Functional Somatic Syndromes: “Fibromyalgia” and the Like

Nothing can pierce the soul as the uttermost sigh of the body.

—George Santayana, The Life of Reason, 1905-1906

By the time I came to write the Second Edition, functional somatic syndromes were important in the scholarship that relates to occupational musculoskeletal disorders. Sadly, they are now pivotal. “Fibromyalgia” (FM) in particular is increasingly used as a label for disabling illness. It is increasingly used as a label for illness consequent to injury inside and outside the workplace. As such, it is ever more contentious in the arena of tort litigation. I am aware of three evidentiary hearings relating to the latter in which it was argued whether FM could be a consequence of a motor vehicle accident or a slip and fall in a supermarket, or could arise out of and in the course of employment and therefore be compensable. These arguments will be discussed in Section III (in each instance the court found for the defense). Fortunately, the growth in relevance of the “FM” construct brings with it a growth in the explanatory science. The subject is so considerable in scope that this chapter will be subdivided:

Labeling Woefulness: This is a discussion of the traditional approach to the topic. It was developed at length in the Second Edition. This is the update.
Tender Points and the Fickle Finger of Faith: This discussion demystifies and debunks the “sign” on which advocacy for “FM” relies.
Medicalization of Misery: This is a discussion of the dynamic that underlies the Labeling of Woefulness.
The Social Construction of FM: This is the state of the art and science.
Preventing FM: Prevention, rather than treatment, holds therapeutic promise.

LABELING WOEFULNESS

Fortunately, most of us, most of our lives, are “well.” To be well is not the same as to feel well. It means that even when faced with some physical symptoms, or certain psychologic stresses, or some degrees of traumatic injury, we remain convinced we are basically well. The “flu,” a sprained ankle, the sporadic headache, a pain in the neck or shoulder or back, a change in bowel habits, heartburn, heartache, and the like may give us pause, but seldom seem insurmountable. To be “well” requires a sense of invincibility.

Sometimes we are less certain. The morbid event may be familiar, but this episode is more dramatic, intense, or persistent. If the event is unfamiliar, it is
always more trying. We draw on personal resources such as the advice of a spouse, extrapolation from seemingly relevant information garnered somewhere in the past, or denial. Usually, our patience, our coping, is rewarded by spontaneous regression of the vexation. This homeostasis is inherently delicate; for some it is tenuous. There are those among us who reach the end of every day relieved they made it that far.

Whenever the sense of vulnerability exceeds our personal resources for coping, most of us take recourse with a health care provider of some ilk. The patient is seldom in a position to weigh the influences that drive the decision to seek medical care. Persistence or intensification of the symptoms is the reason, but do the symptoms reflect progression of the underlying disease? Are the symptoms rendered less tolerable by confounding events in our lives? Or both? The contract implicit in the modern physician-patient relationship downplays the multivariate causation of all illness; rather, in choosing to be a patient, one is taking recourse in the pledge of scientific medicine to define the biologic cause of the symptoms and the promise to apply a remedy if at all possible. In choosing to be a patient, the person has outstripped his or her own homeostatic reserve, has commenced his or her own differential diagnosis with whatever sophistication he or she can muster, and has turned to a physician to get the job done.

Not every day is a good day. All of us have days when we are indisposed. These “bad” days can be characterized in that they share many, if not all, of the features in Table 3.1. Bad days come and go most of the time without causing most of us to pause. But what really makes them bad? How many of the components in Table 3.1
need to be present before all of us would be “under the weather”? The category of external events is insufficient in and of itself or most of us would bemoan a diminished quality of life. The gastrointestinal symptoms in and of themselves are insufficient. After all, alternating diarrhea and constipation are accepted as normal for as many as 22% of us, only a small percentage of whom feel a need to seek medical attention.¹,² Similar insights pertain to component II, the musculoskeletal symptoms. Several surveys show that 20% of us are experiencing morning stiffness, lasting as long as 30 minutes, as a matter of course without seeking medical attention. And 50% of us can be made aware of focal tender points, particularly in the muscles of the pectoral girdle, when we are in robust health.³

