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Posted to Co-Cure Sat, 16 Sep 2000 18:50:02 -0700 by Melissa O'Toole

Decreased bone mineral density during low dose glucocorticoid administration

Full Title: Decreased bone mineral density during low dose glucocorticoid administration in a randomized, placebo controlled trial.
Journal: J Rheumatol 2000 Sep;27(9):2222-6
Authors: McKenzie R, Reynolds JC, O'Fallon A, Dale J, Deloria M, Blackwelder W, Straus SE
Affiliation: Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, Maryland , USA.
NLM Citations: PMID: 10990237, UI: 20443644

OBJECTIVE: While osteoporosis and bone fractures are clearly recognized side effects of high dose glucocorticoids, the effect of low dose glucocorticoids remains controversial. We investigated the effect of 3 months of low dose hydrocortisone on bone mineral density (BMD).

METHODS: Subjects, 18 to 55 years old with chronic fatigue syndrome and no medical or psychiatric illness requiring medication, were randomized in a double blind, placebo controlled trial to receive oral hydrocortisone, 13 mg/m2 body surface area every morning and 3 mg/m2 every afternoon (25 to 35 mg/day, equivalent to about 7.5 mg prednisone/day) or placebo for 12 weeks. Before and after treatment BMD of the lumbar spine was measured by dual energy x-ray absorptiometry.

RESULTS: We studied 23 subjects (19 women, 4 men). For the 11 hydrocortisone recipients there was a mean decrease in BMD: mean change from baseline of the lateral spine was -2.0% (95% CI -3.5 to -0.6. p = 0.03) and mean change of the anteroposterior spine was -0.8% (95% CI -1.5 to -0.1, p = 0.06). Corresponding changes for the 12 placebo recipients were +1.0% (95% CI -1.0 to 3.0, p = 0.34) and +0.2% (95% CI -1.4 to 1.5, p = 0.76).

CONCLUSION: A 12 week course of low dose glucocorticoids given to ambulatory subjects with chronic fatigue syndrome was associated with a decrease in BMD of the lumbar spine. This decrease was statistically significant in lateral spine measurements and nearly so in anteroposterior spine measurements.

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Posted to Co-Cure Sat, 16 Sep 2000 18:46:58 -0700 by Melissa O'Toole

Effect of growth hormone treatment in patients with CFS: a preliminary study

Full Title: Effect of growth hormone treatment in patients with chronic fatigue syndrome: a preliminary study.
Journal: Growth Horm IGF Res 1998 Apr;8 Suppl B:131-3
Authors: Moorkens G, Wynants H, Abs R
Affiliation: Department of Internal Medicine, University Hospital Antwerp, Belgium.
NLM citations: PMID: 10990148, UI: 20443555

The efficacy of growth hormone (GH) therapy was evaluated in patients with chronic fatigue syndrome (CFS) who had peak serum GH levels below 10 microg/l during stage-controlled sleep.

Twenty patients (7 men, 13 women; age range, 30-60 years) with CFS were randomized to receive placebo or GH therapy, 6.7 microg/kg/day (0.02 IU/kg/day), for 12 weeks. Following this double-blind treatment period, the 17 patients remaining in the study were given GH therapy at the above dose for an open period of 9 months. Mean (+/- SD) serum levels of insulin-like growth factor I (IGF-I) increased during GH treatment, from 173 +/- 46 microg/I to 296 +/- 89 microg/l (P < 0.001); IGF-I SDS values increased from -0.45 +/- 1.14 to +1.43 +/- 1.09 (P < 0.001). Fat-free mass and total body water were significantly increased after 12 months of treatment.

Although quality of life, as assessed using two different questionnaires, did not improve significantly during GH treatment, four patients were able to resume work after a long period of sick leave.

