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Fibromyalgia

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Written by: Dr Jeremy Steinberg ā€“ created: 31 March 2021; last modified: 27 April 2025

This page is probably complete!
It is awaiting peer review
Both ascending and descending pathways can influence pain sensitivity in Fibromyalgia.
Fibromyalgia
Epidemiology 2-4% of the population
Causes Combination of genetic and environmental influences
Pathophysiology Dysregulation of central pain processing.
Classification Can be primary or secondary to another pain condition.
Risk Factors Family history, environmental stressors, and certain medical conditions like RA and AS.
Clinical Features Chronic widespread pain, increased pain sensitivity, fatigue and other cognitive difficulties, and sleep disturbance.
Diagnosis ACR diagnostic criteria
Tests Limited laboratory testing to rule out other conditions.
Treatment Non-pharmacological and pharmacological
Prognosis Usually a lifelong condition
This page or section deals with a controversial topic.
Please use your clinical judgement.

Fibromyalgia is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. It is usually a lifelong disorder. It is the prototypical centralised pain state where there is a fundamental problem with augmented pain or sensory processing and manifests in different parts of the body over time. While mental health complaints are common, the pain itself is not psychosomatic in nature.

Epidemiology

Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. It is the second most common rheumatological disorder after osteoarthritis. 10-15% of the population have chronic widespread pain, and there is no clear boundary separating those that have chronic widespread pain from those that have fibromyalgia.

The peak onset is 20-50 but it can occur at any age. and is about twice as common in women. In clinical practice it is predominantly diagnosed in women in late middle age. Other risk factors are increasing age, family history of chronic pain, obesity, and poor mental and/or physical health. It occurs in all countries and ethnicities.

Natural History

Patients with fibromyalgia have roughly double the healthcare utilization compared to matched controls for at least a decade prior to diagnosis. Visits increase rapidly three years prior to diagnosis, then slightly decline after diagnosis, and rise again three years post-diagnosis, remaining at levels comparable to diagnosis but never reaching the level of two years prior to diagnosis. The overall benefit of the diagnostic process and medical input appears questionable at the population level.[1]

Nearly all patients that are eventually diagnosed with fibromyalgia have a long history of having bouts of chronic regional pain various body regions over their lifetime dating back to adolescence.[2] The most common reasons for clinical visits to GPs in order of frequency are depression, fatigue, chest pain, headache, sleep disturbance, dizziness, and IBS.[1]

Risk Factors

There is often a strong familial predisposition to pain. Twin studies show that the risk of developing fibromyalgia is 50% genetic and 50% environmental. First degree relatives are more than 8 times as likely to also have fibromyalgia compared to controls. Many of the genes discovered thus far are involved in the regulation of neurotransmitters that modulate pain sensitivity, but genetic studies are not universally consistent and pain sensitivity is polygenic.[2]

Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction,[3] however it is not a psychosomatic condition. Environmental stressors are often identified, particularly those where there is acute pain that lasts a few weeks. For example motor vehicle accidents or certain infections.

Fibromyalgia is frequently observed as a comorbidity in other chronic pain conditions such as OA, RA, and lupus. About 15-30% of individuals with these rheumatic disorders meet FM criteria, and more individuals do not meet the criteria but display some FM elements, indicating the presence of pathophysiological abnormalities in CNS pain processing. The term "centralized pain" rather than "central sensitisation" is preferred when CNS factors play a significant role in magnifying pain and leading to other somatic symptoms.[2]

Aetiology

While the exact cause remains uncertain, several factors appear to contribute to the development of FM.

  • Genetic Predisposition: A familial component is evident, with first-degree relatives of affected individuals having an eight-fold increased risk. Polymorphisms in genes related to monoamine transport or metabolism have also been associated with a higher risk of developing FM.[4]
  • Environmental and Biological Triggers: Various factors have been implicated as potential triggers, including physical trauma (particularly to the neck and trunk), infections (such as Lyme disease and Epstein-Barr virus), and significant psychosocial stressors.

