FIBROMYALGIA 1999-2000

SUMMARY: Injury may or may not be responsible for subsequent FibroMyalgia Syndrome. Determination of Causation requires more far-reaching multidisciplinary assessment than is often undertaken. FMS appears to be Caused by a pathologically lowered pain threshold. Nerve cells may be chemically sensitised to pain signals. Various treatments have a limited effect on prognosis. Psychosocial factors are more powerful predictors of improvement or recovery.

Assessment

Injury may or may not be responsible for subsequent Fibromyalgia Syndrome (FMS). Medical expert witnesses are of least use to the court if they believe that either a) FMS is meaningless terminology, or b) the complaint of chronic widespread pain means disablement.

Although these extreme positions are seen in defence and claimant experts respectively all too frequently, they represent pre-judgments that belie a meaningful analysis of an individual claim.

How they address standard questions ¹ will reveal the prejudices and depth of analysis of medical expert witnesses.

Determination of Causation requires more far-reaching multidisciplinary assessment than is often undertaken.

Not only must pre-injury records for 5 years or more be reviewed for evidence for undiagnosed pre-existing FMS, but various medical specialties should be considered for diagnostic input. As well as rheumatologist and occupational physician, psychiatric assessment should be routine, and other specialties contribute as necessary - gastroenterology, neurology and general internal medicine.

Causation

FibroMyalgia Syndrome appears to be Caused by a pathologically lowered pain threshold. The central clinical abnormality in FibroMyalgia Syndrome is chronic, widespread allodynia - pain arising from a stimulus that is not normally experienced as painful ². Sufferers have a lowered threshold for pain and tenderness.

Just as birthweight and blood-pressure fall in a range that is roughly normally distributed ("bell-shaped curve"), so do dolorimetry scores ³ - the average amount of local pressure required to cause transition from sensation of pressure to sensation of pain.

Just people whose blood pressures are at the upper end of the range have more illness and higher death-rates, those who have high dolorimetry scores have greater pain and more disability.

On this illness model, a constitutionally low pain threshold ("thin skull") may be further lowered in response to adverse conditions, including physical and/or psychological trauma. If the resultant allodynia is unrelieved, physical deconditioning and daily minor trauma complete the vicious circle and cause self-perpetuating (legal) Impairment and Handicap.

Nerve cells may be chemically sensitised to pain signals. The mechanism of this lowered threshold for appreciation of pain (nociception) and tenderness appears to involve a primary abnormality of neurochemicals, messengers that amplify (pro-nociceptive) or suppress (anti-nociceptive) pain signals ⁴.

Animal experiments ^{5, 6} have shown that the pro-nociceptive chemical known as Substance P normally alerts nerve cells in the spinal cord to incoming pain signals.

In the CerebroSpinal Fluid (CSF) that bathes the brain and spinal cord, concentrations of Substance P are characteristically increased in FMS ⁷. In patients tested on two occasions, an average of a year apart, their symptoms and the concentrations of Substance P in the CSF increased in tandem⁶.

There is a recent unconfirmed report that FMS patients also have increased CSF concentrations of Nerve Growth Factor ⁸. This neurotransmitter is believed to enchance the growth of nerve cells that contain Substance P.

There is also accumulating evidence² that various anti-nociceptive substances are in short supply in FMS patients.

Prognosis

The majority of patients diagnosed with FibroMyalgia Syndrome (FMS) are gainfully employed¹. Severity of symptoms does not determine employment status, and the impact of therapeutic interventions is widely variable.

Various treatments have a limited effect on prognosis.

Thrice weekly aerobic exercise has been further confirmed as reducing tender-point tenderness and possibly pain ^{9, 10}, but only in the short-term¹⁰.

For long-term benefit, various alternative therapies materially improve prognosis for some clients - biofeedback, hypnotherapy, and Cognitive-Behavioural Treatment. Acupuncture benefits some and worsens others^{9, 11, 12}. There is only weak evidence for the effect of chiropractic and massage therapies¹².

Antidepressant medication of the Amitryptiline type (tricyclic), but not of the Prozac variety (Selective Serotonin Reuptake Inhibitors, SSRI), has a definite beneficial effect in 25-30% of patients^{9, 13, 14}. It is probable, but not certain, that this benefit on FMS is independent of the improvement in depression ¹³.

However, the benefits of tricyclic antidepressant medication are usually lost by 2-3 months ¹⁵. A 2-4 week drug holiday using an alternative medication may re-establish effectiveness ¹⁶.

Tranquillisers of the Valium type (benzodiazepines) can be used for such a drug holiday, as they too have been shown to be effective in reducing tenderness and improving functional and psychological status ¹⁷. Such medications are unsuitable for long-term use because they readily cause psychological and physical dependence, including withdrawal seizures.

Narcotics such as Demerol may prove to be effective for intractable non-cancer pain, but they should similarly be avoided in a chronic condition such as FMS, because of the addiction potential.

Various other pharmacological agents, some of which are frequently prescribed, have now been tested and found to be ineffective in FMS⁹: Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), Cortisone-like medication s (corticosteroids), and injected local anesthetics such as Xylocaine.

Psychosocial factors are more powerful predictors of improvement or recovery. Medical experts on prognosis for both claimant and defence should be asked to address explicitly the impact of various pre-existing factors ¹⁸ on outcome:

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