Fibromyalgia: Difference between revisions
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Fibromyalgia is a chronic medical condition that is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. In the field of musculoskeletal medicine in New Zealand, the highly subjective nature of the diagnostic criteria has meant that it is a controversial diagnosis in this specialty. Recent work has found that 40-50% of patients have [[Small Fibre Neuropathy|small fibre neuropathy]].<ref name="Maslinska">Maslinska et al. Small fibre neuropathy as a part of fibromyalgia or a separate diagnosis? Int. J. Clin. Rheumatol. (2018) 13(6), 353-359. [https://www.openaccessjournals.com/articles/small-fiber-neuropathy-as-a-part-of-fibromyalgia-or-a-separate-diagnosis.pdf Full Text]</ref> | Fibromyalgia is a chronic medical condition that is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. In the field of musculoskeletal medicine in New Zealand, the highly subjective nature of the diagnostic criteria has meant that it is a controversial diagnosis in this specialty. Recent work has found that 40-50% of patients have [[Small Fibre Neuropathy|small fibre neuropathy]].<ref name="Maslinska">Maslinska et al. Small fibre neuropathy as a part of fibromyalgia or a separate diagnosis? Int. J. Clin. Rheumatol. (2018) 13(6), 353-359. [https://www.openaccessjournals.com/articles/small-fiber-neuropathy-as-a-part-of-fibromyalgia-or-a-separate-diagnosis.pdf Full Text]</ref> | ||
==Epidemiology== | ==Epidemiology== | ||
Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. | Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. The peak onset is 20-50 and is more common in women. | ||
==Pathophysiology== | ==Pathophysiology== | ||
A popular hypothesis is that fibromyalgia is a [[Central Sensitisation|centralised pain syndrome]]. This hypothesis describes fibromyalgia patients as having augmented pain, and augmented sensory processing in the brain. There is increased connectivity to pro-nociceptive brain regions, and decreased connectivity to anti-nociceptive regions. Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction.{{#pmid:30238382|manuel}} | A popular hypothesis is that fibromyalgia is a [[Central Sensitisation|centralised pain syndrome]]. This hypothesis describes fibromyalgia patients as having augmented pain, and augmented sensory processing in the brain. There is increased connectivity to pro-nociceptive brain regions, and decreased connectivity to anti-nociceptive regions. Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction.{{#pmid:30238382|manuel}} | ||
Fibromyalgia has also been described as a sympathetically maintained or dysautonomia-related neuropathic pain syndrome. The pain has neuropathic features, and is independent of stimulus, and may be accompanied by allodynia and paraesthesias. Nociceptive fibres may be sensitised.<ref name="manuel"/> | Fibromyalgia has also been described as a sympathetically maintained or dysautonomia-related neuropathic pain syndrome. The pain has neuropathic features, and is independent of stimulus, and may be accompanied by allodynia and paraesthesias. Nociceptive fibres may be sensitised.<ref name="manuel" /> | ||
== | ==Clinical Features== | ||
The | The patient may report persistent pain for over three months, pain in more than one region, intrusive fatigue, impaired memory ("fibro fog"), sleep disturbance, and gastrointestinal disturbance. Other symptoms include increased pain sensitivity (e.g. pain with hugging), muscle stiffness, headaches, anxiety, depression, and irregular periods. | ||
== Diagnosis== | |||