Pathophysiology

The pain "set point" or "volume control" of an individual is determined partially by the levels of neurotransmitters on the left that amplify pain signals and those on the right that dampen pain signals. Therefore, an increase in neurotransmitters on the left or a decrease in those on the right may result in diffuse hyperalgesia, which is a common symptom of chronic pain conditions. The chart displays the levels of these neurotransmitters in the cerebrospinal fluid of fibromyalgia (FM) patients, with the arrows indicating the direction of abnormality. The opioidergic system is the "odd one out" being increased. Modified from Hochberg.[2]

The pathophysiology of fibromyalgia (FM) is complex and not fully understood, though it is widely considered a centralised pain syndrome. This central sensitization hypothesis suggests that individuals with FM experience augmented pain and sensory processing within the brain. Clinically, this manifests as increased pain in response to normally painful stimuli (diffuse hyperalgesia), pain provoked by normally non-painful stimuli (allodynia), and deficient conditioned pain modulation (normally only tested within quantitative sensory testing)

Central Mechanisms

Altered Brain Activity and Connectivity: Functional magnetic resonance imaging (fMRI) studies support the concept of amplified pain processing. Individuals with FM show pain-related brain activation patterns in response to mild pressure or heat stimuli that most people would perceive merely as touch. Other imaging studies indicate increased connectivity between brain regions involved in promoting pain transmission and decreased connectivity within key anti-nociceptive (pain-inhibiting) regions. See related topic Temporal Summation of Pain.

Neurotransmitter Imbalances: An imbalance between excitatory and inhibitory neurotransmitters is observed. Levels of excitatory neurotransmitters involved in nociception, such as glutamate, substance P, and nerve growth factor, are often increased in the cerebrospinal fluid. This may explain the efficacy of medications like gabapentinoids, which likely reduce glutamatergic activity. Conversely, there is often a decrease in neurotransmitters that inhibit pain or sensory processing, including serotonin, norepinephrine, and GABA. Treatments like y-hydroxybutyrate and low doses of alcohol might counteract low GABA levels.

Dysfunctional Pain Modulation: The descending pain modulatory pathways, which normally regulate pain signals, appear dysfunctional in FM (See related topic Conditioned Pain Modulation).

  • The diffuse noxious inhibitory control (DNIC) response ā€“ a phenomenon where a sustained painful stimulus normally triggers widespread analgesia ā€“ is reduced in FM patients. This reduction might stem from dysfunction in descending opioidergic and serotonergic-noradrenergic pathways. Conditioned Pain Modulation is the clinical analogue of DNIC.
  • The endogenous opioid system shows alterations[5], including potentially increased activity leading to reduced mu-opioid receptor availability. Paradoxically, this can contribute to increased pain sensitivity. Low-dose naltrexone is thought to target this pathway.

Neuroendocrine and Autonomic Disturbances: Disturbances in the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system are frequently described in FM patients, although study findings on their prevalence and precise nature are inconsistent.[6][7] The role these disturbances play in the condition's pathogenesis is still unclear, but multiple psychosocial factors can influence these systems.[2] Some researchers describe FM as potentially representing a common final pathway for the persistent, unresolved activation of an evolutionarily conserved stress response.

Peripheral Mechanisms

Small Fibre Neuropathy (SFN): A significant proportion (around 40-50%) of FM patients exhibit small fiber neuropathy, characterized by damage to small nerve fibers in the skin, peripheral nerves, and autonomic nervous system. Studies, such as those by Oaklander et al., have found objective evidence of SFN in a substantial percentage of both adult and pediatric patients diagnosed with FM or similar widespread pain conditions, compared to healthy controls.[8][9]

Integrating Central and Peripheral Findings

The relationship between central sensitization and SFN in FM is debated. Some proponents of the central sensitization framework suggest SFN might be a consequence rather than a primary cause, potentially arising from peripheral nervous system changes driven by central nervous system sensitization. However, this view is not universally accepted. Researchers like Manuel et al. propose that FM could be related to a persistent hyper-adrenergic state causing dorsal root ganglia hyper-excitability and neuropathic pain, noting the potential role of specific dorsal root ganglia sodium channel variants.

