Presentation on theme: "Painful Myotendinous Disorders: Our duty to diagnose A Critique of the Fibromyalgia Hypothesis James H. Lampman, MD."— Presentation transcript:
Painful Myotendinous Disorders: Our duty to diagnose A Critique of the Fibromyalgia Hypothesis James H. Lampman, MD
Goals of this presentation To refresh your understanding of clinically relevant myotendinous ailments To introduce the concept of resiliency disorders in the force chains of the locomotor system. To critically appraise the fibromyalgia hypothesis and to cast doubt on the existence of a neurologic state of pain unexplained by musculoskeletal biomechanics.
Myotendinous pain disorders are anatomically rational, whether seen singly or in several locations. They are a shared human experience and are a necessary and common consequence of our biomechanical locomotor structure. The clinician’s duty: concretely examine locomotor anatomic structures from head to toe. This easily deconstructs and clarifies pain sources, even when several such disorders together flood the patient’s emotive description and are perceived as “pain all over.” Theme
Examples of biomechanical disorders of myotendinous force units Rotator cuff impingement Achilles tendonopathy and tears Trapezial, levator, rhomboid strains Trochanteric pain syndrome (gluteus medius tendon) Iliac crest pain/lumbago (axial tendons/aponeuroses) humeral epicondylitis (tennis and golfer’s elbow) Biceps tendinopathy (with or without rupture) DeQuervain wrist (thumb ext & abductor tendons) Trigger finger (finger flexor tendonopathy) Thoracic cage pain syndromes Auto-traumatic disorders of myotendinous resiliency
What is the locomotor system? An effector system for movement and posture Muscles, tendons, aponeuroses, fascia, tethers and pulleys, bursae Numerous balanced “power trains” allow the locomotor system to activate and position the body The numerous and diverse myotendinous chains are vulnerable to biomechanical injury
What is the locomotor system? Zones of relative weakness exist at key points in each force chain The locomotor system, a living mechanism, continuously self-injures, self-heals, and remodels in its normal duties. When we are comfortable, it is only because we operate the system inside the limits of resilience of numerous force chains. A good portion of the human race discovers, regrettably, the severe discomfort and threat of doing otherwise
Finger flexor tendonopathy “trigger finger” A miniature version of the myotendinous resiliency issue Anatomic substrate: tendon and sheath are channeled within 5 annular and 3 cruciate pulleys of the finger Use-related fibrous adhesions along the flexor tendon sheath create obstructive painful dysfunction of the tendon as it passes through the A-1 pulley Delayed appearance of symptoms; exquisite pain; “mystery ailment” for the patient
Gluteus medius tendonopathy (sometimes a tear). A strain/overuse disorder of the lateral hip sometimes called greater trochanteric pain disorder.
Trapezius: a multiply-attached muscle with clinical relevance in upper back, neck, shoulder girdle A common deep myotendinous ache extending to the subocciput, often accompanied by myalgic cranial pain
The resiliency concept The limited and varied biomechanical resilience from point to point along each power train creates the possibility of discrepancy and dysfunction Pathology will appear first at the points of least resiliency (often but not always at or near the enthesis) The phase “everyday enthesopathy*” has been used to describe the numerous and common disorders of the attachment sites. Findings may include: pain, tenderness, swelling, heat, redness, or rupture (but in many cases are submerged). The majority of patients are truly unaware of their anatomy and its weak links. They are often mystified as to what went wrong – and need to be told “your strong part hurt the weaker part.” Sartorius (tendonopathy or avulsion at ASIS in athletes) *Littlejohn
A clinical observation : “I hurt all over” is a common complaint when 2,3,or 4 focal myotendinous disorders are present.
