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Psychiatric diagnoses in patients with fibromyalgiaComment on the article by Aaron et al.

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LETTERS
Psychiatric diagnoses in patients with fibromyalgia:
comment on the article by Aaron et al
To the Editor:
In their carefully done study, Aaron et a1 compared the
frequency of lifetime psychiatric diagnoses, current psychological symptoms, number of tender points, pain threshold, severity of fatigue, and pain intensity in 3 groups of subjects:
patients with an established diagnosis of fibromyalgia syndrome (FMS) who sought medical care for their symptoms
(FMS patients); community residents who had symptoms of
FMS for which they had not previously sought medical care,
and who had confirmation by a rheumatologist that they
fulfilled the diagnostic criteria for FMS (FMS nonpatients);
and community residents who had reported that they were
healthy and had no muscular aches o r pains (controls) (1). The
authors found that FMS patients had more tender points, a
lower pain threshold, more fatigue, more intense pain, and
more current anxiety and/or depression than FMS nonpatients
or controls, and that FMS nonpatients had more of all of these
characteristics than controls.
Using a structured psychiatric interview, FMS patients
were found to have more lifetime psychiatric diagnoses than
FMS nonpatients or controls, but FMS nonpatients did not
have more psychiatric diagnoses than controls. The authors use
this last observation to “strongly suggest that psychiatric illness
is not intrinsically associated with the FMS syndrome” [sic] (1).
They dismiss the difference in symptoms of anxiety andlor
depression between each of the groups because these symptoms correlate with lower pain thresholds and fatigue, and the
difference may be statistically eliminated by controlling for
pain threshold and fatigue.
W e propose a different interpretation of these results,
one that suggests that psychiatric symptoms in fibromyalgia
patients are as much a part of the syndrome as pain and
fatigue. To us, the fact that differences in psychiatric symptoms
between groups may be eliminated by controlling for other
measures of disease severity suggests that these symptoms are
associated with FMS, not the opposite.
Many of these same authors have previously reported
low regional cerebral blood flow and generalized low pain
thresholds in women with FMS, and used that evidence to
suggest “a functional abnormality within the central nervous
system” (2). In that article, Moumtz et a1 succinctly summarized
some of the evidence further supporting a pathogenic hypothesis for FMS involving abnormalities of the neuroendocrine
system and various neurotransmitters. Similar neurologic abnormalities have been found in affective disorders, suggesting
a hypothesis that such behavioral disturbances may be an
intrinsic part of FMS, with the symptoms of pain, fatigue, sleep
disturbance, and psychological distress all sharing a common
pathogenic mechanism. Surely we do not need to be convinced
that neurochernical factors are as much responsible for the
behavior of our patients as for their pain or sleep patterns.
We believe that Hudson et al’s concept of affective
spectrum disorders is on the right track (3), and that the
syndrome of fibromyalgia includes chronic myalgia, decreased
pain thresholds, fatigue, sleep disturbance, and undesirable
behavioral patterns characterized variously as depression, anxiety, or psychological distress. In such a model, we would
expect that the people most sick with this illness would be most
likely to go to the doctor and would have the worst symptoms.
People less sick would be less likely to seek health care and
would have similar, but less severe, symptoms. Individuals who
identify themselves as healthy would have the fewest symptoms
and would wisely stay out of our clutches.
Eric M. Ruderman, M D
Harvey E. Golden, M D
Rush Medical College
Chicugo, IL
Aaron LA, Bradley LA, Alarcon GS, Alexander RW, TrianaAlexander M, Martin MY, Alberts KR: Psychiatric diagnoses in
patients with fibromyalgia are related to health care-seeking behavior rather than to illness. Arthritis Rheum 39:436-445, 1996
Mountz JM, Bradley LA, Modell JG, Alexander RW, TrianaAlexander M. Aaron LA, Stewart KE, Alaru5n GS, Mountz JD:
Fibromyalgia in women: abnormalities of regional cerebral blood
flow in the thalamus and the caudate nucleus are associated with
low pain threshold levels. Arthritis Rheum 38:926-938, 1995
Hudson JI, Goldenberg DL, Pope HJ, Keck PJ, Schlesinger L:
Comorbidity of fibromyalgia with medical and psychiatric disorders.