Fibromyalgia appears to result from a complex interplay of genetic predisposition, environmental triggers, central nervous system alterations (including augmented pain processing, neurotransmitter imbalances, and dysfunctional pain modulation), neuroendocrine and autonomic disturbances, and, in many cases, peripheral factors like small fiber neuropathy.

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.

Pain is frequently accompanied by neurologic symptoms e.g. numbness or tingling. It often occurs alongside other chronic pain conditions like migraine, irritable bowel syndrome, endometriosis, and inflammatory arthritis.

A complete rheumatological, orthopaedic, and neurological examination should be performed.

Diagnosis

Fibromyalgia has variably been characterised as being under-diagnosed, over-diagnosed, and mis-diagnosed.[10] In one study in the US, the majority of individuals with a clinical diagnosis of fibromyalgia do not fulfil the diagnostic criteria.[11]

2010 Criteria

Fibromyalgia Diagnostic Criteria 2010.pdf

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

  1. Widespread Pain Index (WPI) ā‰„ 7/19 and Symptom Severity Scale (SSS) Score ā‰„ 5/12 or WPI between 3ā€“6/19 and SSS ā‰„ 9/12
  2. Symptoms being present at a similar level for at least 3 months
  3. 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

Fibromyalgia diagnostic criteria 2016.pdf

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. WikiMSK has a calculator using this diagnostic criteria. Three criteria must be met

  1. WPI ā‰„ 7 and SSS ā‰„ 5 OR WPI 4 to 6 and SSS ā‰„ 9
  2. Generalized pain: at least 4/5 regions
  3. Have the symptoms in section 3 and pain been present at a similar clinical level for at least 3 months?

Differential Diagnosis

The differential diagnosis must be viewed from two different perspectives. The first perspective is recognising that fibromyalgia type symptoms can occur as a co-morbidity alongside another condition. Fibromyalgia occurs alongside 15-30% of individuals with any autoimmune or chronic musculoskeletal pain condition when there is ongoing nociceptive input. This includes Rheumatoid Arthritis (12-20%), Spondyloarthritis (11-50%), lupus erythematosus (5-25%)[12], Ehlers-Danlos syndrome, sickle cell disease, and cancer pain.

The second perspective is understanding that some conditions can mimic the symptoms and so the patient has a different diagnosis entirely, and fibromyalgia is not a comorbidity. Examples of this are Polymyalgia Rheumatica, hypothyroidism, and some neuromuscular conditions like statin-induced myopathy.[2]

A problem occurs when considering another disease that has clinical features that can be similar to those with fibromyalgia. An obvious example is metastatic cancer.

Differential Diagnosis of Widespread Pain

Differentiating clinically between Small Fibre Neuropathy and Fibromyalgia is challenging. Indicators of SFN are higher pain intensity, length dependent pain pattern (in 80%), stabbing pain and paraesthesia, allodynia; dry eyes/mouth, changed pattern or sweating on body, skin colour alterations/modifications, reduced hair/nail growth on lower extremities, and warm or cold hypoesthesia. Headache and TMJ pain are more common in fibromyalgia.[13] The DN4 questionnaire can be used.[14]

Investigations

First line screening tests to exclude somatic disease are FBC, CRP, CK, calcium, TSH. Other tests to consider are ESR, 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. ANA can be considered if there are consistent clinical features.

Vitamin D levels are low in the majority of patients with chronic pain, but this test is not funded in NZ.[2]

fMRI studies are very accurate at identifying fibromyalgia however it is not available in clinical practice.[15] The sensitivity is 92% and specificity 94%.[16]

Treatment

There is no highly effective treatment. In general pharmacological therapies are targeted towards symptoms, and non-pharmacological therapies are targeted towards dysfunction.

