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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent controlled studies suggest a physiologic basis for FMS, which should be diagnosed by its own characteristic features and not by exclusion of other conditions alone. Diffuse musculoskeletal aching, accompanied by multiple TPs in the absence of an underlying arthritic or systemic condition, are the key features for diagnosis. Based on our controlled study, guidelines for diagnosis are provided in Table 5. Successful management of an FMS patient is often challenging, but frequently gratifying if approached with a positive and caring attitude. The most important aspects of management are a firm diagnosis, reassurance regarding the benign nature of the condition, help in changing patient behavior in order to accept pain and increase functional activities and exercise tolerance, and the use of tricyclic agents. Overall, management of fibromyalgia is an art that requires the combined ingredients of patience, understanding, and firmness in helping patients to assume responsibility for their pain management through behavior modifications.
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PMID:Diagnosis, etiology, and management of fibromyalgia syndrome: an update. 328 8

FMS is a complex condition mainly characterized by the presence of chronic pain. The nature of this complaint thus demands assessment in a hierarchal fashion of the various components of the pain system ranging from the nociceptor through to complex central pain-processing mechanisms. The condition is common and represents the most important defined chronic pain syndrome. Elucidation of the mechanisms and better management of FMS will result in improved knowledge of a whole range of related chronic pain syndromes. The database in FMS is necessarily large but does need to be focused according to the need of the person constructing the database and the need of the individual with FMS. As our understanding of FMS evolves, better ways of assessing the various dimensions of the problem will be devised. Perhaps the challenge we face is to bring all the parts together. In doing so, we may find there is a single essential component that links all the clinical features together, which correlates well with severity, disability and outcome, which is amenable to treatment programs, and which is measurable. The search for the soul of the "elephant" of FMS continues.
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PMID:A database for fibromyalgia. 763 Oct 42

The conclusion is that no one single mechanism can explain FMS and is thus in that sense a compromise. FMS in some patients may start in the muscle, in other patients in the brain. The combination of peripheral and central factors is the key to the pathogenesis of FMS as long as FMS is defined as a pain syndrome.
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PMID:Chronic muscular pain: aetiology and pathogenesis. 785 Aug 76

Since the first comprehensive description of the symptoms of FMS by Yunus et al (1981), numerous investigations have confirmed that FMS is a clinical entity. However, the aetiology of the syndrome is still not fully elucidated. It seems, however, logical to place the origin of the disorder in the muscle. Muscle pain, especially at the muscle-tendon junctions, fatigue and stiffness are the first symptoms. A malfunction of energy metabolism has been detected in part of the muscle fibres. However, it has to be considered that the muscle is not an isolated entity. Its activity is controlled by segmentally arranged motor units of the ventral horn of the spinal cord in response to proprioceptive afferent signals arising in the muscle spindles or in other sensory elements including nociceptors. Together with supraspinal descending inputs, the spinal motor neurone pool is the common final pathway for segmental and suprasegmental inputs, making the motor system extremely powerful for adaptive adjustments but also vulnerable if deficits occur in either of these input levels. A second, recently discovered abnormality seen in FMS is a lowered serotonin level in peripheral and most likely also central structures. The underlying mechanism seems to be defective absorption of the precursor amino acid tryptophan from the gut. Serotonin is involved centrally in the regulation of the sleep pattern, and at the spinal level it acts as a 'gain setter' of motoneurone excitability and suppresses signal transmission of noxious stimuli in dorsal horn neurones. Either of these two disturbances, muscle energy depletion or serotonin deficiency, could by itself evoke many of the symptoms of FMS, and their combined appearance will perpetuate the disease. Depressed levels of somatomedin C, caused by a deficit of stage 4 sleep-dependent release of GH, might represent an additional factor in preventing proper development or repair of myoskeletal structures. Malabsorption of certain amino acids, possibly due to a genetic disorder of gut transport mechanisms, may constitute an additional deleterious factor. The abnormalities found in the HPA and HPT axis may be seen as an attempt of the organism to restore homeostasis. The stimulus eliciting this counter-regulatory reaction may be pain or other afferent signals which normally do not reach the central nervous system. It is doubtful whether the unspecific activation of the HPA axis in a non-inflammatory disease is beneficial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuromediator and hormonal perturbations in fibromyalgia syndrome: results of chronic stress? 785 Aug 79

We performed a combined manual and computer search of the FMS literature to identify controlled clinical trials in FMS from 1980 to June 1994 inclusive. Our specific objectives were: 1) to determine which outcome measures have been used in clinical trials for FMS, and the methods utilized to measure these outcomes; 2) to identify which outcome measures were most and least sensitive in distinguishing between treatment groups, and 3) to identify weakness in trial design. Our analysis of 24 clinical trials demonstrates the large diversity of outcome measures and measurement instruments that have been used to detect differences between treatment and placebo in the management of FMS. Whereas certain outcomes, such as self-reported pain and sleep quality, were frequently measured, other clinically important outcomes, such as functional and psychological status, were infrequently included in data collection. Finally, we identified several significant potential sources of bias, including potential flaws in subject selection and group allocation, inadequate randomization, incomplete blinding, errors in outcome measurement, and inappropriate analysis of data.
Pain 1996 Feb
PMID:An analytical review of 24 controlled clinical trials for fibromyalgia syndrome (FMS). 874 May 97