TABLE 3.1. COMPONENTS OF THE SYNDROME OF OUT-OF-SORTS

I. Loss of the sense of well-being:

Decreased energy
Easy fatiguability
Bitemporal heaviness/achiness
Inexplicable anxiousness
Perception of a sleep debt
Vigilance as to unusual symptoms

II. Musculoskeletal symptoms:

Diffuse achiness
Disconcerting stiffness, often in the morning
Sense of swelling, particularly about small joints
Tenderness often about the neck, shoulders, and low back
Intermittent numbness of the hands and/or feet
Jaw pain

III. Gastrointestinal symptoms:

Increased or decreased stool frequency
Keen awareness of bowel function

IV. Peculiar associations of well-being with external events:

Improvement with exercise
Exacerbation with stress
Exacerbation on gloomy, damp, and cold days

The inescapable conclusion is that the sine qua non of “feeling poorly” is component I, the loss of a sense of well-being, of invincibility, and, pari passu, the acquisition of a sense of growing vulnerability. The other components may define subsets or they may be coincidental, far from a trivial distinction. This distinction underlies a tremendous amount of medical care and occupies the attention of a good deal of lay literature. Do we experience component I because of overpowering difficulties with one or another of the other components? Or is it that component I causes us to be cognizant of the others, to focus on the others, and to use the others as surrogate complaints?

For the chronically vulnerable, there are few good days. No doubt there is a bad day lurking in the future of each and every one of the rest of us as well. Most of us will be nonplused. But if there are too many days in series, or if recurrences cause us to worry whether some insidiously progressive deterioration is to be our fate, few of us can maintain equanimity. Then all of us will cast around for insights. Many are proffered by the lay medical press and by practitioners hawking their services in the various media. Some of us get better. Some of us devise schemes for coping; schemes that may entail changes in self-image or alterations in interactions in our psychosocial milieu. And some of us, early or late, seek medical guidance.

These worried people are never passive patients. They enter the physician’s office already embroiled in the diagnostic exercise. After all, it is their failure at the diagnostic exercise that drives them to be patients and to contract their physician to orchestrate the quest for the answer. Many of them are sore, many are stiff, many consider each bowel movement a setback, and all are wretched. All are meticulously tuned into their bodily functions, and all are as medically sophisticated as their intellect and resources permit.

As part of the exercise of diagnosis, the physician will restructure the patient’s perceptions according to an algorithm designed to test pathophysiologic hypotheses in sequence. Some sort of review of systems is used. A physical examination follows again to serve hypothesis testing. The “red flags” of systemic illness, of serious pathology, are not discerned: no fever, anorexia, weight loss, or clues to destructive, neoplastic, or dystrophic disorders on physical examination. Bowel complaints do not include nocturnal diarrhea, hematochezia, or tenesmus. Musculoskeletal complaints are discordant from signs of inflammation. Hints fuel hypotheses, but nothing
to hang one’s hat on. Diagnostic uncertainty furrows the brow of the physician and is rapidly taken to heart by the patient.

Should not every clinical enigma be a match for modern diagnostics? Who could refuse any study that is suggested? Blood is drawn, and imaging is scheduled. The patient leaves the office a changed person. Every available waking moment offers another opportunity to pursue the diagnostic exercise. Self-awareness is taken to extremes; any nuance in bodily function is noted, even recorded. Some of the testing is intrusive, uncomfortable, surrealistic, and time-consuming. All the while, the patient is worried and actively attempting to make the pivotal observation. Precious few get better during this process. The quest for diagnosis is consuming and subsumes the experience of illness. Results slowly trickle in; they are often negative. When they are “positive,” the inference is blunted by limitations inherent to any test with imperfect specificity when it is used to screen for any disease with a low prevalence. The patient begins to speak in the jargon of the differential diagnosis, think in this mode, and participate in the workup with consuming attention. The differential diagnosis narrows as myositis, myasthenia, lupus, rheumatoid arthritis, Lyme disease, Crohn disease, ulcerative colitis, and other possibilities are discarded by specialists with some conviction. All were exceedingly unlikely given the quality of the symptoms on presentation and the normality of the results of the physical examination. But by now, months have passed. The illness is magnified, and the anxiety about the label has become a way of life.

