Painful Myotendinous Disorders: - PowerPoint Presentation

Slide1

Painful Myotendinous Disorders:Our duty to diagnose

A Critique of the Fibromyalgia Hypothesis

James H. Lampman, MDSlide2

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.Slide3

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.”

ThemeSlide4

Examples of

biomechanical disorders

of

myotendinous force unitsRotator cuff impingement

Achilles tendonopathy and tears

Trapezial, levator, rhomboid strainsTrochanteric 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 syndromesAuto-traumatic disorders of myotendinous resiliencySlide5
Slide6

Muscle architecture types: exuberant diversity

From: Gray’s AnatomySlide7

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 bodyThe numerous and diverse myotendinous chains are vulnerable to biomechanical injurySlide8

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 otherwiseSlide9

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 patientSlide10

Gluteus medius tendonopathy

(sometimes a tear).

A strain/overuse disorder of the lateral hip sometimes called greater trochanteric pain disorder.Slide11

Patellar

Achilles

Hamstring

SupraspinatusSlide12

PlantarisSlide13

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 painSlide14

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)

*LittlejohnSlide15

Joint map

Muscle-tendon mapSlide16

Worksheet for office evaluation*

(43 commonly seen non-inflammatory myotendinous disorders)Slide17

Example: patient with multiple

pain sources

Humeral

epicondylitisFinger flexor tendonopathy

Supraspinatus

tendonopathy

Trapezial strainTrochanteric

pain (glut

medius

)Slide18

A clinical observation:

“

I hurt all over

” is a common complaint when 2,3,or 4 focal myotendinous disorders are present.Slide19

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 tendinitisvariable trapezio-cervical strain and myalgic headacheGluteus medius tendonopathy (left more than right)Slide20

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

: Slide21

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 painSlide22

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. Slide23

Treatment of Resiliency Disorders

Force re-duction, posture retraining

Finger flexor

tendonopathy

x

x

xxxx

x

Elbow epicondylitis

xxxx

xx

?

??

Rotator cuff impingement

xxx

xx

xxx

Xx?

Trapezial-cervical pain

xxxxx

x

Jaw clenching disorder

xxxxx

x

Costochondritis/costosternal

xx

x

Lumbago/iliac crest pain

xxx

x

x

Trochanteric pain syndrome

xxx

x

xxx

Subcalcaneal heel pain

xx

xx

Achilles strain

xxx

xxx

injection

surgery

Splinting, heat, PT-OT

Note on systemic medication: If used at all, select only the safest.Slide24

Myotendinous

pain

is

rationaleven 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.Slide25

Part IISlide26

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.Slide27

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.Slide28

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!Slide29

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.Slide30

Examples of leading studies advancing the fibromyalgia hypothesis

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

Primary fibromyalgia (fibrositis): Clinical study of 50 patients with matched normal controls . Yunus M.

Seminars in Arthritis and

Rheumatism

1981; 151–171. 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]

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 1994

Fibromyalgia in women.

Mountz

JM et al. Arthritis & Rheumatism

1995;

38

: 926–938

.

Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia.

Gracely, Clauw etc 2002 A&R.. Arthritis & Rheumatism 2002; 46: 1333–1343. Evidence of Augmented Central Pain Processing in Idiopathic Chronic Low Back Pain. 2004

Giesicke, Gracely, Clauw etc

Arthritis & Rheumatism 2004; 50: 613–623

.

Fibromyalgia family study: a genome-scan linkage study. Arnold L et al. A & R 2013;65:1122-28.Slide31

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.

Disproportionate influence on the later mythos of fibromyalgia; nearly always quoted in reviews and texts.

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.Slide32

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.Slide33

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. Slide34

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.Slide35

Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome.

Russell IJ.

Arth

Rheum 1994; 37:1593-1601In 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.Slide36

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.Slide37

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.Slide38

Evidence of Augmented Central Pain Processing in Idiopathic Chronic Low Back Pain

.

Giesecke

T et al. Arth Rheum 2004;50;613–623a 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. Slide39

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? Slide40

Dr. Lampman’s

personal conclusions about the literature on this subject from 1968-2014

100 publications were examined for issues of study design and credibilitySlide41

“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.Slide42

“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.Slide43

Why the neurologic hypothesis of fibromyalgia is profoundly obscurantist

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.Misrepresentation of the patient complaint of “hurting all over,” and obscuring the critical differential diagnosis

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 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.

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]

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.

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.Slide44

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 sustainedThe 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.Slide45

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.Slide46

I

Disorders of

myotendinous

resiliency Stereotypical array of ailments related to locomotor force chains

The profound and humbling lesson of having such a disorder

“Hurting all over” usually means two or more specific painful disorders are present. [No human disorder literally causes musculoskeletal pain everywhere]

Clinician’s duty:

concretely examine

, authenticate,

prognose, and treat each ailment]

II

Fibromyalgia: a failed neurologic

hypothesis

Disconnects itself from the

locomotor

system and all recognized facts of anatomy, neurology, and musculoskeletal pathology (bubble of diagnostic

mis

-attribution)

Flawed scientific foundation of unproven claims

Damaging to patient care, research, and clinical reasoningSlide47

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.

 Slide48

End

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