Fibromyalgia—pathways and neurotransmitters

Stahl, Stephen M.

doi:10.1002/hup.1029

Cited by 51 publications

(46 citation statements)

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“…In addition, research studies over the past 20 years have shown that FMS is a pain amplification disorder with clear evidence for a pathogenesis within the central nervous system [10,11]. For example, in ours and other studies, it has been reported that there were elevated levels of substance P and nerve growth factor in the cerebrospinal fluid (CSF) of patients with FMS [7,12,13].…”

Section: Introductionmentioning

confidence: 84%

A brain-derived neurotrophic factor polymorphism Val66Met identifies fibromyalgia syndrome subgroup with higher body mass index and C-reactive protein

2011

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A common single nucleotide polymorphism (SNP) in the gene of brain-derived neurotrophic factor (BDNF) results from a substitution at position 66 from valine (Val) to methionine (Met) and may predispose to human neuropsychiatric disorders. We proposed to determine whether these BDNF gene SNPs were associated with fibromyalgia syndrome (FMS) and/or any of its typical phenotypes. Patients with FMS (N = 95) and healthy normal controls (HNC, N = 58) were studied. Serum high-sensitivity C-reactive protein (hsCRP) levels were measured using an enzyme-linked immunosorbent assay (ELISA). The BDNF SNPs were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).The BDNF SNP distribution was 65 (68%) Val/Val, 28 (30%) Val/Met, and 2 (2%) Met/Met for FMS and 40 (69%), 17(29%), and 1 (2%) for HNC, respectively. The serum high-sensitivity C-reactive protein (hsCRP)and body mass index (BMI) in FMS were higher than in HNC. The FMS with BDNF Val66Val had significantly higher mean BMI (P = 0.0001) and hsCRP (P = 0.02) than did FMS carrying the Val66Met genotype. This pattern was not found in HNC. Phenotypic measures of subjective pain, pain threshold, depression, or insomnia did not relate to either of the BDNF SNPs in FMS. The relative distribution BDNF SNPs did not differ between FMS and HNC. The BDNF Val66Met polymorphism is not selective for FMS. The BDNF Val66Val SNP identifies a subgroup of FMS with elevated hsCRP and higher BMI. This is the first study to associate a BDNF polymorphism with a FMS subgroup phenotype.

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Section: Introductionmentioning

confidence: 84%

A brain-derived neurotrophic factor polymorphism Val66Met identifies fibromyalgia syndrome subgroup with higher body mass index and C-reactive protein

2011

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“…Hastalığın etyolojisi ve farmakopatolojisi yeterince anlaşılamamıştır. Ağrının santral modulasyonu ile inen inhibitör sistemde bozukluk ve substans P hiperaktivitesini ile açıklanmaktadır 6 . Santral ağrı yolaklarının disfonksiyonunun yol açtığı jeneralize ağrı sensitizasyonundan kaynaklandığı düşünülmektedir.…”

Section: Fibromiyalji Etyopatogeneziunclassified

“…Amerikan Romatizma Savaş (ACR) Derneği Sınıflama Kriterlerine göre diğer bölgelere kıyasla daha ağrılı bulunan 18 tipik hassas nokta kabul edilmiştir. Sınıflama amaçlı her iki kriteri de karşılıyor olması gereklidir 6,7,8,10 .…”

Section: Fibromiyaljide Klinik Bulgularunclassified

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Fibromiyaljide Kognitif Disfonksiyon