Recently, fibromyalgia (FMS) was shown to be a disorder associated with an altered functioning of the stress response system. FMS patients display a hyperreactive pituitary adrenocorticotropic hormone (ACTH) release in response to corticotropin-releasing hormone (CRH) and to insulin-induced hypoglycemia. We suggested that negative feedback of cortisol could be deranged. Therefore we investigated the properties and function of the glucocorticoid receptors (GR) in FMS patients and compared the results with those of healthy persons and patients with chronic low back pain (LBP a localized pain condition). Forty primary FMS patients (F:M = 36:4), 28 LBP patients (25:3) and 14 (12:2) healthy, sedentary control persons were recruited for the study. Urinary free cortisol excretion in FMS and LBP patients was lower compared to controls. Only FMS patients displayed lower CBG and basal serum cortisol concentrations when compared to controls. However, plasma free cortisol concentrations were similar in the three groups. There was no difference in the number of GR per cell among the three groups (FMS: 6498 +/- 252, LBP: 6625 +/- 284, controls: 6576 +/- 304), but the dissociation constant (Kd) of the FMS (14.5 +/- 0.9 nmol/l) and LBP (14.7 +/- 1.3 nmol/l) subjects was significantly higher than that of the controls (10.9 +/- 0.8 nmol/l) (p < .05). The maximal stimulation of the lymphocytes, as measured by the maximal thymidine incorporation (in the absence of cortisol) in the FMS group was approximately 1.5 times higher (p < .05) than in the control or LBP group. The ED50 (the cortisol concentration giving 50% inhibition of the thymidine incorporation), however, was identical in all three groups. We conclude that FMS patients have a mild hypocortisolemia, increased cortisol feedback resistance in combination probably with a reduced CRH synthesis or release in the hypothalamus. The role of the GR and mineralocorticoid receptor (MR) in the CRH regulation in the FMS patients remains to be solved.
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PMID:Glucocorticoid receptors, fibromyalgia and low back pain. 948 5

In contrast with the situation just a few years ago, the most widely accepted model for the pathogenesis of FMS now invokes CNS mechanisms like nociception and allodynia rather than pathologically painful muscles. The levels of platelet serotonin and CSF substance P appear to be abnormal in directions that could logically amplify pain perception. The extent to which these mechanisms are unique to FMS will be critical in determining the direction that future research should take. Certainly, a better understanding of the cause of FMS could represent an important step toward the development of more effective therapy.
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PMID:Neurochemical pathogenesis of fibromyalgia. 1002 86

Fibromyalgia patients hardly suffer from major psychiatric illnesses. Most often, persistent somatoform pain disorder (ICD-10) and dysthymia are identified by psychiatric assessment. Features of "pain proneness" can also be found regularly, which can explain the elevated levels of stress observed in FMS. Repeated traumatic experiences during childhood and as adults can be discovered in many cases, which helps to understand some of the difficulties met in psychotherapy with FMS patients. Modified psychotherapy techniques are recommended using pain-centered behavioral methods initially, and progressing only later to an insight orientated approach.
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PMID:Psychological and psychiatric aspects of fibromyalgia syndrome (FMS). 1002 94

We developed several kinds of fentanyl-loaded poly(L-lactide-co-glycolide) (PLGA) microspheres (FMS) for sustained release of fentanyl. FMS were prepared by an emulsion solvent-evaporation method. In this study, the influences of several preparation parameters, such as initial drug loading, polymer concentration, and solvent volume on the release patterns of fentanyl were investigated. Furthermore, it has been well noted that the detection of fentanyl is extremely difficult because its clinical dose level is very low, about 1-3 ng/ml, in cancer-patient treatment. Therefore, we also developed a rapid and sensitive determination method for fentanyl in systemic circulation by employing gas chromatography (GC) system. Fentanyl was slowly released from FMS over 15 days with a quasi-zero order property. From the results, our FMS may be good formulations to deliver the analgesics and suitable for the treatment of severe pain over long periods.
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PMID:Preparation and characterization of fentanyl-loaded PLGA microspheres: in vitro release profiles. 1183 50

The objective of the present study was to evaluate instruments used to assess pain in patients with fibromyalgia (FMS). Participants were 602 patients with FMS. Pain was measured with five scales: a visual analog scale (VAS), the Pain Rating, Present Pain, and Number of Words Chosen Indexes from the McGill Pain Questionnaire; and intensity of pain obtained from a manual tender point exam. The VAS had the highest correlations with other measures of pain and with self-efficacy for pain, physical functioning, fatigue, and stiffness. The correlations between the VAS and fatigue and stiffness were significantly higher than those of other pain measures (p < .01). Our findings suggest that the easy-to-administer VAS may be the most useful measure of pain with patients with FMS.
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PMID:A comparison of pain measures used with patients with fibromyalgia. 1204 70


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