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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent epidemiological surveys in general populations of different countries of the world found lifetime prevalence rates of major depressions between 3.3% and 17%. For dysthymia (depressed mood over a period of at least two years with at least two concomitant depressive symptoms) the prevalence rate was found to be between 2% and 7%. The prevalence rates of major depressions and dysthymia are usually higher for females than for males. Bipolar disorders can be observed in about 1% of a general population over lifetime, and they seem to be somewhat more common among males than females. Divorced and separated persons have a higher risk of suffering from major depressions than married persons. Major depressions are thought to be more common among members of the lowest social class than among people belonging to the upper classes. Major depressions usually start between the age of 25 and 30 years, and the age of onset of bipolar disorders is between the age of 18 and 30 years. For western industrial nations a secular trend towards an increase in the prevalence of major depressions may be presumed. However, such a secular trend has not yet been confirmed, owing to biases associated with methodological problems. A notable comorbidity of major depressions can be observed with all anxiety disorders, obsessive-compulsive disorders, eating disorders, post-traumatic stress disorder, disorders of impulse control, abuse and dependence of alcohol and of other legal and illegal drugs, pathological gambling, migraine, fibromyalgia and irritable bowel syndrome. This observation has led to the concept of an "affective spectrum". This phenomenon has to be kept in mind during the diagnostic process and treatment.
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PMID:[Epidemiology and comorbidity of depressive disorders]. 1073 97

Functional somatic illness is a clinical concept used to define medically unexplained somatic symptoms considered to express psychological distress. Functional somatic illness may express underlying psychiatric disorders (e.g. fibromyalgia due to non-fearful panic disorder, irritable bowel syndrome due to bipolar disorder). Sustained physiological activation caused by stressful life events combined with catastrophic thinking may be another cause. Functional somatic illness may also be caused by classic conditioning of physiological responses that may have been triggered by biological or emotional stimuli. Operant conditioning may also be a cause. The therapeutic alliance relies on acceptance of the reality of the subjective complaints, without a priori acceptance of the patient's attribution of the cause of the symptoms. We recommend initial exploration of the patient's own ideas about aetiology, including appropriate medical tests. The physician should then change the agenda to a biopsychosocial perspective and identify current stressors and psychosocial variables that reinforce symptoms. Only a few randomised trials have been performed. They suggest that psychological treatment should be systematic and structured, with a focus on information, alternative ways of perception, and problem solving. Active forms of physiotherapy and psychopharmacological drugs may be of some benefit in selected patients.
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PMID:[Functional somatic diseases--a review]. 1209 7

It has long been recognized that the symptom complex of fibromyalgia can be seen with hypothyroidism. Hypothyroidism may been categorized, like diabetes, into type I (hormone deficient) and type II (hormone resistant). Most cases of fibromyalgia fall into the latter category. The syndrome is reversible with treatment, and is usually of late onset. It is likely more often acquired than due to mutated receptors. Now that there is evidence to support the hypothesis that fibromyalgia may be due to thyroid hormone resistance, four major questions appear addressable. First, can a simple biomarker be found to help diagnose it? Second, what other syndromes similar to Fibromyalgia may share a thyroid-resistant nature? Third, in non-genetic cases, how is resistance acquired? Fourth, what other methods of treatment become available through this new understanding? Preliminary evidence suggests that serum hyaluronic acid is a simple, inexpensive, sensitive, and specific test that identifies fibromyalgia. Overlapping symptom complexes suggest that chronic fatigue syndrome, Gulf war syndrome, premenstrual syndrome, post traumatic stress disorder, breast implant silicone sensitivity syndrome, bipolar affective disorder, systemic candidiasis, myofascial pain syndrome, and idiopathic environmental intolerance are similar enough to fibromyalgia to merit investigation for possible thyroid resistance. Acquired resistance may be due most often to a recently recognized chronic consumptive coagulopathy, which itself may be most often associated with chronic infections with mycoplasmids and related microbes or parasites. Other precipitants of thyroid resistance may use this or other paths as well. In addition to experimentally proven treatment with supraphysiologic doses of thyroid hormone, the thyroid-resistant disorders might be treatable with anti-hypercoagulant, anti-infective, insulin-sensitizing, and hyaluronolytic strategies.
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PMID:A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone. 1288