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Posted to Co-Cure Sat, 16 Sep 2000 18:43:33 -0700 by Melissa O'Toole

Secretion of growth hormone in patients with CFS

Full Title: Secretion of growth hormone in patients with chronic fatigue syndrome. Journal: Growth Horm IGF Res 1998 Apr;8 Suppl B:127-9
Authors: Berwaerts J, Moorkens G, Abs R
Affiliation: Department of Endocrinology, Middelheim Hospital, Antwerp, Belgium.
NLM citations: PMID: 10990147, UI: 20443554

Decreased serum levels of insulin-like growth factor I (IGF-I) are common in patients with fibromyalgia, which is frequently associated with chronic fatigue syndrome (CFS).

Twenty patients with CFS (7 men, 13 women; age range, 30-60 years) and age- and sex-matched controls were tested for peak GH responses to insulin-induced hypoglycaemia and arginine administration. Nocturnal secretion of GH and serum levels of IGF-I were also measured. Serum IGF-I SDS (+/- SD) was significantly lower in patients with CFS than in controls (SDS, -0.39 +/- 1.07 vs 0.33 +/- 0.84; P = 0.02).

Patients with CFS also tended to have reduced nocturnal secretion of GH (area under the curve, 32.4 +/- 18.3 vs 62.7 +/- 43.7 microg/l/15 minutes; P= 0.06), but peak GH responses to insulin-induced hypoglycaemia and arginine administration did not differ significantly between the two groups.

It is not clear whether the tendency for impaired spontaneous nocturnal GH secretion in patients with CFS is a cause or an effect of the condition.

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Posted to Co-Cure Fri, 15 Sep 2000 00:29:00 -0400 by Kimberly Hare

Acute abstinence syndrome following abrupt cessation of long-term use of tramadol

Full Title: Acute abstinence syndrome following abrupt cessation of long-term use of tramadol (Ultram(R)): a case study.
Journal: Eur J Pain 2000 Sep;4(3):307-311
Authors: Freye E, Levy J
Affiliation: Pain Center, Extension of the Heinrich-Heine-University of Dusseldorf, Graf-Adolf-Strasse 16, Dusseldorf, 40211, Germany
NLM Citation: PMID: 10985875

We report on a patient who had taken the centrally acting analgesic tramadol for over 1 year. The compound had proven to be sufficient to treat her painful episodes related to fibromyalgia. Due to lack of supply while being on a trip, intake of the drug was stopped abruptly, resulting in the development of classical abstinence-like symptoms within 1 week.

Abstinence-like symptoms consisted of restlessness and insomnia for which the benzodiazepine lorazepam was given. Diarrhoea and abdominal cramps were treated with the peripherally active opioid loperamide, while bouts of cephalgia were treated with sumatriptan. Diffuse musculoskeltal-related pain and restless leg syndrome (RLS) were treated with dextromethorphan. All these different medications proved to be efficacious as they resulted in the cessation of symptoms. Within 1 week symptoms ceased and the patient regained her normal activities without any sequelae.

Although tramadol is considered a non-habit- and non-dependence-forming analgesic, abstinence symptoms are likely to develop following abrupt cessation of intake, especially when the compound had been taken over 1 year. Therefore patients should be advised of such an effect whenever they decide to stop intake or their physician is planning to switch to another medication. To avoid abstinence-like symptoms doses should be slowly tapered down.

Copyright 2000 European Federation of Chapters of the International Association for the Study of Pain.

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Posted to Co-Cure Mon, 11 Sep 2000 18:23:21 -0400 by Fred Springfield

Decrease in Pressure Pain Thresholds of Latent Myofascial Trigger Points ...

Decrease in Pressure Pain Thresholds of Latent Myofascial Trigger Points in the Middle Finger Extensors Immediately After Continuous Piano Practice
Journal of Musculoskeletal Pain, Vol. 8(3) 2000 pp. 83-92
Authors: Shu-Min Chen,MD; Jo-Tong Chen, MD; Ta-Shen Kuan, MD; Judith Hong; Chang-Zern Hong, MD

ABSTRACT.
Objectives: This study is designed to investigate the change of the pressure pain threshold [PPT] of latent myofascial trigger points [MTrPs], immediately after rapid repetitive contraction of the involved muscle.

