon as a potential virus eradicating agent. Also, recog-
nizing fibromyalgia in patients with HCV will prevent misinterpreta-
tion of fibromyalgia symptoms as part of the liver disease and will
enable the physician to reassure the patient about these symptoms
and to alleviate them (Buskila et al., 1997).
histocompatibility linkage: A few studies have reported familial ag-

gregation of fibromyalgia (see GENETICS), and Yunus (1998) and
Yunus et al. (1999) have documented a weak association between fi-
bromyalgia and the human leukocyte antigen (HLA) gene region.
homeopathy: Patients with rheumatic syndromes often seek alterna-

tive therapies, with homeopathy being one of the most frequent
(Jonas et al., 2000). Although homeopathy is one of the most fre-
quently used complementary therapies worldwide, clinical trials in-
volving its effects on fibromyalgia are warranted.
homocysteine: Regland et al. (1997) found increased homocysteine

levels in the central nervous system in twelve patients fulfilling the
criteria for both fibromyalgia and chronic fatigue syndrome. Cerebro-
spinal homocysteine levels correlated with fatiguability and vitamin
B12 levels. Vitamin B12 deficiency causes a deficient remethylation
of homocysteine and is, therefore, probably contributing to the in-
creased homocysteine levels found in this patient group.
hyaluronic acid: Barkhuizen and Bennett (1999) and Yaron et al.

(1997) reported that serum levels of hyaluronic acid, a breakdown
product of collagen, in fibromyalgic women were significantly ele-
vated compared to healthy controls and rheumatoid arthritis patients
(see COLLAGEN).
hydrocortisone: Low-dose hydrocortisone injections have been

tested for the treatment of chronic fatigue syndrome and fibro-
myalgia, but more evidence for this therapeutic modality needs to be
garnered, and it may only partially benefit a subset of patients
(Teitelbaum et al., 1999).
hyperkalemic periodic paralysis: Gotze et al. (1998) reported that a

forty-three-year-old woman with hyperkalemic periodic paralysis
was erroneously diagnosed as having fibromyalgia based on the cri-
teria of the American College of Rheumatology. Her son and three
close relatives also had histories of muscle pain and fatigue increas-
ing with age.
hyperparathyroidism: The symptoms of hyperparathyroidism are

vague and often similar to symptoms of depression, irritable bowel
syndrome, fibromyalgia, or stress reaction (Allerheiligen et al.,
1998). Hyperparathyroidism is a common cause of hypercalcemia.
The hypercalcemia usually is discovered during a routine serum
chemistry profile. Often, there has been no previous suspicion of this
disorder. In most patients initially believed to be asymptomatic, pre-
viously unrecognized symptoms resolve with surgical correction of
the disorder.
hypervigilance: It has been postulated that the enhanced pain sensi-

tivity in fibromyalgia results from a higher pain magnitude in re-
sponse to nociceptive stimuli (hyperalgesia) or from a general per-
ceptual amplification of sensations (hypervigilance). A study of
twenty fibromyalgia patients by McDermid et al. (1996) supported
the hypervigilance model of pain perception in fibromyalgia by doc-
umenting that fibromyalgia patients have a heightened sensitivity to
pain (e.g., low threshold and tolerance) because of increased atten-
tion to external stimulation and a preoccupation with pain sensations.
However, no evidence for hypervigilance for innocuous electro-

cutaneous signals was found in a study of thirty fibromyalgia pa-
tients; they did not show superior detection of electrical stimuli either
under single or dual task conditions when compared to thirty con-
trols. Also, no differences were found between patients and controls
on the body vigilance questionnaire (Peters et al., 2000). Lorenz
(1998) also challenged the hypervigilance model by failing to find
differences in auditory perception among fibromyalgia patients.
hypnosis: Hypnosis is a powerful tool in pain therapy, and fibro-

myalgia patients experience less pain during hypnotically induced
analgesia than during resting wakefulness (Wik et al., 1999). Wik
et al. (1999) showed that hypnotic analgesia is associated with a bilat-
erally increased cerebral blood flow in the orbitofrontal and subcal-
losial cingulate cortices, the right thalamus, and the left inferior pari-
etal cortex, and bilaterally decreased flow in the cingulate cortex.
I Immunology: Unlike chronic fatigue syndrome patients,

fibromyalgia patients do not show clear evidence of immu-
nological derangements. For instance, in a study of four-
teen fibromyalgia patients, Bonaccorso et al. (1998) found
no evidence of activation of cell-mediated immunity, and Samborski
et al. (1996) found no differences in lymphocyte immunophenotypes
(percentage of CD3, CD19, CD4, CD8, CD3/HLA-DR, and
CD4/CD45RA) in fibromyalgia patients as compared to healthy con-
trols (see also NATURAL KILLER CELLS). Despite the apparent lack of
chronic immunological changes in fibromyalgia, several studies have
used immunological markers as correlates for fibromyalgia symp-
tomatology or for variables that affect it. In this respect, pain and
stiffness in fibromyalgia may be accompanied by a suppression of
some aspects of the inflammatory response system (higher sgp130
and lower soluble CD8 serum levels), and the presence of clinically
significant depressive symptoms in fibromyalgia is associated with
some signs of inflammatory response system activation (higher solu-
ble IL-6 receptor and IL-1 receptor antagonist serum levels) (Maes et
al., 1999). Smart et al. (1997) found that fibromyalgia patients who
test positive for antinuclear antibodies represent a subgroup of fibro-
myalgia patients with a more pronounced inflammatory response
profile than those patients who test negative for antinuclear antibod-
ies. Samborski et al. (1996) found evidence for allergies in 50 percent
of fibromyalgia patients and evidence of CD8 cell suppression of im-
munoglobulin E production in these patients. Cole et al. (1999)
showed that among individuals with functional bowel disease and fi-
bromyalgia, those who were socially inhibited exhibited, under high
but not low engagement conditions, significantly increased
induration in response to intradermal tetanus toxoid, an observation
that indicates heightened delayed-type hypersensitivity response
with social inhibition.
inflammatory bowel disease: Rheumatological complications of in-

flammatory bowel disease (Crohn’s disease and ulcerative colitis) in-
clude peripheral arthritis and spondylitis, and soft tissue rheumatism,
specifically fibromyalgia. In a study by Buskila et al. (1999), fibro-
myalgia was documented in 30 of 113 patients with inflammatory
bowel disease (30 percent), specifically in 49 percent of patients with
Crohn’s disease and 19 percent with ulcerative colitis; in controls, the
rate was 0 percent. Subjects with Crohn’s disease exhibited more ten-
derness and reported more frequent and more severe fibromyalgia as-
sociated symptoms than subjects with ulcerative colitis. Recognizing
fibromyalgia in patients with inflammatory bowel disease will pre-
vent misdiagnosis and ensure correct treatment.
inflammatory spinal pain: Patients are said to have inflammatory

spinal pain if they fulfill at presentation four of the following five cri-
teria: duration of spinal discomfort for at least three months, spinal
morning stiffness, age less than forty, insidious onset of symptoms,
and no relief from pain with rest, but improvement with exercise. In-
flammatory spinal pain is typical of the spondylarthropathies. Only
in a minority of the cases is it found in other rheumatic disorders,
such as rheumatoid arthritis, fibromyalgia, infectious spondylitis, or
tuberculous spondylitis (Cantini et al., 1998).
insulin-like growth factor-1: Some of the clinical features of fibro-

myalgia resemble the ones described in the adult growth hormone-
deficiency syndrome (Leal-Cerro et al., 1999), and serum levels of
insulin-like growth factor-1 (IGF-1), also known as somatomedin C,
have been found to be decreased in fibromyalgia patients (Bennett
et al., 1997), suggesting that disruption of the growth hormone-IGF-1

axis might explain the link between muscle pain and poor sleep. Leal-
Cerro et al. (1999) found that fibromyalgia patients exhibit a marked
decrease in spontaneous growth hormone secretion but normal pitu-
itary responsiveness to exogenously administered growth hormone-
releasing hormone (GHRH), an observation that suggests the exis-
tence of an alteration at the hypothalamic level in the neuroendocrine
control of growth hormone and IGF in these patients. Leal-Cerro
et al. (1999) also found that growth hormone treatment over four days
led to increased IGF-1 and IGF-binding protein-3 (IGFBP3) levels.
Despite the clinical similarities between fibromyalgia and chronic
fatigue syndrome (CFS), Bennet et al. (1997) found that serum IGF-1
levels are elevated in the latter syndrome, an observation that sug-
gests that fibromyalgia and CFS may be associated with different ab-
normalities of sleep and/or of the somatotropic neuroendocrine axis.
However, Buchwald et al. (1996) found no differences in serum IGF-1
and IGFBP3 levels among patients with fibromyalgia, CFS, CFS and
fibromyalgia, and controls. Jacobsen et al. (1995) and Romano (1996)
failed to find major secretory deficiencies of growth hormone and
IGF-1 in fibromyalgia. Several factors could contribute to the differ-
ences in findings among the studies. For instance, Dessein et al.
(1999) reported that IGF-1 serum levels were lower in obese patients
as compared to nonobese patients.
In terms of the origin of the relationship between low IGF-1 levels
and pain and sleep problems in fibromyalgia, Older et al. (1998)
found that three nights of delta-wave sleep interruption caused no
significant lowering of pain thresholds or serum IGF-1 in healthy vol-
unteers, which caused them to conclude that the low levels of IGF-1
seen in fibromyalgia patients may result from chronic rather than
acute delta-wave sleep interruption or may be dependent on factors
other than disturbances of delta-wave sleep. In support of the latter
possibility, Jacobsen et al. (1995) reported that although fibromyal-
gia patients had more sleep problems than controls, no major differ-
ences in IGF-1 levels were apparent.
interferon-alpha: In two reports, Russell, Michalek, et al. (1999)
and Russell, Vipraio, et al. (1999) documented that daily sublingual
interferon-alpha at different doses (15, 50, or 150 IU) was not associ-
ated with significant improvement or adverse events in fibromyalgia
patients. Interferon-alpha is used for the treatment of viral hepatitis

C-associated disease.
interstitial cystitis: Interstitial cystitis is a relatively uncommon dis-

order characterized by pain in the bladder and pelvic region, typically
accompanied by urinary urgency and frequency (Clauw et al., 1997).
Although genitourinary and musculoskeletal symptoms predominate
in interstitial cystitis and fibromyalgia, respectively, both disorders
share a number of features, including similar symptomatology (dif-
fusely increased peripheral nociception and increased pain sensitiv-
ity), demographics, natural history, aggravating factors, overlapping
conditions (allergies, irritable bowel syndrome), and efficacious ther-
apy (Clauw et al., 1997). In comparison to the general population, in-
dividuals with interstitial cystitis are 100 times more likely to have in-
flammatory bowel disease and 30 times more likely to have systemic
lupus erythematosus (Alagiri et al., 1997).
intramuscular stimulation: In retrospective analyses of two and six

patients, Chu (2000a,b) showed that automated twitch-obtaining in-
tramuscular stimulation (ATOIMS) and electrical twitch-obtaining
intramuscular stimulation (ETOIMS) methods are promising in the
control of radiculopathy-related myofascial pain and fibromyalgia.
Reduction of mechanical tension through muscle relaxation is the
proposed basis for the pain relief.
irritable bowel syndrome: Irritable bowel syndrome and fibromyal-

gia are considered chronic syndromes of altered visceral and somatic
perception, respectively (Chang, 1998; Chang et al., 2000; Chun et
al., 1999; Mayer et al., 1998; Sivri et al., 1996). As many as 70 per-
cent of patients with fibromyalgia complain of the symptoms of irri-
table bowel syndrome, and approximately 35 percent of patients with
irritable bowel syndrome also have fibromyalgia (Barton et al., 1999;
Chang, 1998). The diagnostic criteria of fibromyalgia syndrome in-
clude irritable bowel syndrome, and, hence, a common etiopatho-
physiology has been suggested (Azpiroz et al., 2000; Sperber, Atzmon,
et al., 1999; Sperber, Carmel, et al., 1999). Similar to fibromyalgia, a
large proportion of irritable bowel syndrome patients also complain
of other functional disorders, such as headache, noncardiac chest
pain, low back pain, sicca complex, and dysuria (Chang, 1998;
Mayer et al., 1998). Sperber, Atzmon, et al. (1999), Sperber, Carmel,

et al., (1999), Sperber et al. (2000), and Chang et al. (2000) found that
patients with both irritable bowel syndrome and fibromyalgia have
increased severity of symptoms. However, both hypervigilance and
somatic hypoalgesia contribute to the altered somatic perception in
irritable bowel syndrome patients, while comorbidity with fibromy-
algia results in somatic hyperalgesia in irritable bowel syndrome pa-
tients (Chang, 1998; Chang et al., 2000). Another distinctive feature
was pointed out by the study of Chun et al. (1999), which found that
although patients with fibromyalgia and sphincter of Oddi dysfunc-
tion, type III, share many demographic and psychosocial characteris-
tics with patients with irritable bowel syndrome (Chun et al., 1999),
the latter have significantly lower rectal pain thresholds and in-
creased levels of psychologic distress compared to con-
trols.
J joint hypermobility: The estimated prevalence of gener-
alized hypermobility in the adult population is 5 to 15 per-
cent, and hypermobile individuals may be predisposed to soft tissue
trauma and subsequent musculoskeletal pain and rheumatism (Hud-
son et al., 1995, 1998). Some patients who have clinical symptoms of
fibromyalgia but do not exactly meet the American College of
Rheumatology criteria could in fact have joint hypermobility, and
these patients may be misdiagnosed as having fibromyalgia. Wide-
spread pain is associated with joint hypermobility in women under
age fifty, and fibromyalgia and joint hypermobility may coexist
(Acasuso-Diaz and Collantes-Estevez, 1998; Fitzcharles, 2000;
Klemp, 1997). Karaaslan et al. (2000) reported that the frequency of
joint hypermobility was 8 percent in patients with fibromyalgia and 6
percent in subjects without fibromyalgia. Acasuso-Diaz et al. (1998)
and Hudson et al. (1995) reported that 27 to 30 percent of fibromyal-
gia patients suffered joint hyperlaxity. In a review of the medical
charts of 2,500 female patients seen in a rheumatology practice, Lai
et al. (2000) documented that joint hypermobility was independently
associated with both fibromyalgia and with breast implantation, but
fibromyalgia and breast implantation were not found to be independ-
ently associated with each other.
juvenile fibromyalgia: The frequency of chronic pain syndromes in

pediatric rheumatology has increased over the past twenty-five years.
Diagnosis is complex: underlying organic illness, somatization, and
growing pains are all possibilities (Cassidy, 1998). Fibromyalgia has
also been recognized in children and adolescents as juvenile fibro-
myalgia (JF) (Buskila, 1996; Clark et al., 1998; Kulig, 1991; Sherry,
1997; Tayag-Kier et al., 2000). Juvenile rheumatoid arthritis (JRA)
and juvenile fibromyalgia can coexist (Schikler, 2000). For the pa-
tient with an initial diagnosis of either JRA or JF whose clinical
response to therapy is not in keeping with expectations or physical
examination findings or whose clinical course worsens without ex-
planation, reevaluation to determine if JF in the JRA patient has de-
veloped or JRA in the JF patient has emerged is warranted.
The clinical spectrum of fibromyalgia in children (diffuse aching,
headaches, sleep disturbances, and, less commonly, stiffness, subjec-
tive joint swelling, fatigue, abdominal pain, joint hypermobility, diz-
ziness, and depression) is similar to that of adults but with better out-
comes (Gedalia et al., 2000; Mikkelsson, Salminen, et al., 1997;
Mikkelsson, Sourander, et al., 1997; Mikkelsson, 1999; Rusy et al.,
1999; Sieb et al., 1997; Siegel et al., 1998). Tayag-Kier et al. (2000)
also demonstrated, in sixteen children and adolescents with JF, ab-
normalities in sleep architecture, including periodic limb movement
in sleep, similar to those seen in adult fibromyalgia patients. How-
ever, Breau et al. (1999) consider that fibromyalgia and chronic fa-
tigue syndrome may be related in children and may not be duplicates
of the adult disorders; that psychological and psychosocial factors are
unlikely contributors to the etiology of these disorders; and that the
evidence is increasingly pointing to a role for genetic factors in their
etiology. Roizenblatt et al. (1997) reported a significant concordance
of fibromyalgia diagnosis and significant correlations between poly-
somnographic indexes, sleep anomalies, and pain manifestations in
children and their mothers.
Gedalia et al. (2000) reported that active exercise programs seem
to correlate with better outcomes in JF. Kujala et al. (1999) point out
that, in addition to its likely long-term health benefits, vigorous phys-
ical activity causes musculoskeletal pains during adolescence, which
should be considered as a confounder in epidemiological studies on
fibromyalgia and related issues. In terms of other factors that affect
JF symptomatology, Schanberg et al. (1998) found that family envi-
ronment and parental pain history may be related to how children

cope with JF. Behavioral interventions targeting the family may im-
prove the long-term functional status of children with JF (Haavet and
Grunfeld, 1997; Schanberg et al., 1996). In this respect, Reid et al.
(1997) point out that disability among children with fibromyalgia or
JRA is a function of the children’s psychological adjustment and
physical state, and of the parents’ physical state and method of cop-
ing with pain.
K keratoconjunctivitis sicca: Patients with fibromyalgia

often describe the presence of dry eyes and other ocular
symptoms (Barton et al., 1999), and it has been claimed
that a subgroup of fibromyalgia patients might have features sugges-
tive of primary Sjogren’s syndrome (see also SJOGREN’S SYN-
DROME). However, Gunaydin et al. (1999) found that chronic
blepharitis and the use of tricyclic antidepressants may play a role in
developing keratoconjunctivitis sicca among fibromyalgia patients,
and the rate of the latter disorder does not increase in fibromyalgia
patients who probably have objective ocular findings comparable
with the normal population.
ketamine: Graven-Nielsen et al. (2000) showed that mechanisms in-

volved in referred pain, temporal summation, muscular hyperalgesia,
and muscle pain at rest were attenuated by intravenous injection of
the N-methyl-D-aspartate (NMDA) receptor antagonist ketamine
(0.3 mg/kg, Ketalar) in fibromyalgia patients. Whether the latter effect
is specific for fibromyalgia patients or a general phenomena in painful
musculoskeletal disorders is not known. A single sub-anaesthetic dose
of ketamine causes a long-term depression of pain intensity in some,
but not in all, patients suffering chronic pain (Oye et al., 1996). This
effect is distinctly different from the short-lasting (10 to 30 minutes)
analgesic effect in cases of acute nociceptive pain. The long-term de-
pression of the intensity of chronic pain states may be due to a rever-
sal of NMDA receptor-dependent long-term potentiation of synapses
in central pain pathways.
Klebsiella: No evidence for the existence of disease-specific