What is it? We must know soon and for certain. After all, the patient is getting more ill, and scientific therapeusis must be structured by the diagnostic possibilities. Enter the next round of labels: FM, chronic fatigue syndrome (CFS), irritable bowel syndrome (IBS), temporomandibular joint dysfunction (TMJ) syndrome, chronic Epstein-Barr virus infection, chronic Lyme disease, and more.

Patients with the illness captured in Table 3.1 are seldom balanced in all four components. Either they perceive a weighting or the diagnostic evaluation is instructive in this regard. The latter may reflect the perception on the part of the patient or the primary physician of the more telling of the symptoms. If the inference is not communicated directly; it is tacit and reflected in the pattern of consultation to be undertaken. If the musculoskeletal components of the illness come to the fore, the consulting rheumatologist is likely to ply a label like FM. If you are seen by a gastroenterologist, you will not escape without the lumen of your viscera escaping scrutiny. If the lumen divulges no secret, you and your illness will be labeled with IBS. If neither referral is made, and your Epstein-Barr virus and Lyme titers are unremarkable, your illness will be characterized as mainly components I and IV, and the label CFS will be bandied about. In fact, if one examines the literature defining these three labels, little about them is mutually exclusive.⁴

Each diagnostic label is promulgated by a clinical school generally claiming to be championing the scientific cause of the patients they attend to. To initiate studies of natural history or intervention, each school has formulated clinical criteria, which, as one might surmise, have much in common while pivoting on a special feature. In each instance, the criteria have since been worked and reworked by “working groups” of experts trying to hone in on the very essence of the condition by the
application of statistics and consensus with varying degrees of rigor. There is always a mandate to exclude inflammatory or neoplastic diseases as a cause of the illness. Even with the latest generation of criteria, a formal analysis of the symptom profiles of patients who meet accepted criteria for CFS or FM documents far greater similarities than differences.⁵ The overlap is such a predominent feature of all these putative diagnostic labels that it was argued cogently a decade ago that they are a single “affective spectrum disorder.”⁶ However, for reasons that will become clear shortly, each putative entity has advocacy among the groups of patients so labeled and their treating physicians. Such advocacy fuels disease-specific research that marches on in lockstep between the labels.

Chronic Fatigue Syndrome

Researchers who are focused on CFS continue to probe the microbiologic, psychosocial, neuroendocrine, and therapeutic fronts with a tenacity that belies their progress.⁷,⁸ Unfortunately, particularly if patients have multiple somatic complaints or a history of a dysthymic order, the prognosis for these people to ever feel well again is dismal.⁹ Equally distressing is the fact that most patients who satisfy the criteria for CFS have spent 15 years repeatedly seeking medical attention for a wide variety of complaints,¹⁰ indicating that they are mired in the world of the vulnerable people discussed in the beginning of this chapter. The labeling does little to extricate them. Perhaps they would do as well to remain among the 0.5% of people in the community¹¹ who would qualify for the diagnosis, by all “criteria,” if they decided they wanted to be patients.