Methods: Forty 8-19 year-old students who had taken piano lessons for longer than one year. Three consecutive measurements of PPT were obtained on the latent MTrPs of bilateral extensor digitorium communis muscles 20 minutes before, immediately before, immediately after, and 20 minutes after continuous piano practice of fast music pieces for 20 minutes.

Results: Mean pain threshold was significantly [P < 0.01] reduced immediately after piano practice, and returned to original value 20 minutes after practice. There was no statistically significant difference between the mean value of 20 minutes before practice and immediately before practice [control values]. There was no significant difference between the right and the left hands. Age and experience were not significantly correlated with the changes of pain threshold.

Conclusion: A latent MTrP in a muscle may increase the irritability after rapid repetitive use [over loading of that muscle]. Usually, this change is a temporary phenomenon after an adequate rest period. Therefore, adequate rest may be important to reduce the probability in the development of an active MTrP.

KEYWORDS. Myofascial trigger point, pain threshold, repetitive muscle contraction, music injury

INTRODUCTION
Myofascial trigger point [MTrP] is a characteristic of myofascial pain syndrome, which is one of the most common painful muscular disorders (1-5). An MTrP is a very sensitive spot within a taut band of skeletal muscle fibers that is painful on compression and that can give rise to characteristic referred pain, tenderness, and autonomic phenomena (1). An active MTrP always produces clinical symptoms [spontaneous pain], while a latent MTrP is usually subclinical [painful in response to compression only] (1-5). There may be one or more sensitive spots in a normal muscle, and the most sensitive [tender] spot in a palpable taut band is the latent MTrP (1-6). Almost every skeletal muscle in the body has one or more MTrPs. The important characteristics of a MTrP include (1-4): 1. Localized tender spot in a palpable taut band [tight and firm muscle fibers]; 2. Consistent and characteristic referred pain pattern; and 3. Local twitch response [a brisk twitching contraction of the muscle fibers, induced by snapping palpation on MTrPs in some muscles, or by needling of MTrPs in most muscles].

The reliability of MTrP identification has been studied by Gerwin et al. (5). It has been concluded that hands-on training is essential to achieve a reliable MTrP examination. The presence of spot tenderness in a palpable taut band is highly indicative of a latent or active MTrP (4,5). Addition of pain recognition is diagnostic of an active trigger point (4,5). The additional finding of a referred pain and/or local twitch response confirms the presence of an MTrP, particularly during MTrP injection (5).

The pathophysiology of the MTrP is now much clearer based on recent clinical and basic science studies (6). There are multiple basic MTrP units in an MTrP region. This basic unit contains a sensory component [sensitive locus] and a motor component [active locus]. The sensitive locus is probably sensitized nociceptors and the active locus is considered to be dysfunctional endplates (3,4,6). Theoretically, accumulation of nociceptors in the vicinity of dysfunctional end- plates of skeletal muscle may potentially evolve to an MTrP. Latent MTrP may develop progressively in early life as a consequence of chronic repetitive trauma (3,6). Active MTrPs are produced by activation of latent MTrPs in response to acute trauma or prolonged repetitive minor trauma (1,3,4,6). Therefore, for example, if someone plays piano continuously for hours, the latent MTrPs of the involved muscles may become active ones and may cause pain or discomfort especially in children [our clinical observation in Taiwan]. In a study by Farrell and Littlejohn (7), it was found that task content including repetition frequency, static muscle work, force and action variety, can influence probability of reduced pressure pain threshold [PPT] in normal subjects. The PPT in an active MTrP is much lower than the latent one (8). The PPT is a good indicator of the irritability [or sensitivity] of an MTrP (8,9).