Klebsiella species was obtained by Toivanen et al. (1999) when ana-
lyzing, either separately or simultaneously according to somatic

serotypes (O groups), capsular (K) serotypes, and biochemically
identified species, feces from 187 ankylosing spondylitis patients
and 195 fibromyalgia or rheumatoid arthritis patients.
L laser therapy: Longo et al. (1997) showed that two-thirds

of 846 patients with fibromyositic rheumatisms, untreat-
able with other therapies, responded to therapy with de-
focalized laser beams (analgesic and antiphlogistic ef-
fects). This form of therapy needs standardization.
leiomyosarcoma: A retroperitoneal leiomyosarcoma was reported in

a patient who had been diagnosed with fibromyalgia (De Tomas
Palacios et al., 1995).
lidocaine: The antinociceptive effects of systemically administered

local anesthetics have been shown in various conditions, such as neu-
ralgia, polyneuropathy, fibromyalgia, and postoperative pain (Koppert
et al., 1998). Injection of low-dose local anesthetics, such as lido-
caine, are also useful in pain states, such as fibromyalgia, which are
dominated by hyperalgesia. In this respect, increasing painfulness
during sustained pinching has been attributed to excitation and simul-
taneous sensitization of particular Adelta- and C-nociceptors. This
hyperalgesic mechanism seems to be particularly sensitive to low
concentrations of injected lidocaine (Koppert et al., 1998). In contrast
to the latter observation, Scudds et al. (1995) found no efficacy in pain
reduction when using 4 percent topical lidocaine in sphenopalatine
blocks in forty-two fibromyalgia patients and nineteen with myo-
fascial pain syndrome. Moreover, Figuerola et al. (1998) showed an
increase in plasma metenkephalin levels ten minutes after either local
injection of lidocaine hydrochloride, local injection of saline, or dry
needling.
light treatment: In a randomized ten-week crossover study compar-

ing the effects of four weeks of “visible electromagnetic fields”
(light condition; mean 4,750 lux, SD 2,337 lux) to four weeks of
“nonvisible electromagnetic fields” (no light condition) in fourteen
fibromyalgia patients reporting seasonality of symptoms, Pearl et al.
(1996) found no significant differences between the light and no-

light conditions on pain, mood, or sleep. However, Tabeeva et al.
(1998) reported that phototherapy of fibromyalgia patients was asso-
ciated with an increase of total sleep duration, and a decrease of the
time of falling asleep, the latent period of the phase of fast sleep, acti-
vated movement index, intensivity of movements, and arousal time
during sleep. A distinction should be made between fibromyalgia and
seasonal affective disorder.
M magnesium: In a study of ninety-seven patients, Moorkens

et al. (1997) found no association between magnesium defi-
ciency and chronic fatigue syndrome or fibromyalgia. How-
ever, serum magnesium levels were significantly lower in
those patients with spasmophilia. Eisinger et al. (1996) also
failed to find magnesium deficiency in twenty-five fibromyalgia pa-
tients studied.
massage: A study by Brattberg (1999) of forty-eight individuals di-

agnosed with fibromyalgia (twenty-three in the treatment group and
twenty-five in the reference group) showed that a series of fifteen
treatments with connective tissue massage conveys a pain-relieving
effect of 37 percent, reduces depression and the use of analgesics, and
positively affects quality of life. The treatment effects appeared grad-
ually during the ten-week treatment period. Three months after the
treatment period, about 30 percent of the pain-relieving effect was
gone, and six months after the treatment period, pain was back to
about 90 percent of the baseline value.
masticatory myofascial pain: Cimino et al. (1998) reported several

similarities between fibromyalgia and masticatory myofascial pain in
forty-six patients affected by craniomandibular disorders, the most
striking of which were pain during mandibular function, articular
noises, and headache. Both groups had similar mean scores of muscle
pain upon palpation, mean values of active mouth opening, and mean
values of passive opening. Cimino and colleagues recommend that
the physician should be alert to the need to conduct interdisciplinary
evaluations in the diagnosis and management of fibromyalgia and of
masticatory myofascial pain.
medicinal baths: In a randomized, comparative, and investigator-

blinded study of thirty outpatients with generalized fibromyalgia
undergoing therapy consisting of either ten whirl baths with plain wa-
ter or with the addition of pine oil or valerian, Ammer and Melnizky
(1999) found that plain-water baths modify the pain intensity while
medicinal baths improve well-being and sleep.
melatonin: Desynchronization of circadian systems has been postu-

lated in the etiology of fibromyalgia. The pineal hormone melatonin
is involved in synchronizing circadian systems, and the use of exoge-
nous melatonin has become widespread in patients with fibromyalgia
and chronic fatigue syndrome (Webb, 1998). However, Korszun et al.
(1999) found that although nighttime plasma melatonin levels were
significantly higher in fibromyalgia patients compared to controls,
there were no differences in the timing of cortisol and melatonin se-
cretory patterns and no internal desynchronization of the two rhythms
in fibromyalgia patients compared to controls. Raised plasma mela-
tonin concentrations have been documented in several other condi-
tions that are associated with dysregulation of neuroendocrine axes,
and increased melatonin levels may represent a marker of increased
susceptibility to stress-induced hypothalamic disruptions (see also
NEUROENDOCRINOLOGY). Although the latter data indicate that
there is no rationale for melatonin replacement therapy in fibro-
myalgia patients, in a preliminary four-week pilot study of treatment
with melatonin (3 mg at bedtime) in nineteen fibromyalgia patients,
Citera et al. (2000) reported significant improvements after thirty
days in median values for the tender point count and severity of pain
at selected points, patient and physician global assessments, and
sleep. Also, unlike Korszun et al. (1999), Wikner et al. (1998), found
a 31 percent lower nighttime melatonin secretion in eight fibro-
myalgia patients as compared to healthy subjects and proposed that
this deficiency may contribute to impaired sleep at night, fatigue dur-
ing the day, and changed pain perception. However, Press et al.
(1998) found that nocturnal urine 6-sulphatoxymelatonin levels were
similar in thirty-nine fibromyalgia patients and controls.
mitochondrial myopathy: Mitochondrial myopathy can also mimic

fibromyalgia and should be included in the differential (Benito-Leon
et al., 1996; Villanova et al., 1999).
moclobemide: A four-center, twelve-week study by Hannonen et al.

(1998) of 130 female fibromyalgia patients without psychiatric disor-
ders showed that although moclobemide (450 to 600 mg) improved
pain, the improvement was invalidated by the poor success of the
drug with regard to sleep.
motor cortical dysfunction: In a study of thirteen fibromyalgia pa-

tients using single and double magnetic stimulation, Salerno et al.
(2000) demonstrated motor cortical dysfunction involving excitatory
and inhibitory mechanisms, an observation that supports the hypoth-
esis of aberrant central pain mechanisms. Similar observations were
made in five rheumatoid arthritis patients, a finding which suggests
that the lesions were not specific and could be related to chronic pain
disorders within the central nervous system. Ivanichev and Staro-
sel’tseva (2000) proposed a model based on proprioceptive desaffer-
entation which promotes disinhibition of neurons and formation of
the generators of pathologically increased irritation with positive
feedback on rubro-segmental, pallido-thalamic, strio-piramidal, and
parietal-premotor levels of the construction of the movement. More-
over, based on a comparison of the movement disorders in fibromyal-
gia patients to those found in akinetic syndromes that are secondary
to disturbances in the functions of the cortico-thalamo-nigro-striatal
system and associated areas, Burgunder (1998) proposes that since
basal ganglia also play a role in pain, a comparative study of their in-
volvement in movement disorders and nociception seems to be fruit-
ful, especially in devising new therapeutic strategies.
mud packs: Bellometti and Galzigna (1999) reported that mud packs
together with antidepressant treatment (trazodone) are able to influ-
ence the hypothalamic-pituitary axis, stimulating increased levels of
adrenocorticotropic hormone, cortisol, and beta-endorphin serum
levels. The discharge of corticoids in the blood and the increase in
beta-endorphin serum levels are followed by a reduction in pain
symptoms, which is closely related to an improvement in ability, de-
pression, and quality of life. It seems that the synergistic association
between a pharmacological treatment (trazodone) and mud packs
acts by helping the physiological responses to achieve homeostasis
and to rebalance the stress response system.
muscle abnormalities: An assessment of maximal and explosive

strength characteristics of the leg muscles and a comparison of acute
neuromuscular fatigue during heavy resistance loading and short-
term recovery from fatigue failed to demonstrate lower dynamic or
isometric muscle strength characteristics in eleven premenopausal
women with fibromyalgia as compared to twelve matched healthy fe-
male controls (Hakkinen et al., 2000). The latter observations strongly
support normal muscle structure and neuromuscular function in fi-
bromyalgia patients (Simms, 1996).
Some earlier studies disagree with the latter conclusion of normal
structure and muscle function in fibromyalgia. For instance, Pongratz
and Spath (1998) found that the most common morphological finding
in muscle biopsies in long-standing fibromyalgia is type II fiber atro-
phy, a change that can be found in many other conditions, such as dis-
use atrophy, affections of the corticospinal tracts, steroid atrophy, and
other different neuromuscular disorders. Pongratz and Spath (1998)
also found that an increase in lipid droplets and a slight proliferation
of mitochondria in type I muscle fibers correlated with the duration of
fibromyalgia and that some fibromyalgia patients with ragged red fi-
bers, which histochemically show a pronounced accumulation of
lipids and mitochondria and single fiber defects of cytochrome-c-
oxidase, had deletions of the mitochondrial genome. However, al-
though Norregaard (1998), Norregaard et al. (1995), and Borman
et al. (1999) reported reduced quadriceps muscle strength and sub-
maximal aerobic performance in fibromyalgia patients, there was no
relation between the decreased muscle performance and clinical find-
ings, including pain severity, number of tender points, and duration of
the symptoms. Graven-Nielsen et al. (1997) suggest that modulation
of muscle activity by muscle pain could be controlled via inhibition
of muscles agonistic to the movement and/or excitation of muscles
antagonistic to the movement.
Simms (1996) points out that the studies which indicated morph-
ologic abnormalities in fibromyalgia patients had major problems
with patient selection and lacked adequate control groups. Jacobsen
(1998) and Olsen and Park (1998) reinforced that there are no signs
of specific muscle pathology in fibromyalgia and that alterations in
muscle function may reflect effects of deconditioning or inhibition of
contraction due to spinal or supraspinal mechanisms. Moreover,
phosphorus magnetic resonance spectroscopy has been used in the
investigation of muscle energy metabolism (Argov et al., 2000;

Strobel et al., 1997) and, although Sprott et al. (2000) found increases
in the levels of phosphodiesterase and inorganic phosphate in the
fibromyalgic muscle tissue of fifteen patients as compared to seven-
teen healthy controls, the latter authors suggest that the latter meta-
bolic differences may have been related to weakness and fatigue in
the fibromyalgia patients, and they do not fully explain the fibromy-
algia symptoms. Park et al. (1998) also studied the biochemical status
of muscle in eleven fibromyalgia patients and showed that patients
had significantly lower than normal phosphocreatinine and ATP lev-
els and phosphocreatinine to inorganic phosphate ratios in the quad-
riceps muscles during rest, metabolic abnormalities that are consis-
tent with weakness and fatigue. Studies of muscle blood flow and
motor unit recruitment also demonstrate abnormalities that can be ex-
plained by deconditioning alone (Simms, 1996; Vestergaard-Poulsen
et al., 1995). Thorsteinsdottir et al. (1998) found no difference in
ubiquinone concentration of muscles and blood in fibromyalgia pa-
tients and healthy controls.
Based on the observation of an increased sensitivity of the flare re-
action in fibromyalgia patients, Sann and Pierau (1998) suggest that
the hyperalgesia characteristic of fibromyalgia might be partly due to
altered functions of C-fiber nociceptors. Local efferent functions of
C-fiber nociceptors, such as vasodilation and the axon reflex flare re-
action, are mediated via a local release of substance P, neurokinin A,
and calcitonin gene-related peptide (CGRP) from the peripheral end-
ing. CGRP is the main mediator of the capsaicin-induced flare reac-
tion in mammalian skin. The latter theory of the genesis of pain in
fibromyalgia syndrome is that excessive muscle tension leads to in-
creased excitability of nociceptors in muscle, which in turn leads to
muscle hypertension and chronic pain. Furthermore, defective sym-
pathetic control (Wachter et al., 1996) is proposed to result in dis-
turbed microcirculation and nociceptor excitation. In aggregate, how-
ever, studies using EMG techniques show no evidence of excessive
muscle tension or defective sympathetic nervous function (Simms,
1996). Therefore, although muscular pain has been a central feature
of fibromyalgia syndrome (Henriksson et al., 1996), controlled stud-
ies of muscle fail to support a convincing role for muscle in the
pathophysiology of the condition. Muscle tenderness in fibromyalgia
cannot be explained on the basis of primary muscle abnormalities, ei-

ther structural or functional.
mycoplasma: More than 60 percent of patients with chronic fatigue

syndrome/fibromyalgia syndrome, as compared to 15 percent in con-
trols, have mycoplasmal blood infections, such as Mycoplasma fer-
mentans infection (Choppa et al., 1998; Nasralla et al., 1999). The
role of Mycoplasma as an etiological agent for fibromyalgia or
chronic fatigue syndrome remains controversial.
myoadenylate deaminase deficiency: Marin and Connick (1997)

described a patient who was treated unsuccessfully for fibromyalgia
for many years and who ultimately was diagnosed with a rare benign
skeletal muscle metabolic disorder caused by myoadenylate deamin-
ase deficiency.
myofascial pain syndrome: Myofascial pain syndrome (MPS) is a

very common localized—sometimes also polytopic—painful mus-
culoskeletal condition associated with trigger points for which, how-
ever, diagnostic criteria established in well-designed studies are still
lacking (Cimino et al., 1998; Pongratz and Spath, 1998). Fibro-
myalgia should be included in the differential diagnosis for myo-
fascial pain of the masticatory or facial muscles (Aronoff, 1998;
Bernstein, 1997; Bohr, 1996; Dao et al., 1997; Fishbain and Roso-
moff, 1996; Galer, 1997; Gantz and Fukuda, 1997; Goldenberg,
1996; Long, 1997; Nye, 1997; Perle, 1996; Romano, 1997).
Harden et al. (2000) surveyed American Pain Society members,
and 88.5 percent of respondents reported that MPS is a legitimate di-
agnosis, with 81 percent describing MPS as distinct from fibromyal-
gia. The only signs and symptoms described as essential to the diag-
nosis of MPS by greater than 50 percent of the sample were regional
location, presence of trigger points, and a normal neurologic exami-
nation. Regarding the signs and symptoms considered to be essential
or associated with MPS, more than 80 percent of respondents agreed
on regional location, trigger points, normal neurologic examination,
reduced pain with local anesthetic or “spray and stretch,” taut bands,
tender points, palpable nodules, muscle ropiness, decreased range of
motion, pain exacerbated by stress, and regional pain described as
“dull,” “achy,” or “deep.” Sensory or reflex abnormalities, scar tissue,
and most test results were considered to be irrelevant to the diagnosis

of MPS by a large proportion of the respondents.
Some patients may exhibit both MPS and fibromyalgia (Dao et al.,
1998). For instance, of the 162 female participants with a history of
myofascial face pain, Raphael et al. (2000) found that thirty-eight
(23.5 percent) reported a history of fibromyalgia. Patients who have
myofascial face pain and a history of widespread pain suggestive of
fibromyalgia are likely to have more persistent and debilitating myo-
fascial face pain and to have higher rates of depression and somat-
ization symptoms than those who have no history of widespread pain.
Raphael and Marbach (2000) also found reduced fertility among
women with myofascial face pain, but this was restricted to those
who self-report a history of fibromyalgia.
The most important criteria for differential diagnosis are the pres-
ence of tender points (TePs) and widespread, nonspecific, soft tissue
pain in fibromyalgia, compared with regional and characteristic re-
ferred pain patterns with discrete muscular trigger points (TrPs) and
taut bands of skeletal muscle in MPS. Myofascial TrPs are found
within a taut band of skeletal muscle and have a characteristic “nodu-
lar” texture upon palpation. TrPs are thought to develop after trauma,
overuse, or prolonged spasm of muscles. Local treatment applied to
TePs is ineffective, yet specific treatment of TrPs is often dramati-
cally effective.
Fibromyalgia is a systemic disease process, apparently caused by
dysfunction of the limbic system and/or neuroendocrine axis, and of-
ten requiring a multidisciplinary treatment approach, while MPS is a
condition that arises from the referred pain and muscle dysfunction
caused by TrPs, which often respond to manual treatment methods
such as ischemic compression and various specific stretching tech-
niques (Schneider, 1995).
natural killer cells: Natural killer (NK) cells are mostly

large granular lymphocytes and are constitutively cyto-
N cidal against tumor-transformed and virus-infected cells,

an activity that does not require immunization (Patarca
et al., 1995). Although several studies revealed impaired
NK cell function in chronic fatigue syndrome patients as
assessed by cytotoxic activity against K562 target cells (Barker et al.,
1994; DuBois, 1986; Gupta and Vayuvegula, 1991; Kibler et al.,
1985; Klimas et al., 1990; Morrison et al., 1991; Ojo-Amaise et al.,

1994; See et al., 1997; Straus et al., 1985; Whiteside and Friberg,
1998), Russell et al. (1999) found no difference in the natural killer
cell activity or response to interferon-alpha in fibromyalgia patients
as compared to controls.
NK cell activity is known to be decreased by stress and, partly rep-
licating previous data in healthy volunteers, Lekander et al. (2000)
found that natural killer cell activity in fibromyalgia patients corre-
lated negatively with right hemisphere activity in the secondary
somatosensory and motor cortices as well as the thalamus. Moreover,
natural killer cell activity was negatively and bilaterally related to ac-
tivity in the posterior cingulate cortex. The latter findings illustrate
that immune parameters are related to activity in brain areas involved
in pain perception, emotion, and attention (Lekander et al., 2000).
neck support: Ambrogio et al. (1998) found inconclusive evidence

in a study of thirty-five fibromyalgia patients who tried three types of
neck support (Shape of Sleep pillow, two neck ruffs with one stan-
dard pillow, and a single standard pillow). However, from a patient’s
perspective, neck support is an important part of a comprehensive
physiotherapy program.
nerve growth factor: Giovengo et al. (1999) found elevated levels of

the neuropeptide nerve growth factor in the cerebrospinal fluid of pri-
mary, but not secondary, fibromyalgia patients (41.8 +/–12.7 pg/mL
versus 9.1 +/–4.1 pg/mL in controls), an observation that reinforces
the notion of a central mechanism in the pathogenesis of fibro-
myalgia.
neuroendocrinology: The neuroendocrine axes are essential physio-

logic systems that allow for communication between the brain and
the body (Crofford, 1998a,b; Morand et al., 1996). Interconnections
among the neuroendocrine axes coordinate regulation of these sys-
tems in both a positive and negative fashion (Crofford, 1998a,b).
Changes in neuroendocrine transmitters such as serotonin, substance
P, growth hormone, and cortisol suggest that dysregulation of the au-
tonomic and neuroendocrine systems are associated with fibromyalgia
(Bellometti and Galzigna, 1999; Bradley et al., 2000; Clauw and
Chrousos, 1997; Crofford et al., 1996; Dessein et al., 2000; Griep et al.,
1998; Heim et al., 2000; Millea and Holloway, 2000; Pillemer et al.,
1997; Russell, 1998; Scott and Dinan, 1999). Almost all of the hor-
monal feedback mechanisms controlled by the hypothalamus are al-
tered in fibromyalgia, as evinced by elevated basal values of adreno-
corticotropic hormone (ACTH), follicle-stimulating hormone (FSH),
and cortisol, as well as lowered basal values of insulin-like growth
factor-1 (IGF-1, somatomedin C), free triiodothyronine (FT3), and
estrogen (Bennett et al., 1997; Clauw and Chrousos, 1997; Griep
et al., 1998; Neeck, 2000; Riedel et al., 1998). In fibromyalgia pa-
tients, the systemic administration of corticotropin-releasing hormone
(CRH), growth hormone-releasing hormone (GHRH), thyrotropin-
releasing hormone (TRH), and luteinizing hormone-releasing hor-
mone (LHRH) leads to increased secretion of ACTH and prolactin,
whereas the degree to which thyroid-stimulating hormone (TSH) can
be stimulated is reduced (Neeck and Riedel, 1999; Netter and Hennig,
1998; Riedel et al., 1998). The stimulation of the hypophysis with
LHRH in female fibromyalgia patients during their follicular phase
results in a significantly reduced luteinizing hormone response (Neeck
and Riedel, 1999; Riedel et al., 1998). Based on the latter observa-
tions, it has been proposed that the alterations in set points of hor-
monal regulation that are typical for fibromyalgia patients can be ex-
plained as a primary stress activation of hypothalamic CRH neurons
caused by chronic pain or other factors (Crofford and Demitrack,
1996; Lentjes et al., 1997; Neeck, 2000; Netter and Hennig, 1998;
Oye et al., 1996; Stanton, 1999; Torpy and Chrousos, 1996;
Winfield, 1999). In addition to the stimulation of pituitary ACTH se-
cretion, CRH activates somatostatin on the hypothalamic level,
which in turn inhibits the release of GH and TSH at the hypophyseal
level. The lowered estrogen levels could be accounted for both via an
inhibitory effect of the CRH on the hypothalamic release of LHRH or
via a direct CRH-mediated inhibition of the FSH-stimulated estrogen
production in the ovary. Serotonin (5HT), precursors such as
tryptophan (5HTP), drugs that release 5HT or act directly on 5HT re-
ceptors stimulate the hypothalamic-pituitary-adrenal (HPA) axis, in-
dicating a stimulatory serotonergic influence on HPA axis function.
Therefore, activation of the HPA axis may reflect an elevated
serotonergic tonus in the central nervous system of fibromyalgia pa-
tients. Defects in the HPA axis have also been observed in autoim-
mune and rheumatic diseases, chronic inflammatory disease, and
chronic fatigue syndrome (Anisman et al., 1996; Crofford et al.,