Am J Med 92:363-367. 1992
Reply
To the Editor:
We greatly appreciate the thoughtful response of Drs.
Ruderman and Golden to our article concerning the frequency
of lifetime psychiatric diagnoses among patients and nonpatients with FMS as well as healthy controls. We expected that
this article would generate disagreement among some readers
of Arthritis & Rheumatism because our data are not in accord
with Hudson et al’s model. which posits that FMS is part of a
spectrum of genetically based affective disorders (1). Since
disagreement generally produces advances in science, we welcome the opportunity to examine the genetic model of FMS
favored by Drs. Ruderman and Golden, and to discuss the
meaning of our data in the context of this model.
Hudson et al’s genetic model is based primarily on the
results of 2 studies of small groups of patients with FMS seen
at university-based rheumatology clinics (1,2). Hudson and
colleagues chose to examine the frequency of lifetime psychiatric diagnoses in FMS patients using reliable, structured
psychiatric interviews rather than questionnaire-based measures of psychological symptoms, because the latter may be
influenced by numerous illness-related and social factors.
Their studies showed that clinic patients with FMS are characterized by high frequencies of lifetime diagnoses of affective
disorders; the first symptoms of these diagnoses generally
appeared prior to the onset of FMS (1,2). Hudson et a1 noted
that these psychiatric diagnoses are also found often in patients
who have other chronic disorders, such as migraine headache,
irritable bowel syndrome (IBS), and chronic fatigue syndrome,
which tend to overlap with FMS. It was suggested, then, that
these chronic disorders and the affective disorders may share a
genetic abnormality (1). Moreover, this genetic abnormality
was considered to b e a necessary condition for the occurrence of any of these disorders, which were thought to
LETTERS
represent a spectrum of genetically based affective disorders
(see ref. 1, p. 366).
If Hudson et al’s model is valid, we would expect to
find frequent lifetime diagnoses of affective disorders among
persons with FMS, regardless of their health care-seeking
status. Indeed, using a structured psychiatric interview, we
performed a cross-sectional investigation that replicated Hudson and colleagues’ finding of high frequencies of affective
disorder that usually appeared prior to pain onset in our
rheumatology clinic patients with primary FMS. These patients
generally met criteria for multiple psychiatric disorders and
reported high levels of psychological distress on standardized
questionnaires. However, our nonpatients with FMS, who had
not sought health care for their pain in the past 10 years,
showed a pattern of results that was not consistent with
Hudson et al’s genetic model; i.e., the nonpatients reported
relatively high levels of psychological distress, but they did not
differ from healthy controls in the frequency of their lifetime
diagnoses of affective disorders or any other psychiatric illnesses. The nonpatients and controls usually had no more than
1 lifetime psychiatric diagnosis. It is interesting to note,
however, that the nonpatients’ psychiatric disorders generally
appeared before their FMS symptoms began.
Since the publication of these findings, we have prospectively examined the health care-seeking behavior of 40
nonpatients with FMS over a 30-month period (3). Ten
nonpatients obtained medical treatment for FMS pain during
this time. The most powerful predictor of seeking treatment
was a history of >1 lifetime psychiatric diagnosis at baseline.
Hudson et al’s model cannot readily account for the
absence of differences between nonpatients and controls in
psychiatric morbidity in our original cross-sectional study,
because the model views high frequencies of affective disorders as evidence that all persons with FMS, IBS, or migraine
headache share a genetic abnormality. Thus, the most parsimonious explanation for our cross-sectional and longitudinal
findings is that the presence of psychiatric illness that begins
early in the lives of persons with FMS does not reflect the
influence of a genetic abnormality common to all individuals
with FMS, IBS, migraine headache, or affective disorders.
Instead, early history of multiple psychiatric illnesses is an
important factor associated with seeking medical care for FMS
at a tertiary health center.