Fibromyalgia is over diagnosed. In one study in the US, the majority of individuals with a clinical diagnosis of fibromyalgia do not fulfil the diagnostic criteria.<ref>Walitt B, Katz RS, Bergman MJ, Wolfe F. Three-Quarters of Persons in the US Population Reporting a Clinical Diagnosis of Fibromyalgia Do Not Satisfy Fibromyalgia Criteria: The 2012 National Health Interview Survey. PLoS One. 2016 Jun 9;11(6):e0157235. doi: 10.1371/journal.pone.0157235. PMID: 27281286; PMCID: PMC4900652.</ref> | |||
===2010 Criteria=== | |||
{{PDF|Fibromyalgia Diagnostic Criteria 2010.pdf|Fibromyalgia Diagnostic Criteria ACR 2010}} | |||
In 2010 the American College of Rheumatology (ACR) revamped the diagnostic criteria. There is no requirement for a tender point examination like in the ACR 1990 classification. Three criteria must be met for the diagnosis | |||
#Widespread Pain Index (WPI) ≥ 7/19 and Symptom Severity Scale (SSS) Score ≥ 5/12 or WPI between 3–6/19 and SSS ≥ 9/12 | #Widespread Pain Index (WPI) ≥ 7/19 and Symptom Severity Scale (SSS) Score ≥ 5/12 or WPI between 3–6/19 and SSS ≥ 9/12 | ||
#Symptoms being present at a similar level for at least 3 months | #Symptoms being present at a similar level for at least 3 months | ||
#The patient does not have another disorder that would otherwise sufficiently explain the pain. | #The patient does not have another disorder that would otherwise sufficiently explain the pain. | ||
Conditions 1 and 2 are assessed by the Fibromyalgia Survey Questionnaire. | Conditions 1 and 2 are assessed by the Fibromyalgia Survey Questionnaire. | ||
{{PDF| | ===2016 Criteria=== | ||
{{PDF|Fibromyalgia diagnostic criteria 2016.pdf|Fibromyalgia Diagnostic Criteria ACR 2016}} | |||
The criteria were modified in 2016. A major change was that other conditions don't need to be ruled out and it can be diagnosed irrespective of other diagnoses. | |||
==Differential Diagnosis == | |||
{{DDX Box|ddx-title=Differential Diagnosis of Widespread Pain|ddx-text={{Widespread Pain DDX}}}} | |||
==Small Fibre Neuropathy== | ===Small Fibre Neuropathy=== | ||
{{main|Small Fibre Neuropathy}} | {{main|Small Fibre Neuropathy}} | ||
There has been a large amount of research confirming the presence of [[Small Fibre Neuropathy|small fibre neuropathy (SFN)]] in some fibromyalgia patients. Overall it appears that around 40-50% of fibromyalgia patients actually have SFN - a neuropathic pain syndrome. | There has been a large amount of research confirming the presence of [[Small Fibre Neuropathy|small fibre neuropathy (SFN)]] in some fibromyalgia patients. Overall it appears that around 40-50% of fibromyalgia patients actually have SFN - a neuropathic pain syndrome. | ||
For example, Oaklander et al found that in 41 patients with unexplained widespread pain that started before the age of 21, 59% of children at definite SFN, 17% had probable SFN, and 22% had possible SFN.<ref>{{#pmid:23478869}}</ref> They then found that in a group of 27 fibromyalgia patients and 30 matched controls, 41% of fibromyalgia patients had definite SFN, compared to 3% in the control group.<ref>{{#pmid:23748113}}</ref> See Manuel et al for a summary.<ref name="manuel"/> | For example, Oaklander et al found that in 41 patients with unexplained widespread pain that started before the age of 21, 59% of children at definite SFN, 17% had probable SFN, and 22% had possible SFN.<ref>{{#pmid:23478869}}</ref> They then found that in a group of 27 fibromyalgia patients and 30 matched controls, 41% of fibromyalgia patients had definite SFN, compared to 3% in the control group.<ref>{{#pmid:23748113}}</ref> See Manuel et al for a summary.<ref name="manuel" /> | ||