Irritable Bowel Syndrome

Thanks to the pioneering work of Drossman and colleagues, the concept of IBS is far less mired in debates about organicity.¹,² As mentioned previously, the symptoms that signify IBS need not be abnormal. They are not even disconcerting for a significant minority of people. Given that there are no disease-specific markers, diagnosis is entirely symptom-based. The latest attempt to hone diagnostic criteria resulted in “The Rome Criteria” for the functional gastrointestinal disorders.¹² Despite the honings, little new of substance has been forthcoming. There may be underlying abnormalities in the physiology of the colon; those that have been demonstrated are subtle,¹³ not uniformly present, and highly unlikely to evolve into any classic organic bowel disease.¹⁴ Nonetheless, the illness these patients experience can be pervasive,¹⁵ and the prognosis can be poor. Gastroenterologists have a long tradition of plying patients with concoctions that perturb bowel motility. No wonder IBS is a seductive therapeutic challenge. Gastroenterologists are stymied, although not totally, by a condition that inherently alternates between diarrhea and constipation. They have found that smooth muscle relaxants are beneficial for the component of IBS that is painful¹⁶ and that loperamide is effective for diarrhea.¹⁷ Enter alosetron (Lotronex), the Glaxo (Research Triangle Park, NC) drug that has been approved, then withdrawn, and then approved with limited indications for
IBS by the Food and Drug Administration. This is the first major assault of “Big Pharma” on IBS. Alosetron has a rocky but very telling history. It was originally approved for IBS until it became clear that ischemic colitis was a rare but real threat in those patients with diarrhea as the principal manifestation. This is an example of a drug toxicity in which the frequency and severity of a life-threatening adverse reaction was weighted against the value of palliating a symptom. The drug was withdrawn only to reemerge as the agent touted to be useful for treating the symptom of constipation in the setting of IBS. Since approval for this indication, alosetron is marketed for treating constipation in other settings. However, there is a large placebo effect—so large as to call into question any indication for this agent.¹⁸

Labeling Whatever

Before we turn to the focus of this chapter, FM, a short digression is called for. There is no field of medicine that is not ready and willing to label a medically inexplicable symptom with a chauvinistic rubric. Patients with IBS, CFS, or the like can and will report difficulties and disturbances with body image or function for nearly every anatomic site. Cardiology has evolved to surmount the possibility of a medically inexplicable symptom with an aggressive empiric posture that will leave very few without angioplasty, stenting, or coronary artery bypass grafting.¹⁹ Most other fields have some reservations about empiricisms, allaying their uncertainties with labels that seem valid but are no more than hypothesis. For example, orofacial pain is often ascribed to TMJ by dentists willing to overlook the fact that their patients are plagued by symptoms in multiple organ systems that could not possibly have anything to do with the TMJ²⁰,²¹ and despite the fact that TMJ pathoanatomy is not associated with such illness behaviors.²² Patients labeled with “interstitial cystitis” are beleagured with nonbladder-related symptoms,²³ as are patients who complain of dry eyes and mouth in the absence of Sjögren’s Syndrome.²⁴

Fibromyalgia

As I first detailed nearly 20 years ago,²⁵ the advocates of fibrositis as a diagnosis and concept have been faced with criticism and uneven acceptance since the term was coined in 1904. This continues today²⁶ despite the fact that the concept garnered the implicit sanction of the American College of Rheumatology (ACR) more than a decade ago by virtue of the promulgation of “criteria” for diagnosis of the illness to be labeled FM, rather than the older label fibrositis.²⁷ The criteria were formulated and promulgated as an aid to research, including research into the pathogenesis of the illness, rather than as an assertion that the pathogenesis is understood. Unfortunately, the criteria were established by a form of circular reasoning; physicians who were dedicated labelers sought features that distinguished the patients whom they had already labeled with FM. One can never test a hypothesis using the same data that were used to generate the hypothesis in the first place. The criteria have proved neither specific nor reliable. Even Wolfe, who was instrumental
in the criteria’s formulation, has decried their use in the clinical setting.²⁸ Nonetheless, the criteria have swayed many a practitioner into thinking that FM is an established entity. There is no debate that there are many individuals whose pervasive illness is consonant with the illness denoted by the FM label. The debate rages over whether the illness is a consequence of an underlying organ-system dysfunction or the illness is a form of illness behavior magnified by the medical model for care. I am of the latter opinion.