A typical example: a 43 year-old woman seeks evaluation for 6 years of “hurting all over,” worse in past 6 months. Findings : Fluctuating mild right rotator cuff tendinitis variable trapezio-cervical strain and myalgic headache Gluteus medius tendonopathy (left more than right)
P atient perceptions may or may not correlate precisely with pathophysiology Bilateral rotator cuff impingement R Lateral epicondylitis Iliac crest strain R Gluteus medius tendinopathy R Subcalcaneal pain Example of accurate correlation 57 year-old woman who was thought to have “fibromyalgia” Findings on anatomic examination Pain Diagram:
53 year-old active farm wife. 5 years of variable pain (“all over”) worse in past 6 months. Diagnosed elsewhere as “fibromyalgia.” Anatomic examination findings: Trapezial-cervical strain Left rotator cuff impingement Bilateral trochanteric pain Lumbar/iliac crest pain
Treatment tactics After concrete exam and authentication, each lesion calls for specifically directed treatment from a matched menu of interventions. Opportunities and options: injection, medication (systemic and topical), surgery, splinting, physical & occupational therapy modalities. Recognize that promising “quick relief” from medication or injection may mislead the patient into returning to provocative activities. Place responsibility with the patient to modify the imprudent forces, repetitions and postures which caused the problems. Natural healing occurs slowly and relapses are common. This is a hard lesson to accept but it’s a deep, humbling, and true message everyone has to accept one way or another.
Treatment of Resiliency Disorders Force re- duction, posture retraining Finger flexor tendonopathyxxxxxxx Elbow epicondylitisxxxxxx??? Rotator cuff impingementxxxxxxxxXx? Trapezial-cervical painxxxxxx Jaw clenching disorderxxxxxx Costochondritis/costosternalxxx Lumbago/iliac crest painxxxxx Trochanteric pain syndromexxxx Subcalcaneal heel painxx Achilles strainxxx injectionsurgery Splinting, heat, PT-OT Note on systemic medication: If used at all, select only the safest.
Myotendinous pain is rational even when perceived as “all over” Occurs in recognizable stereotypical patterns Based on resiliency discrepancies along one or more muscle-tendon locomotor units (“one part is strong enough to hurt the next part down the chain”) All ages and all walks of life, especially in dynamic midlife when physical expectations exceed declining resiliency. Usually arises because of insufficient sensitivity to dynamic misuse as it happens, with delayed onset of symptoms. “A mystery surprise.” Even a single ailment of this type should deliver a profound message to the sufferer – courtesy of the astute clinician.
Fibromyalgia: a radical hypothesis from the borderlands of science What do its proponents say it is? A unique or prototypical generalized intrinsic pain state. Commonly pictured as tender points in anatomy-free “3 Graces” or as a diagram of sensory information ascending, descending, traversing interconnected CNS regions. Independent of specific anatomic basis in the body, though it is perceived as musculoskeletal pain. It is signaled abstractly by (or even defined by) bodily tender points of which the patient is said often to be unaware; and/or by widely distributed enduring pain loci which need not have local pathology Its special “chronicity” sets it apart from the mundane pain we know day by day The amorphous widely perceived pain, the chronicity, tender points, and reduced sensory thresholds are said to be expressions of some form of dysregulation of pain processing residing in the central nervous system. The pain state of fibromyalgia is said to be part of a larger rubric of ill-defined somatic and cognitive dysfunctions.
The central axiom of fibromyalgia: “Central” pain or central augmentation of pain Evidently started as an extrapolation from the lesional central pain known to neurologists --e.g. central post-stroke; cord injuries; CNS diseases (MS etc) Central pain felt as a regional burning, searing, itching, allodynic. Not especially similar to musculoskeletal pain No loci in brain which map downstream to body pain (as in somatosensory homunculus) Pain a complex subjective cognitive/emotive/psychosocial experience involving multiple brain regions Modified to refer to neurotransmitter-based influence on ascending & descending pathways and interconnected regions within brain Would be able to diminish sensory thresholds, leading to hyperalgesia, allodynia, and deep tissue pain; capable of creating signal tender points and faulty transmissions perceived as severe musculoskeletal pain; would also permit any other organs or the brain itself to malfunction or be perceived as malfunctioning. Would be accessible to study via: imaging the brain; measuring neurotransmitters; using brief acute-pain “sonar pings”; using electrophysiological sensory testing, etc. Would provide a rationale for neuro-active drugs, cognitive-behavioral therapy, magnets etc.