1996; Crofford and Demitrack, 1996; Demitrack, 1997; Demitrack
and Crofford, 1998; Scott and Dinan, 1999; Torpy and Chrousos,
1996).
Administration of interleukin (IL)-6 (3 g/kg of body weight sub-
cutaneously), a cytokine capable of stimulating CRH, to thirteen fe-
male fibromyalgia patients yielded exaggerated norepinephrine (NE)
responses and heart rate increases, as well as delayed ACTH release
(Torpy et al., 2000). The latter observations are consistent with a de-
fect in hypothalamic CRH neuronal function and abnormal regula-
tion of the sympathetic nervous system. The excessive heart rate re-
sponse after IL-6 injection in fibromyalgia patients may be unrelated
to the increase in NE, or it may reflect an alteration in the sensitivity
of cardiac beta-adrenoceptors to NE. These responses to a physio-
logic stressor support the notion that fibromyalgia may represent a
primary disorder of the stress system (Torpy et al., 2000).
Not all studies agree with the assessment of endocrine function de-
scribed previously. For instance, in a study of fifteen premenopausal
women with fibromyalgia, Samborski et al. (1996) failed to find sig-
nificant differences in the levels of ACTH, substance P, and TSH in
fibromyalgia patients compared to controls. Adler et al. (1999) re-
ported that although twenty-four-hour urinary free cortisol levels and
diurnal patterns of ACTH and cortisol were normal, as also found by
Maes et al. (1998), there was a significant (approximately 30 percent)
reduction in the ACTH and epinephrine responses to hypoglycemia
in women with fibromyalgia compared with controls. Prolactin,
norepinephrine, cortisol, and dehydroepiandrosterone responses to
hypoglycemia were similar in the two study groups. In subjects with
fibromyalgia, the epinephrine response to hypoglycemia correlated
inversely with overall health status as measured by the fibromyalgia
impact questionnaire. Adler et al. (1999) concluded that fibromy-
algia patients have an impaired ability to activate the hypothalamic-
pituitary portion of the hypothalamic-pituitary-adrenal (HPA) axis as
well as the sympathoadrenal system, leading to reduced ACTH and
epinephrine responses to hypoglycemia.
Hapidou and Rollman (1998) reported that the number of tender
points identified by palpation was greater in the follicular (post-
menstrual) phase of the cycle as compared to the luteal (inter-
menstrual) phase in normally cycling women but not in users of oral
contraceptives. Although the latter and other studies mentioned sug-
gest that sex hormones have a role in fibromyalgia symptomatology

(Akkus et al., 2000; Anderberg, 2000), and Raphael and Marbach
(2000) found reduced fecundity among women with myofascial face
pain who also reported a history of fibromyalgia, a study by Korszun
et al. (2000) of nine premenopausal women with fibromyalgia or
eight with chronic fatigue syndrome found no indication of abnormal
gonadotropin secretion or gonadal steroid levels (no significant dif-
ferences in follicle-stimulating hormones, progesterone, or estradiol
levels in patients versus controls, and no significant differences in
pulsatile secretion of luteinizing hormone).
There is little direct information as to how the specific HPA axis
perturbations seen in fibromyalgia can be related to the major symp-
tomatic manifestations of pain, fatigue, sleep disturbance, and psy-
chological distress. Interventions providing symptomatic improve-
ment in patients with fibromyalgia and CFS can directly or indirectly
affect the HPA axis. These interventions include exercise, tricyclic
antidepressants, and selective serotonin reuptake inhibitors (Crofford,
1998a,b). Moreover, in a study of thirty-six fibromyalgic women pa-
tients (with forty pregnancies total), Ostensen et al. (1997) found that
all women described worsening fibromyalgia symptoms during preg-
nancy, with the last trimester experienced as the worst period. A new
change of fibromyalgia symptoms within six months after delivery
was reported for thirty-seven of the forty pregnancies, to the better in
four and to the worse in thirty-three cases, resulting in a prolonged
sick leave for fourteen patients. An increase in depression and anxi-
ety was a prominent problem in the postpartum period. Fibromyalgia
had no adverse effect on the outcome of pregnancy or the health of
the neonate. In the majority of fibromyalgia patients, hormonal
changes connected with abortion, use of hormonal contraceptives,
and breast-feeding did not modulate symptom severity. A premen-
strual worsening of symptoms was recorded by 72 percent of the pa-
tients. Comparing the twenty-six patients who had borne children
during disease with eighteen patients who had all their children be-
fore the onset of fibromyalgia revealed a negative effect of pregnancy
and the postpartum period of fibromyalgia and increased functional
impairment and disability in the twenty-six patients (Ostensen et al.,
1997).
neurogenic inflammation: Enestrom et al. (1997) found that skin

biopsies from twenty-five fibromyalgia patients had significantly
higher values of immunoglobulin (Ig)G deposits in the dermis and
vessel walls, showed a higher reactivity for collagen III, and had a
higher mean number of mast cells. There was a correlation between
the percentage of damaged/degranulated mast cells and the individ-
ual IgG immunofluorescence scores. These findings support the hy-
pothesis of neurogenic inflammation involvement in fibromyalgia
(see also CHEMICAL INTOLERANCE).
neuroimaging: Mountz et al. (1995) reported that regional cerebral

blood flow (rCBF) in the left and right hemithalami or the left and
right heads of the caudate nucleus is significantly lower in women
with fibromyalgia than in normal controls. Compared with controls,
the women with fibromyalgia also were characterized by signifi-
cantly lower cortical rCBF and lower pain threshold levels at both
tender points and control points. San Pedro et al. (1998) confirmed
the findings of lower rCBF and its relationship to pain in fibromyal-
gia patients. The latter findings support the hypothesis that abnormal
pain perception in women with fibromyalgia may result from a func-
tional abnormality within the central nervous system (Yang et al.,
1999).
neuropeptide Y: Crofford et al. (1996) initially found that the plasma

levels of neuropeptide Y (NPY), a peptide colocalized with nor-
epinephrine in the sympathetic nervous system, are low in fibromyal-
gia patients (Crofford et al., 1996), while in a more recent report
Anderberg et al. (1999) found that NPY levels were significantly ele-
vated in fibromyalgia patients compared to the controls. Several fac-
tors affect NPY levels. For instance, Anderberg et al. (1999) reported
that NPY levels are higher during the luteal phase, and NPY levels cor-
relate with anxiety but not depression. Fibromyalgia patients may,
therefore, have an altered activity in the NPY system, most likely due
to prolonged and/or repeated stress, and may also be affected by the
hormonal state and time of the menstrual cycle.
nociceptin: Anderberg et al. (1998) showed that the levels of the

neuropeptide nociceptin were lower in fibromyalgia patients than in
controls, a finding that may be linked to other neuroendocrine abnor-
malities reported for fibromyalgia patients (see NEUROENDOCRIN-

OLOGY).
nonsteroidal anti-inflammatory drugs (NSAIDs): Through a

mailed questionnaire survey of 1,799 patients with osteoarthritis,
rheumatoid arthritis, or fibromyalgia who were participating in a
long-term outcome study, Wolfe et al. (2000) found a considerable
and statistically significant preference for NSAIDs compared with
acetaminophen among different groups of rheumatic disease pa-
tients. Although this preference decreased slightly with age and was
less pronounced in osteoarthritis patients, the preference was noted
among all categories of patients and was not altered by disease sever-
ity. Wolfe et al. (2000) concluded that if safety and cost are not issues
there would hardly ever be a reason to recommend acetaminophen
over NSAIDs, since patients generally preferred NSAIDs and fewer
than 14 percent preferred acetaminophen. Vachtenheim (1995) also
reported on the efficacy of a nonsteroidal anti-inflammatory oint-
ment, Mobilisin, which contains flufenamic acid, in fibromyalgia pa-
tients. If safety and costs are issues, then the recommendation of the
American College of Rheumatology that acetaminophen be tried first
seems correct, since 38.2 percent found acetaminophen to be as ef-
fective or more effective than NSAIDs (Wolfe et al., 2000).
nursing: Nurses can enhance patients’ quality of life by helping them

to cope with pain, establish sleep patterns, take exercise, manage
stress, improve concentration and memory, and fight isolation
(Edmands et al., 1999; Ryan, 1995).
O omega-3 fatty acids: As for other rheumatic diseases,

Ozgocmen et al. (2000) reported that omega-3 fatty acids
may also be useful in the treatment of fibromyalgia.
opioids: Opioids are prescribed for the management of pain associ-

ated with fibromyalagia. Quang-Cantagrel et al. (2000) showed that
if a patient receiving chronic opioid therapy experiences an intolera-
ble side effect or if the drug is ineffective, changing to a different
opioid may result in a lessening or elimination of the side effect
and/or improved analgesia. In terms of which opioid to prescribe,
Quijada-Carrera et al. (1996) reported that treatment with tenoxicam

(20 mg) plus bromazepan (3 mg) can be effective for some patients
with fibromyalgia, but the overall differences between the treated
group and the placebo group were neither clinically nor statistically
significant.
orofacial pain: Heir (1997) and Bailey (1997) stress that pain prob-
lems associated with the orofacial region need to be evaluated thor-
oughly because the differential diagnosis is broad-ranging, including
diseases such as Lyme disease and fibromyalgia.
osteomalacia: Reginato et al. (1999) point out that osteomalacia is

usually neglected when compared with other metabolic bone dis-
eases and may present with a variety of clinical and radiographic
manifestations mimicking other musculoskeletal disorders, includ-
ing fibromyalgia.
osteoporosis: Fibromyalgia is considered a risk factor and has been

associated with osteoporosis. Early detection and implementation of
appropriate nutritional supplementation (calcium/vitamin D), resis-
tive and weight-bearing exercise, and specific bone mineral enhanc-
ing pharmacological therapy may be indicated in pre-, peri-, and
postmenopausal subjects (Dessein and Stanwix, 2000; Swezey and
Adams, 1999).
P pain: Fibromyalgia is associated with chronic widespread

pain and decreased threshold for pain, features that are
nonspecific (also present in other rheumatic conditions,
such as rheumatoid arthritis), ill-defined and not well understood,
and require careful evaluation for differential diagnosis (Alvarez-
Lario et al., 1999; Atkins et al., 1995; Drewes, 1999; Ferguson and
Ahles, 1998; Forseth et al., 1999; Friedman and Nelson, 1996;
Gustafsson and Gaston-Johansson, 1996; Henriksson et al., 1996;
MacFarlane et al., 1996; MacFarlane, 1999; Mountz et al., 1998;
Nicassio et al., 1995; Reilly, 1999; Rubio Montanes et al., 1995;
Smythe et al., 1997; Turk and Okifuji, 1997; Weigent et al., 1998;
White and Harth, 1999; Zetterberg, 1996). Persistent pain in fibromy-
algia is often difficult to understand and to treat, maybe because it is
partially or wholly of nonnociceptive afferent origin (Bassoe, 1997;
Bendtsen et al., 1997; Bengtsson and Henriksson, 1996; Houvenagel,

1999; Kosek et al., 1996; Kramis et al., 1996; Lidbeck, 1999; Lorenz
et al., 1996; Sartin, 2000; Sorensen et al., 1998). Nonnociceptive pain
is often an important component of pain associated with peripheral
and central neuropathy, fibromyalgia, trauma-induced pain, idio-
pathic low back pain, and chronic regional pain syndrome.
Nonnociceptive pain is often dependent upon central sensitization in-
duced by prior or ongoing nociception.
Chronic pain often differs from acute pain. The correlation be-
tween tissue pathology and the perceived severity of the chronic pain
experience is poor or even absent. Furthermore, the sharp spatial lo-
calization of acute pain is not a feature of chronic pain; chronic pain
is more diffuse and often spreads to areas beyond the original site.
Also of importance: chronic pain seldom responds to the therapeutic
measures that are successful in treating acute pain. Physicians who
are unaware of these differences may label the patient with chronic
pain as being neurotic or even a malingerer (Bennett, 1999).
Morris et al. (1998) used capsaicin-induced secondary hyperalgesia
as a marker of abnormal nociceptive processing in fibromyalgia pa-
tients (Arner et al., 1998) and found enhanced sensitivity of nocicep-
tive neurons at a spinal level, thereby supporting the concept of a gen-
eralized disturbance of pain modulation in this disorder (Bradley
et al., 1997). Lautenbacher and Rollman (1997) also found that fibro-
myalgia patients had significantly lower heat pain thresholds than
healthy subjects, but similar electrical detection and pain thresholds.
Although repeatedly applied electrical stimuli resulted in a degree of
perceptual adaptation that was similar between the two groups, con-
current tonic thermal stimuli, at both painful and nonpainful levels,
significantly increased the electrical pain threshold in the healthy
subjects but not in the fibromyalgia patients.
Integration of nociceptive signaling comprises peripheral, spinal,
and supraspinal sites of the nervous system, and various excitatory or
inhibitory neurotransmitter and modulator systems participate in
pain processing and modulation (Schadrack and Zieglgansberger,
1998). The role of different neuroendocrine mediators in pain associ-
ated with fibromyalgia has been the subject of intense study (Russell,
1998; Weigent et al., 1998). For instance, Ernberg et al. (2000) re-
ported that injection of serotonin (5HT) into the masseter muscle
leads to pain and allodynia/hyperalgesia in healthy female controls
but not in female fibromyalgia patients. Pain perception, therefore,

appears to be differentially modulated in fibromyalgia patients (Brad-
ley et al., 1997). In this respect, Kosek and Hansson (1997) found that
although fibromyalgia patients did not differ from healthy controls in
their response to vibratory stimulation in the forearm, no modulation
of pressure pain was induced by heterotopic noxious conditioning
stimulation, as opposed to controls, suggesting a dysfunction in sys-
tems subserving diffuse noxious inhibitory controls. Sorensen et al.
(1997) also reported that different patient subgroups may show ab-
normalities in different pain-processing mechanisms.
Pain in fibromyalgia has several consequences. Agargun et al.
(1999) reported that there is a negative correlation between pain and
sleep disturbance: increased pain sensitivity is associated with greater
sleep disturbance. Also, poor sleep results in increased pain severity
and increased pain attention (Affleck et al., 1996).
pain syndromes: Pain syndromes can be divided anatomically into

those that cause generalized pain, such as fibromyalgia syndrome
and myofascial pain syndromes, and those that are confined to one re-
gional anatomical area (Carette, 1996). The latter group comprise
those of the neck, shoulder, elbow, wrist/hand, hip, knee, and ankle/
foot (Linaker et al., 1999). Diffuse pain syndromes, such as fibromy-
algia, are more common in women and also some, such as fibromyal-
gia and polymyalgia rheumatica, in older persons (Gowin, 2000). Fi-
bromyalgia also may be a secondary phenomenon associated with
some of the other diffuse pain syndromes, such as those of neoplastic
or endocrinological etiology.
Several chronic pain syndromes may mimic fibromyalgia by (1) the
occurrence of widespread pain, (2) the chronicity of complaints,
(3) the preponderance of females in some of these, and (4) the lack of
objective data to be derived from imaging techniques and laboratory
tests (Menninger, 1998). Differential diagnosis requires examination
of the locomotor system under biomechanical auspices both at rest
and during movement to diagnose hyper- and hypomobility syn-
dromes; treatment of these conditions is guided by principles to im-
prove biomechanical function. In addition, the skin needs to be exam-
ined to detect panniculosis (also called cellulitis), which may be
mixed with fibromyalgia due to its preferential occurrence in peri- or
postmenopausal women (Menninger, 1998). Vertebral fractures and
fibromyalgia, although very different and unrelated clinical condi-

tions, are common pain conditions that can, at times, be difficult to
diagnose and manage (Hall, 1999). Distinction between fibromyalgia
and other chronic pain syndromes is also relevant in terms of progno-
sis, as illustrated by a study by MacFarlane et al. (1996), which found
that although chronic widespread pain in the community has a gener-
ally good prognosis, those with additional symptoms associated with
fibromyalgia were more likely still to have chronic widespread pain
two years later.
pentazocine-induced fibrous myopathy: A case report by Sinsa-

waiwong et al. (1998) on a forty-seven-year-old woman who had a
four-year history of intramuscular pentazocine injections in the lower
extremities and who developed gradual stiffness and weakness of the
lower extremities illustrates that caution in long-term usage and early
recognition of pentazocine toxicity as a neuromuscular complication
are important in order to prevent irreversible drug-induced fibrous
myopathy and localized neuropathy. The latter condition should also
be differentiated from fibromyalgia.
Persian Gulf War syndrome: Since the Persian Gulf War ended in
1991, veterans have reported an increased prevalence, as compared to
contemporary military personnel who were not deployed, of diverse,
unexplained symptoms, including some consistent with chronic fa-
tigue syndrome, fibromyalgia, and multiple chemical sensitivity
(Alloway et al., 1998; Hodgson and Kipen, 1999; Nicolson and
Nicolson, 1998; “Self-Reported Illness and Health Status Among
Gulf War Veterans: A Population-Based Study,” 1997). Although
some veterans have wondered if their development of systemic lupus
erythematosus, amyotrophic lateral sclerosis, or fibromyalgia might
be related to Gulf War service, an examination by Smith et al.
(2000) of hospitalizations of regular, active-duty service personnel
deployed to the Persian Gulf War (n = 551,841) compared with
nondeployed Gulf War-era service personnel (n = 1,478,704) did not
support Gulf War service and disease associations. Other controlled
epidemiological studies in Gulf War veterans and controls describe
significant excesses of symptoms that were not clearly associated
with pathologic disease (Hodgson and Kipen, 1999).
Grady et al. (1998) reported that of 250 Gulf War veterans evalu-
ated, 139 (56 percent) were referred for rheumatology consultation,
which was the most common elective subspecialty referral. Of the pa-
tients evaluated, 82 (59 percent) had soft tissue syndromes, 19 (14 per-
cent) had rheumatic disease, and 38 (27 percent) had no rheumatic
disease. The most common soft tissue syndromes were patellofemoral
syndrome (33 patients [24 percent]), mechanical low back pain (23
patients [17 percent]), and fibromyalgia (22 patients [16 percent]).
Grady et al. (1998) concluded that the rheumatic manifestations in
Gulf War veterans are similar to symptoms and diagnoses described
in previous wars and are not unique to active-duty soldiers. After ana-
lyzing the rheumatic manifestations of 145 Persian Gulf War veter-
ans, Escalante and Fischbach (1998) found that although the most
common diagnosis was fibromyalgia (33.8 percent), followed by var-
ious soft tissue problems (17.2 percent), clinical or radiographic
osteoarthritis (11.0 percent), and nonspecific arthralgias (9.6 per-
cent), no specific rheumatic diagnosis is characteristic of Gulf War
veterans with unexplained illness. However, pain is common and
widespread in these patients, and their health-related quality of life is
poor. Further research is necessary to determine the cause of the
symptoms of veterans of the Gulf War.
phenobarbital: A case report by Goldman and Krings (1995) illus-

trates fibromyalgia induced by the anticonvulsant phenobarbital in a
female swimming instructor who was seen with chronic bilateral
shoulder pain and loss of range of motion. The patient, who was tak-
ing medication for tonic/clonic seizures, recalled that her symptoms
began after her anticonvulsant medication was switched from hy-
dantoin sodium to phenobarbital.
phosphate diabetes: Based on measurements of phosphate reabsorp-

tion by the proximal renal tubule, phosphate clearance, and renal
threshold phosphate concentration, nine out of eighty-seven CFS pa-
tients in one study also fulfilled the diagnostic criteria for phosphate
diabetes (phosphate depletion due to abnormal renal reabsorption of
phosphate by the proximal tubule) (De Lorenzo et al., 1998). De
Lorenzo and colleagues concluded that phosphate diabetes should be
considered in the differential diagnosis of CFS. Laroche and Tack
(1999) also pointed out that hypophosphoremia secondary to moder-
ate idiopathic phosphate diabetes should be included in the differen-

tial diagnosis of primary fibromyalgia.
physical therapy: Physical therapy for fibromyalgia is aimed at

disease consequences such as pain, fatigue, deconditioning, muscle
weakness, sleep disturbances, and other disease consequences (Meng-
shoel, 1997). A review by Offenbacher and Stucki (2000) concluded
that, based on evidence from randomized controlled trials, cardiovas-
cular fitness training significantly improves cardiovascular fitness,
both subjective and objective measures of pain, as well as subjective
energy and work capacity, and physical and social activities. More-
over, based on anecdotal evidence of small observational studies,
physiotherapy may reduce overloading of the muscle system, im-
prove postural fatigue and positioning, and condition weak muscles.
platelet alpha-2-adrenoreceptors: In the search for disease mark-

ers, Maes et al. (1999) found that fibromyalgia, particularly in the
early phase of illness, is accompanied by lowered affinity of platelet
alpha-2-adrenoreceptors. Further studies are needed to assess the
usefulness of the latter observation.
polymyalgia rheumatica: Polymyalgia rheumatica (PMR) is a