Education

When explaining the condition a useful analogy is an electric guitar. Pain processing is a lot like an electric guitar. To make an electric guitar louder you can either strum the strings harder or turn up the amplifier. The strings in the guitar are equivalent to all the different nerves in different parts of the body.

All the information (pain, temperature, pressure, etc) comes up through the amplifier which is the spinal cord and the brain. If the amplifier is set high enough - through a combination of genetics and environmental stressors - then pain will occur. Everyone has their own amplifier setting on a range of 0-100. If you happen to have a setting of 70 that is higher than average, but less than fibromyalgia, you will feel more pain. While in fibromyalgia the amplifier is set to 95 or more. Fibromyalgia is not something that either exists or doesn't, but rather there is a degree of "fibromyalgia-ness."

The amplifier in fibromyalgia is not only set higher for pain processing, but for all sensory processing. For example there is increased sensitivity to sounds, lights, smells, and side effects from drugs. Fatigue, insomnia, and memory problems also often occur.

Non-pharmacologic Therapies

This includes exercise (aerobic +/- strength training), stress management, sleep management, and CBT. If obese then undertaking a calorie restricted diet is effective at improving symptoms of pain and fatigue, particularly if 10% or more weight loss is achieved.[17]

There is modest evidence for manual therapy[18], massage, yoga, Tai chi, hypnotherapy, biofeedback, balneotherapy, neuromodulation (rTMS and tDCS). Trigger point injections have weak evidence.

Medication

Best evidence: TCAs, gabapentinoids. Also cyclobenzaprine (at night), duloxetine, and milnacipran but these are not available in NZ.

Modest evidence: Tramadol, older less selective SSRIs, low dose naltrexone[19], cannabinoids (CBD alone or low dose THC. Low dose THC may be more effective than high dose). Also gamma hydroxybutyrate but this is not available in NZ.

Not generally effective: Opioid don't tend to work possibly due to reduced mu-opioid receptor availability. In fact, opioids can make fibromyalgia pain worse. NSAIDs, corticosteroids, benzodiazepines are also generally not effective. Ketamine is not effective for fibromyalgia.[20]

Surgery Considerations

The degree of "fibromyalgia-ness" (even sub-threshold fibromyalgia) is highly predictive of surgical failure and opioid non-responsiveness in patients undergoing arthroplasty and hysterectomy.[21][22][23] Each one point increase in fibromyalgia-ness leads to 8mg greater opioid requirement during acute hospitilisation, and 20-25% greater likelihood of surgical failure for knee or hip arthroplasty (success being 50% improvement or much better or very much better on global impression of change).

Resources

Fibromyalgia Diagnostic Criteria 2016 Article - Wolfe 2016.pdf
Fibromyalgia year in review 2020.pdf
Fibromyalgia year in review 2021.pdf
Fibromyalgia year in review 2022.pdf
Fibromyalgia year in review 2023.pdf
Fibromyalgia year in review 2024.pdf

See Also

History of the condition

See review by Hauser and colleagues.[12]