How would you test the “central pain” axiom? Start with finding a study subject group of enduring pain patients for whom the best clinical explanation is that they have nothing medically or biomechanically wrong. Assemble comparison groups with known enduring pain sources such as joint disease, chronic pancreatitis, metastatic cancer, burns, or painful neuropathies such as postherpetic neuralgia. Employ any method you desire to look at differences in pain perception and processing. Determine if your patients have any kind of neurologic aberrancy compared to the normal way any chronic pain patient processes pain. Such experiments have not been either advocated or done!
Review of 4 decades of the trajectory of fibromyalgia “Fibromyalgia” misappropriated the concept of central pain from neurology, it manufactured its own terminology, its own physical examination, its own methods of investigation, its own peer review. Above all it presented itself not as a hypothesis to be tested but as a revealed axiomatic truth. “Extraordinary claims require extraordinary proof” did not apply. A belief system whose advocates built a “protected zone” against effective scientific scrutiny Decades into it, there is not the least bit of credible evidence of anything different or aberrant about the “pain processing” of those labeled fibromyalgia, compared to any enduring pain disorder. Repeat: it has never been shown that “FM” pain processing and brain function is anything other than the normal and routine way the normal nervous system deals with pain. There is no actual evidence or active line of investigation which legitimately supports the “neuro- interpretive” concept underlying FM nor any of the associated concepts.
Examples of leading studies advancing the fibromyalgia hypothesis 1.Musculoskeletal Symptoms and Non-REM Sleep Disturbance in Patients with "Fibrositis Syndrome" and Healthy Subjects HARVEY MOLDOFSKY, MD, PHILLIP SCARISBRICK, BS ROBERT ENGLAND, BA, AND HUGH SMYTHE, MD Psychosomatic Medicine Vol. 37, No. 4 (July-August 1975) and Induction of neurasthenic musculoskeletal pain syndrome by selective sleep stage deprivation. Moldovsky H and P Scarisbrick. Psychosomatic Medicine Vol. 38, No. 1 (January-February 1976 2.Primary fibromyalgia (fibrositis): Clinical study of 50 patients with matched normal controls. Yunus M. Seminars in Arthritis and Rheumatism 1981; 151–171.Seminars in Arthritis and Rheumatism 3.Electron microscopic studies of muscle biopsy in primary fibromyalgia syndrome: a controlled and blinded study. Yunus M et al. The Journal of Rheumatology [1989, 16(1):97-101]The Journal of Rheumatology 4.Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. IJ Russell Arthritis & Rheumatism Volume 37, Issue 11, pages 1593–1601, November 1994Volume 37, Issue 11, 5.Fibromyalgia in women. Mountz JM et al. Arthritis & Rheumatism 1995; 38: 926–938. 38 6.Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Gracely, Clauw etc 2002 A&R.. Arthritis & Rheumatism 2002; 46: 1333–1343. 46 7.Evidence of Augmented Central Pain Processing in Idiopathic Chronic Low Back Pain. 2004 Giesicke, Gracely, Clauw etc Arthritis & Rheumatism 2004; 50: 613–623. 8.Fibromyalgia family study: a genome-scan linkage study. Arnold L et al. A & R 2013;65:1122-28.