Some central sensitisation framework proponents claim that the presence of small fibre neuropathy has unclear relevance, and may be a consequence not a cause of fibromyalgia, with peripheral nervous system changes in response to central nervous system sensitisation. This view is not universally shared. Manuel et al believe fibromyalgia to be related to a persistent hyper-adrenergic state, leading to dorsal root ganglia hyper-excitability, and neuropathic pain. They note the role of dorsal root ganglia sodium channel variants in the condition.<ref name="manuel" /> | |||
== Investigations == | |||
Screening tests include FBC, ESR, CRP, CK, LFTs, TFTs, LFTs, glucose, UEC | |||
If there is suspicion of axial [[spondyloarthritis]] then consider HLA-B27, and RF if psoriatic. | |||
If there is suspicion of [[Rheumatoid Arthritis]] then include anti-CCP, and RF. | |||
== Treatment == | |||
Exercise is first line, medication is second line. | |||
==Resources== | |||
{{PDF|Fibromyalgia Diagnostic Criteria 2016 Article - Wolfe 2016.pdf}} | |||
{{Members link}} | |||
==See Also== | ==See Also== | ||
| Line 35: | Line 59: | ||
==References== | ==References== | ||
<references/> | <references /> | ||
{{Reliable sources}} | {{Reliable sources}} | ||
[[Category:Widespread]] | [[Category:Widespread]] | ||
[[Category:Rheumatology]] | [[Category:Rheumatology]] | ||
Revision as of 20:10, 5 April 2022
Fibromyalgia is a chronic medical condition that is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. In the field of musculoskeletal medicine in New Zealand, the highly subjective nature of the diagnostic criteria has meant that it is a controversial diagnosis in this specialty. Recent work has found that 40-50% of patients have small fibre neuropathy.[1]
Epidemiology
Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. The peak onset is 20-50 and is more common in women.
Pathophysiology
A popular hypothesis is that fibromyalgia is a centralised pain syndrome. This hypothesis describes fibromyalgia patients as having augmented pain, and augmented sensory processing in the brain. There is increased connectivity to pro-nociceptive brain regions, and decreased connectivity to anti-nociceptive regions. Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction.[2]
Fibromyalgia has also been described as a sympathetically maintained or dysautonomia-related neuropathic pain syndrome. The pain has neuropathic features, and is independent of stimulus, and may be accompanied by allodynia and paraesthesias. Nociceptive fibres may be sensitised.[2]
Clinical Features
The patient may report persistent pain for over three months, pain in more than one region, intrusive fatigue, impaired memory ("fibro fog"), sleep disturbance, and gastrointestinal disturbance. Other symptoms include increased pain sensitivity (e.g. pain with hugging), muscle stiffness, headaches, anxiety, depression, and irregular periods.
Diagnosis
Fibromyalgia is over diagnosed. In one study in the US, the majority of individuals with a clinical diagnosis of fibromyalgia do not fulfil the diagnostic criteria.[3]
2010 Criteria
In 2010 the American College of Rheumatology (ACR) revamped the diagnostic criteria. There is no requirement for a tender point examination like in the ACR 1990 classification. Three criteria must be met for the diagnosis
- Widespread Pain Index (WPI) ≥ 7/19 and Symptom Severity Scale (SSS) Score ≥ 5/12 or WPI between 3–6/19 and SSS ≥ 9/12
- Symptoms being present at a similar level for at least 3 months
- The patient does not have another disorder that would otherwise sufficiently explain the pain.
Conditions 1 and 2 are assessed by the Fibromyalgia Survey Questionnaire.
2016 Criteria
The criteria were modified in 2016. A major change was that other conditions don't need to be ruled out and it can be diagnosed irrespective of other diagnoses.