Drs. Ruderman and Golden criticize this interpretation of our findings on the grounds that we did not pay
sufficient attention to data regarding neuroendocrine abnormalities and psychological distress in patients with FMS (4).
They note that neuroendocrine abnormalities similar to those
found in FMS patients (e.g., serotonin deficiency) are also
found in patients with affective disorders. Thus, Drs. Ruderman and Golden suggest that these neuroendocrine abnormalities account for the strong relationship between measures of
disease severity and psychological distress found in our patients and nonpatients with FMS, and reflect the operation of
a pathogenetic mechanism common to FMS and affective
disorders. We agree with Drs. Ruderman and Golden that
symptoms of psychological distress in persons with FMS may
be related in part to some neuroendocrine abnormalities
common to FMS and depression. However, psychological
distress also may represent a response to the chronic pain,
fatigue, and other symptoms of FMS that are influenced by
2087
social factors, individual coping repertoires, and the lack of
effective remedies for the symptoms. Therefore, a relationship
between psychological distress and disease severity measures
cannot be regarded as evidence for a genetic abnormality
common to FMS and the affective disorders, because the
causal direction of the relationship has not been established.
Moreover, it should be noted that there also are
several biologic abnormalities associated with FMS that are
not related to affective disorders, such as functional abnormalities in the thalamus and caudate nucleus (4)and high cerebrospinal fluid (CSF) levels of substance P (5). Indeed, preliminary findings in our laboratory suggest that high CSF levels
of substance P are found in both patients and nonpatients with
FM. It is likely, then, that abnormal levels of substance P are
more highly associated with the pathogenetic mechanisms
underlying FMS than are affective disorders.
In summary, Hudson et al’s work represents one of the
first attempts to develop a model of the pathogenesis of FMS.
It is appealing because the central role ascribed to affective
disorders that begin early in life is consistent with the high
frequencies of psychiatric illnesses observed in clinic patients
with FMS. However, we believe that advances in the understanding and treatment of FMS will be hindered if we accept a
model that can account only for the psychiatric histories of
persons who seek medical treatment in tertiary care centers.
We hope that our work will contribute to the development of
a pathogenetic model of FMS that will be valid for all persons
with FMS, regardless of their health care-seeking status or the
settings in which they obtain treatment for FMS and other
chronic disorders.
Leslie A. Aaron, M A
Laurence A. Bradley, PhD
Graciela S. Alarcon, MD, MPH
Ronald W. Alexander, M A
Mireya Triana-Alexander, BA
Michelle Y. Martin, MA
Kristin R. Alberts, BA
The University of Alabama at Birmingham
1. Hudson JI, Goldenberg DL, Pope HG, Keck PJ, Schlesinger L
Comorbidity of fibromyalgia with medical and psychiatric disorders.
Am J Med 92363-367, 1992
2. Hudson JI, Hudson MS, Pliner LF, Goldenberg DL, Pope HG:
Fibromyalgia and major affective disorder: a controlled phenomenology and family history study. Am J Psychiatry 142441-448, 1985
3. Aaron LA, Bradley LA, Alexander MT, Alexander RW, Martin
MY, Alberts KA, Alarc6n GS: Prediction of health-care seeking for
fibromyalgia symptoms among community residents with FM (abstract). Arthritis Rheum 38 (suppl 9):S230, 1995
4. Mountz JM, Bradley LA, Modell JG, Alexander RW, TrianaAlexander M, Aaron LA, Stewart KE, Alarcdn GS, Mountz JD:
Fibromyalgia in women: abnormalities of regional cerebral blood
flow in the thalamus and caudate nucleus are associated with low
pain threshold levels. Arthritis Rheum 38:926-938, 1995
5. Russell IJ, Orr MD, Littman 9, Vipraio GA, Alboukrek D,
Michalek JE: Lopez Y, MacKillip F: Elevated cerebrospinal fluid
levels of substance P in patients with the fibromyalgia syndrome.
Arthritis Rheum 37:1593-1601, 1994
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