Bipolar disorder is characterized by chronic and recurrent symptoms including mania, hypomania, and depressive and mixed episodes, with approximately 5.7 million Americans over age 18, or 2.6% of the U.S. population, suffering from the illness. The prevalence of the disorder may be higher due to its chronic and recurrent nature. Individuals with bipolar disorder often first present in general medical settings with depressive symptomatology. Long-term management typically occurs in mental health settings by psychiatrists or other mental health specialists. While there have been major advances in pharmacotherapy for bipolar disorder, evidence-based information on drug effectiveness is not always easily accessible to prescribers in daily practice. Available information has sometimes led to inappropriate use of various classes of drugs, specifically antiepileptic drugs (AEDs), for bipolar disorder. Originally approved in 1993 by the U.S. Food and Drug Administration (FDA) only for adjunctive treatment of partial complex seizures, the manufacturer of gabapentin (Neurontin), an AED, promoted its off-label use for treatment of psychiatric disorders, including bipolar disorder. The efficacy of the drug for this indication had not been demonstrated, nor had the manufacturer sought FDA approval for the indication. In 2004, 50 Attorneys General settled consumer protection claims regarding alleged deceptive off-label marketing practices of Pfizer subsidiary Warner-Lambert. At about the same time, a consortium of State Medicaid agencies funded a drug class review to compare effectiveness and adverse event profiles of AEDs in the treatment of bipolar mood disorder, neuropathic pain, and fibromyalgia. This article presents a summary of the findings from the drug class review related to prescription of the AEDs in bipolar disorder.
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PMID:Effectiveness of antiepileptic drugs for the treatment of bipolar disorder: findings from a systematic review. 1903 5

Despite the high prevalence of insomnia in the primary care setting, only a small proportion of patients report sleep problems to their physician. Evidence shows that treatment of insomnia can ameliorate the high socioeconomic burden associated with the disorder, as well as improve patient outcomes in coexistent diseases such as depression, bipolar disorder, rheumatoid arthritis, and fibromyalgia. The first strategy for improving diagnosis of insomnia is heightened awareness of the condition. As the first point of contact for most patients, primary care physicians are in a unique position to improve rates of detection and treatment. All patients should be screened for sleep disorders with such questions as "How is your sleep?" "Do you have trouble getting to sleep or staying asleep?" and "Do you get drowsy during the day or at inappropriate times?" Medical history and physical examination may also reveal possible coexistent psychiatric and medical illnesses that put patients at higher risk for insomnia, as well as suggest involvement of prescription and nonprescription medications and environmental factors that contribute to insomnia. Diagnostic tools such as the Epworth Sleepiness Scale and the Sleep Hygiene Self-Test can aid patients and physicians in recognizing sleep problems, assessing their severity, and measuring improvement after treatment.
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PMID:Practical diagnostic strategies and tools for insomnia. 1966 87

Fibromyalgia is a chronic musculoskeletal pain condition of unknown etiology that predominantly affects women. Lifetime mood and anxiety disorders are common in patients with fibromyalgia and affect the course and severity of fibromyalgia. Recent fibromyalgia clinical trials have included clinical assessments to identify comorbid psychiatric disorders and determine the impact of comorbidity on treatment response. Options for the treatment of fibromyalgia patients with comorbid major depressive disorder or anxiety disorders include antidepressants with dual effects on serotonin and norepinephrine (eg, venlafaxine, duloxetine), which reduce pain in patients with fibromyalgia and have antidepressant and anxiolytic activity. Other possible treatments for anxiety or sleep disturbances associated with fibromyalgia include the alpha-2-delta ligands (eg, pregabalin, gabapentin) that reduce pain in fibromyalgia patients, have anxiolytic effects, and enhance slow-wave sleep. Antidepressants or alpha-2-delta ligands should be combined with established mood stabilizers in patients with comorbid fibromyalgia and bipolar disorder. There is also evidence to support exercise and cognitive-behavioral therapy in the treatment of fibromyalgia and mood or anxiety disorders. Many patients would likely benefit from combinations of pharmacologic and nonpharmacologic treatments.
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PMID:Management of psychiatric comorbidity in fibromyalgia. 1981 76