disease of unknown etiology characterized by severe myalgia and
stiffness in shoulder girdle and pelvic girdle muscles and by normal
serum creatine kinase levels. Marked elevation of erythrocyte sedi-
mentation rate, acute onset within two weeks, and appearance in the
aged are also additional characteristics of PMR. Ten to 50 percent
of PMR patients have a concomitant temporal arteritis (giant cell
arteritis). For the differential diagnoses of PMR, rheumatoid arthritis,
polymyositis, fibromyalgia, malignancies, infections, and depression
should be considered (Nishikai, 1999) (see also AGING AND GERIAT-
RICS).
postcardiac injury rheumatism: Another disorder listed in the dif-

ferential diagnosis for fibromyalgia is postcardiac injury rheumatism
(PIR) (Mukhopadhyay et al., 1995). In a study by Mukhopadhyay
et al. (1995), out of the 249 patients who survived cardiac surgery,
twenty (8 percent) and twenty-two (9 percent) patients had early and
late PIR, respectively. Earlier onset (within two weeks of surgery),
milder articular involvement, absence of constitutional features and

laboratory abnormalities, and good response to analgesics were char-
acteristics of early PIR. In contrast, late PIR, which occurred between
the third and fourteenth week after surgery, was associated with more
marked articular involvement along with systemic and laboratory ab-
normalities and required longer analgesic therapy, steroid support, or
prolonged physiotherapy in different combinations.
post-Lyme disease syndrome: Despite antibiotic treatment, a sequel

of Lyme disease (or Lyme borreliosis) may be a post-Lyme disease
syndrome characterized by persistent arthralgia, fatigue, and neuro-
cognitive impairment that is probably induced by Lyme disease.
Bujak et al. (1996) found that of twenty-three patients with post-
Lyme disease syndrome, seven (30 percent) had fibromyalgia, three
(13 percent) had chronic fatigue syndrome, and ten (43 percent) had
similar but milder symptoms but did not meet the criteria for either.
Late Lyme disease or post-Lyme disease syndrome must be distin-
guished by clinical characteristics from fibromyalgia (the most com-
mon source of misdiagnosis in several studies) (Berman and Wenglin,
1995; Ellenbogen, 1997; Rahn and Felz, 1998). A case can be defined
as borreliosis only if either the typical erythema migrans is reliably
identified by a physician or if a characteristic late manifestation of
Lyme disease is accompanied by unequivocal serological and/or bac-
teriological evidence of Borrelia burgdorferi infection (Frey et al.,
1995, 1998; Graninger, 1996; Nadelman et al., 1999; Sigal, 1995).
Within the musculoskeletal system, the only reliable characteristic
symptom is true synovitis, as defined by the palpable swelling of a
joint. Mere joint pain or the subjective pain syndrome of fibromyal-
gia do not constitute a defining symptom for borreliosis (Graninger,
1996). Fallon et al. (1999) reported increased Fibromyalgia Impact
Questionnaire total score, muscle pain, and joint pain in fibromyalgia
patients as compared to post-Lyme disease syndrome patients.
postpolio syndrome: Fibromyalgia may mimic some of the symp-

toms of postpoliomyelitis syndrome, a disorder characterized by new
weakness, fatigue, and pain decades after paralytic poliomyelitis
(Trojan and Cashman, 1995). Trojan and Cashman (1995) found that
ten (10.5 percent) of ninety-five postpolio patients met the criteria for
fibromyalgia, and another ten patients (10.5 percent) had borderline
fibromyalgia. Postpolio syndrome patients with fibromyalgia were

more likely than patients without fibromyalgia to be female (80 percent
versus 40 percent) and to complain of generalized fatigue (100 per-
cent versus 71 percent) but were not distinguishable in terms of age at
presentation to clinic, age at polio, length of time since polio, physi-
cal activity, weakness at polio, motor strength scores on examination,
and presence of new weakness, muscle fatigue, or joint pain. Approx-
imately 50 percent of postpolio syndrome patients in both the fibro-
myalgia and borderline fibromyalgia groups responded to low-dose,
nighttime amitriptyline therapy.
post-traumatic stress disorder: Traumatic events can result in a set

of symptoms including nightmares, recurrent and intrusive recollec-
tions, avoidance of thoughts or activities associated with the trau-
matic event, and symptoms of increased arousal such as insomnia and
hypervigilance. These post-traumatic stress disorder (PTSD)-like
symptoms are frequently observed in persons with chronic pain syn-
dromes. Approximately 56 percent of a sample of ninety-three fibro-
myalgia patients studied by Sherman et al. (2000) reported clinically
significant levels of PTSD-like symptoms (PTSD+). The PTSD+
patients reported significantly greater levels of pain, emotional dis-
tress, life interference, and disability than did the patients without
clinically significant levels of PTSD-like symptoms (PTSD–). Over
85 percent of the PTSD+ patients, compared with 50 percent of the
PTSD– patients, demonstrated significant disability. Based on re-
sponse to the Multidimensional Pain Inventory, a significantly lower
percentage of PTSD+ patients were classified as adaptive copers
(15 percent) compared with the PTSD– group (48.2 percent) (Sherman
et al., 2000). Amir et al. (1997) also documented that PTSD subjects
suffering from fibromyalgia were more tender and reported more pain,
lower quality of life, and higher functional impairment, and suffered
more psychological distress than the PTSD patients without fibromy-
algia. Therefore, clinicians should assess the presence of these symp-
toms, as the failure to attend to them in treatment may impede success-
ful outcomes.
propyl endopeptidase: Maes et al. (1998) found that fibromyalgia

patients have significantly lower serum activities of prolyl endo-
peptidase (PEP) but normal activities of dipeptidyl peptidase IV
(DPP IV). Serum PEP activity was negatively correlated with sever-
ity of pressure hyperalgesia and the nonsomatic, cognitive symptoms
of the Hamilton Depression Rating Scale. Fibromyalgia patients with
severe pressure hyperalgesia had significantly lower PEP activity
than normal controls and fibromyalgia patients with less severe
hyperalgesia, observations that are consistent with a relationship be-
tween low PEP activity and abnormal pain perception. Fibromyalgia
patients with severe nonsomatic depressive symptoms had signifi-
cantly lower serum PEP activity than normal volunteers. Lower serum
PEP activity may play a role in the biophysiology of fibromyalgia
through diminished inactivation of algesic and depression-related
peptides (Maes et al., 1998).
prostaglandin D synthase: Prostaglandin D synthase (PGD syn-

thase) or beta-trace protein is a major constituent of human cerebro-
spinal fluid (CSF), representing 3 percent of the total CSF protein.
Normally, PGD synthase levels in CSF are approximately thirty-five-
fold higher than those of serum, with a median concentration of
11,299 g/L. Melegos et al. (1997) found no statistical difference
between PGD synthase concentrations in the CSF or the serum of pa-
tients with different diseases, such as multiple sclerosis, HIV/AIDS-
related neuropathies, viral meningitis, and fibromyalgia. Therefore,
PGD synthase measurement has no clinical utility in diagnosing neu-
rological disorders in adulthood.
protein peroxidation: Eisinger et al. (1996) demonstrated increased

protein peroxidation (elevated protein carbonyls) in twenty-five fibro-
myalgia patients. The relevance of this observation needs further sub-
stantiation.
psychiatry: Patients with chronic widespread pain (CWP) have been

reported to have a greater prevalence of mental disorders and somat-
ization than that found in the general population (Avina-Zubieta
et al., 1997; Ben-Zion et al., 1996; Ruderman and Golden, 1996). A
population-based case-control study by Benjamin et al. (2000) of 710
subjects, although unable to demonstrate a cause-and-effect relation-
ship, showed that 16.9 percent of those with CWP were estimated to
have a psychiatric diagnosis, suggesting that these disorders should
be identified and treated. Offenbaecher et al. (1998) found clinically
relevant depression in 27 percent of 304 fibromyalgia patients stud-

ied. Meyer-Lindenberg and Gallhofer (1998) proposed that the sub-
group of fibromyalgia patients with depressive symptoms may be
pragmatically classified as suffering from somatized depression, and
Keel (1998) pointed out that fibromyalgia patients most often present
with persistent somatoform pain disorder (ICD-10) and dysthymia
than with major psychiatric disorders. In a multicenter study of sev-
enty-three individuals, Epstein et al. (1999) found that fibromyalgia
patients exhibited high levels of some lifetime or current psychiatric
disorders (mainly depression, 22 percent, and panic disorders, 7 per-
cent) and significant current psychological distress. A study by Aaron
et al. (1996) yielded similar results. Current anxiety level appears to
be an important correlate of functional impairment in fibromyalgia
patients (Epstein et al., 1999). Repeated traumatic experiences dur-
ing childhood and as adults can be discovered in many cases, which
helps in understanding some of the difficulties met in psychotherapy
with fibromyalgia patients (Keel, 1998).
Antidepressant treatment is generally beneficial in fibromyalgia,
but improvement in symptomatology does not necessarily correlate
with treatment of comorbid psychiatric conditions (Dunne and Dunne,
1995; Gruber et al., 1996; Hudson and Pope, 1996) (see also ANTIDE-
PRESSANTS), an observation that curtails those who favor a psychiat-
ric etiology of diffuse pain syndromes. In this respect, a study by Katz
and Kravitz (1996) suggests that the tendency toward depression in
fibromyalgia patients may be a manifestation of a familial depressive
spectrum disorder (alcoholism and/or depression in family mem-
bers), not simply a “reactive” depression secondary to the pain and
other symptoms.
psychosocial factors: In fibromyalgia, psychosocial factors are rele-

vant at different levels (predisposing, triggering, and stabilizing/
“chronifying” factors) (Affleck et al., 1998; Anderberg, 1999; Eich
et al., 2000; Rosenfeld and Walco, 1997; Walker et al., 1997). Hall-
berg and Carlsson (1998) found that individuals with insecure attach-
ment styles are overrepresented among patients with chronic pain.
Wolfe and Hawley (1998) pointed out that psychosocial distress and
psychological abnormality occurs frequently in fibromyalgia pa-
tients (Jamison, 1999a,b) (see AFFECTIVE DISTRESS AND ANXIETY).
Patterns of decreased levels of education and increased rates of di-
vorce, obesity, and smoking have been noted in clinical and epidemi-
ological studies (Neumann and Buskila, 1998). Links to physical and
sexual abuse have been noted as well (see ABUSE). Major depression
as well as increased rates of depression, anxiety, and somatization are
also commonly found in fibromyalgia (see DEPRESSION, PSYCHIA-
TRY). Turk et al. (1998) suggest that customizing
fibromyalgia treatment based on patients’ psychosocial
Q needs will lead to enhanced treatment efficacy.
quality of life: Quality of life is significantly affected in

patients with rheumatic diseases, such as fibromyalgia, rheumatoid
arthritis, and Sjogren’s syndrome (Buskila et al., 1997; Ruiz Moral et
al., 1997; Strombeck et al., 2000). Comorbid conditions such as anxi-
ety and depression further affect quality of life (Kurtze et al., 1999).
Schlenk et al. (1998) found that fibromyalgia patients had compara-
ble quality-of-life scores to patients with chronic obstructive pulmo-
nary disease, AIDS, or urinary incontinence, and worse than patients
with prostate cancer or hyperlipidemia. Wolfe and Hawley (1997)
found that fibromyalgia patients have lower quality-of-life scores
compared to patients with rheumatoid arthritis or osteoarthritis. Pa-
tients’ perceptions and coping styles also determine quality of life
(Soderberg et al., 1997). Neumann and Buskila (1997) reported that
the quality of life and physical functioning of the relatives of fibro-
myalgia patients were impaired, especially for female relatives and
those with undiagnosed fibromyalgia, a finding that may be attrib-
uted to the psychological distress in families of fibromyalgia patients
and to the high prevalence (25 percent) of undiagnosed fi-
bromyalgia among relatives.
R Raynaud’s phenomenon: Raynaud’s phenomenon has

also been reported among patients with fibromyalgia (Grassi
et al., 1998).
rehabilitation: After an extensive review of the literature,

Karjalainen et al. (2000) concluded that there appears to be little sci-
entific evidence for the effectiveness of multidisciplinary rehabilita-
tion for musculoskeletal disorders, including fibromyalgia. However,
multidisciplinary rehabilitation is a commonly used intervention for

chronic musculoskeletal disorders (Epifanov and Epifanov, 2000),
which cause much personal suffering and substantial economic loss
to the society (Berg et al., 1998). Buckelew et al. (1996) found that
higher levels of self-efficacy are associated with better outcome and
may mediate the effectiveness of rehabilitation-based treatment pro-
grams for fibromyalgia. There is a need for high quality trials in this
field.
rhinitis: Rhinitis symptoms are present in approximately 70 percent

of subjects with fibromyalgia and chronic fatigue syndrome (FM/
CFS). Because only 35 percent to 50 percent have positive allergy
skin tests, nonallergic mechanisms may also play a role. Baraniuk
et al. (1998) found no differences in the basal secretion of markers of
vascular permeability, submucosal gland serous cell secretion, and
eosinophil and neutrophil degranulation in nonallergic FM/CFS sub-
jects. Irritant rhinitis has been associated with FM/CFS (Baraniuk et
al., 2000).
ritanserin: Ritanserin is a long-acting serotonin (5-hydroxy-

tryptamine) 2 (5-HT2)-receptor blocker. In a sixteen-week study of
fifty-one female fibromyalgia patients, Olin et al. (1998) found that,
at the end of the study, there was an improvement in feeling refreshed
in the morning in the ritanserin-treated group and that headache was
also significantly improved compared with the placebo group. There
was no difference in pain, fatigue, sleep, morning stiffness, anxiety,
and tender point counts in the ritanserin and placebo groups. Fifty-
one percent of the fifty-one patients had at least one of the three anti-
bodies to 5-HT, Gm1, and phospholipids. The incidence and activity
of these antibodies were not influenced by ritanserin or placebo. The
observation that ritanserin has only a small effect on clinical symp-
toms indicates that disturbances in serotonin metabolism or uptake
may be only one factor in the pathogenesis of the disease.
rubella vaccines: The National Vaccine Injury Compensation Pro-

gram and the United States Court of Federal Claims have accepted a
causal relationship between currently used rubella vaccine in the
United States and some chronic arthropathy with an onset between
one week and six weeks after vaccine administration. Fibromyalgia
was reported in four out of seventy-two subjects with chronic

arthropathy developing between one week and six weeks after the ru-
bella vaccination, and in eleven out of fifty-two individuals in whom
chronic arthropathy developed in less than one week or greater than
six weeks postvaccination (Weibel and Benor, 1996).
S S-adenosyl-L-methionine: A short-term crossover study

by Volkmann et al. (1997) on thirty-four fibromyalgia pa-
tients showed no effect of intravenous administration of
600 mg for ten days of S-adenosyl-L-methionine (SAMe). Tavoni et
al. (1998) also failed to demonstrate statistically significant effects of
SAMe on secondary fibromyalgia.
saliva: Because of accessibility, measurement of neuropeptides in

human saliva could provide a valuable tool for study of patients with
chronic painful disorders, such as rheumatoid arthritis, osteoarthritis,
and fibromyalgia (Fischer et al., 1998).
sarcoid arthritis: Gran and Bohmer (1996) reported the develop-

ment of secondary fibromyalgia in two patients with sarcoid arthritis.
Although acute sarcoid arthritis is usually a self-limiting joint dis-
ease, recurrences may occasionally occur and some cases develop
chronic sarcoidosis of the lungs.
scleritis: Fan and Florakis (1996) presented a case report of a patient

with scleritis and fibromyalgia and proposed that additional cases
might suggest that fibromyalgia be added to the list of etiologies of
scleritis.
selective serotonin reuptake inhibitors (fluoxetine, citalopram):

Several authors have recommended the use of selective serotonin
reuptake inhibitors (SSRIs), such as fluoxetine (Prozac), in the man-
agement of chronic pain and fibromyalgia (Anderbeg et al., 2000;
Chambliss, 1998; Nerhood, 1998). However, Norregaard et al. (1995)
failed to find a positive effect for citalopram in fibromyalgia, and
Smith (1998) suggests that there is little evidence for the replacement
of tricyclic antidepressants with SSRIs in pain management. Based
on a review of the literature, Jung et al. (1997) concluded that it is un-
clear whether SSRIs are beneficial for migraine headaches, tension

headaches, diabetic neuropathy, or fibromyalgia and recommended
that it may be reasonable to reserve SSRIs for those who fail to re-
spond to other medications or who are intolerant of their side effects.
In a four-week trial of 20 mg fluoxetine and 25 mg of amitriptyline,
alone or in combination, Goldenberg et al. (1996) found that both
medications are effective treatments for fibromyalgia (pain, well-
being, sleep), and they work better in combination than either medi-
cation alone.
selenium: Reinhard et al. (1998) reported decreased serum concen-

trations of selenium among sixty-eight fibromyalgia patients in Ger-
many, although there was overlap in the range of concentrations as
compared to ninety-seven controls.
self-esteem: Johnson et al. (1997) in a study of thirty-six depressed

fibromyalgia patients found that they had a high need to gain self-
esteem through competence and others’ approval. This was com-
bined with a low basic sense of self-esteem. Nondepressed fibromy-
algia patients did not display this self-esteem pattern. Based on the
latter observations, Johnson et al. (1997) suggest that an emphatic
competence-dependent self-esteem is one vulnerability factor that, in
proper genetic and environmental conditions, increases susceptibility
to fibromyalgia and depression.
serotonin: Ernberg, Hedenberg-Magnusson, Alstergren, and Kopp,

(1999) found that serotonin is present in the human masseter muscle
both immediately following puncture and also in a subsequent steady
state and that it is associated with pain and allodynia. The origin of
the serotonin seems to be partly the blood, but peripheral release also
occurs (Sprott et al., 1998). Allodynia of orofacial muscles in patients
with temporomandibular disorder is significantly related to serotonin
concentration (Ernberg, Hedenberg-Magnusson, Alstergren, Lunde-
berg, et al., 1999). Ernberg et al. (1998) also found that there is a re-
duction of the ratio between initial serotonin and steady state level in
the painful masseter muscle after intramuscular glucocorticoid ad-
ministration to fibromyalgia patients, a reduction not present in local-
ized myalgia patients. Serotonin seems to be involved in the modula-
tion of local muscle microcirculation in fibromyalgia patients and in
hyperalgesia in localized myalgia patients (Ernberg et al., 1998; Wolfe

et al., 1997). A defect in serotonergic analgesia and a hyperalgesic
state are proposed as features common to headache and fibromyalgia
(Nicolodi et al., 1998). The benefit to both migraine and fibromyalgia
from inhibiting ionotropic N-methyl-D-aspartate receptor activity
implies that redundant hyperalgesia-related neuroplastic changes are
crucial for severe or chronic migraine and primary fibromyalgia
(Nicolodi et al., 1998). Serotonin substrate supplementation, via
L-tryptophan or 5-hydroxytryptophan, has been shown to improve
symptoms of depression, anxiety, insomnia, and somatic pains in a
variety of fibromyalgia patient cohorts (Juhl, 1998).
serotonin 3-receptor antagonists (Tropisetron, Ondansetron):

