Abstract
Fibromyalgia has always struggled to be taken seriously. The vague mixture of aches, pains, stiffness and fatigue with no clear clinical or investigational findings has led many to doubt its very existence. Evidence is accumulating, however, of demonstrable abnormalities of pain processing and psychosocial factors in fibromyalgia subjects. These may ‘prove’ its existence, but do they suggest it is rheumatological?
British Society for Rheumatology Conference 2010. An excellent fibromyalgia session.
The neurologist demonstrated that fibromyalgia is a neurological syndrome; the psychologist demonstrated that it is also a psychological syndrome. The rheumatologist asserted the rheumatologist was the ideal person to manage it. And you had to ask … why?
Fibromyalgia has always struggled to be taken seriously. Starting life as ‘fibrositis’, a catch-all for unexplained pains, it came to stand for a subset syndrome of pains and morning stiffness plus systemic complaints such as fatigue and sleep disturbance. The American College of Rheumatology criteria of 1990 1 – widespread pain plus 11 positive out of 18 possible ‘tender points’ – were a welcome formalization of the diagnosis, but still subjective, hardly dispelling suspicions that fibromyalgia was not a distinct entity.
So, to answer the title's question, I propose we progress through three stages. Does fibromyalgia exist?… If so, is it rheumatological? … If it isn't, should rheumatologists look after it anyway? …
Does fibromyalgia exist?
In 1975, Moldofsky and colleagues demonstrated that 10 fibromyalgia sufferers had poor ‘delta-wave sleep’, nocturnal electroencephalograms showing ‘alpha-wave intrusion’ into, or complete absence of, this deepest, most restorative sleep. This might be cause or effect, but by preventing delta-wave sleep in six healthy young subjects, they induced the pains and fatigue of fibromyalgia, 2 significantly increased during the periods of deprivation.
Reappraisal has thrown some doubt on these findings,
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but by this time more evidence of neurological abnormalities in fibromyalgia subjects had followed. Their pain threshold was lower. One study of 85 patients versus 40 controls showed decreased tolerance to cold, heat and electrical stimuli – both by subjective tests and by measuring an involuntary leg muscle reflex response to pain.
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Other workers used functional magnetic resonance imaging (MRI) to highlight brain areas involved in pain appreciation. One group compared nine fibromyalgia sufferers with nine controls, and showed increased activity in these areas in the fibromyalgia group – including a clear contralateral effect – following both painful and nonpainful stimuli.
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Extensive reviews6,7 of these and other data on inhibitory pathways, N-methyl-
If so, is it rheumatological?
The above evidence would argue – no. Any differences between fibromyalgia patients and controls seem neurological, not rheumatological. No joint abnormalities have been shown, while a flurry of interest in altered muscle ‘energy metabolism’ was found to be based on abnormalities reflecting normal deconditioning of underused muscles by Simms et al., 8 who used MRI spectroscopy in 13 patients compared with carefully selected sedentary controls. Simms 9 went on to analyze all the available muscle data in a 1998 review confidently entitled ‘Fibromyalgia is Not a Muscle Disorder’.
Fibromyalgia subjects do differ from controls in their premorbid personality 10 and experiences such as family illness during teenage years. 11 Mood and anxiety disorders, and true psychiatric diagnoses are more common in fibromyalgia patients than those with rheumatoid arthritis. 12 Reviewing such findings 13 adds a psychological layer to the neurological paradigm, but moves us even further from rheumatology. The evidence suggests fibromyalgia is a neuropsychological syndrome.
Approaches to treatment now work from this premise. Up-to-date systematic 14 and narrative 15 reviews of current therapies begin by stating fibromyalgia is ‘a common pain disorder’, 14 or ‘an abnormal central processing pain disorder’. 15 None suggest it is a rheumatic disease. This is not just the scientists’ viewpoint, it is mainstream. A recent NURSING review states ‘FMS [fibromyalgia syndrome] isn't a musculoskeletal syndrome’. 16 The prediction in 1988 of Dudley Hart, 17 doyen of rheumatology, who wrote ‘… a disorder of pain modulation – a pain amplification syndrome – would seem to fit the facts best … no signs of any arthritic or rheumatic disease are present,’ appears to have been correct.
… Should rheumatologists look after it anyway?
Possible Reasons
Symptoms include pain and stiffness and you get that in arthritis. By this logic, patients with abdominal migraine would attend gastroenterologists. It is important that rheumatologists see and assess these patients to ‘exclude’ rheumatic disease, but once done, it does seem illogical for them to manage a neuropsychiatric condition.
Tradition. We certainly do not want to lose the knowledge and expertise of current rheumatology enthusiasts, but there is now no reason to view jobbing rheumatologists as fibromyalgia specialists. Understanding of the disease has moved on. We do not send peptic ulcers to general surgeons, to agonize between omeprazole and a highly selective vagotomy.
There is no-one else. Neurologists and psychiatrists are presumably no more able to look after all the ‘unexplained symptoms’ cases than rheumatologists. But there is a solution. Fibromyalgia is neither life-threatening nor investigation-intensive. A recent excellent Arthritis Research Campaign leaflet, written by a general practitioner (GP), addresses these aspects and the importance of non-pharmacological treatment and family dynamics. He concludes it is a disease of primary care, 18 and I agree. Backup for GPs is, of course, needed. The rheumatologist should be available to exclude rheumatic problems, but any management advice should come from other specialties. The helpful modalities – cognitive therapy, biofeedback … tricyclics, serotoninergics, gabapentin, cyclobenzaprine, tramadol, duloxetine, milnacipran, pregabalin 15 – are largely alien to rheumatologists (steroids do not work! 19 ). How can we assume that someone trained in anti-inflammatories and anti-tumour necrosis factors is able to juggle serotonins, calcium channels and gamma-amino butyric acid?
Thus we have a syndrome with no suggestion of joint or muscle abnormality, but with accumulating evidence of neurological dysfunction and psychological overlay, whose pharmacological treatment consists of various antidepressants and psychoactive drugs … and sufferers attend rheumatology clinics.
It does not make sense. And it is important. In my view, presenting fibromyalgia as a rheumatological disease does it a disservice. People will believe a ‘pain syndrome’ caused by aberrant neurological processes; they will not accept a ‘disease of muscles and joints’ where muscles and joints are entirely normal. If we wish fibromyalgia to be taken seriously, we must stop pretending we think it is a rheumatic disease.