Between 1990 and 2011 the following fifteen new antiepileptic drugs (AEDs) were approved: eslicarbazepine acetate, felbamate, gabapentin, lacosamide, lamotrigine, levetiracetam, oxcarbazepine, pregabalin, retigabine, rufinamide, stiripentol, tiagabine, topiramate, vigabatrin, and zonisamide. These AEDs (except felbamate) offer appreciable advantages in terms of their favorable pharmacokinetics, improved tolerability and lower potential for drug interactions. All AEDs introduced after 1990 that are not second generation drugs (with the exception of vigabatrin and tiagabine) were developed empirically (sometimes serendipitously) utilizing mechanism-unbiased anticonvulsant animal models. The empirical nature of the discovery of new AEDs in the last three decades coupled with their multiple mechanisms of action explains their diverse chemical structures. The availability of old and new AEDs with various activity spectra and different tolerability profiles enables clinicians to better tailor drug choice to the characteristics of individual patients. With fifteen new AEDs having entered the market in the past 20years the antiepileptic market is crowded. Consequently, epilepsy alone is not attractive in 2011 to the pharmaceutical industry even though the clinical need of refractory epilepsy remains unmet. Due to this situation, future design of new AEDs must also have a potential in non-epileptic CNS disorders such as neuropathic pain, migraine prophylaxis and bipolar disorder or fibromyalgia as demonstrated by the sales revenues of pregabalin, topiramate and valproic acid. This review analyzes the effect that the emerging knowledge on the chemical properties of the old AEDs starting from phenobarbital (1912) has had on the design of subsequent AEDs and new therapeutics as well as the current approach to AED discovery.
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PMID:Chemical properties of antiepileptic drugs (AEDs). 2221 Feb 79

Persons with single copies of common alpha-1-antitrypsin polymorphisms such as S and Z are often considered "silent carriers". Published evidence however supports a complex behavioral phenotype or trait - intense creative energy ("ICE")-associated with A1AT polymorphisms. We now confirm that phenotype and present an association of fibromyalgia syndrome (FMS) and A1AT in a consecutive series of neurological patients. This is a retrospective case control series of 3176 consecutive patients presenting to Duke University Memory Clinic (747 patients) and to regional community-based Caldwell Hospital Neurology and Memory center (2429 patients). Work-up included medical history and examination, psychological evaluation, and genetic analysis. Chronic widespread pain (CWP) or FMS were diagnosed according to clinical guidelines, mostly as secondary diagnoses. Neurological patients carrying A1AT polymorphisms were common (ca 16% prevalence) and carriers had significantly higher use of inhaler and anxiolytic medications. Patients with ICE phenotype had a significantly higher proportion of A1AT polymorphisms (42%) compared to non-ICE patients (13%). Presence of CWP or FMS was common (14-22%) with average age at presentation of 56 years old and mostly female gender (82%). Patients with CWP/FMS had again significantly higher proportion of A1AT polymorphisms (38%) compared to other neurological patients (13%). Patients with anxiety disorders, bipolar I or bipolar II disorders or PTSD also had increased proportion of A1AT polymorphisms and significant overlap with ICE and FMS phenotype. Significant reductions in CWP/FMS prevalence are seen in apolipoprotein E4 carriers and methylene tetrahydrofolate reductase (MTHFR) mutation homozygotes. Since ICE phenotype is reported as a lifelong behavioral attribute, the presumption is that A1AT carriers have fundamental differences in brain development and inflammatory response. In support of this concept is finding those persons reporting a diagnosis of juvenile rheumatoid or idiopathic arthritis (JRA, JIA) had a significantly high proportion of A1AT polymorphisms (63%), suggesting a spectrum for JRA to later FMS presentations. Likewise, persons reporting a history of attention deficit disorder (ADD) had an increased proportion of A1AT polymorphisms (26%) compared to non-ADD persons (13%). Toxic environmental exposures are common (23%) and associated with diagnoses of PSP, PPA, FTD, FTD-PD, PD and ADVD. A1AT carriers were increased in cases of toxic exposure and PSP, PPA and FTD-PD. Our findings support the ICE behavioral phenotype for A1AT polymorphism carriers and the reported association with anxiety and bipolar spectrum disorders. We now extend that phenotype to apparent vulnerability to inflammatory muscle disease in a spectrum from JRA to fibromyalgia (FMS) and specific behavioral subsets of ADD, PTSD, and specific late onset neurological syndromes (FTD-PD and PPA). High and low risk FMS subsets can be defined using A1AT, MTHFR and APOE genotyping. Clinical diagnoses associated with A1AT polymorphisms included fibromyalgia, JRA/JIA, bipolar disorder, PTSD, primary progressive aphasia and FTDPD, but not most Alzheimer Disease subtypes. These results support an extended phenotype for A1AT mutation carriers beyond liver and lung vulnerability to selective advantages: ICE phenotype and disadvantages: fibromyalgia, affective disorders, and selected late onset neurological syndromes.
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PMID:Fibromyalgia, mood disorders, and intense creative energy: A1AT polymorphisms are not always silent. 2241 31