Musculoskeletal Symptoms and Non-REM Sleep Disturbance in Patients with Fibrositis Syndrome and Healthy Subjects MOLDOFSKY H, et al. Psychosomatic Medicine 1975; 37:341-351 and Induction of neurasthenic musculoskeletal pain syndrome by selective sleep stage deprivation. Moldovsky H et al. Psychosomatic Medicine 1976;38:35-44. No rule of science left unbroken in proposing a pet theory about sleep dysfunction & fibrositis Pre-emptive de-selection of patients who did not display the desired results before the study (3 discarded, 6 used) Unblinded evaluators who had a vested interest in outcome No actual control group for claimed EEG abnormalities (comparison was made to partial EEG results in middle- aged men published by others several years prior) Unvalidated questionnaire and dolorimeter methods Very low subject numbers (6 in the sleep deprivation phase); subjects different age & gender than those in clinical syndrome Extreme sleep deprivation resulting in “overwhelming physical tiredness, heaviness, or sluggishness to the point of experiencing difficulty with walking or standing up.” In these pre-selected normal young individuals deprived of slow-wave delta sleep, the authors state that they found a reversible modest reduction in pain threshold at dolorimeter points, and vague physical complaints including achiness. No distinct clinical ailment. In other words, The results of severe deprivation of restorative sleep temporarily made some healthy people miserable. o Disproportionate influence on the later mythos of fibromyalgia; nearly always quoted in reviews and texts. o For 20 years thereafter no one attempted even to replicate findings. A few attempts later gave indeterminate results. In 40 years, no one has been able to show a primary sleep disturbance, nor that sleep disruption is anything but secondary to pain.
Primary fibromyalgia (fibrositis): Clinical study of 50 patients with matched normal controls. Yunus M. Semin. Arth Rheum 1981;11:151-171 “Detailed clinical study of 50 patients with primary fibromyalgia and 50 normal matched controls has shown a characteristic syndrome. Primary fibromyalgia patients are usually females, aged 25–40 yr, who complain of diffuse musculoskeletal aches, pains or stiffness associated with tiredness, anxiety, poor sleep, headaches, irritable bowel syndrome, subjective swelling in the articular and periarticular areas and numbness. Physical examination is characterized by presence of multiple tender points at specific sites and absence of joint swelling.” A seminal study helping to define FM, confidently putting forward tender points and non-locomotor symptoms. Comparison group: healthy normal people selected to be free of all symptoms. Therefore all the features in the preselected group labeled “fibromyalgia” will characterize the syndrome you’ve already identified. Thus it’s circular and trivial and useless to even bother with such a control group – This study modeled a design motif frequently used in FM reports, of attributing specificity to findings in pre-diagnosed cases by comparing them to normal controls. Standard anatomic, biomechanical exam findings of musculoskeletal system not given. Such findings never reappear in all future publications relating to fibromyalgia. This study was a bellwether of future research design: normal controls, irrelevant controls, never controls who closely matched clinical exam features, and extinction of concern with standard anatomic/physiologic examination.
What does it mean in this setting to have a “healthy normal” control group”? Your test group subjects are selected to suit your preferences, preconceptions, and pre- defined criteria of abnormalities. The normal control group by definition has none of the pre-defined abnormalities. Every difference found will simply confirm your preconceptions in a circular way. It is disingenuous to use such a control group as if it adds a sheen of science. And it is trivial and useless.
Electron microscopic studies of muscle biopsy in primary fibromyalgia syndrome: a controlled and blinded study. Yunus M et al. J. Rheum 1989;16:97-101 Electron microscopic evaluation of trapezius muscle tissue: after finding subtle abnormalities in a 1986 study of muscles from fibromyalgic-labelees, he studied again in 1989 and this time compared normal controls: all had the same minor changes However this study became important since it sealed the case, for much of the FM research community, that peripheral body tissue could not the source of the wide-ranging pain of their subjects. It escaped notice that the pain could originate in other elements of the locomotor force chain such as tendons, myotendinous transitions, enthetic structures, aponeuroses, pulley structures etc. It suited the preconception perfectly and thus the author and his friends were not “called out” about the inadequacy of the concept underlying this study. This was another giant step down the corridors of illogic. Interestingly, some investigators still seem to be looking for relevant abnormalities in muscle (Srikuaea/Crofford 2013) or in small-fiber nerves in skin and vessels (Oaklander 2013, Albrecht 2013), in all cases however comparing their FM labelees to normals and drawing equally unwarranted conclusions.
Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Russell IJ. Arth Rheum 1994; 37:1593-1601 In this paper it was determined that CSF substance P was 3-fold elevated in 32 patients with fibromyalgia, compared to 30 normal controls. A side result was that among the FM patients with a spectrum of tender point counts, Substance P levels did not correlate with the tender point count. Pain severity not graded: ?correlation. Anatomic findings not disclosed: ?correlation. Note: this study, as does the vast majority of studies in FM, compares healthy normal volunteers instead of “positive controls” and thus one does not know if CSF transmitter molecules are just nonspecifically elevated in anyone with pain, or whether there’s something specific about FM. Also – no relevant physical findings or severity sorting. However, this study is quoted regularly and authoritatively as if it has value to the profession and the public.