Koca¹

2015

Arşiv Kaynak Tarama Dergisi

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The primary symptom of fibromyalgia is widespread pain with muscle tenderness to light palpation. However many patients report a wide range of symptoms including pain, dyscognition, sleep disturbances, fatigue and mood disorders (frequently depression). Such symptoms seem to be related to one another. Besides, a decrease in concentration and memory disorder has recognised as an independent symptom yet; added into literature under the terms 'dyscognition' and 'fibrofog'. Recently clinicians interested in investigations about dyscognition in fibromyalgia syndrome. Cognitive symptoms may be exacerbated by the presence of depression, anxiety, sleep dysorders, endocrine disregulations and pain; but the relationship is unclear. Additionally some of recent studies suggest that insulin resistance may represent a risk factor for memory impairment in these patients. There is lack of standardized tests, treatment methods and studies for understanding pathophysiologic pathways of cognitive problems (memory, concentration) in fibromyalgia. Key words: Dyscognition, fibromyalgia syndrome, insulin resistance, sleep disorder ÖZET Fibromiyalji'de asıl semptom hafif palpasyon ile olan kas hassasiyeti ve yaygın ağrıdır. Bununla birlikte hastalar ağrı, kognitif disfonksiyon, uyku bozukluğu, yorgunluk ve duygudurum bozuklukları (sıklıkla depresyon) gibi geniş bir yelpazedeki semptomlardan yakınırlar. Bu semptomlar birbirleri ile ilişkili gibi görünmektedir. Bunların yanında konsantrasyonda azalma ve hafıza bozukluğu artık bağımsız bir semptom olarak ele alınmakla birlikte literatüre 'kognitif disfonksiyon' ve 'fibro-fog' terimleri adı altında eklenmiştir. Son yıllarda klinisyenler fibromiyalji sendromundaki kognitif disfonksiyon hakkındaki araştırmalara ilgi duymaya başlamışlardır. Kognitif semptomlar depresyon, anksiyete, uyku bozuklukları, endokrin dengesizlikler ve ağrı varlığında artış göstermektedir. Ek olarak yeni bazı çalışmalarda insülin direncinin bu hastalarda hafıza bozukluğu için risk faktörü olabileceğini

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“…15 Dysfunction in these descending pathways is thought to result in the hyperalgesic (heightened sensitivity to pain) and allodynic (painful response to nonpainful stimuli) states experienced by patients with FM and other related central sensitization syndromes such as IBS and TMD. 16,17 The potential benefit of milnacipran in the treatment of FM was further supported by analgesic effects of SNRIs in animal models of pain, 18 as well as findings showing decreased cerebrospinal fluid levels of serotonin and norepinephrine metabolites in patients with FM. 19 Moreover, therapeutic benefits in FM had already been observed with drugs that inhibit the reuptake of both serotonin and norepinephrine, such as the TCA, amitriptyline.…”

Section: Introductionmentioning

confidence: 95%

Role and rationale for the use of milnacipran in the management of fibromyalgia

Kranzler¹,

Gendreau

2010

NDT

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Fibromyalgia (FM) is a complex syndrome characterized by chronic widespread musculoskeletal pain which is often accompanied by multiple other symptoms, including fatigue, sleep disturbances, decreased physical functioning, and dyscognition. Due to these multiple symptoms, as well as high rates of comorbidity with other related disorders, patients with FM often report a reduced quality of life. Although the pathophysiology of FM is not completely understood, patients with FM experience pain differently from the general population, most likely due to dysfunctional pain processing in the central nervous system leading to both hyperalgesia and allodynia. In many patients with FM, this aberrant pain processing, or central sensitization, appears to involve decreased pain inhibition within the spinal tract, which is mediated by descending pathways that utilize serotonin, norepinephrine, and other neurotransmitters. The reduced serotonin and norepinephrine levels observed in patients with FM suggest that medications which increase the levels of these neurotransmitters, such as serotonin and norepinephrine reuptake inhibitors (SNRIs), may have clinically beneficial effects in FM and other chronic pain conditions. Milnacipran is an SNRI that has been approved for the management of FM. In clinical trials, treatment with milnacipran for up to 1 year has been found to improve the pain and other symptoms of FM. Because FM is characterized by multiple symptoms that all contribute to the decreased quality of life and ability to function, the milnacipran pivotal trials implemented responder analyses. These utilized a single composite endpoint to identify the proportion of patients who reported simultaneous and clinically significant improvements in pain, global disease status, and physical function. Other domains assessed during the milnacipran trials include fatigue, multidimensional functioning, mood, sleep quality, and patient-reported dyscognition. This review article provides information intended to help clinicians make informed decisions about the use of milnacipran in the clinical management of patients with FM. It draws primarily on results from 2 of the pivotal clinical trials that formed the basis of approval of milnacipran in the United States by the Food and Drug Administration.

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Fibromyalgia—pathways and neurotransmitters

Cited by 51 publications

References 47 publications

A brain-derived neurotrophic factor polymorphism Val66Met identifies fibromyalgia syndrome subgroup with higher body mass index and C-reactive protein

A brain-derived neurotrophic factor polymorphism Val66Met identifies fibromyalgia syndrome subgroup with higher body mass index and C-reactive protein

Fibromiyaljide Kognitif Disfonksiyon

Role and rationale for the use of milnacipran in the management of fibromyalgia

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