This study aims to further confirm that the PPT of a latent MTrP in a muscle is reduced after repetitive contraction of that muscle. The pressure algometer developed by Fischer (10-12) has proven to be a reliable and valid way to measure the pain threshold of an MTrP (13-16). We used the same pressure algometer applied by Fisher (10-12) to assess the changes of PPT of latent MTrPs in bilateral middle finger extensors [extensor digitorium communis muscles] 20 minutes before, immediately before, immediately after, and 20 minutes after continuous piano practice for 20 minutes.

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: mailto:getinfo@haworthpressinc.com .]


Shu-Min Chen, MD, Jo-Tong Chen, MD, Ta-Shen Kuan, MD, and Judith Hong are affiliated with the Department of Physical Medicine and Rehabilitation, National Cheng-Kung University Hospital, Tainan, Taiwan.

Chang-Zern Hong, MD, is affiliated with the Department of Physical Medicine and Rehabilitation, University of California Irvine, Medical Center, 101 The City Drive, Orange, CA 92688 USA.

Address correspondence to: Shu-Min Chen, MD, Department of Physical Medicine and Rehabilitation, National Cheng-Kung University Hospital, 138 Sheng-Li Road, Tainan 704, Taiwan.

This article has been presented in the 8th World Congress of the International Rehabilitation Medicine Association in Kyoto, August 31-September 4, 1997.

Submitted: November 24, 1998.
Revision accepted: June 14, 1999.

© 2000 by The Haworth Press, Inc. All rights reserved.

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Posted to Co-Cure Mon, 11 Sep 2000 03:40:19 -0400

St. John's Wort

[Moderator's Note: This rather extensive review of St. John's Wort might be of interest because of the reported use of St. John's Wort within our patient populations.]

The latest in clinical trials, indications, and toxicology.
UpToDate (C) 2000

Read it Here

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Posted to Co-Cure Fri, 8 Sep 2000 23:26:10 -0400 by Fred Springfield

No Increased Neuromuscular Jitter at Rabbit Skeletal Muscle Trigger Spot Spontaneous Electrical Activity Sites

Journal of Musculoskeletal Pain, Vol. 8(3) 2000 pp. 69-82
Authors: Ta-Shen Kuan, MD, MS; Thy-Sheng Lin, MD, MS; Jo-Tong Chen, MD; Shu-Min Chen, MD; Chang-Zern Hong, MD

ABSTRACT.
Objective: One of the important characteristics of myofascial trigger point [MTrP] is spontaneous electrical activity [SEA]. Spontaneous electrical activity is recorded from an active locus [a basic unit] of MTrP and has been considered as an abnormal endplate potential, which might be due to excessive acetylcholine release in neuromuscular junction. This study is designed to test the hypothesis that active loci in MTrPs are related to neuromuscular transmission disorder.

Methods: Twenty-one adult New Zealand rabbits were anesthetized and their biceps femoris were exposed to localize myofascial trigger spot [MTrS, equivalent to MTrP in human]. A monopolar needle electrode was first used for searching SEA in an MTrS region. Then, a single fiber electromyography [SFEMG] electrode was used to collect the neuromuscular jitter at the site where SEA was recorded. The same procedure was performed at the normal muscle site [no SEA recorded] in contralateral limb to collect the neuromuscular jitter as a control. Mean value of consecutive differences [MCD] of 100 successive inter- potential intervals was calculated to express the neuromuscular jitter.

Results: There was no statistically significant difference [P> 0.05] in MCD of MTrS between the active loci and control sites.

Conclusion: It appears that the neuromuscular transmission of endplate in MTrS in rabbits is not impaired based on this SFEMG study using jitter as the sole criteria. Spontaneous electrical activity is not related to neuromuscular transmission abnormality. Further studies are required to clarify the mechanism of dysfunctional endplates in relation to MTrP.

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: getinfo@haworthpressinc.com .]