Because the ACR criteria carry the patina of authority, they are worthy of inspection. In 1986, 22 clinicians and clinical investigators, all proponents of the fibrositis concept, formed a committee to establish diagnostic criteria of measured sensitivity and specificity. Sixteen members of this committee deemed themselves a “consortium” and agreed to participate in the actual investigation. They identified 293 patients in their practices whom they had labeled with primary or secondary FM. The concept of secondary or concomitant FM is difficult at best; for me it is impossible. It is the concept that in the setting of another rheumatic disease (e.g., rheumatoid arthritis with its polyarthritis, polymyalgias, and systemic symptomatology), one can still discern FM as a discrete entity. Nonetheless, they compared their 293 patients with FM with 265 age- and sex-matched controls. The controls were their patients whom they had labeled as having regional musculoskeletal illnesses or rheumatologic complaints that suggested the possibility of systemic rheumatic disease but were too subtle to allow for a definitive diagnosis. All control patients had musculoskeletal symptoms. The patients with FM and the control patients with rheumatic disease were compared for all the features in the classic criteria for fibrositis. The only distinction they detected, and therefore the “criteria” they formulated, are presented in Table 3.2. To be labeled with FM by these clinicians in their practices, you have to be hurting in a peculiar widespread distribution and have lots of special points about your pectoral and pelvic girdle and knees and elbows that are tender when probed by these examiners. Hurting alone was insufficient, because approximately 70% of the referent patients were hurting to this degree. The diagnosis is based on “tender points.” As I said previously, there is a circularity to the establishment of these criteria by these believers in patients they had already labeled. But tautology is but one of the shortcomings of the “ACR criteria.”

The criteria are subjective because there are absolutely no reproducible, specific, biochemical, immunologic, electrodiagnostic, or histopathologic correlates with the diagnosis of FM. That fact is not for lack of trying; the literature is littered with false starts, and the effort continues apace in recent years.²⁹ Many a “finding” is
likely to be a secondary phenomenon.³⁰ In a study performed a decade ago,³¹ elevated levels of the nociceptive neurotransmitter substance P were demonstrated in the cerebrospinal fluid of patients with FM compared with healthy controls.³¹ This finding is held by most who are committed to the hypothesis that FM is a disease demonstrating a specific derangement in biology. The small difference between healthy patients and patients with FM in regard to the levels of substance P in the spinal fluid is reason to be cautious in interpreting the finding. The fact that the substance P levels do not correlate with the magnitude of symptomatology in FM also made we wary of imputing too much to the observation as it stands. Finally, the fact that the FM levels were compared with levels in healthy volunteers offers no insight about whether the finding is specific to FM. Perhaps the same would be found in patients who are depressed or experience chronic pain for some other reason. The finding has proven reproducible in a more recent study with assay methods that are vastly improved.³² The comparison, again, was with healthy controls. The difference, again, was small and anything but compelling. In fact, the values of the patients with FM were within the range of those of the healthy controls, albeit in the upper half of that range.

TABLE 3.2. THE 1990 AMERICAN COLLEGE OF RHEUMATOLOGY CRITERIA FOR FIBROMYALGIA

Widespread pain (pain on the right and left as well as above and below the waist) AND Tenderness at 11 or more of 18 specific tender point sites.

Nonrestorative, disordered sleep is a feature of the FM syndrome. It was traditionally a minor criterion and is so nonspecific that it was not elevated to the status of ACR criteria (Table 3.2). Nonetheless, it has been held as a important clue to pathogenesis by committed investigators for more than 20 years. They argue that disturbed sleep architecture leads to abnormal neuroendocrine responses that, in turn, provoke the symptoms of FM.³³ These investigators and their data have encountered considerable challenge about whether the symptoms of disordered sleep are secondary phenomenon, whether the putative electroencephalogram “abnormalities” are sensitive³⁴ or specific,³⁵ and even whether there is any abnormality in sleep architecture.³⁶

