A rhetorical question posed by the bard leads Prof Muhammad Yunus (no, not the Nobel Laureate – this guy was merely responsible for the pioneering 1982 study of fibromyalgia) to muse: “…anything that is not currently viewed as a disease is viewed as predominantly or exclusively psychological and benign and is not taken seriously by the health care providers”. For fibro’s status to be promoted from a syndrome to a disease requires an understanding of causality. That would allow treatment of cause, rather than merely alleviating symptoms.
Wherever symptoms outweigh evidence from signs the patient is relegated to a diagnostic dumping ground of functional somatic syndromes. Somatization disorder sufferers are characterized by pain and headaches resulting from distress. The recent version of Diag & Stats Manual of Mental Disorders (DSM-5) has grouped these along with hypochondriacs into the category Somatic Symptom Disorder. Other simplifications result in broadening the size of the SSD patient market sixfold over DSM-IV criteria (Rief et al 2011). Thankfully it advises that many individuals with fibromyalgia would not satisfy the criterion necessary to diagnose somatic symptom disorder (ie any one of either: Disproportionate and persistent thoughts about the seriousness of one’s symptoms, Persistently high level of anxiety about health or symptoms, or Excessive time and energy devoted to these symptoms or health concerns.©) Otherwise anyone on disability benefits, or income protection insurance could be critically judged by their practitioner as catastrophising. But of course, fibromites have rheumatology specialists managing their treatment, otherwise secondary care escalation would be straight to psychiatrists and everyone would be on anti-depressants [cue hollow laughter].
How much of fibro is in your head remains enigmatic, just as much so as attempting to explain specificity due to exact locations of the 18 tender points in the 1990 ACR criteria (this week I’m bagging psychs, not rheumys since I need help in understanding enthesopathy!). The selectivity of the blood brain barrier means that the hormone and neurotransmitter levels that matter won’t ever be measured in blood serum. Not that this affects the presumption of a dysregulated hypothalamus-pituitary-adrenal axis , and hypothesized low levels of serotonin (in) or cortisol (out) aren’t seen as necessary to be monitored in order to be prescribed a serotonin reuptake inhibitor. The anti-depressant drug mechanism relies upon lifting the use-by time for the chemical to come in for recycling and thus ensures plenty of serotonin. Blind trust & guesswork are valuable skills in applying neuroendocrinology theories to each individual, and the patients & research consultants to pharma have these attributes respectively …. in spades ♠