Fibromyalgia in women. Mounts JM et al. Arth Rheum 1995; 38:962-938 An early study of cerebral imaging using 10 fibromyalgia labelees and 7 healthy normals: dolorimeter pain threshold at tender points and control points as well as regional blood flow to thalamus and caudate as seen in SPECT were both abnormal in the women with pain compared to pain-free individuals. The journal allowed the study to conclude: “The findings of low regional cerebral blood flow and generalized low pain thresholds support the hypothesis that abnormal pain perception in women with FM may result from a functional abnormality within the central nervous system.” Here we see useless information again, in view of the design calling for normal controls instead of comparison with “positive controls” with one or another sort of recognized peripheral pain A proper “positive” control group of women with one or more different pain disorders would likely have revealed that the “FM” women did not have a “functional abnormality within the CNS” but instead were processing just the way the human race does in other pain disorders. Further, detection of correlation of imaging with physical exam findings or severity not possible in view of lack of data.
Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arth Rheum 2002;46:1333-1343.. Gracely RH, et al. 16 FM labelees vs 16 healthy normals. Thumbnail pressure/fMRI study. Equal pinch pressure and equal pinch pain-perception phases: Comparison of 19 regions in brain revealed that 13 were more active in FM and 1 more active in normal controls. Journal allowed the authors to conclude “.. supports the hypothesis that FM is characterized by cortical or subcortical augmentation of pain processing..” Author’s later review: “These observations provided the first fMRI-based evidence for central augmentation of pain sensitivity in fibromyalgia.” This not justified since a positive (chronic pain) control group (e.g. osteoarthritis, metastatic cancer, or multiple tendonosis) was not looked at to determine if in fact it was “normal” for any chronic pain to affect processing in this fashion. What if any and all chronic pain conditions are “characterized” by the same fMRI findings? And again, ?correlation with pain severity and/or distribution of physical findings.
Evidence of Augmented Central Pain Processing in Idiopathic Chronic Low Back Pain. Giesecke T et al. Arth Rheum 2004;50;613–623 a remarkable study Effects of thumbnail pressure pain on fMRI brain imaging in 11 healthy controls, 16 FM labelees, and 11 patients with at least 3 months of lumbar pain “unexplained” by Xrays or MRIs. On thumb-screw pain application designed to equalize perception of pain, The FM labelees lit up 5 brain areas associated with pain processing compared to 1 such area for normal controls, and did so at average lower force levels. An additional group was studied --lumbar pain (called “idiopathic” although most had some degree of disk degeneration, endplate changes, or vertebral height reduction). Acute pain processing findings on fMRI were identical to the fibromyalgia labelees! For me, this study simply means that acute pain applied to those with lumbar pain is processed the same as for those with multiple areas of myotendinous pain. That’s just the way acute pain looks in anyone with chronic pain. The authors however, seriously stated that the lumbar pain patients had nothing much wrong physically and were thus victims of central pain. For them it was proof that lumbar pain and “fibromyalgia” were both due to aberrancy in central pain processing! The journal editors allowed them to conclude that there is “augmented pain processing in patients with chronic low back pain. Once again, standard physical exam findings were not described for any of the patients. Nor was severity of symptoms sorted. This study was the closest anyone has come to showing by direct comparison that there is not an aberrancy in central processing in patients labeled as FM.