The clinical investigations exploring the neuroscience and endocrinology in patients labeled with FM is revealing. As just discussed, the findings, by and large, have proven inconsistent, irreproducible, subtle, and nonspecific. This is not for lack of trying to find biologic markers.³⁷ The latest assault on the secrets of the biology of FM recruited state-of-the-art cerebral imaging techniques: single-photon emission computed tomography³⁸ and functional magnetic resonance imaging (MRI).³⁹ In the positron emission tomography study, the comparison was between 17 women labeled with FM and 22 women labeled as healthy. In the MRI study, 15 women and 1 man labeled with FM were compared with matched controls labeled as healthy. In the positron emission tomography study, subtle differences were detected in the perfusion of several discrete brain structures. In the MRI study, images were compared before and after the thumbnails of the subjects were painfully squeezed. There was considerable alteration in cerebral blood flow and “activation” detected in both groups, with some subtle differences. Time will tell if these differences are reproducible. Science will tell if they are meaningful. Epidemiology will tell if they speak to more than the fact that patients labeled with FM have a distinctive neurophysiologic construct.

Could it be that there are no qualitatively distinctive markers? Could it be that the analysis of the biology of medically inexplicable, persistent, widespread pain will have to wait for the technology that allows for the dissection of the fine structure of neurophysiologic constructs and the epidemiology that can cope with individual differences? If so, the wait may prove interminable.

Pain and Suffering

In the past decade there have been important advances in our understanding of the neurophysiology of pain, including advances relevant to consideration of the pathophysiology of FM. The advances of earlier decades related to nociception, the transduction and processing of impulse traffic consequent to tissue damage. Awareness and emotional responses were seen to be secondary to the sensory input, involving the highly variable recruitment of limbic system and thalamic functions. In the past decade, neurophysiologists have been rethinking this model.⁴⁰ Echoing Kant, a “constructivist” theory has emerged suggesting that awareness is a result of parallel processes that create our personal reality from the nociceptive sensory input. This theory of constructivism pertains to memory as well as to pain. In this way, the neurophysiologic responsiveness is conditioned by prior experience playing out on the genetics of the possible. There are animal models in which manipulation of the genetic control of opioid neuropeptides produces a state of allodynia.⁴¹ However, science is a long way from that level of insight in humans. Furthermore, there is every reason to expect a range of mechanisms and individual differences rather than a pivotal gene.

Nonetheless, there is no doubt that there are neurophysiologic constructs that account for much that metaphysics consider to be the “mind.” There is no doubt that our emotions, educational accomplishments, tightly held beliefs, and much more reflect neurophysiologic constructs. There is no doubt that the fashion in which we respond to life’s joys and challenges reflect the idiosyncratic nature of these constructs. There is no doubt that this is true of acute and chronic stress and distress with consequences that can be more dramatic than simply perturbations in our neuroendocrine physiology⁴² and immunomodulation⁴³; there can be perturbations in our longevity.⁴⁴ There is no doubt that there is a wide range of individual differences, heritable differences, in this biology, all of which warrant being considered normal. Much is homeostatic. Much is the joy of humanity. Some is its sorrow.

Understanding neurophysiologic constructs is one of science’s great frontiers. Important inroads have been forthcoming about basic mechanisms. Clinical investigation is stymied by the bluntness of the available methodology and the need to define a referent population, one that is either “normal” or distinctive. The literature that relates to FM is illustrative in this regard.

As stated previously, there is no doubt that patients with FM have sets of neurophysiologic constructs that support their illness. They are living life under a pall and are in such distress that they have sought care. In so doing, they have acquired illness behaviors and a distinctive sick role. There must be special fine structures to their neurophysiologic constructs. Some will be shared by others who
live life under a pall but do not experience persistent widespread pain, or if they do, they do not choose to be patients. Some of these people have plenty of “tender points” and probably share the “evidence for central sensitization” that patients labeled with FM exhibit.⁴⁵ Neither group likes to be poked or prodded. If one wants to probe the distinctiveness of the neurophysiologic construct that is labeled FM, what is the proper comparison group? Certainly, randomly chosen “healthy” people would be no more appropriate than selecting people of the blithest of spirits. Could it be that patients with FM are healthy people who have learned adverse illness behaviors?