Serotonin (5-HT) 3-receptor antagonists are potent and highly selec-
tive competitive inhibitors of the 5-HT3-receptor with negligible af-
finity for other receptors. They are rapidly absorbed and penetrate the
blood-brain barrier easily (Wolf, 2000). 5-HT3-receptor antagonists
do not modify any aspect of normal behavior in animals or induce re-
markable changes of physiological functions in healthy subjects.
They are well tolerated over wide dose ranges; the most common side
effects in clinical use are headache and obstipation. Clinical efficacy
was first established in chemotherapy-induced emesis, and other es-
tablished indications are radiotherapy-induced and postoperative
emesis. Antiemetic efficacy results from a simultaneous action at pe-
ripheral and central 5-HT3-receptors. Other peripheral actions include
reduction of secretion and diarrhea caused by increased intestinal se-
rotonin content (e.g., in carcinoid syndrome), a limited antiarrhyth-
mic activity and a reduction of experimentally induced pain. CNS ef-
fects comprise anxiolysis, attenuation of age-associated memory
impairment, reduction of alcohol consumption in moderate alcohol
abuse, and an antipsychotic effect in patients with Parkinson psycho-
sis. In migraine, 5-HT3-receptor antagonists show moderate efficacy,
as well. Repeatedly demonstrated efficacy of 5-HT3-receptor antago-
nists in patients suffering from fibromyalgia raises the question for
the mechanism of action involved. Ligand binding at the 5-HT3-
receptor causes manifold effects on other neurotransmitter and neuro-
peptide systems. In particular, 5-HT3-receptor antagonists diminish
serotonin-induced release of substance P from C-fibers and prevent
unmasking of NK2-receptors in the presence of serotonin (Wolf,
2000). The effect of the 5-HT3-receptor antagonists is probable pri-

marily to limit the release of substance P, which acts as a pain and in-
flammatory mediator, and is itself released by the neurogenic inflam-
mation that occurs after the binding of serotonin to its corresponding
receptor (Stratz and Muller, 2000a,b). Intraarticular injection of the
5-HT3-receptor antagonist, tropisetron, results in improvement on dif-
ferent types of local rheumatic pain and inflammatory processes
(Stratz and Muller, 2000a,b). Intravenous administration of 2 mg of
tropisetron or oral administration of 5 mg daily are well tolerated and
result in reduction of pain associated with fibromyalgia (Farber et al.,
2000; Haus et al., 2000; Muller and Stratz, 2000; Papadopoulos et al.,
2000; Samborski et al., 1996) and improvement of comorbid depres-
sion (Haus et al., 2000). However, there are no clear biochemical
markers (including serum concentrations of serotonin, somatomedin
C, oxytocin, calcitonin-gene-related peptide, calcitonin, and chole-
cystokinin) associated with the effect of tropisetron in fibromyalgia
(Hocherl et al., 2000; Stratz and Muller, 2000a). Hrycaj et al. (1996)
found that the 5-HT3-receptor antagonist ondansetron also appears to
be effective in about 50 percent of fibromyalgia patients.
serotonin receptor gene: The T102 allele of the serotonin2A-recep-

tor gene might be involved in the complex circuits of nociception. Al-
though a study of 168 fibromyalgia patients failed to evince that the
T102C polymorphism is directly involved in the etiology of fibromy-
algia, it might be in linkage dysequilibrium with the true functional
variant, which has to be unraveled (Bondy et al., 1999).
serotonin transporter gene: A higher frequency of the S/S genotype

of the serotonin transporter gene (5-HTT) was found among sixty-
two fibromyalgia patients compared with 110 healthy controls (31 per-
cent versus 16 percent). The S/S subgroup exhibited higher mean lev-
els of depression and psychological distress. These results support
the notion of altered serotonin metabolism in at least a subgroup of fi-
bromyalgia patients (Offenbaecher et al., 1999).
serum nucleotide pyrophosphohydrolase: Another possible marker

tested for fibromyalgia was not specific per the study by Cardenal et al.
(1998), who found elevated levels of serum nucleotide pyrophospho-
hydrolase in patients with degenerative arthritis whether or not calcium
pyrophosphate crystals were present, in patients with either scleroderma

or fibromyalgia, and in patients receiving hemodialysis therapy or tak-
ing cyclosporine.
Sjogren’s syndrome: Sjogren’s syndrome, the second most common

autoimmune rheumatic disease, refers to keratoconjunctivitis sicca
and xerostomia resulting from immune lymphocytes that infiltrate
the lacrimal and salivary glands (Fox et al., 2000). Sjogren’s syn-
drome is included in the differential for the diagnosis for fibro-
myalgia, and the distinction between fibromyalgia patients with low
titer antinuclear antibodies and primary Sjogren’s syndrome remains
difficult (Fox, 1997; Fox et al., 1998). Giles and Isenberg (2000) re-
ported that fibromyalgia was present in nine out of seventy-four
(12 percent) patients with primary Sjogren’s syndrome compared
with eleven of 216 (5 percent) lupus patients and none of secondary
Sjogren’s syndrome patients. Giles and Isenberg (2000) also reported
that fatigue in patients with primary or secondary Sjogren’s syn-
drome is not due to the coexistence of fibromyalgia in most cases.
Dohrenbusch et al. (1996) found a higher prevalence of fibromyalgia
in Sjogren’s syndrome (44 percent among primary and 5 percent
among secondary Sjogren’s syndrome patients).
skinache syndrome: Chronic pain of unknown etiology, and charac-

terized by cutaneous trigger points, has been coined skinache syn-
drome (Bassoe, 1995). In contrast to fibromyalgia, skinache syndrome
has a simple and effective cure: subcutaneous injection of lidocaine.
sleep: Nonrestorative sleep is a prominent feature of fibromyalgia;

unrefreshing sleep occurs in 76 to 90 percent of fibromyalgia patients
compared with 10 to 30 percent of controls (Campbell et al., 1983;
Green, 1999; Hemmeter et al., 1995; Hench, 1996; Kempenaers
et al., 1994; Lugaresi et al., 1981; Moldofsky, 1989; Moldofsky et al.,
1975; Reilly and Littlejohn, 1993; Roizenblatt et al., 2001; Schaefer,
1995; Smythe, 1995; Smythe and Moldofsky, 1977; Wolfe and Cathey,
1983; Wolfe et al., 1990; Yunus et al., 1981). Fibromyalgia patients
report early morning awakenings, awakening feeling tired or un-
refreshed, insomnia, as well as mood and cognitive disturbances;
they may also experience primary sleep disorders, including sleep
apnea (Harding, 1998). Sleep disturbances contribute to overnight
pain and stiffness exacerbation and increased pain sensitivity in fi-

bromyalgia and other chronic musculoskeletal pain conditions
(Affleck et al., 1996; Agargun et al., 1999; Croft et al., 1994; Green-
berg et al., 1995; Hemmeter et al., 1995; Hirsch et al., 1994; Kryeger,
1995; Kryger and Shapiro, 1992; Leigh et al., 1998; Mahowald et al.,
1989; Moldofsky and Scarisbrick, 1976; Older et al., 1998; Roizen-
blatt et al., 1997; Scharf et al., 1998; Walsh et al., 1994; Wittig et al.,
1982), and poor sleep is associated with psychological distress and
cognitive dysfunction (Affleck et al., 1996; Côte and Moldofsky,
1997; Hansotia, 1996; Hyyppa and Kronholm, 1995; Paiva et al.,
1995; Phillips and Cousins, 1986; Pilowski et al., 1985; Shaver et al.,
1997).
Among the disruptions in sleep architecture in fibromyalgia pa-
tients, there is evidence for prolonged sleep latencies (Branco et al.,
1994; Horne and Shackeel, 1991), low sleep efficiency (Touchon
et al., 1988; Wittig et al., 1982), an increased amount of stage 1
non–rapid eye movement (non-REM) sleep (Anch et al., 1991; Branco
et al., 1994; Harding, 1998; Moldofsky et al., 1975; Sergi et al., 1999;
Shaver et al., 1997), the presence of alpha electroencephalographic
activity during non-REM sleep (Branco et al., 1994; Drewes, Gade,
et al., 1995; Drewes, Nielsen, et al., 1995; Flanigan et al., 1995; Har-
ding, 1998; MacFarlane et al., 1996; Moldofsky et al., 1975; Perlis et
al., 1997; Roizenblatt et al., 1997, 2001; Ware et al., 1986), a reduc-
tion in slow-wave sleep (Branco et al. 1994; Drewes et al., 1995,
1996; Horne and Shackeel, 1991; Touchon et al., 1988) and in REM
percentages (Branco et al., 1994), an increased number of arousals
(Branco et al., 1994; Clauw et al., 1994; Harding, 1998; Horne and
Shackeel, 1991; Molony et al., 1986; Shaver et al., 1997; Staedt et al.,
1993; Touchon et al., 1988), periodic breathing (Sergi et al., 1999) and
arterial oxygen desaturations (Alvarez-Lario et al., 1996), and restless
leg movements (Atkinson et al., 1988; Wittig et al., 1982; Yunus and
Aldag, 1996).
Lentz et al. (1999) reported that disruption of slow-wave sleep in
healthy volunteers, without reducing total sleep or sleep efficiency,
for several consecutive nights is associated with decreased pain
threshold, increased discomfort, fatigue, and the inflammatory flare
response in skin. Also, deep pain induced during sleep in normal con-
trols causes the alpha frequency rhythm, termed alpha-delta sleep
anomaly, which is seen in fibromyalgia patients and in normal con-

trols during stage 4 sleep deprivation (Fischler et al., 1997; Harding,
1998). These results suggest that disrupted sleep is probably an im-
portant factor in the pathophysiology of symptoms in fibromyalgia.
The association between sleep disturbances and pain and other
fibromyalgia symptoms has been challenged by several studies. Older
et al. (1998) found that three nights of delta-wave sleep interruption
caused no significant lowering of pain thresholds or serum insulin-
like growth factor 1 (IGF-1) in healthy volunteers, thereby conclud-
ing that the low levels of IGF-1 seen in fibromyalgia patients may re-
sult from chronic rather than acute delta-wave sleep interruption, or
may be dependent on factors other than disturbances of delta-wave
sleep. Tishler et al. (1997) also reported that sleep abnormalities and
fibromyalgia in primary Sjogren’s syndrome patients are frequent
and that their etiology might involve other mechanisms besides joint
pain or sicca symptomatology. Donald et al. (1996) reported that al-
though fibromyalgia was uncommon (2.7 percent) in patients with a
primary complaint of disturbed sleep and, in particular, patients with
sleep apnea, reduced physical activity was strongly associated with
reported pain symptoms.
Harding (1998) recommends that before prescribing pharmaco-
logic compounds aimed at modifying sleep, adequate pain control
and sleep habits should be achieved; tricyclic antidepressants, trazo-
done, zopiclone, and selective serotonin reuptake inhibitors may be
required (Touchon, 1995).
smoking: Ostensen and Schei (1997) reported that smoking was sig-
nificantly more frequent for Norwegian women reporting fibro-
myalgia. Anxiety and depression in fibromyalgia was associated with
higher consumption of cigarettes (Kurtze et al., 1998, 1999). Tobacco
use may adversely affect fibromyalgia (Aaron and Buchwald, 2000;
Jay, 2000).
social networks: In a cross-sectional, retrospective, case-control

study of twenty-five female fibromyalgia patients, Bolwijn et al.
(1996) found that, compared to twenty-five healthy controls, the so-
cial networks of fibromyalgia patients presented more linkages with
intimate friends, family members, and health care providers.
sphenopalatine blocks: Although sphenopalatine blocks have been

used to treat pain for more than eighty years, Janzen and Scudds
(1997), in a double-blind placebo-controlled study on sixty-one pa-
tients (forty-two with fibromyalgia and nineteen with myofascial
pain syndrome) failed to find support for this technique by showing
no statistical differences between the lidocaine and the placebo
groups.
spinal tracts: In the spinal cord, long descending pathways are

known to exist which modulate pain sensations by either inhibiting or
facilitating the discharges of spinal nociceptive neurons. Mense
(1998, 2000) has proposed that a dysfunction of the descending in-
hibitory pathways could mimic, to a large extent, the pain of fibromy-
algia. Dorsal descending systems are tonicly active and have a partic-
ularly strong inhibitory action on neurons that mediate pain from
deep tissues, and an impairment of their function is likely to lead to
spontaneous deep pain (because of an increased background activity
in nociceptive neurons supplying deep tissues); tenderness of deep
tissues (because of a lowered mechanical threshold of the same neu-
rons); and hyperalgesia of deep tissues (because of increased neuronal
responses to noxious stimuli).
Staphylococcus toxoid vaccine: Several studies have shown a posi-

tive effect of Staphylococcus toxoid vaccine in patients with fibromy-
algia and chronic fatigue syndrome (Andersson et al., 1998). For in-
stance, in a placebo-controlled study of twenty-eight patients who
fulfilled the criteria for both fibromyalgia and chronic fatigue syn-
drome, significant improvements in fatiguability and pain were seen.
In a follow-up study of twenty-three patients, the vaccine treatment
was continued for two to six years. Fifty percent were rehabilitated
successfully and resumed half-time or full-time work (Andersson
et al., 1998).
substance P: Substance P is a putative nociceptive transmitter. The

finding of significantly high levels of substance P in the cerebrospinal
fluid of fibromyalgia patients (Larson et al., 2000; Liu et al., 2000)
supports the impact of this neurotransmitter on both nociceptive and
antinociceptive mechanisms (Pongratz and Sievers, 2000). Sub-
stance P levels are also elevated in the serum of fibromyalgia patients
(Sprott et al., 1998). Schwarz et al. (1999) documented a strong nega-

tive correlation between serum substance P and 5-hydroxyindolacetic
acid (5-HIAA) as well as between substance P and tryptophan in
fibromyalgia patients. High serum concentrations of 5-HIAA and
tryptophan showed a significant relation to low pain scores. More-
over, 5-HIAA was strongly related to good quality of sleep, while
substance P was related to sleep disturbance (Schwarz et al., 1999).
In contrast to fibromyalgia, Evengard et al. (1998) found normal
levels of substance P in the cerebrospinal fluid of fifteen patients with
chronic fatigue syndrome, an observation that supports the notion
that fibromyalgia and chronic fatigue syndrome are different dis-
orders despite overlapping symptomatology.
Super Malic: In a study of twenty-four fibromyalgia patients who

were randomized to a fixed dose (3 tablets b.i.d.), placebo-controlled,
four-week-course pilot trial, followed by a six-month, open-label,
dose escalation (up to 6 tablets b.i.d.) trial, Russell et al. (1995) found
that Super Malic, a proprietary tablet containing malic acid (200 mg)
and magnesium (50 mg), is safe and may be beneficial in the treat-
ment of fibromyalgia patients. Further studies are necessary.
surgeries: ter Borg et al. (1999) found no differences in the fre-

quency of abdominal surgery between eighty newly diagnosed fe-
male fibromyalgia and forty-seven rheumatoid arthritis patients per-
formed before the formal diagnosis. In the rheumatoid arthritis group
more cholecystectomies were performed, probably due to the older
age of these patients, whereas in the fibromyalgia group there were
more hysterectomies (Wagener et al., 1997) and appendectomies
than in the rheumatoid arthritis group.
systemic lupus erythematosus: Fibromyalgia and systemic lupus

erythematosus (SLE) may be comorbid conditions (Bennett, 1997;
Godfrey et al., 1998; Handa et al., 1998; Lopez-Osa et al., 1999;
Romano, 1995, 1997; Wallace, 1995), and patients with SLE may be
at increased risk to develop secondary fibromyalgia (Grafe et al.,
1999). SLE is in the differential in the diagnosis of fibromyalgia
(Calvo-Alen et al., 1995). Health-related quality of life is impaired
both among women with fibromyalgia or SLE and with fibromyalgia
patients reporting greater impairment along several dimensions
(Da Costa et al., 2000). Bruce et al. (1999) documented that in an out-
patient population of SLE patients (eighty-one studied), fatigue se-
verity correlates with poor health status and a higher tender point
count. Wang et al. (1998) also reported that fatigue in SLE patients is
highly correlated with the presence of fibromyalgia and not with
lupus disease activity. In patients with SLE, factors associated with
quality of life and fibromyalgia seem to have a greater influence on
the severity of reported fatigue than does the level of current disease
activity (Abu-Shakra et al., 1999; Bruce et al., 1999; Gladman et al.,
1997; Petri, 1995). Akkasilpa et al. (2000) found that SLE patients
with fibromyalgic tender points are less likely to be good “copers.”
Although fibomyalgia and SLE may coexist, Gladman et al. (2000)
found that patients with inactive SLE demonstrate neurocognitive
dysfunction that is not associated with comorbid fibromyalgia or
with specific organ involvement or organ damage. Moreover, Taylor
et al. (2000) reported that only a minority (10 percent of 216 as-
sessed) of lupus patients with fatigue fulfill the American College of
Rheumatology criteria for fibromyalgia. In one study, fibromyalgia
symptomatology did not correlate with lupus severity
(Grafe et al., 1999).
T temporomandibular disorder: Patients with chronic fa-

tigue syndrome, fibromyalgia, myofascial pain syndrome,
and temporomandibular disorder (TMD) share many clini-
cal illness features such as myalgia, fatigue, sleep disturbances, im-
pairment in ability to perform activities of daily living as a conse-
quence of these symptoms, and other comorbid conditions (such as
irritable bowel syndrome, interstitial cystitis, and others) (Aaron et
al., 2000). Fibromyalgia and myofascial pain syndrome are causes of
TMD, and fibromyalgia patients often suffer from symptoms of
TMD with the intensity of local pain correlating with that of general
body pain (De Laat, 1997; Hedenberg-Magnusson et al., 1997, 1999;
Pennacchio et al., 1998; Stohler, 1999). Conversely, patients with
TMD and chronic facial pain may also manifest pain or increased
pain sensitivity at remote sites outside of the head and neck region
that may be secondary to impaired endogenous opioid systems
(Kashima et al., 1999; Korszun et al., 1998; Wright et al., 1997) or to
dysregulations in the hypothalamic-pituitary axis (Auvenshine,
1997). Miller et al. (1997) documented an unusual case of

temporomandibular disorder in the presence of both fibromyalgia
and Ehlers-Danlos syndrome. Plesh et al. (1996) point out that de-
spite the overlap between fibromyalgia, myofascial pain syndrome,
and temporomandibular disorder, they are distinct clinical entities,
and TMD patients show less evidence of distress than fibromyalgia
patients.
tender point pathophysiology: Tender points are areas of tender-

ness occurring in muscles, muscle-tendon junctions, bursa, or fat
pads. When tender points occur in a widespread manner, they are
usually considered characteristic of fibromyalgia, and the presence of
eleven out of eighteen tender points in defined locations in the body
serves as part of the diagnostic criteria for fibromyalgia (Quimby et
al., 1998; Sigal et al., 1998). Tender point examination is considered
superior to dolorimetry (Wolfe, 1997). However, Tunks et al. (1995)
reported that both dolorimetry and palpation are sufficiently reliable
to discriminate control patients from patients with myofascial pain
and fibromyalgia, but may not discriminate patients with myofascial
pain from those with fibromyalgia.
McIntosh et al. (1998) reported that at least three subjects should
be examined using three standards of reliability (80 percent, 85 per-
cent, and 90 percent) before certification is granted to a health care
professional. To minimize intrarater and interobserver variation in
tender point examination, Smythe (1998) developed a training pro-
gram that focused on learning to deliver 4 kg force as the pressure
used in tender point examinations. Smythe (1998) recommends that
these skills should be periodically refreshed to prevent drift into error.
Okifuji et al. (1997) also developed a standardized tender point ex-
amination protocol (Manual Tender Point Survey [MTPS]) as a diag-
nostic procedure to evaluate the tender point criterion for fibro-
myalgia syndrome (sensitivity of 88.57 percent and specificity of
71.43 percent, comparable to the sensitivity and specificity of the
1990 multicenter study). Based on a study of eighty-four fibromyal-
gia patients, Wolfe (1998) points out that positive control points are a
common feature (63 percent) in fibromyalgia and appear to be a
marker for a generally low pain threshold rather than a disproportion-
ate increase in severe symptoms or distress. Control point positivity
should not be used to disqualify a diagnosis of fibromyalgia, and
Wolfe (1998) suggests that their assessment should be abandoned in

the manual tender point examination.
Tender point scores are related to generalized pain and pain behav-
ior tendencies in fibromyalgia patients and do not independently re-
flect generalized psychological distress (Fassbender et al., 1997;
Nicassio et al., 2000) as had been suggested by some authors (Croft
et al., 1996; McBeth et al., 1999; Wolfe, 1997). In this respect, based
on a study of 113 fibromyalgia patients, Jacobs et al. (1996) con-
cluded that tender point scores and self-reported pain represent very
different aspects of pain in fibromyalgia, the former being a more ob-
jective finding less prone to be affected by the patient’s distress level.
In a study of twenty fibromyalgia patients, Jeschonneck et al. (2000)
found that vasoconstriction occurs in the skin above tender points in
fibromyalgia patients, an observation that supports the hypothesis
that fibromyalgia is related to local hypoxia in the skin above tender
points. In another study of twenty fibromyalgia patients, Sprott et al.
(2000) showed that acupuncture led to normalization of clinical pa-
rameters with improvement in microcirculation above tender points.
The latter observations stand in contrast with an earlier study of six-
teen fibromyalgia patients by Kosek et al. (1995), who found that
pressure-induced pain sensibility in fibromyalgia patients is not most
pronounced in muscle tissue and does not depend on increased skin
sensibility.
Tender points and fibromyalgia may be precipitated by infections
(Rea et al., 1999). Although tender points are a common, transient
finding associated with acute infectious mononucleosis, fibromyal-
gia is an unusual long-term outcome (Rea et al., 1999). Hormonal
changes may also affect tender points. For instance, Hapidou and
Rollman (1998) documented that the number of tender points identi-
fied by palpation was greater in the follicular (postmenstrual) phase
of the cycle as compared to the luteal (intermenstrual) phase in nor-
mally cycling women but not in users of oral contraceptives.
thyroid microsomal antibodies: In a cross-sectional study of forty-