References

  1. ā†‘ 1.0 1.1 Hughes, Gwenda; Martinez, Carlos; Myon, Eric; TaĆÆeb, Charles; Wessely, Simon (2006-01). "The impact of a diagnosis of fibromyalgia on health care resource use by primary care patients in the UK: an observational study based on clinical practice". Arthritis and Rheumatism. 54 (1): 177ā€“183. doi:10.1002/art.21545. ISSN 0004-3591. PMID 16385513. Check date values in: |date= (help)
  2. ā†‘ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Hochberg. Fibryomyalgia In: Rheumatology. 2019
  3. ā†‘ MartĆ­nez-LavĆ­n. Fibromyalgia and small fiber neuropathy: the plot thickens!. Clinical rheumatology 2018. 37:3167-3171. PMID: 30238382. DOI.
  4. ā†‘ Williams, David A.; Clauw, Daniel J. (2009-08). "Understanding Fibromyalgia: Lessons from the Broader Pain Research Community". The Journal of Pain. 10 (8): 777ā€“791. doi:10.1016/j.jpain.2009.06.001. ISSN 1526-5900. Check date values in: |date= (help)
  5. ā†‘ Schrepf, Andrew; Harper, Daniel E.; Harte, Steven E.; Wang, Heng; Ichesco, Eric; Hampson, Johnson P.; Zubieta, Jon-Kar; Clauw, Daniel J.; Harris, Richard E. (2016-10). "Endogenous opioidergic dysregulation of pain in fibromyalgia: a PET and fMRI study". Pain. 157 (10): 2217ā€“2225. doi:10.1097/j.pain.0000000000000633. ISSN 1872-6623. PMC 5028286. PMID 27420606. Check date values in: |date= (help)
  6. ā†‘ MartĆ­nez-LavĆ­n, Manuel (2021). "Fibromyalgia in women: somatisation or stress-evoked, sex-dimorphic neuropathic pain?". Clinical and Experimental Rheumatology. 39 (2): 422ā€“425. doi:10.55563/clinexprheumatol/0c7d6v Check |doi= value (help). ISSN 0392-856X. PMID 32940205.
  7. ā†‘ Lyon, Pamela; Cohen, Milton; Quintner, John (2011-08). "An evolutionary stress-response hypothesis for chronic widespread pain (fibromyalgia syndrome)". Pain Medicine (Malden, Mass.). 12 (8): 1167ā€“1178. doi:10.1111/j.1526-4637.2011.01168.x. ISSN 1526-4637. PMID 21692974. Check date values in: |date= (help)
  8. ā†‘ Oaklander & Klein. Evidence of small-fiber polyneuropathy in unexplained, juvenile-onset, widespread pain syndromes. Pediatrics 2013. 131:e1091-100. PMID: 23478869. DOI. Full Text.
  9. ā†‘ 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.
  10. ā†‘ HƤuser, Winfried; Sarzi-Puttini, Piercarlo; Fitzcharles, Mary-Ann (2019). "Fibromyalgia syndrome: under-, over- and misdiagnosis". Clinical and Experimental Rheumatology. 37 Suppl 116 (1): 90ā€“97. ISSN 0392-856X. PMID 30747096.
  11. ā†‘ 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.
  12. ā†‘ 12.0 12.1 HƤuser, Winfried; Sarzi-Puttini, Piercarlo; Fitzcharles, Mary-Ann (2019). "Fibromyalgia syndrome: under-, over- and misdiagnosis". Clinical and Experimental Rheumatology. 37 Suppl 116 (1): 90ā€“97. ISSN 0392-856X. PMID 30747096.
  13. ā†‘ Bailly, Florian (2021-12). "The challenge of differentiating fibromyalgia from small-fiber neuropathy in clinical practice". Joint Bone Spine. 88 (6): 105232. doi:10.1016/j.jbspin.2021.105232. ISSN 1778-7254. PMID 34082128. Check date values in: |date= (help)
  14. ā†‘ Di Carlo, Marco; Cesaroni, Pietro; Salaffi, Fausto (2021). "Neuropathic pain features suggestive of small fibre neuropathy in fibromyalgia syndrome: a clinical and ultrasonographic study on female patients". Clinical and Experimental Rheumatology. 39 Suppl 130 (3): 102ā€“107. doi:10.55563/clinexprheumatol/r0kho4 Check |doi= value (help). ISSN 0392-856X. PMID 33666162.