Fibromyalgia family study: a genome-scan linkage study. Arnold L et al. Arth Rheum 2013;65:1122-28 Study patients were those labeled with central pain/FM. Multi-case families were selected and relatives added up and compared to a background population prevalence of 2%. No control group as such. In this study enriched for familial cases, one result suggested “ a strong genetic component of fibromyalgia.” a) Is that circular? What if probands were not preselected to have an affected relative? ; b) what if additional family members had been also mistakenly been told “fibromyalgia” by MDs in the same community; c) would the genetic aggregation still be seen if 2.5%, 3% or 4% population prevalence were used? – “sensitivity analysis” needed in case they had low-balled the population prevalence There was a “suggestive linkage of familial cases to the chromosome 17p11.2-q11.2 region.”. Note:.. Paper is dense with statistics and molecular genetics, but no actual description or quantitation of clinical features of case material. (?were the worst cases more likely to have linkage?) No control group and especially no control group of multicase families with multiple locomotor disturbances… would the genetic studies of this group be identical to those labeled “fibromyalgia?” Are they in fact the same people?
Dr. Lampman’s personal conclusions about the literature on this subject from 1968-2014 100 publications were examined for issues of study design and credibility
“Not even wrong” All investigators were easily able to recruit many pain subjects in whom they could not detect convincing explanatory anatomic findings. None of the studies set out to test the hypothesis that fibromyalgia-labeled patients had a pain-processing mechanism different from that of any other chronic pain patients. Virtually all the studies matched the description the physicist Wolfgang Pauli used for some investigations: “Not even wrong.” Their design makes them irrelevant right out of the gate.
“Not even wrong” (more) One study inadvertently landed on a useful design. It showed acute pain processing fMRI’s to be identical in lumbar pain and “fibromyalgia.” However, the authors obtusely provided a completely wrong-headed conclusion. When studies showed acute pain in osteoarthritis and irritable bowel patients to be processed differently than that in healthy normals, thought leaders similarly and obtusely conclude that such disorders must have the same central aberrancy and augmentation as “fibromyalgia.” And when effective treatment of peripheral pain sources in “FM” cases normalized their pain processing and thresholds, this simply to them means that tonic input of the “central pain” was being maintained by peripheral sources. In neither case was there concern for the simpler but forbidden idea that the FM hypothesis itself could be a complete failure. None of the authors seems willing to deal with anything that challenges the central axiom that fibromyalgia is a unique or at least prototypical central pain augmentation disorder. It is not on the research agenda. Nor will they test the concern that the apparent linkage of irritable colon, bladder etc are anything other than an illusion of case selection, care- seeking, and other biases.
Why the neurologic hypothesis of fibromyalgia is profoundly obscurantist 1. Failure to properly examine patients using anatomic principles; promoting faulty and nonphysiologic concepts such as “chronic widespread pain” and the “tender point” examination; misapplying neurology’s central pain concept, and dismissing the locomotor system from consideration. 2.Misrepresentation of the patient complaint of “hurting all over,” and obscuring the critical differential diagnosis 3.Insisting on the uniqueness of fibromyalgic pain and its neurologic processing but failing to compare it to other sorts of pain – in other words, mistaking for “aberrant” the way any pain is processed by someone already in pain 4.Arbitrarily asserting an “omnium-gatherum” set of non-locomotor corollary symptoms (attached to index cases mainly by care-seeking sampling bias) said to have idiopathic, functional, psychosomatic, neurologic origins which link them to fibromyalgia --such as interstitial cystitis, irritable bowel, TMJ disorder, sleep disorder, headache, fatigue, cognitive alterations and depression. 5.In investigations, failing to accurately and quantitatively describe the subjects and failing to sort or grade the results according to clinical descriptors [clouding and concealing presence or lack of dose effect or limit effect] 6.Extending the preoccupation with “aberrancy” into the genetic realm, claiming support for the integrity of the FM diagnosis if able to show “labelees” may have genetic/familial aggregation -- in the meantime, failing to assess aggregation in a proper control group consisting of multiple tendonopathy cases and their families. 7.When facts demonstrate that FM-labelee pain is no different than various nociceptive pain states (e.g. osteoarthritis), deceptively generalizing “central augmentation” to numerous common kinds of pain and widely extending the hypothesis, thus diverting attention from the underlying theoretical weakness of the entire field, and promoting ever-widening CNS drug treatment of questionable rationality.