to forty-two-year-old men and women (737 and 771, respectively),
Aarflot and Bruusgaard (1996) found that the prevalence of thyroid
microsomal antibodies was significantly higher in persons with
chronic widespread musculoskeletal complaints compared to those
without (16.0 percent versus 7.3 percent). The increase was restricted
to women, while thyroid function tests did not differ significantly be-
tween the two groups. Aarflot and Bruusgaard (1996) concluded that
the association between chronic widespread musculoskeletal pain
complaints and thyroid antibodies in women may reflect a subgroup
of patients in which thyroid autoimmunity, rather than thyroid func-
tion, is important.
tramadol: In a double-blind crossover study of twelve fibromyalgia

patients, Biasi et al. (1998) documented that during the first treatment
cycle effective control of spontaneous pain was achieved with the
centrally acting analgesic tramadol (100 mg ampule in 100 mL given
intravenously in 15 minute doses), which determined a reduction of
20.6 percent while with the placebo spontaneous pain increased by
19.8 percent. As a cautionary note, Freye and Levy (2000) reported
on a fibromyalgia patient who had taken tramadol for over one year
and stopped abruptly, resulting in the development of classical absti-
nence-like symptoms within one week. Patients should be advised of
such effects whenever they decide to stop intake or when their physi-
cian is planning to switch them to another medication. To avoid absti-
nence-like symptoms, doses should be slowly tapered down.
trauma: The concept that fibromyalgia may follow trauma is cur-

rently an area of intense debate within the medical field (Bohr, 1995;
Ferrari and Kwan, 1999; Ferrari and Russell, 1998; Fishbain and
Rosomoff, 1998; Link et al., 1996; “Nonarticular Rheumatism, Sports-
Related Injuries, and Related Conditions,” 1997; Pinals, 1997; Smith,
1998; White, Carette, et al., 2000; White, Ostbye, et al., 2000;
Wigley, 1998), and Aaron et al. (1997) and Gardner (2000) stress that
it is driven to a large extent by social and legal issues. Jenzer (1995)
reported that whiplash injury to the cervical spine rarely results in
disability, and, if so, it is only minor. Other authors support the lack of
an association between whiplash injury and fibromyalgia (Cohen and
Quintner, 1998; Gordon, 1997) despite an original article by Buskila
et al. (1997).
In a study by White et al. (2000), random samples of 287 Canadian
general practitioners, 160 orthopedists, 160 physiatrists, and 160
rheumatologists were surveyed as to whether they agreed with a diag-
nosis of fibromyalgia in a case scenario mailed to them, and what fac-
tors they considered to be important in the development of chronic,

generalized posttraumatic pain. More recent medical school gradu-
ates were more likely to agree with the fibromyalgia diagnosis. Or-
thopedists (28.8 percent) were least likely to agree, while rheuma-
tologists (83.0 percent) were most likely to agree. On multivariate
analysis, three factors predicted agreement with the diagnosis of fi-
bromyalgia: (1) number of fibromyalgia cases diagnosed by the re-
spondent per week; (2) patient’s sex; and (3) severity of initial inju-
ries. Two factors predicted disagreement: (1) force of initial impact;
and (2) patient’s precollision psychiatric history. The authors con-
cluded that future studies of the association between trauma and fi-
bromyalgia should identify potential cases outside of specialty clin-
ics, and baseline assessments should include some measurement of
personality, stress, and precollision physical and mental health.
treatment: Treatment of fibromyalgia is largely empirical, palliative

rather than curative, and symptom focused, although experience and
small clinical studies have proved the efficacy of some pharmacolog-
ical and nonpharmacological interventions from both conventional
and alternative medicine sources, usually in a combination that is also
sensitive to psychosocial factors (Akama, 2000; Bennett, 1995, 1996;
Bennett et al., 1996; Burckhardt et al., 1998; Buskila, 1999; Clauw,
2000; Cohn, 2000; Eisinger and Dupond, 1996; Huppert, 2000; Keel,
1999; Keel et al., 1998; Lamberg, 1999; Langer, 1995; Leventhal,
1999; Littlejohn, 1995; Lloyd, 2000; Louis et al., 1998; Mason et al.,
1998; McCain, 1996; Millea and Holloway, 2000; Muilenburg, 2000;
Muller et al., 2000; Parziale, 1999; Reilly, 1999; Richards and Cleare,
2000; Rossy et al., 1999; Russell, 1996; Sandstrom and Keefe, 1998;
Schachna and Littlejohn, 1999; Sim and Adams, 1999; Strobel et al.,
1998; Tanum and Malt, 1995; Thomas et al., 1999; Turk et al., 1998;
Wolfe, 2000; Zborovskii and Babaeva, 1996) (each therapeutic mo-
dality is discussed under the pertinent subheading). The presence of
fibromyalgia affects the effectiveness of pharmacologic treatment of
other diseases, such as rheumatoid arthritis (Wolfe, 1995). Develop-
ment of treatment outcome assessment instruments is also an intense
area of study (Alarcon and Bradley, 1998; Bakker et al., 1995; Finckh
et al., 1998; Hewett et al., 1995; Rutten-van Molken et al., 1995;
Zucker et al., 1997). Potential sources of bias in clinical trials include

flaws in subject selection and group allocation, inadequate random-
ization, incomplete blinding, errors in outcome measurement, and in-
appropriate analysis of data (White and Harth, 1996).
trigger points: Trigger points are defined as areas of muscle that are
painful to palpation and are characterized by the presence of taut
bands and the generation of a referral pattern of pain, while tender
points are areas of tenderness occurring in muscles, muscle-tendon
junctions, bursa, or fat pads. Trigger points, which typically occur in
a more restricted regional pattern than tender points, are indicative of
myofascial pain syndrome (Borg-Stein and Stein, 1996; Schneider,
1995). In some patients the two phenomena may coexist, and over-
lapping syndromes can occur (Hong and Hsueh, 1996). In appropri-
ately selected patients, it appears that myofascial trigger point injec-
tions can be helpful in decreasing pain and improving range of
motion in conjunction with a comprehensive exercise and rehabilita-
tion program (Hong and Hsueh, 1996; Jayson, 1996; Potter, 1997). In
contrast to tender points, trigger points often respond to manual treat-
ment methods, such as ischemic compression and various specific
stretching techniques (Schneider, 1995).
tryptophan: Tryptophan is the amino acid precursor of serotonin,

and the serotonergic system has been proposed to be connected to
pathophysiology of fibromyalgia (see NEUROENDOCRINOLOGY). In
agreement with the latter proposal, Schwarz et al. (1999) reported a
strong negative correlation between serum levels of serotonin and
tryptophan, and high serum concentrations of tryptophan showed a
significant relation to low pain scores. Therapeutic administration of
5-hydroxytryptophan (5-HTP), the intermediate metabolite of the es-
sential amino acid L-tryptophan in the biosynthesis of serotonin, has
been shown to be effective in treating a wide variety of
conditions, including depression, fibromyalgia, binge eat-
U ing associated with obesity, chronic headaches, and in-

somnia (Birdsall, 1998).
urine: Fibromyalgia may be associated with an increase
V presence of bacteria in the urine (Xie et al., 1998), an ob-

servation that has not been studied broadly.
venlafaxine: Dwight et al. (1998) reported that out of

eleven fibromyalgia patients who completed an open
eight-week trial with the antidepressant venlafaxine, six (55 percent)
experienced a greater or equal to 50 percent reduction of fibromyal-
gia symptoms. The presence of lifetime psychiatric disorders, partic-
ularly depressive and anxiety disorders, predicted a positive response
to venlafaxine. These findings suggest that it is important to assess
for comorbid psychiatric disorders in patients with fibromyalgia and
that venlafaxine may be helpful to some of these patients (Dryson,
2000).
virology: Buchwald et al. (1996) reported that seroprevalence and/or

geometric mean titer of antibodies to herpes simplex virus 1 and 2,
rubella, adenovirus, human herpesvirus 6, Epstein-Barr virus, cyto-
megalovirus, and Coxsackie B virus, types 1-6 were not useful in
evaluating patients presenting with chronic fatigue or in
any subset of these patients, including those with chronic
W fatigue syndrome or fibromyalgia.
weather: Quick (1997) points out that many people be-

lieve that weather conditions can influence joint pain, but
science offers no proof. If the phenomenon were real, cause-and-ef-
fect mechanisms might provide clues that would aid joint pain treat-
ment. Literature on the subject is sparse, conflicting, and vulnerable
to bias, and further physiologic investigations are not likely to pro-
duce useful information. However, for patients who believe that
weather can influence their pain, the causes may be un-
known, but the effect is real (Quick, 1997).
Z zolpidem: A dose-ranging, double-blind, placebo-con-

trolled, modified crossover study by Moldofsky et al.
(1996) concluded that although short-term treatment (six-
teen nights) with zolpidem (5 to 15 mg orally at bedtime) does not af-

fect the pain of fibromyalgia, it is useful for sleep and daytime energy
in this patient population (Rothschild, 1997).
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Berg D; Berg LH; Couvaras J; Harrison H. (1999). Chronic fatigue syndrome

and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: An
explanatory model and approach to laboratory diagnosis. Blood Coagulation
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Anticardiolipin antibodies in childhood rheumatic disorders. Lupus 7(8):551-
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Heller U; Becker EW; Zenner HP; Berg PA. (1998). [Incidence and clinical rele-
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relevanz von antikorpern gegen phospholipide, serotonin und ganglioside bei
patienten mit horsturz und progredienter innenohrschwerhorigkeit. HNO 46(6):
583-586.
Antipolymer Antibodies
Angell M. (1997). Antipolymer antibodies, silicone breast implants, and fibromyal-

gia. Lancet 349(9059):1171-1172; discussion 1172-1173.
Edlavitch SA. (1997). Antipolymer antibodies, silicone breast implants, and fibro-
myalgia. Lancet 349(9059):1170.
Ellis TM; Hardt NS; Atkinson MA. (1997). Antipolymer antibodies, silicone breast
implants, and fibromyalgia. Lancet 349(9059):1173.
Everson MP; Blackburn WD Jr. (1997). Antipolymer antibodies, silicone breast im-
plants, and fibromyalgia. Lancet 349(9059):1171; discussion 1172-1173.
Korn JH. (1997). Antipolymer antibodies, silicone breast implants, and fibromyal-
gia. Lancet 349(9059):1171.
Lamm SH. (1997). Antipolymer antibodies, silicone breast implants, and fibromy-
algia. Lancet 349(9059):1170-1171; discussion 1172-1173.
Wilson RB; Gluck OS; Tesser JR; Rice JC; Meyer A; Bridges AJ. (1999).
Antipolymer antibody reactivity in a subset of patients with fibromyalgia corre-
lates with severity. Journal of Rheumatology 26(2):402-407.
Antiserotonin Antibodies
Coplan JD; Tamir H; Calaprice D; DeJesus M; de la Nuez M; Pine D; Papp LA;

Klein DF; Gorman JM. (1999). Plasma anti-serotonin and serotonin anti-
idiotypic antibodies are elevated in panic disorder. Neuropsychopharmacology

20(4):386-391.
583-586.
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antikorper beim fibromyalgie-syndrom—ausdruck einer neuroendokrinologi-
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Olin R; Klein R; Berg PA. (1998). A randomised double-blind 16-week study of
ritanserin in fibromyalgia syndrome: Clinical outcome and analysis of auto-
antibodies to serotonin, gangliosides and phospholipids. Clinical Rheumatology
17(2):89-94.
Artists and Musicians
Hingtgen CM. (1999). The painful perils of a pair of pianists: The chronic pain of
Clara Schumann and Sergei Rachmaninov. Seminars in Neurology 19 (Suppl. 1):
29-34.
Martinez-Lavin M; Amigo MC; Coindreau J; Canoso J. (2000). Fibromyalgia in
Frida Kahlo’s life and art. Arthritis and Rheumatism 43(3):708-709.
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Ascorbigen
Bramwell B; Ferguson S; Scarlett N; Macintosh A. (2000). The use of ascorbigen in

the treatment of fibromyalgia patients: A preliminary trial. Alternative Medical
Reviews 5(5):455-462.
Attributions
Neerinckx E; Van Houdenhove B; Lysens R; Vertommen H; Onghena P. (2000).

Attributions in chronic fatigue syndrome and fibromyalgia syndrome in tertiary
care. Journal of Rheumatology 27(4):1051-1055.
Autoimmune Fatigue Syndrome
Itoh Y; Fukunaga Y; Igarashi T; Imai T; Yoshida J; Tsuchiya M; Fujino O;

Murakami M; Yamamoto M. (1998). Autoimmunity in chronic fatigue syn-
drome in children. Japanese Journal of Rheumatology 8(4):427-429.
Itoh Y; Hamada H; Imai T; Saki T; Igarashi T; Yuge K; Fukunaga Y; Yamamoto M;
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Autoimmunity 25(4):243-250.
Itoh Y; Igarashi T; Tatsuma N; Imai T; Yoshida J; Tsuchiya M; Murakami M;
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Itoh Y; Igarashi T; Tatsuma N; Imai T; Yoshida J; Tsuchiya M; Murakami M;
Fukunaga Y. (2000). Immunogenetic background of patients with autoimmune
fatigue syndrome. Autoimmunity 32:193-197.
Autonomic Dysfunction
Bou-Holaigah I; Calkins H; Flynn JA; Tunin C; Chang HC; Kan JS; Rowe PC.
(1997). Provocation of hypotension and pain during upright tilt table testing in
adults with fibromyalgia. Clinical and Experimental Rheumatology 15(3):239-
246.
Cohen H; Neumann L; Shore M; Amir M; Cassuto Y; Buskila D. (2000). Auto-
nomic dysfunction in patients with fibromyalgia: Application of power spectral
analysis of heart rate variability. Seminars in Arthritis and Rheumatism
29(4):217-227.
Kelemen J; Lang E; Balint G; Trocsanyi M; Muller W. (1998). Orthostatic sympa-
thetic derangement of baroreflex in patients with fibromyalgia. Journal of
Martinez-Lavin M; Hermosillo AG. (2000). Autonomic nervous system dysfunc-
tion may explain the multisystem features of fibromyalgia. Seminars in Arthritis
and Rheumatism 29(4):197-199.
Martinez-Lavin M; Hermosillo AG; Mendoza C; Ortiz R; Cajigas JC; Pineda C;
Nava A; Vallejo M. (1997). Orthostatic sympathetic derangement in subjects
with fibromyalgia. Journal of Rheumatology 24(4):714-718.
Martinez-Lavin M; Hermosillo AG; Rosas M; Soto ME. (1998). Circadian studies
of autonomic nervous balance in patients with fibromyalgia: A heart rate vari-
ability analysis. Arthritis and Rheumatism 41(11):1966-1971.
Sendrowski DP; Buker EA; Gee SS. (1997). An investigation of sympathetic hyper-
sensitivity in chronic fatigue syndrome. Optometry and Visual Sciences
74(8):660-663.
Tougas G. (1999). The autonomic nervous system in functional bowel disorders.
Canadian Journal of Gastroenterology 13 (Suppl. A):15A-17A.
Wilke WS; Fouad-Tarazi FM; Cash JM; Calabrese LH. (1998). The connection be-
tween chronic fatigue syndrome and neurally mediated hypotension. Cleveland
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Behcet’s Syndrome
Yavuz S; Fresko I; Hamuryudan V; Yurdakul S; Yazici H. (1998). Fibromyalgia in

Behcet’s syndrome. Journal of Rheumatology 25(11):2219-2220.
Benzodiazepine-Induced Hip Fracture
Robb-Nicholson C. (1998). I read in your June 1997 publication that one of the risk
factors for hip fracture is current use of long-acting benzodiazepines. Could you
list exactly which medications these are? I take Xanax and doxepin for fibromy-
algia. My pharmacist could find no evidence that either of these drugs depletes
bone calcium. How do they place me at increased risk for osteoporosis? Harvard
Women’s Health Watch 5(5):8.
Biofeedback
Buckelew SP; Conway R; Parker J; Deuser WE; Read J; Witty TE; Hewett JE; Mi-
nor M; Johnson JC; Van Male L; McIntosh MJ; Nigh M; Kay DR. (1998). Bio-
feedback/relaxation training and exercise interventions for fibromyalgia: A
prospective trial. Arthritis Care Research 11(3):196-209.
Mur E; Drexler A; Gruber J; Hartig F; Gunther V. (1999). [Electromyography bio-
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Wien Medizinishe Wochenschrift 149(19-20):561-563.
Sarnoch H; Adler F; Scholz OB. (1997). Relevance of muscular sensitivity, muscu-
lar activity, and cognitive variables for pain reduction associated with EMG bio-
feedback in fibromyalgia. Perception and Motor Skills 84(3 Pt. 1):1043-1050.
Borna Disease Virus
Kitani T; Kuratsune H; Fuke I; Nakamura Y; Nakaya T; Asahi S; Tobiume M;

Yamaguti M; Machii T; Inagi R; Yamanishi K; Ikuta K. (1996). Possible corre-
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fatigue syndrome. Microbiology and Immunology 40(6):459-462.
Nakaya T; Kuratsune H; Kitani T; Ikuta K. (1997). Demonstration on borna disease
virus in patients with chronic fatigue syndrome. Nippon Rinsho—Japanese
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Nakaya T; Takahashi H; Nakamura Y; Asahi S; Tobiume M; Kuratsune H; Kitani
T; Yamanishi K; Ikuta K. (1996). Demonstration of Borna disease virus RNA in
peripheral blood mononuclear cells derived from Japanese patients with chronic
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Wittrup IH; Christensen LS; Jensen B; Danneskiold-Samsoe B; Bliddal H; Wiik
(2000). A. Search for Borna disease virus in Danish fibromyalgia patients. Scan-
dinavian Journal of Rheumatology 29:387-390.
Botulinum Toxin
Paulson GW; Gill W. (1996). Botulinum toxin is unsatisfactory therapy for fibro-
myalgia. Movement Disorders 11(4):459.
Breast Implants
Angell M. (1997). Antipolymer antibodies, silicone breast implants, and fibromyal-

gia. Lancet 349(9059):1171-1172; discussion 1172-1173.
Blackburn WD Jr; Grotting JC; Everson MP. (1997). Lack of evidence of systemic
inflammatory rheumatic disorders in symptomatic women with breast implants.
Plastic and Reconstructive Surgery 99(4):1054-1060.
Bridges AJ; Anderson JD; Burns DE; Kemple K; Kaplan JD; Lorden T. (1996).
Autoantibodies in patients with silicone implants. Current Topics in Microbiol-
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Brown SL; Langone JJ; Brinton LA. (1998). Silicone breast implants and autoim-
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Cuellar ML; Gluck O; Molina JF; Gutierrez S; Garcia C; Espinoza R. (1995). Sili-
cone breast implant—associated musculoskeletal manifestations. Clinical Rheu-
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Edlavitch SA. (1997). Antipolymer antibodies, silicone breast implants, and fibro-
myalgia. Lancet 349(9059):1170.
Ellis TM; Hardt NS; Atkinson MA. (1997). Antipolymer antibodies, silicone breast
implants, and fibromyalgia. Lancet 349(9059):1173.
Everson MP; Blackburn WD Jr. (1997). Antipolymer antibodies, silicone breast im-
plants, and fibromyalgia. Lancet 349(9059):1171; discussion 1172-1173.
Friis S; Mellemkjaer L; McLaughlin JK; Breiting V; Kjaer SK; Blot W; Olsen JH.
(1997). Connective tissue disease and other rheumatic conditions following
breast implants in Denmark. Annals of Plastic Surgery 39(1):1-8.
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Korn JH. (1997). Antipolymer antibodies, silicone breast implants, and fibromyal-
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Lai S; Goldman JA; Child AH; Engel A; Lamm SH. (2000). Fibromyalgia, hyper-
mobility, and breast implants. Journal of Rheumatology 27(9):2237-2241.
Lamm SH. (1997). Antipolymer antibodies, silicone breast implants, and fibro-
myalgia. Lancet 349(9059):1170-1171; discussion 1172-1173.
Levenson T; Greenberger PA; Murphy R. (1996). Peripheral blood eosinophilia,