KEYWORDS. Myofascial pain syndrome, trigger point, single fiber electromyography


Ta-Shen Kuan, MD, MS; Jo-Tong Chen, MD; and Shu-Min Chen, MD, all are affiliated with the Department of Physical Medicine and Rehabilitation, National Cheng-Kung University Hospital, Tainan, Taiwan, R.O.C.

Thy-Sheng Lin, MD, MS is affiliated with the Department of Neurology, National Chen-Kung University, Tainan, Taiwan, R.O.C.

Chang-Zern Hong, MD is affiliated with the Department of Physical Medicine and Rehabilitation, University of California Irvine, Medical Center, 101 The City Drive, Orange, CA 92688 USA.

Address correspondence to: Ta-Shen Kuan, MD, MS, Department of Physical Medicine and Rehabilitation, National Cheng-Kung University Hospital, No. 138, Sheng-Li Road, Tainan, 704, Taiwan, R.O.C.

Supported by National Science Council [Taiwan] Grant NSC-87-2314-B006-02.
Submitted: March 23, 1999.
Revision accepted: August 22, 1999.

© 2000 by The Haworth Press, Inc. All rights reserved

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Posted to Co-Cure Fri, 8 Sep 2000 23:28:12 -0400

Cerebral perfusion in chronic fatigue syndrome and depression

Authors: Machale SM, Lawrie SM, Cavanagh JT, Glabus MF, Murray CL, Goodwin GM, Ebmeier KP
Affiliation: University Department of Psychiatry, Royal Edinburgh Hospital.
British Journal of Psychiatry 2000 Jun;176:550-6
NLM citations: PMID: 10974961, UI: 20430660

30 people with CFS (PWCs), 12 with depression, and 15 healthy volunteers were assessed for regional cerebral perfusion at rest. PWCs and depressed patients showed increased perfusion in the right thalamus, pallidum and putamen. CFS patients also had increased perfusion in the left thalamus. Depressed patients had relatively less perfusion of the left prefrontal cortex than PWCs. The authors were unable to test for reduced perfusion of the brain-stem in PWCs due to limits in the spatial resolution of SPECT. The authors state that the main limitation of their study was that their CFS subjects had high levels of depression. They also state that their method of choosing subjects may mean that the PWC and control groups were not representative of those groups in clinics and in the community. Almost all the depressed subjects and half of the PWCs were medicated for depression, and psychotropic medication may alter cerebral perfusion, although the authors state that their findings in PWCs did not appear to be explained by medication effects.

Full Text

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Posted to Co-Cure Mon, 4 Sep 2000 20:12:05 -0400 by Fred Springfield

The Effects of Controlled Delta Sleep Deprivation on Experimental Pain in Healthy Subjects

The Effects of Controlled Delta Sleep Deprivation on Experimental Pain in Healthy Subjects
Journal of Musculoskeletal Pain, Vol. 8(3) 2000 pp. 49-67
Asbjørn Mohr Drewes, MD, PhD, DSc; Kim Dremstrup Nielsen, MSc, PhD; Cuno Rasmussen, MSc; Taro Arima, DDS; Peter Svensson, DDS; Petra Rössel, MD; Lars Arendt-Nielsen, MSc, PhD, DSc

ABSTRACT.
Objectives: The interaction between sleep and pain is important in patients suffering from rheumatic illness. Not only can pain disturb sleep, but alterations in the deeper sleep stages induced by the disease process may have the potential to decrease the pain threshold. Previous studies however, have shown diverging results. In the current experiment we studied the effects of deep sleep deprivation using a standardized, computer-assisted system on subjective symptoms and pain elicited by different experimental modalities.