What are the origins of the fibromyalgia hypothesis? The power of the cultural matrix “Holy Seven” psychosomatic disorders (1930-50): Rheumatoid, Asthma, Ulcerative Colitis, Hypertension, Hyperthyroidism, Eczema, Gastric Ulcers. Trend of misuse of the Specificity Theory of neurology “focus on identifying and interrupting pain pathways” e.g. cutting tracts in CNS (Parris) Modern neurology’s mapping of the body’s somatosensory structure back to modules in the brain (Penfield 1950) Concern that ideas may cause drastic physical symptoms and neurobehavioral aberrations (conversion disorders, “hysteria”). Freudianism: the potency of dysfunctions traced to their roots in infancy. 19 th Century concepts of neurasthenia and female weakness, part of a structure by which gender inequality was explained, legitimized, and sustained The modern cultural narrative of the abused, degraded, anxious, or depressed woman in physical pain due to psychological baggage. Mind-body medicine with its correlations in mystical Eastern philosophy, demon-preoccupied cults and religions, and voodoo medicine. Over-application of “bio-psychosocial” model. Pharmaceutical industry sponsorship and definition of the pain problem and the research goals.
After 4 decades of fibromyalgia promotion: Thousands of useless speculative publications, all starting with an unmoored neurologic assertion and improper experimental design Collapse of the integrity of peer review and editorial control systems Failure of sound critique from rheumatology, neurology Breach of duty in diagnosis and care of our patients No useful scientific progress A free-for-all of industrially-marketed disinformation and unworthy treatments aimed at vulnerable patients Overall: a signature achievement of the confabulatory wing of science. The public is frequently skeptical: “This is what doctors say when they can’t figure out what is wrong!” Fibromyalgia, in fact, is what you say when you have not provided your patient with an anatomically informed assessment.
I Disorders of myotendinous resiliency a.Stereotypical array of ailments related to locomotor force chains b.The profound and humbling lesson of having such a disorder c.“Hurting all over” usually means two or more specific painful disorders are present. [No human disorder literally causes musculoskeletal pain everywhere] d.Clinician’s duty: concretely examine, authenticate, prognose, and treat each ailment] II Fibromyalgia: a failed neurologic hypothesis a.Disconnects itself from the locomotor system and all recognized facts of anatomy, neurology, and musculoskeletal pathology (bubble of diagnostic mis-attribution) b.Flawed scientific foundation of unproven claims c.Damaging to patient care, research, and clinical reasoning
Conclusion By now, however, the full shape, the trajectory, and historical meaning of the fibromyalgia hypothesis is only too evident. It was inspired and imaginative – but not in a good way. Right out of the gate in the 1970’s, the fibromyalgia hypothesis entered an endless closed corridor of medical illogic. As the years wore on by, it could not produce anything other than faulty foundational evidence. Its culturally- entwined prejudices could not escape the psychosomatic model, its applicability to the individual patient has been misleading, its treatment program ineffective, and its research program unproductive, scattered, and confused. Despite gaining a pseudo-orthodoxy through endless repetition, its flaws have led to its collapse into untenability. It has earned its status, I believe, as the 8 th of the “Holy Seven” disorders falsely attributed to mysterious cerebral control of the body. The fibromyalgia hypothesis has been an embarrassment to rheumatology and to the practice of good medicine. You are under no obligation to accept the authority of its proponents. I believe that, misinformed by the fibromyalgia hypothesis, many physicians have breached their duty to diagnose and care properly for their patients. That’s why I take this subject very seriously, and why I, as a modest country doctor unversed in technical science, bring it to your attention and consideration. My conclusion and my advice to you as clinicians is to simply do a normal history of each specific pain complaint, do a conventional anatomic physical examination, and fulfill your duty of diagnosis and care to the patient. If you do that I believe you will never find patients whom you can honestly classify as fibromyalgia. And you will do your patients right, by telling them the truth and directing them into rational treatment for a set of problems that anatomic destiny requires the human race to suffer.
End To receive a copy of this presentation contact Dr. Lampman at: JHL1946@gmail.com or inquire at the Medical Education office.