hyperimmunoglobulinemia A and fatigue: Possible complications following
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Levine P; Clauw DJ; Claman HC; Robertson AD; Ketch L. (2000). Silicone breast
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Martin L. (1999). Silicone breast implants: The saga continues. Journal of
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Peters W; Smith D; Fornasier V; Lugowski S; Ibanez D. (1997). An outcome analy-
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Romano TJ. (1996). Breast implants and connective-tissue disease. Journal of the
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Rosenberg NL. (1996). The neuromythology of silicone breast implants. Neurology
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Silverman S; Gluck O; Silver D; Tesser J; Wallace D; Neumann K; Metzger A;
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tomatic patients with breast implants and patients with fibromyalgia. Current
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Thomas WO III; Harper LL; Wong SW; Michalski JP; Harris CN; Moore JT;
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63(5):421-429.
Vasey FB. (1997). Clinical experience with systemic illness in women with silicone
breast implants: Comment on the editorial by Rose. Arthritis and Rheumatism
40(8):1545.
Vasey FB; Aziz N. (1995). Breast implants and connective-tissue diseases. New
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Wolfe F. (1999). “Silicone-related symptoms” are common in patients with fibro-
myalgia: No evidence for a new disease. Journal of Rheumatology 26(5):1172-
1175.
Wolfe F; Anderson J. (1999). Silicone-filled breast implants and the risk of fibro-
myalgia and rheumatoid arthritis. Journal of Rheumatology 26(9):2025-2028.
Young VL; Nemecek JR; Schwartz BD; Phelan DL; Schorr MW. (1995). HLA typ-
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Breathing
Alvarez-Lario B; Viejo Banuelos JL. (1997). [Sleep respiratory disorders in

fibromyalgia syndrome] Trastornos respiratorios del sueno en el sindrome de
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Ozgocmen S; Ardicoglu O. (1999). Reduced chest expansion in primary
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Sergi M; Rizzi M; Braghiroli A; Puttini PS; Greco M; Cazzola M; Andreoli A.
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Weiss DJ; Kreck T; Albert RK. (1998). Dyspnea resulting from fibromyalgia. Chest
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Calcitonin
Bessette L; Carette S; Fossel AH; Lew RA. (1998). A placebo controlled crossover
trial of subcutaneous salmon calcitonin in the treatment of patients with
fibromyalgia. Scandinavian Journal of Rheumatology 27(2):112-116.
Cancer Chemotherapy
Simonson N. (1996). [Can tamoxifen relieve fibromyalgia?] Kan tamoxifen lindra

fibromyalgi? Lakartidningen 93(5):340.
Warner E; Keshavjee al-N; Shupak R; Bellini A. (1997). Rheumatic symptoms fol-
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Carpal Tunnel Syndrome
Cimmino MA; Parisi M; Moggiana G; Accardo S. (1996). The association between

fibromyalgia and carpal tunnel syndrome in the general population. Annals of
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Perez-Ruiz F; Calabozo M; Alonso-Ruiz A; Ruiz-Lucea E. (1997). Fibromyalgia
and carpal tunnel syndrome. Annals of Rheumatic Diseases 56(7):438-439.
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Chemical Intolerance
Bell IR; Baldwin CM; Russek LG; Schwartz GE; Hardin EE. (1998). Early life
stress, negative paternal relationships, and chemical intolerance in middle-aged
women: Support for a neural sensitization model. Journal of Women’s Health
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Bell IR; Baldwin CM; Schwartz GE. (1998). Illness from low levels of environmen-
tal chemicals: Relevance to chronic fatigue syndrome and fibromyalgia. Ameri-
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Bell IR; Patarca R; Baldwin CM; Klimas NG; Schwartz GE; Hardin EE. (1998). Se-
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Bell IR; Szarek MJ; Dicenso DR; Baldwin CM; Schwartz GE; Bootzin RR. (1999).
Patterns of waking EEG spectral power in chemically intolerant individuals dur-
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Csef H. (1998). [The non-specific environmental syndromes MCS (multiple chemi-
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Fiedler N; Kipen HM; DeLuca J; Kelly-McNeil K; Natelson B. (1996). A controlled
comparison of multiple chemical sensitivities and chronic fatigue syndrome.
Psychosomatic Medicine 58(1):38-49.
Gibson PR; Cheavens J; Warren ML. (1998). Social support in persons with self-
reported sensitivity to chemicals. Research in Nursing and Health 21(2):103-
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Lohmann K; Prohl A; Schwarz E. (1996). Multiple chemical sensitivity disorder in
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Miller CS. (1999). Are we on the threshold of a new theory of disease? Toxicant-
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Rowat SC. (1999). Paraoxonase/MCS. Environmental Health Perspectives
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Shanklin DR; Stevens MV; Hall MF; Smalley DL. (2000). Environmental
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Slotkoff AT; Radulovic DA; Clauw DJ. (1997). The relationship between fibromy-
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Chiari Malformation
Bradley LA; Alarcon GS. (1999). Is Chiari malformation associated with increased
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Muller W; Kelemen J; Stratz T. (1998). Spinal factors in the generation of
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Chiropractic Treatment
Blunt KL; Rajwani MH; Guerriero RC. (1997). The effectiveness of chiropractic
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Hains G; Hains F. (2000). A combined ischemic compression and spinal manipula-
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Harper A; Liu D. (1998). The effectiveness of chiropractic management of
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Schneider M. (1998). The effectiveness of chiropractic management of fibromyal-
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Chlamydia
Machtey I. (1997). Chlamydia pneumoniae antibodies in myalgia of unknown

cause (including fibromyalgia). British Journal of Rheumatology 36(10):1134.
Chlorella Pyrenoidosa
Merchant RE; Carmack CA; Wise CM. (2000). Nutritional supplementation with
Chlorella pyrenoidosa for patients with fibromyalgia syndrome: A pilot study.
Phytotherapy Research 14(3):167-173.
Chronic Fatigue Syndrome
Baschetti R. (1997). Etiology of chronic fatigue syndrome. American Journal of

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Bazelmans E; Vercoulen JH; Swanink CM; Fennis JF; Galama JM; van Weel C;
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Bertolin JM; Calvo J. (1997). Chronic fatigue syndrome. To be or not to be?
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Buchwald D. (1996). Fibromyalgia and chronic fatigue syndrome: Similarities and
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Butler C; Rollnick S. (1996). Missing the meaning and provoking resistance: A
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Chalder T; Power MJ; Wessely S. (1996). Chronic fatigue in the community: A
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Cheung F; Lin KM. (1997). Neurasthenia, depression and somatoform disorder in a
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Clauw DJ; Chrousos GP. (1997). Chronic pain and fatigue syndromes: Overlapping
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Index
Index
5-HT3-receptor, 84-85 Alternative medicine, 5

5-hydroxyindolacetic acid (5-HIAA), Ambrogio, N., 64
89-90 American College of Rheumatology,
5-hydroxytrytophan (5-HTP), 96 criteria for fibromyalgia, 37,
IGF-1, 39, 43, 50-51 38
P450IID6 oxidative enzyme, 26 and acetaminophen use, 69
T102 allele, 85 and Behcet’s syndrome, 12
and disability, 30
and epidemiology, 33
Aarflot, T., 93 and fatigue, 91
Aaron, L.A., 79, 94 and fibromyalgia diagnosis, 48, 53
Abuse, 1 and hyperkalemic periodic paralysis,
Acasuso-Diaz, M., 53 48
Acetaminophen, 69 and joint hypermobility, 53
Acupuncture, 2-3, 5 American Pain Society, 62
Acute fatigue, 36 Amir, M., 77
Acute pain, 71 Amitriptyline, 6, 83
Adenosine 3'5'-phosphate Ammer, K., 58
phosphodiesterase, cyclic, 33 Amyotrophic lateral sclerosis, 73
Adenovirus, 97 ANA-negative children, 11
Adler, G.K., 66 ANA-positive children, 11
Adrenal androgens, hyposecretion of, Anderberg, U.M., 1, 68
26 Ankylosing spondylitis, 25
Adrenocorticotropic hormone (ACTH), Anthraquinones, 5
59, 65 Antibodies, 6-10
Adult growth hormone deficiency, 50 Anti-B2GPI antibodies, 8
Aerobic endurance, 35 Anticardiolipin antibody, 6-7
Affective distress and anxiety, 3 Antidepressants, 7, 79, 88, 97
Agargun, M.Y., 72 Antiganglioside antibodies, 9-10, 43
Agents, chemical intolerance, 17 Antinuclear antibody (ANA), 8, 11, 49
Aging, 4 Antiphospholipid antibodies, 8-9, 10, 43
Akinetic syndrome, 59 Antipolymer antibodies, 9
Akkasilpa, S., 24, 91 Anti-Sa, 11
Alcohol, 4 Antiserotonin antibodies, 9-10, 43
Alexander, R.W., 1 Anxiety, 3, 15, 42
Allergy, 4, 49-50 Ardicoglu, O., 15
Allodynia, 83 Arnold, L.M., 7
Aloe, 4-5 Arthralgias, absence of and EMS, 31
Aloe vera gel, 4-5 Arthritis, rheumatoid, 1, 9, 14, 25, 27
Alpha anomaly, 41, 87 Arthritis Impact Measurement Scales,
Alpha-adrenergic dominance, 33 28
191
Arthritis Self-Efficacy Scales, 28 Bolwijn, P.H., 88
Artist, 10 Bonaccorso, S., 49
Ascorbigen, 10 ter Borg, E.J., 90
Asthma, 25 Borman, P., 60
ATP level, 61 Borna disease virus, 13
Attributions, 10-11 Borrelia burgdorferi infection, 76
Atypical neurologic disease syndrome, Botulinum toxin, 13
15 Bou-Holaigah, I., 11
Atypical neurologic multiple sclerosis- Bramwell, B., 10
like syndrome, 15 Brattberg, G., 57
Audiovestibular dysfunction, 22 Breau, L.M., 54
Auditory perception, 49 Breast cancer, 16
Autoantibodies, presence of, 39 Breast implants, 9, 13-15, 39, 53
Autoantibody pattern, 7, 42 Breathing, 15-16
Autoimmune fatigue syndrome, 11 Bridges, A.J., 14
Autoimmunity, 14 Broccoli powder, 10
Automated twitch-obtaining Bromazepan, 69
intramuscular stimulation Bruce, I.N., 90
(ATOIMS), 52 Bruusgaard, D., 93
Autonomic dysfunction, 11-12 Buchwald, D., 51, 97
Avoidance of thoughts, and PTSD, 77 Buckelew, S.P., 13
Avon, S.L., 26 Bujak, D.I., 76
Burgunder, J.M., 59
Buskila, D., 42, 50, 80, 94
Back pain. See Lower back pain
Bailey, D.R., 70
Barkhuizen, A., 47
Barth, H., 31 Calcitonin, 16
Basal ganglia, 59 Calcitonin gene-related peptide
Behavioral intervention, 25, 54 (CGRP), 61
Behcet’s syndrome, 12 Canadian general practitioners, 94
Bellometti, S., 59 Cancer chemotherapy, 16
Bendtsen, L., 44 Capen, Karen, 29
Benign joint hypermobility syndrome, Capsular (K) serotypes, 55
39 Carbon monoxide, transfer pattern, 15
Benjamin, S., 78 Cardenal, A., 85
Bennett, A.L., 51 Cardiorespiratory fitness, 40
Bennett, R.M., 43, 47 Carlsson, S.G., 3, 79
Benzodiazepine-induced hip fracture, 12 Carpal tunnel syndrome, 15, 16, 47
Berg, D., 8 Cashman, N.R., 76
Berg, P.A., 7, 9, 42, 46 Castiglione delle Stiviere (Mantova,
Beta-endorphin serum level, 59 Italy), 32
Biasi, G., 94 CD8 cell suppression, 50
Biochemically identified species, 56 Celiker, R., 3
Biofeedback/relaxation, 13 Cell-mediated immunity, 49
Blackburn Jr., W.D., 14 Cellulitis, 72
Bladder pain, 52 Centers for Disease Control and
Blepharitis, 55 Prevention (CDC), 20
Blood pressure, drop in, 12 Central nervous system, chronic pain
Bohmer, E., 82 within, 59
Index 193
Central nervous system serotonin Corticotropin-releasing hormone
neuronal alterations, 10 (CRH), 65
Cerebrospinal fluid (CSF), 78 Cortisol, 25, 59, 64, 65
C-fiber nociceptors, 61 Coxsackie B virus, 97
Chang, L., 52 Crofford, L.J., 68
Chemical intolerance (CI), 16-18, 39 Crohn’s disease, 50
Chemotherapy, 16 Cryotherapy, 25-26
nausea, 2 Cyclosporine, 85
Chest pain, noncardiac, 52 Cytochrome-c-oxidase, 60
Chiari malformation, 18 Cytomegalovirus, 97
Childhood abuse, 1
Chiropractic treatment, 18-19
Chlamydia, 19
Chlorella pyrenoidosa, 19 De Lorenzo, F., 74
Chronic fatigue immune dysfunction Debrisoquine/sparteine polymorphism,
syndrome, 20 26
Chronic fatigue syndrome, 19-22 Deconditioning, 60, 61
Chronic pain, 71 Dehydroepiandrosterone sulphate, 26, 65
and childhood abuse, 1 Delayed-type hypersensitivity response,
Chronic widespread pain (CWP), 78 50
Chu, J., 52 Delta-wave sleep interruption, 51
Chun, A., 53 Dental pain, postoperative, 2
Cimino, R., 57 Dentistry, 26
Circadian system, desynchronization Deoxypyridinoline (Dpyd), 24
of, 58 Department of Veterans Affairs, 30
Citalopram, 82-83 Depression, 3, 7, 13, 15, 23, 27, 79
Citera, G., 58 Dermatomyositis, 15
Clark, P., 32 Dessein, P.H., 26, 51
Clifford, P., 25 Diabetes, 74
Clinical trials, bias in, 95 Diffuse pain syndromes, 72
Cogan I syndrome, 22 Dinser, R., 43
Cognitive function, 23-24 Dipeptidyl peptidase IV (DPP IV), 77
Cognitive impairment, 14 Disability, 27-30
Cognitive-behavioral therapy, 22-23 Disorders
Cole, S.W., 50 in CI patients, 17
Collagen, 24 and fibromyalgia, 39
Collagen vascular disease, 13 Distress, 3
Compensation, insurance, 29-30 Dizziness, 30-31
Complementary medicine, 5 Dohrenbusch, R., 46, 86
Conditioning, behavioral mechanism, 17 Donald, F., 88
Connick, E., 62 Dorsal descending system, 89
Contaminated L-tryptophan intake, 31 Dry eyes, 55
Control point positivity, 92 Dry needling, 2, 56
Coordination, lack of, 10 Dupuytren’s contractures, 4
Coping, 24-25, 91 Dwight, M.M., 97
Coplan, J.D., 10 Dyspnea, 16
Copper, 25 Dysthymia, 79
Cortico-thalamo-nigro-striatal system, 59 Dysuria, 52
Edema, and EMS, 31 Finestone, H.M., 1
Educational/attention control program, Fischbach, M., 74
13 Fischler, B., 3
Effort, 31 Fitness, 40
Ehlers-Danlos syndrome, 31, 91 Fitzcharles, M.A., 5, 38
Eisinger, J., 57, 78 Flare reaction, 61
Elderly, 4 Florakis, G.J., 82
Electrical stimuli, detection of, 49 Fluoxetine, 82-83
Electrical twitch-obtaining Follicle-stimulating hormone (FSH), 65
intramuscular stimulation Free triiodothyronine (FT3), 65
(ETOIMS), 52 Frequent urination, 52
Electroacupuncture, 2-3 Freye, E., 94
Electromyography (EMG), 13 Functional bowel disease, 50
Enestrom, S., 67 Functional Impact Questionnaire, 28
Eosinophilia-myalgia syndrome (EMS), Functional impairment, 27-30
31 Functional somatic syndromes, 41
Epidemiology, 31-33
Epstein, S.A., 79
Epstein-Barr virus, 20, 33, 97
Erb gene, 33-34 G proteins, inhibitory, 33
Ergonomics, 34 Gallhofer, B., 27, 78
Ernberg, M., 43, 71, 83 Galzigna, L., 59
Erythrocyte sedimentation rate (ESR), Gamma-hydroxybutyrate, 41
8, 34 Ganglioside, 7
Escalante, A., 74 Gardner, G.C., 94
Esdaile, J.M., 5, 38 Gastrointestinal problems, 11, 12
Estrogen, 65 Gedalia, A., 8, 54
Evaluation of Daily Activity Gender, 41-42
Questionnaire (EDAQ), 28 Generalization, behavior mechanism,
Evengard, B., 19, 90 17
Exercise, 13, 34-35, 54, 70 Generalized pain, 72
Genetics, 8, 25, 38, 42-43
and hystocompatibility linkage, 47
Geriatrics, 4
Fallon, J., 76 Gibson, T., 33
Family members, of CFS patients, 8 Giles, I., 86
and genetics, 42-43 Gill, W., 13
Fan, N.I., 82 Giovengo, S.L., 64
Farooqi, A., 33 Gladman, D.D., 91
Fatigue, 8, 11, 14, 20, 35-36 Glucocorticoid, 43
Fatty acids, 5 Goldberg, R.T., 1
Federal University of Sao Paulo, Goldenberg, D., 83
Rheumatology Division, 30 Goldman, S.I., 74
Feldman, D., 29 Goossens, M.E., 23
Female gender, 1, 41-42 Gordon, D.A., 28
and Behcet’s syndrome, 12 Gotze, F.R., 48
and gynecology, 44 Gowans, S.E., 35
Fibromyalgia, 36-40 Grace, G.M., 23
Fibromyalgia Impact Questionnaire, 76 Grady, E.P., 73
“Fibrositis,” 39 Gran, J.T., 32, 82
Figuerola, M.L., 56 Graven-Nielsen, T., 55, 60
Index 195
Growing pains, 54 Hydrocortisone, 48
Growth hormone (GH), 43-44, 50, 64 Hydroxypyroline (Hyp), 24
Growth hormone-insulin-like growth Hyperalgesia, 45, 56, 61
factor-1 (IGF-1) axis, 39, 43 Hypercalcemia, 48
Growth hormone-releasing hormone Hyperkalemic periodic paralysis, 48
(GHRH), 51, 65 Hypermobility, 53
Gulf War syndrome, 17, 20, 39, 73-74 Hypersensitivity myofascial syndrome,
Gunaydin, I., 55 2
Gynecology, 44 Hyperthyroidism, 48
Hypervigilance, 48-49, 53
Hypnosis, 49
Hair electrolytes, 44 Hypnotic analgesia, 49
Hallberg, L.R., 3, 79 Hypoalgesia, 53
Hamilton Depression Rating Scale, 77 Hypocortisolism, 25
Hannonen, P., 59 Hypoglycemia, 66
Hansson, P., 72 Hypothalamic-pituitary-adrenal (HPA)
Hapidou, E.G., 66, 93 axis, 18, 25, 59, 65
Harden, R.N., 62
Harding, S.M., 88
Hawley, D.J., 29, 79, 80 IgE level, 4
Headache, 34, 44-45, 52 IGF-binding protein-3 (IGFBP3) levels,
Hearing, 45-46 51
Hearing loss, 10 Immunoglobulin (Ig)G deposits, 68
Heart rate, increase in, 66 Immunology, 49-50
Heir, G.M., 70 Impaired detoxification, 26
Helfenstein, M., 29 Impaired porphyrin metabolism, 18
Heller, U., 9, 10, 46 Infection, tender points and, 93
Hellstrom, O., 24 Inflammatory bowel disease, 50
Hemodialysis therapy, 85 Inflammatory eye changes, 22
Henriksson, C., 28 Inflammatory response system
Hepatitis C virus (HCV), 46-47, 51 activation, 49
Herpes simplex virus 1 and 2, 97 Inflammatory spinal pain, 50
Hingtgen, C.M., 10 Insecure attachment, 79
Hip fracture, 12 Insulin-like growth factor-1 (IGF-1),
Histocompatibility linkage, 47 39, 43, 50-51, 65, 88
HLA-B61, 11 Insurance compensation, 29-30
HLA-DR2, 11 Interferon-alpha, 51, 64
HLA-DR9, 11 Interleukin (IL)-6, 14, 65
HLA-DR53, 14 Interleukin-8, 14
Homeopathy, 47 Interstitial cystitis, 52
Homocysteine, 47 Intramuscular stimulation, 52
Hormonal change, tender points Irritable bowel syndrome, 12, 52-53
and, 93 Isenberg, D., 86
Hrycaj, P., 85 Isotonic saline, 16
Huber, M., 29 Itoh, Y., 11
Hudson, N., 53 Ivanichev, G.A., 59
Human adjuvant disease, 15
Human herpesvirus 6, 97
Human leukocyte antigen (HLA) Jacobs, J.W., 93
region, 42, 47 Jacobsen, S., 51, 60
Hyaluronic acid, 47-48 Janzen, V.D., 88
Jenzer, G., 94 Lowe, J.C., 33
Jeschonneck, M., 93 Lower back pain
Johnson, M., 83 and acupuncture, 2
Joint hypermobility, 53 and Chiari malformation, 18
Joint pain, 76, 97 and cryotherapy, 25
Jung, A.C., 82 and ergonomics, 34
Juvenile fibromyalgia (JF), 53-55 and irritable bowel syndrome, 52
Juvenile rheumatoid arthritis (JRA), 54 and Persian Gulf War syndrome, 74
Low-grade fever, 11
Low-intensity walking, 35
Kahlo, Frida, 10 Luteinizing hormone-releasing
Karaaslan, Y., 53 hormone (LHRH), 65
Karjalainen, K., 80 Lyme disease, 70, 76
Katz, R.S., 79 Lymphocytes immunophenotypes, 49
Keel, P., 78
Kelley, P., 25
Keratoconjunctivitis sicca, 55, 86 MacFarlane, G.J., 73
Ketamine, 55 Macrophagic myofasciitis, 38
Kindling, 17 Maes, M., 66, 75, 77
Klebsiella, 55-56 Magnesium, 57, 90
Klein, R., 7, 8, 42, 46 Mailis, A., 29
Korszun, A., 58 Malic acid, 90
Kosek, E., 71, 93 Maltreatment, 1
Kravitz, H.M., 79 Manipulative therapy, 5
Krings, M.S., 74 Mannerkorpi, K., 34
Kujala, U.M., 54 Manual Tender Point Survey (MTPS), 92
Kurtze, N., 3, 27 Marbach, J.J., 63, 67
Marin, R., 62
Martin, L., 35
Lai, S., 53 Martin, M.Y., 24-25
Landro, N.I., 23 Martinez-Lavin, M., 10
Laroche, M., 74 Massage, 57
Laser therapy, 56 Masticatory myofascial pain, 57
Lautenbacher, S., 71 McDermid, A.J., 48
Leal-Cerro, A., 43, 50-51 McIntosh, M.J., 92
Leiomyosarcoma, 56 Medical Outcomes Study Short-Form
Lekander, M., 64 General Health Survey
Lemley, K.J., 35 (SF-36), 28
Lentz, M.J., 87 Medicinal baths, 57-58
Leukocyte count, high and EMS, 31 Meiworm, L., 35
Levy, J., 94 Melatonin, 58
Lidocaine, 56 Melegos, D.N., 78
Liedberg, C., 28 Melnizky, P., 58
Light treatment, 56-57 Memory loss, 14, 23
Lipid droplets, 60 Meningoencephalomyelitis, 13
Long, J.A., 30 Mense, S., 89
Longo, L., 56 Metzger, D., 25
Lorenz, J., 49 Meyer, B.B., 35
Low-affinity thyroid hormone Meyer-Lindenberg, A., 27, 78
receptors, 33 Microcirculation, 2
Index 197
Microscopists, and ergonomics, 34 Natural killer (NK) cells, 63-64
Migraine. See Headache Natvig, B., 40
Miller, C.S., 18 Nausea, 2
Miller, T.A., 36 Neck support, 64
Miller, V.J., 91 Neerinckx, E., 10-11
Mind-body techniques, 5, 23 Nerve growth factor, 64
Mitochondria, 60 Netherlands, fibromyalgia prevalence
Mitochondrial myopathy, 58 in, 32
Mobilisin, 69 Neumann, L., 42, 80
Moclobemide, 7, 59 Neurally mediated hypotension, 39
“Modified job,” 28 Neurasthenia, 20
Modified Stanford Health Assessment Neuroendocrine mediators, 71
Questionnaire, 28 Neuroendocrinology, 64-67
Moldofsky, H., 97 Neurogenic inflammation, 18, 67-68
Mood-altering activity, 6 Neuroimaging, 68
Moorkens, G., 57 Neurokinin A., 61
Morris, V., 71 Neuropeptide Y (NPY), 68
Morriss, R.K., 27 Neuropsychiatric disease, 13
Motor cortical dysfunction, 59 Neurotic anxiety, 42
Mountz, J.M., 68 Nicassio, P.M., 23
Mud packs, 59 Nielens, H., 40
Mukhopadhyay, P., 75 Nightmares, and PTSD, 77
Muller, W., 18 NIH Consensus Conference, 2
Multidimensional Health N-methyl-D-aspartate (NMDA)
Questionnaire, 28 receptor antagonist ketamine,
Multidimensional Pain Inventory, 28, 55
77 Nociceptin, 68
Multifocal motor neuropathy, 15 Nocturnal urine 6-sulphatoxymelatonin
Multiple chemical sensitivity, 16-17, levels, 58
20, 39 Nodular texture, TrPs, 63
Multiple sclerosis, 15 Nonnociceptive pain, 71
Mur, E., 13 Nonphysician practitioners, 5
Muscle abnormalities, 60-62 Nonsteroidal anti-inflammatory drugs
Musculoskeletal disorder, 44 (NSAIDs), 69
Musculoskeletal pain, 8, 12, 53 “Nonvisible electromagnetic fields,” 56
Musicians, pain and, 10 Nordvag, B.Y., 32
“Myalgic encephalomyelitis,” 20 Norepinephrine (NE), 66
Mycoplasma, 62 Norregaard, J., 31, 60, 82
Mycoplasma fermentans infection, 62 Norway
Myoadenylate deaminase deficiency, 62 fibromyalgia prevalence in, 32
Myofascial pain syndrome (MPS), insurance compensation in, 29
62-63 and smoking, 88
Myofascial temporomandibular Nursing, 69
disorder, 42 Nutritional supplements, 19, 70
National Insurance Acts (1991, 1995), Ocular symptoms, 55