Differential Diagnosis
- Autoimmune: Polymyalgia Rheumatica, Sjogren's Disease, Rheumatoid Arthritis, Connective tissue disease (autoimmune), Inflammatory myositis, Sarcoidosis, Celiac disease, Inflammatory Bowel Disease, Sarcoidosis
- Genetic: Heritable Connective Tissue Disorders, Neuromuscular Diseases (e.g. Myotonic Dystrophy type 2, Pompe Disease)
- Idiopathic: Fibromyalgia, Degenerative myopathies, Small Fibre Neuropathy
- Primary Joint disease: Osteoarthritis
- Neoplastic disease: Metastases, Multiple myeloma, Leukaemia, Lymphoma
- Infections: bacterial endocarditis, hepatitis B and C
- Bone disease: Osteomalacia, Osteomyelitis
- Endocrine: Hypothyroidism and hyperthyroidism, Hyperparathyroidism, Acromegaly, Diabetes, Vitamin D deficiency, endocrine myopathies
- Neurological: Parkinson disease, Neuropathies, Motor neurone disease, Chronic Inflammatory Demyelinating Polyneuropathy, Multiple sclerosis, Myalgias in rare disease (e.g., Stiff Person Syndrome), Myalgias with lesions of the central and peripheral nervous system
- Medication: opioids, statins, aromatase inhibitors, carbimazole, ezitimibe, metoprolol, minoxidil, PPIs, salbutamol, amiodarone, colchicine, ACE inhibitors
Small Fibre Neuropathy
- Main article: Small Fibre Neuropathy
There has been a large amount of research confirming the presence of small fibre neuropathy (SFN) in some fibromyalgia patients. Overall it appears that around 40-50% of fibromyalgia patients actually have SFN - a neuropathic pain syndrome.
For example, Oaklander et al found that in 41 patients with unexplained widespread pain that started before the age of 21, 59% of children at definite SFN, 17% had probable SFN, and 22% had possible SFN.[4] They then found that in a group of 27 fibromyalgia patients and 30 matched controls, 41% of fibromyalgia patients had definite SFN, compared to 3% in the control group.[5] See Manuel et al for a summary.[2]
Some central sensitisation framework proponents claim that the presence of small fibre neuropathy has unclear relevance, and may be a consequence not a cause of fibromyalgia, with peripheral nervous system changes in response to central nervous system sensitisation. This view is not universally shared. Manuel et al believe fibromyalgia to be related to a persistent hyper-adrenergic state, leading to dorsal root ganglia hyper-excitability, and neuropathic pain. They note the role of dorsal root ganglia sodium channel variants in the condition.[2]
Investigations
Screening tests include FBC, ESR, CRP, CK, LFTs, TFTs, LFTs, glucose, UEC
If there is suspicion of axial spondyloarthritis then consider HLA-B27, and RF if psoriatic.
If there is suspicion of Rheumatoid Arthritis then include anti-CCP, and RF.
Treatment
Exercise is first line, medication is second line.
Resources
See Also
References
- ↑ Maslinska et al. Small fibre neuropathy as a part of fibromyalgia or a separate diagnosis? Int. J. Clin. Rheumatol. (2018) 13(6), 353-359. Full Text
- ↑ 2.0 2.1 2.2 2.3 Martínez-Lavín. Fibromyalgia and small fiber neuropathy: the plot thickens!. Clinical rheumatology 2018. 37:3167-3171. PMID: 30238382. DOI.
- ↑ Walitt B, Katz RS, Bergman MJ, Wolfe F. Three-Quarters of Persons in the US Population Reporting a Clinical Diagnosis of Fibromyalgia Do Not Satisfy Fibromyalgia Criteria: The 2012 National Health Interview Survey. PLoS One. 2016 Jun 9;11(6):e0157235. doi: 10.1371/journal.pone.0157235. PMID: 27281286; PMCID: PMC4900652.
- ↑ Oaklander & Klein. Evidence of small-fiber polyneuropathy in unexplained, juvenile-onset, widespread pain syndromes. Pediatrics 2013. 131:e1091-100. PMID: 23478869. DOI. Full Text.
- ↑ Oaklander et al.. Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia. Pain 2013. 154:2310-6. PMID: 23748113. DOI. Full Text.
Literature Review
Literature Review
- Reviews from the last 7 years: review articles, free review articles, systematic reviews, meta-analyses, NCBI Bookshelf
- Articles from all years: PubMed search, Google Scholar search.
- TRIP Database: clinical publications about evidence-based medicine.
- Other Wikis: Radiopaedia, Wikipedia Search, Wikipedia I Feel Lucky, Orthobullets,