Methods: Ten healthy males, mean age 22.7 years, were subjected to deprivation of the deeper sleep stages for three nights. Following a baseline recording, sleep was analyzed in 2 s segments with on-line frequency analysis. If any 30 s epoch contained more than seven 2 s segments dominated by low frequency content corresponding to deep sleep, the sleep was disturbed by an acoustic stimulus. The amount of delta power was computed in sleep stages non-rapid-eye-movement [NREM]2-4. Subjects rated different questions regarding their feeling of pain, discomfort and psychological complaints twice a day during the experiment. Experimental pain was assessed with thermal [heat and cold pressor] and electrical stimuli as well as pressure pain thresholds in different areas of the body.

Results: The first night of deep sleep deprivation resulted in a reduction in delta power to 39.3 and 10.5% of the baseline in stages NREM3 and 4, respectively [P 0.005, P = 0.015]. In five subjects the delta power deprivation in stages NREM3 + 4 was 62.2% of baseline in the second deprivation night [P = 0.043]. No consistent changes however, were found for the subjective ratings or the experimental pain assessments following the first deprivation night. For the five subjects who were sufficiently deprived for deep sleep in two nights, the same findings as above were seen following both nights.

Conclusion: Controlled delta power deprivation during sleep did not result in pain in healthy, young males. Although sleep disturbances may interact with pain and other daytime symptoms, we believe that other factors such as premorbid genetic constitution, age, sex, and several external factors are necessary before sleep disturbances per se are able to induce musculoskeletal symptoms.

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: mailto:getinfo@haworthpressinc.com .]

KEYWORDS. Sleep, musculoskeletal pain


Asbjørn Mohr Drewes, MD, PhD, DSc, is Associate Professor, Department of Medicine M, Aalborg Hospital, Aalborg, Denmark and also with the Laboratory for Experimental Pain Research, Center for Sensory-Motor Interaction, Aalborg University, Aalborg, Denmark.

Kim Dremstrup Nielsen, MSc, PhD, is Associate Professor, Cuno Rasmussen, MSc, and Taro Arima, DDS, are PhD Students, and Lars Arendt-Nielsen, MSc, PhD, DSc, is Professor, Laboratory for Experimental Pain Research, Center for Sensory- Motor Interaction, Aalborg University, Aalborg, Denmark.

Peter Svensson, DDS, is Associate Professor, Laboratory for Experimental Pain Research, Center for Sensory-Motor Interaction, Aalborg University, Aalborg, Den mark and also with Royal Dental College, Aarhus University, Aarhus, Denmark.

Petra Rössel, MD, is affiliated with the Department of Medicine M, Aalborg Hospital, Aalborg, Denmark.

Address correspondence to: Asbjørn Mohr Drewes, MD, PhD, DSc, Associate Professor, Department of Medicine M, Aalborg Hospital, DK-9000, Aalhorg, Denmark.

The study was supported by the Danish Rheumatism Association.
Submitted: March 30, 1999.
Revision accepted: August 19, 1999.

Journal of Musculoskeletal Pain, Vol. 8(3) 2000
© 2000 by The Haworth Press, Inc. All rights reserved.

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Posted to Co-Cure Fri, 1 Sep 2000 02:55:33 -0400 by Fred Springfield

A Descriptive Analysis of Fibromyalgia from the Patients' Perspective

A Descriptive Analysis of Fibromyalgia from the Patients' Perspective
Journal of Musculoskeletal Pain, Vol. 8(3) 2000, pp. 35-47
Alice Prince, Ph.D.; Amy L. Bernard, Ph.D., CHES; Patricia A. Edsall, AA

ABSTRACT.
Objective: To collect information directly from fibromyalgia patients on: clinical characteristics, symptom management, other illnesses, and exposure to factors that might be linked to fibromyalgia syndrome [FMS].

Methods: Survey of FMS support group members in Washington state, Illinois, and Pennsylvania [N = 270].

Results: One-third indicated a family history, and three-quarters indicated either an accident or severe stress preceded the onset of symptoms. A wide variety of symptoms were reported as well as fluctuations in symptoms from day to day and seasonally.

Conclusions: More descriptive information needs to be collected from patients in order to determine the factors responsible for the onset of FMS symptoms and to improve clinical management.