We have recently reported that memantine has a clinically relevant antimanic and long-lasting mood-stabilizing effect in treatment-resistant bipolar disorders, both as augmenting agent and as monotherapy. We have also observed an acute antimanic and sustained mood-stabilizing effect in a small number of patients with bipolar I disorder who had had minimal previous pharmacotherapy. In this article, we report the case of a young woman suffering from bipolar II disorder with associated fibromyalgia, in whom memantine showed an acute antimanic and a long-term prophylactic effect on both bipolar disorder as well as the associated fibromyalgia syndrome.
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PMID:Memantine in the treatment and prophylaxis of bipolar II disorder and comorbid fibromyalgia: a case report. 2484 98

In many psychiatric, neurodegenerative and systemic inflammatory disorders circadian melatonin is decreased whilst melatonin enzymes and melatonin receptors are genetic susceptibility factors. Treatment with melatonin is useful in a diverse range of medical conditions, including bipolar disorder, Alzheimer's disease, depression and fibromyalgia. Decreased melatonin effects are classically attributed to lost pineal production. However, melatonin, along with its immediate precursor N-acetylserotonin (NAS), is produced by many, if not all, mitochondrial containing cells, including immune cells and central glia. Here we review the data on local melatonin and NAS production and propose that astrocyte melatonin and NAS efflux is crucial to local central inflammation regulation at the glia-neuronal interface. Melatonin and NAS provide antioxidant and anti-inflammatory effects, as well as increasing mitochondrial oxidative phosphorylation and functioning. Consequently, their decreased production at sites of local inflammation is proposed to underlie melatonin's genetic association with a diverse range of medical conditions. Similarly the benefits of serotonin boosting medications, including antidepressants, across a wide range of conditions are partly mediated by increasing serotonin availability for astrocytic local NAS and melatonin production. Such a conceptualization incorporates a plethora of data across different disorders, especially the commonalities in oxidative and nitrosative stress, anti-oxidants, tryptophan catabolites and mitochondrial dysregulation evident in a diverse array of medical conditions. Glia melatonin and NAS regulation are important treatment targets in psychiatric disorders, neurodegenerative disorders and glioma.
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PMID:Local melatonin regulates inflammation resolution: a common factor in neurodegenerative, psychiatric and systemic inflammatory disorders. 2501 20


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