  15. ā†‘ Gracely, Richard H.; Petzke, Frank; Wolf, Julie M.; Clauw, Daniel J. (2002-05). "Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia". Arthritis and Rheumatism. 46 (5): 1333ā€“1343. doi:10.1002/art.10225. ISSN 0004-3591. PMID 12115241. Check date values in: |date= (help)
  16. ā†‘ LĆ³pez-SolĆ , Marina; Woo, Choong-Wan; Pujol, Jesus; Deus, Joan; Harrison, Ben J.; Monfort, Jordi; Wager, Tor D. (2017-01). "Towards a neurophysiological signature for fibromyalgia". Pain. 158 (1): 34ā€“47. doi:10.1097/j.pain.0000000000000707. ISSN 1872-6623. PMC 5161739. PMID 27583567. Check date values in: |date= (help)
  17. ā†‘ Schrepf, Andrew; Harte, Steven E.; Miller, Nicole; Fowler, Christine; Nay, Catherine; Williams, David A.; Clauw, Daniel J.; Rothberg, Amy (2017-12). "Improvement in the Spatial Distribution of Pain, Somatic Symptoms, and Depression After a Weight Loss Intervention". The Journal of Pain. 18 (12): 1542ā€“1550. doi:10.1016/j.jpain.2017.08.004. ISSN 1528-8447. PMC 5841588. PMID 28847734. Check date values in: |date= (help)
  18. ā†‘ Ughreja, Reepa Avichal; Venkatesan, Prem; Balebail Gopalakrishna, Dharmanand; Singh, Yogesh Preet (2021-11). "Effectiveness of myofascial release on pain, sleep, and quality of life in patients with fibromyalgia syndrome: A systematic review". Complementary Therapies in Clinical Practice. 45: 101477. doi:10.1016/j.ctcp.2021.101477. ISSN 1873-6947. PMID 34507243. Check date values in: |date= (help)
  19. ā†‘ Jackson, Daniel; Singh, Sunita; Zhang-James, Yanli; Faraone, Stephen; Johnson, Brian (2021). "The Effects of Low Dose Naltrexone on Opioid Induced Hyperalgesia and Fibromyalgia". Frontiers in Psychiatry. 12: 593842. doi:10.3389/fpsyt.2021.593842. ISSN 1664-0640. PMC 7921161. PMID 33664680.
  20. ā†‘ Corriger, Alexandrine; Voute, Marion; Lambert, CĆ©line; Pereira, Bruno; Pickering, GisĆØle; OKAPI Consortium (2022-04-01). "Ketamine for refractory chronic pain: a 1-year follow-up study". Pain. 163 (4): 690ā€“701. doi:10.1097/j.pain.0000000000002403. ISSN 1872-6623. PMID 34252909.
  21. ā†‘ Brummett, Chad M.; Janda, Allison M.; Schueller, Christa M.; Tsodikov, Alex; Morris, Michelle; Williams, David A.; Clauw, Daniel J. (2013-12). "Survey criteria for fibromyalgia independently predict increased postoperative opioid consumption after lower-extremity joint arthroplasty: a prospective, observational cohort study". Anesthesiology. 119 (6): 1434ā€“1443. doi:10.1097/ALN.0b013e3182a8eb1f. ISSN 1528-1175. PMC 3867739. PMID 24343289. Check date values in: |date= (help)
  22. ā†‘ Brummett, Chad M.; Urquhart, Andrew G.; Hassett, Afton L.; Tsodikov, Alex; Hallstrom, Brian R.; Wood, Nathan I.; Williams, David A.; Clauw, Daniel J. (2015-05). "Characteristics of fibromyalgia independently predict poorer long-term analgesic outcomes following total knee and hip arthroplasty". Arthritis & Rheumatology (Hoboken, N.J.). 67 (5): 1386ā€“1394. doi:10.1002/art.39051. ISSN 2326-5205. PMC 4414825. PMID 25772388. Check date values in: |date= (help)
  23. ā†‘ Janda, Allison M.; As-Sanie, Sawsan; Rajala, Baskar; Tsodikov, Alex; Moser, Stephanie E.; Clauw, Daniel J.; Brummett, Chad M. (2015-05). "Fibromyalgia survey criteria are associated with increased postoperative opioid consumption in women undergoing hysterectomy". Anesthesiology. 122 (5): 1103ā€“1111. doi:10.1097/ALN.0000000000000637. ISSN 1528-1175. PMID 25768860. Check date values in: |date= (help)

Literature Review

Literature Review

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