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: getinfo@haworthpressinc.com.]

KEYWORDS. Fibromyalgia, descriptive analysis, women’s health, patients

INTRODUCTION

Although a variety of factors have been hypothesized to be responsible for the onset of fibromyalgia syndrome [FMS] symptoms, there is no definitive proof to validate any of these theories (1,2). Currently, the predominant theory is that FMS is genetic, but may require some catalyst such as another illness, stress, or an injury to trigger its symptoms (3-6). Other theories that have been hypothesized include neurohormonal deregulation (7), viral infection (8), dysfunctional spectrum syndrome (9), pain amplification disorder (10), biopsychosocial disorder (10), organ system dysfunction (5), deficiency of stage four sleep (11), and a psychological or psychiatric disorder (10,12,13).

The diagnosis of FMS is made based on the patient’s self-reported symptoms and pain in tender point areas with palpitation (14-18). There are a wide variety of symptoms a FMS patient could present with, including widespread muscle pain and fatigue (3-5,9,12,16,17,19-22), sleep disorders (16,17,20-23), irritable bowel syndrome (19,21,22), chronic headaches (19,21,22), temporomandibular joint dysfunction syndrome (21), multiple chemical sensitivity syndrome (21), pre-menstrual syndrome FPMSI (21,22), anxiety and depression (12,13,22,24-26), stiffness (4,5,17,20,21), cognitive or memory impairment (21,27), and restless leg syndrome (22). Because the factors responsible for triggering FMS symptoms are unknown, there is no cure for FMS, which limits treatment to symptom management. Drug therapy is often used to minimize pain and relieve depression and sleep-disturbances. However, the effectiveness of drug therapy is limited and many of these prescription medications have unwanted side effects (28). Dissatisfaction with drug therapy has led many patients to seek alternative treatments for their FMS symptoms, although most report that nothing they have tried completely alleviates their symptoms (4,17,19,28-33).

In order for the seven to ten million Americans who are suffering from FMS (22) to find any relief from this disease, the underlying factor[s] which trigger the FMS symptoms must be found so that, at a minimum, more effective treatments can be developed for this syndrome and, optimally, a cure can be discovered. Case studies and studies involving patient self-report can assist in reaching this goal. Examining patient characteristics, symptoms, and responses to treatment can lead to information which can assist researchers in pinpointing the factors responsible for FMS symptoms and/or better treatment options. The purpose of this study was to collect information directly from FMS patients regarding disease characteristics and progression, symptoms and their management, other illnesses the patient currently suffers from or has suffered from in the past, and exposure to factors that might be somehow linked to their FMS. Because much of the research conducted to date on FMS has been clinical in nature, this study sought a more patient-driven approach by using survey research to collect the information outlined above and to provide some opportunity for open-ended responses which would allow the subjects to have a voice in the study results.


Alice Prince, PhD, is Assistant Professor, Department of Kinesiology and Health Education, Southern Illinois University at Edwardsville, Edwardsville, IL [E-mail: aprince@siue.edu].

Amy L. Bernard, PhD, CHES, is Assistant Professor, Health Promotion and Education Program, University of Cincinnati, Cincinnati, OH [E-mail: amy.bernard@uc.edu].

Patricia A. Edsall, AA, 107 East Center, Troy, IL 62294.

Address correspondence to: Amy L. Bernard, PhD, CHES, Health Promotion and Education Program, University of Cincinnati, P.O. Box 210002, Cincinnati, OH 45221-0002.

This article was supported by a grant from The College of Education at Southern Illinois University at Edwardsville.
Submitted: October 20, 1998.
Revision accepted: May 26, 1999.

Journal of Musculoskeletal Pain, Vol. 8(3) 2000
© 2000 by The Haworth Press, Inc. All rights reserved.

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Note: All abstract summaries, unless otherwise noted, were prepared by Margaret Bailey.


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