29 Oddi dysfunction, type III, 53
National Vaccine Injury Compensation Offenbaecher, M., 27, 75, 78
Program, 81 Okifuji, A., 44, 92
Older, S.A., 53, 88 Placebo versus amitriptyline, 6
Olin, R., 10, 81 Plain-water baths, 58
Olsen, N.J., 60 Plasma metenkephalin levels, 56
O’Malley, P.G., 7 Platelet alpha-2-adrenoreceptors, 75
Omega-3 fatty acids, 69 Plesh, O., 91
Ondansetron, 84-85 Polyarthritis, 16
Opioids, 69-70 Polyarthropathy, nondestructive, 16
Organic illness, 53 Poly/dermatomyosis, 9
Orofacial pain, 70 Polymyalgia rheumatica (PMR), 4, 75
Orthostatic hypotension, 6 Pongratz, D.E., 60
Orthostatic stress, 11 Postcardiac injury rheumatism (PIR),
Ostensen, M., 67, 88 75-76
Osteoarthritis, 9, 25 Post-Lyme disease syndrome, 76
Osteomalacia, 70 Postoperative nausea, 2
Osteoporosis, 12, 70 Postpartum, and fibromyalgia, 67
Ozgocmen, S., 15, 69 Postpolio syndrome, 76-77
Post-traumatic stress disorder (PTSD),
25, 77
Pain, 70-72 Posture, 18
Pain syndromes, 72-73 Pregnancy, and fibromyalgia, 67
Pain threshold, 48 Premenstruation, and fibromyalgia, 67
Pakistan, fibromyalgia in, 33 Press, J., 58
Pallido-thalamic level, 59 Prolactin, 66
Palmar fasciitis, 4 Proprioceptive desafferentation, 59
Panic disorder, 10 Proprioceptive disturbance, 45
Panniculosis, 72 Propyl endopeptidase (PEP), 77-78
Parietal-premotor level, 59 Prostaglandin D synthase (PGD), 78
Park, J.H., 60, 61 Prostaglandins, 5
Patellofemoral syndrome, 74 Protein peroxidation, 78
Paulson, G.W., 13 Prozac, 82
Pearl, S.J., 56 Psychiatry, 78-79
Pediatric fibromyalgia patients, 7, 9, Psychological stress, 12
11, 30, 53-54 Psychosocial factors, 79-80
Pediatric rheumatology, 53 Psychosomatic disease, fibromyalgia
Pelvic pain, 52 as, 29
Pentazocine-induced fibrous myopathy, Pyridinoline (Pyd), 24
73
Persian Gulf War syndrome, 17, 20, 39,
73-74 Quality of life, 80
Phenobarbital, 74 Quality of Life Scale, 28
Phosphate diabetes, 74 Quang-Cantagrel, N.D., 69
Phosphocreatinine level, 61 Quick, D.C., 97
Phospholipids, 7
Phosphorus magnetic resonance
spectroscopy, 60
Physical assault, 1 Rachmaninov, Sergei Vassilievich, 10
Physical therapy, 74-75 Radiculopathy, 15
Pierau, F.K., 61 Ramsay, C., 35
Pillows, 64 Raphael, K.G., 63, 67
Pima indians, and fibromyalgia, 33 Rapid-eye movement sleep, 6
Index 199
Raynaud’s phenomenon, 80 Saliva, 82
Recall, delayed, 23 Salmon calcitonin, 16
Recollection, and PTSD, 77 Samborski, W., 49, 65
Referrals, fibromyalgia, 32-33 San Pedro, E.C., 68
Reflex changes, 14 Sann, H., 61
Reflex-sympathetic dystrophy, 4 Sarcoid arthritis, 82
Reginato, A.J., 70 Sardini, S., 32
Regional cerebral blood flow (rCBF), Sarnoch, H., 13
68 Savelkoul, M., 24
Regland, B., 47 SBIs (silicone breast implants), 9,
Rehabilitation, 80-81 13-15
Reid, G.J., 55 Schanberg, L.E., 25, 54
Reinhard, P., 83 Schedule for Rating Disabilities,
Respiratory patterns, 15-16 Department of Veterans
Rheumatic conditions Affairs, 30
and disability, 27 Schei, B., 88
and hepatitis C, 46-47 Schepelmann, K., 45
and homeopathy, 47 Schizophrenia, 13
and inflammatory bowel Schlenk, E.A., 80
disease, 50 Schumann, Clara Wieck, 10
and joint hypermobility, 53 Schwarz, M.J., 89, 96
and laser therapy, 56 Scleritis, 82
and juveniles, 53-54 Scleroderma, 85
and Persian Gulf War Scudds, R.A., 56, 88
syndrome, 74 Secondary fibromyalgia, 90
Rheumatoid arthritis Selective serotonin reuptake inhibitors
and abuse, 1 (SSRIs), 82-83
and antipolymer antibodies, 9 Selenium, 83
and breast implants, 14 Self-esteem, 83
and cryotherapy, 25 Self-help group, 11, 35
and disability, 27 Sensory loss, 10, 14
and juveniles, 54 Sergi, M., 15
and quality of life, 80 Serotonergic analgesia, 45
Rheumatoid factor, 8 Serotonin, 7, 64, 71, 83-84
Rhinitis, 81 Serotonin receptor gene, 85
Ridgway, K., 2 Serotonin (5-HT) 3-receptor
Ritanserin, 81 antagonists, 84-85
Roizenblatt, S., 54 Serotonin reuptake inhibitors, 88
Rollman, G.B., 66, 71, 93 Serotonin transporter gene, 42, 85
Romano, T.J., 51 Serotonin2A-receptor gene, 85
Rosenhall, U., 45-46
Rubella vaccines, 81-82, 97 Serum androgen level, decrease in, 26
Rubro-segmental level, 59 Serum nucleotide
Russell, I.J., 51, 64, 90 pyrophosphohydrolase, 85
Rusy, L.M., 30 Sex hormones, 66
Sexual abuse, childhood, 1
Sham acupuncture groups, 2
Shanklin, D.R., 18
Saccharides, 5 Shape of Sleep pillow, 64
S-adenosyl-L-methionine (SAMe), 82 Sherman, J.J., 77
Salerno, A., 59 Short-term pain reduction, 26
Sicca complex, 52 Spondyloarthritis, 38
Sick building syndrome, 17, 39 Spondylosis, 16
Silicone breast implantation (SBIs), 9, “Spray and stretch,” 62
13-15, 39, 53 Sprott, H., 2, 24, 61
Silicone encephalopathy, 15 S/S genotype, 85
Simms, R.W., 60 Staphylococcus toxoid vaccine, 89
Singh, B.B., 23 Starosel’tseva, N.G., 59
Sinsawaiwong, S., 73 Stiffness, 7
Six-minute walk, 28 Stone, R.G., 45
Sjogren’s syndrome, 55, 80, 86 Straub, T.A., 16
Skeith, K.J., 26 Stress, 25
Skevington, S.M., 3 psychological vulnerability to, 1
Skin test, allergic, 4 Stress-response system, 39
Skinache syndrome, 86 Stretching exercises, 35
Sleep, 86-88 Strio-piramidal level, 59
anomaly, 6, 87 Stucki, G., 75
delta-wave interruption, 51 Suarez-Almazor, M.E., 8, 34
and juvenile fibromyalgia, 54 Substance P, 19, 61, 64, 89-90
and light treatment, 56-57 Super Malic, 90
pain and disturbance of, 72 Surgeries, 90
quality of, 7 Switzerland, medical compensation in,
slow-wave, 41, 87 29
and zolpidem use, 97 Sympathoadrenal system, 66
Slow-wave sleep, 41, 87 Synovitis, 76
Smart, P.A., 49 Systemic lupus erythematosus (SLE),
Smith, A.J., 82 90-91
Smith, T.C., 73 and antipolymer antibodies, 9
Smoking, 88 and breast implants, 14
Smythe, H., 92 and coping, 24
Social networks, 88 and gender, 41
Soderberg, S., 30 and interstitial cystitis, 52
Soft tissue rheumatism, 8, 13, 34, 36, and Persian Gulf War syndrome, 73
73 Systemic sclerosis, 9, 41
Soft tissue trauma, 53
Soluble intercellular adhesion
molecule-1, 14 Tabeeva, G.R., 56-57
Soluble intercellular adhesion Tachycardia, 6
molecule-2, 14 Tack, Y., 74
Somatic serotypes (O groups), 55 Tamoxifen, 16
Somatization, 17, 52, 53 Tan, E.M., 8
Somatoform pain disorder Taut bands, 62
(ICD-10), 79 Tavoni, A., 82
Somatotropic axis, 43 Tayag-Kier, C.E., 54
Sorensen, J., 72 Taylor, J., 91
Spasmophilia, 57 Taylor, R.M., 31
Spath, M., 60 Temporomandibular disorder (TMD),
Sperber, A.D., 52 26, 91-92
Sphenopalatine blocks, 88-89 Tender point pathophysiology, 38, 44,
Spinal tracts, 89 92-93
Spiritual intervention, 5 Tender points (TePs), 63
Index 201
Tenderness, 7 Visceral, 52
Tenoxicam, 69 “Visible electromagnetic fields,” 56
Tension headache. See Headache Vitamin B12 deficiency, 47
Thyroid microsomal antibodies, Vlaeyen, J.W., 23
93-94 Volkmann, H., 82
Thyroid-stimulating hormone
(TSH), 65
Thyrotropin-releasing hormone
(TRH), 65 Wacker, H.R., 27
Time-dependent sensitization, 17 Wadsworth, F., 44
Tishler, M., 88 Walter, B., 3
Toivanen, P., 55 Wang, B., 90
“Toxicant-induced loss of tolerance,” Ward, M.H., 35
18 Weather, 97
Training, physical, 34-35 Weiss, D.J., 15
Tramadol, 94 Western Ontario MacMaster
Trauma, 1, 79, 94-95 (WOMAC), 28
Trazodone, 59, 88 Wharton, R.B., 45
Treatment, of fibromyalgia, 95 White, K.P., 33, 94
Tricyclic antidepressant, 6, 55 Whole-body cold therapy, 26
Trigger fingers, 4 Wik, G., 49
Trigger points (TrPs), 38, 62, 63, 96 Wikner, J., 58
Trojan, D.A., 76 Wilson, R.B., 9
Winfeld, J.B., 1
Tropisetron, 84-85 Wolfe, F.
Tryptophan, 96 and disability, 28, 29, 30
Tumor necrosis factor-alpha, 14 and distress, 3, 79
Tuncer, T., 4 and fatigue, 35
Tunks, E., 92 and NSAIDs, 69
Turk, D.C., 80 and positive control points, 92
Type II fiber atrophy, 39, 60 and quality of life, 80
Women. See Female gender
World Health Organization, 37
Ulcerative colitis, 50
United States Court of Federal Claims,
81 Xenobiotic detoxification, 26
Upright tilt, 11, 12
Urine, 96
Yaron, I., 47
Yavuz, S., 12
Vachtenheim, J., 69 Young, V.L., 14
Van Linthoudt, D., 29 Yunus, M.B., 42, 47
Vasoconstriction, 93
Vasodilation, 61
Venlafaxine, 97
Vertebral fracture, 72 Zierhut, M., 22
Victimization, 1 Zolpidem, 97
Virology, 97 Zopiclone, 88
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Roberto Patarca-Montero, MD, PhD, HCLD

The Concise Encyclopedia

“T his encyclopedia provides the

“W ho would need a concise ency-

“T his book enables you to find spe-

The Haworth Medical Press®

CONSERVATION AND PRESERVATION NOTES

Roberto Patarca-Montero, MD, PhD

Concise Encyclopedia of Chronic Fatigue Syndrome by Roberto

Roberto Patarca-Montero, MD, PhD, HCLD

The Haworth Medical Press®

Library of Congress Cataloging-in-Publication Data

Roberto Patarca-Montero, MD, PhD, HCLD, is Assistant Profes-

A cence and in adulthood seem to be very common in those

acupuncture: There are various acupuncture techniques and meth-

also be useful in the treatment of fibromyalgia (White, 1995). How-

affective distress and anxiety: A study in Germany by Walter et al.

aging and geriatrics: The prevalence of fibromyalgia increases with

alcohol: Alcohol consumption may exacerbate symptomatology in

allergy: Tuncer et al. (1997) reported a high frequency of allergy

plant-derived saccharides resulted in a remarkable reduction in initial

alternative and complementary medicine: Fibromyalgia is a

amitriptyline: Amitriptyline is a tricyclic antidepressant agent that

anticardiolipin antibody: Anticardiolipin antibodies occur in a wide

tomyositis, 3 rheumatic fever, 3 vasculitis, 2 scleroderma, and 11

antidepressants: O’Malley et al. (2000) performed a meta-analysis

antiganglioside antibodies: Klein and Berg (1995) reported a de-

fibromyalgia patients and in about 55 percent of chronic fatigue syn-

antinuclear antibodies: A study by Suarez-Almazor et al. (1998) of

antiphospholipid antibodies: Berg et al. (1999) found low level co-

pholipid antibody syndrome among pediatric fibromyalgia patients.

antipolymer antibodies: Wilson et al. (1999) found a higher sero-

antiserotonin antibodies: Klein and Berg (1995) showed the pres-

with fibromyalgia/chronic fatigue syndrome, while antiganglioside

artists and musicians: Martinez-Lavin et al. (2000) reported on the

ascorbigen: In a one-month open-label trial, Bramwell et al. (2000)

attributions: Neerinckx et al. (2000) found that the majority of pa-

with a self-help group because they particularly show external, sta-

autoimmune fatigue syndrome: Itoh et al. (1997) found that among

autonomic dysfunction: Power spectrum analyses of heart rate vari-

Behcet’s syndrome: Yavuz et al. (1998) found a trend for

B syndrome patients. In their study, ten (nine of whom were

benzodiazepine-induced hip fracture: Fibromyalgia patients on

biofeedback: Based on a study of nineteen fibromyalgia patients,

Borna disease virus: Borna disease virus is a neurotropic RNA virus

breast implants: Although some authors in older studies have sug-

combination or in attempts to correlate them with the clinical situa-

breathing: In a study of seventeen fibromyalgia patients, Sergi et al.

diagnosis of dyspnea, and timely diagnosis and treatment may be de-

calcitonin: In a double-blind crossover trial in which

C calcitonin (100 IU s.c.) and isotonic saline (1 cc s.c.) for

cancer chemotherapy: In a study by Warner et al. (1997), of eight

carpal tunnel syndrome: An association between fibromyalgia and

chemical intolerance: Several studies indicate that low level chemi-

ple chemical sensitivity, sick building syndrome, and Persian Gulf

to low-level chemicals in the environment) (Bell, Baldwin, Russek,

Chiari malformation: Muller et al. (1998) point out that distur-

chiropractic treatment: In a preliminary study, Hains and Hains

in pain intensity, sleep disturbance, and fatigue associated with fibro-