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Over the past decade there have been major advances in our understanding of fibromyalgia (FM). The identification of alterations in the levels of many neurotransmitters has resulted in newer targets for therapeutic intervention in this condition.

FM is a chronic disorder characterised by widespread musculoskeletal pain. According to the American College of Rheumatology (ACR) fibromyalgia classification criteria (1990) (1) patients must have a history of widespread pain that has been present for at least 3 months. The pain can be elicited on digital palpation by manual pressure of approximately 4 kg/[cm.sup.2] at 11 or more of the 18 defined tender points. The pain is considered to be widespread if it involves both sides of the body and occurs above and below the waist. In addition, axial skeletal pain (cervical spine, anterior chest, thoracic spine or low back) must be present.
Table I. The 2010 fibromyalgia clinical diagnostic criteria (4)
* Widespread pain index (WPI)
The WPI score depends on the number of sites where the patient had
pain in the last week (score: 0 - 19) The 19 sites are ( R - right;
L - left ):

Shoulder girdle R/L  Hip (buttock, trochanter) R/L  Jaw R/L

Upper arm R/L             Upper leg R/L             Chest

Lower arm R/L             Lower leg R/L             Abdomen

* Symptom severity  (SS)scale

Fatigue                Waking unrefreshed

Cognitive disturbance  General  somatic symptoms

The score for each of the 4 symptoms is allocated as 0 (no problem), 1
(slight), 2 (moderate) and 3 (severe). The total score ranges from 0
to 12

* Patients are classified as having fibromyalgia if: WPI > 7 and
SS score > 5 or WPI between 3 and 6 and SS score > 9 The new diagnostic
criteria do not require a physical examination and can be

These criteria were developed for use in clinical trials. It is increasingly recognised that the diagnosis of FM does not rely solely upon eliciting tender points, and features such as fatigue, sleep disturbance and cognitive dysfunction are prominent. (2)

FM affects mainly middle-aged women; however, adolescents, men and older people are also affected. It is far more prevalent than inflammatory arthritis, e.g. rheumatoid arthritis.

Chronic widespread pain is the characteristic symptom in patients with FM. Only about 50% of patients with chronic widespread pain fulfil the criteria for FM. (3) It is unclear how patients with chronic widespread pain who do not fulfil the tender point criteria should be classified, and the role of the tender points in the diagnosis of FM has been challenged by many authors.


The 2010 fibromyalgia clinical diagnostic criteria (4) were recently proposed by Wolfe and colleagues and depend on the widespread pain index and the symptom severity scale as shown in Table I.


Functional MRI imaging studies have shown that low-intensity stimuli, which would not normally produce pain, activate areas of the brain that process pain and result in pain sensation in FM patients. In addition, areas of the brain which are activated by low-intensity stimuli in FM patients are only activated by high-intensity stimuli in controls. (3)

Biochemical abnormalities that have been noted in FM patients include: (3)

* Substance P is raised 2-3-fold in the CSF. Increased levels lead to heightened awareness of pain.

* Brain-derived neurotropic factor (4-fold increase) and glutamate are elevated.

* Serotonin levels are low. This has been linked to poor sleep, pain perception, headaches and mood disorders.

* Dopamine levels are low. This plays a role in pain perception and natural analgesia.

* Noradrenaline levels are low.

These biochemical abnormalities result in whole body hypersensitivity to pain and suggest that FM is a disorder of central pain processing or a syndrome of central sensitisation. (3) Therefore, in FM, some of the neurotransmitters which increase pain are high and others, which may inhibit pain, are too low.

Clinical aspects

Several risk factors have been identified, including genetic factors, gender, age, poor sleep, physical de-conditioning and neuroendocrine and autonomic dysregulation. Approximately 50% of patients with FM state that their symptoms began after a precipitating event, including chronic stress, emotional trauma, physical injury, surgery and motor vehicle accidents. (3)

The dominant symptoms are widespread muscle and/or joint pain, fatigue, sleep disturbances, impaired memory and concentration, cognitive impairment, depression and paraesthesia.

The spectrum of abnormalities seen in FM extends beyond widespread pain and overlaps with other syndromes, such as: (2), (3)

* regional pain syndromes, e.g. non-cardiac chest pain, dyspepsia, headaches, irritable bowel syndrome, chronic pelvic pain, temporomandibular joint pain

* other central sensitivity syndromes, such as chronic fatigue, irritable bowel, pelvic pain, tension headaches, migraine, restless legs syndrome

* allergic symptoms, such as nasal congestion, hives and welts

* mood disorders, including anxiety, depression and personality disorders.


A thorough history and physical examination is the basis of making a confident diagnosis, as radiological and laboratory tests do not assist in confirming it.

Conditions which must be considered in the differential diagnosis include hypothyroidism, polymyalgia rheumatica, systemic lupus erythematosus, rheumatoid arthritis and myositis. (5)

Patient education. FM should be explained as a symptom, such as headache or backache. It is important for patients to be told that they have a real problem which is a biologically based disorder.

Psychological and behavioural management, including cognitive behavioural therapy and relaxation techniques, should be employed at the outset.

Physical therapy improves pain and functional ability and should include strength training, developing flexibility, balance and endurance.

Diet. Important considerations are vitamin D supplementation, emphasis on bone health and reaching an optimum weight.

Pharmacological management. Evidence for the efficacy of different classes of drugs has been categorised as follows:

* Strong evidence-tricyclics (amitriptyline); dual re-uptake inhibitors (SNRI/NSRI-venlafaxine, duloxetine, milnacipran); alpha-2-delta ligands (pregabalin, gabapentin)

* Modest evidence-tramadol; selective serotonin re-uptake inhibitors (SSRIs); dopamine agonists; gamma-hydroxybutyrate

* Weak evidence-growth hormone; 5-hydroxytryptamine; tropisetron, S-adenosyl-L-methionine

* No evidence-opioids; NSAIDs; corticosteroids; benzodiazepine and nonbenzodiazepine hypnotics; melatonin; guanifenesin; dehydro-epiandrosterone.

References available at


Principal Specialist and Lecturer, Department of Rheumatology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal and Inkosi Albert Luthuli Central Hospital, Durban

GIRISH M MODY, MB ChB, FCP (SA), MD, FRCP (Lond), Fellow of the University of KwaZulu-Natal

Aaron Family Professor and Head of the Department of Rheumatology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal and Inkosi Albert Luthuli Central Hospital, Durban

Correspondence to: N Patel (
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Author:Patel, Neeta; Mody, Girish M.
Publication:CME: Your SA Journal of CPD
Article Type:Disease/Disorder overview
Geographic Code:1USA
Date:Aug 1, 2011
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