TENDER POINTS AND THE FICKLE FINGER OF FAITH

For clinicians inclined to label the woeful with FM, the diagnosis pivots on the tender points. Tender points have a long and venerable history.²⁵ They underlie several traditional forms of massage therapy in Asian cultures. They were recognized by such early 20th-century giants as Sir William Gowers, who coined the term “fibrositis” in 1904, and Sir William Osler, who advocated needling with sterilized “bonnet needles.”⁴⁶ Despite the venerable history and decades of false starts, there is no convincing anatomic, biochemical, or electrophysiologic abnormality demonstrable at these tender points in patients who are hurting. Even more daunting, the majority of individuals who are not hurting have tender points in similar locations³ that are just less tender! Furthermore, if you question patients whose pimary illness is nonrheumatic and who are attending a general medical clinic, the overlap with “fibrositics” in symptoms and tender points is impressive.⁴⁷ The magnitude of the Syndrome of Out-of-Sorts (Table 3.1) that colors the lives of all medical patients, whatever their primary diagnosis from heart failure to HIV infection,⁴⁸ has not escaped the cognizance of wise clinicians and should be more generally appreciated. Ill medical patients, who feel so poorly, do not like to be poked either.

The lack of specificity of the “tender point” has caused those who believe that FM is a discrete clinical entity reflecting a specific and potentially demonstrable pathogenesis to go back to the drawing board. Is there anything special about the “tender points” of the patient with fibrositis other than the degree of tenderness or number of points that distinguishes patients with FM from healthy people with tender points or patients without musculoskeletal symptoms who have tender points? There are those who argue that the more meaningful sign is not the “tender point” but the “trigger point,” which is said to be a marker of the so-called myofascial pain syndrome denoting patients whose pain is less widespread. The distinction relates to whether the point is locally sensitive or there is an element of referral of the pain. However, the entire distinction between “tender” and “trigger” points is muddled in the literature and, like the concept of secondary fibrositis, is yet another point of contention even among clinicians who are proponents of the FM syndrome.⁴⁹ Suffice it to say that whenever the reliability of the assessment of “trigger points” has been put to the test,⁵⁰,⁵¹ the “sign” remains “only accessible to the finger of faith.”⁵² Rather than battle on the quality of the discomfort elicited by
the pressing finger, most of the clinical investigators and rheumatologists interested in FM have turned to attempting to quantify the number of tender points. Quantification of the number of specific points underlies the ACR criteria (Table 3.2). However, the degree of tenderness is critical; if the patient responds to a standard force of 4 kg with an exclamation of discomfort, a flinch, or a “jump sign,” the site is declared a “tender point.” That is why the “consortium” who formulated the ACR criteria undertook training sessions to improve the inter- and intraobserver reliability of quantifying tender points. The 4-kg force is usually applied with thumb pressure or an instrument called a dolorimeter. The accuracy and reliability of dolorimetry in use leaves much to be desired.⁵³ The accuracy and reliability of the probing thumb are worse. In fact, the accuracy of palpation, that is, the ability to reliably exert 4 kg of pressure with one’s thumb, is dismal unless the observers are carefully and repeatedly trained.⁵⁴ Interestingly, the experienced “expert” assessors of tender points in this study of the accuracy of palpation turned out to be less accurate, reliable, and trainable than the naive examiner.

Given the issue of the reliability of the quantification of tenderness, and given the remarkable lack of specificity, I have serious reservations about any assertion that tender points can be used to define a discrete pathophysiologic entity. Many patients with CFS, IBS, and FM, many patients with all sorts of chronic illnesses with end-organ damage, and some subsets of non-patients all find the pressure of the probing thumb particularly uncomfortable. We will shortly discuss recent data indicating that the number of tender points is a feature of the unhappy individuals captured in Table 3.1 whether or not they have a specific “disease.”

However, the clinical community that promulgates the FM concept is not ready to give up on patients’ tender points. Some practitioners persist in treating them. Generations of practitioners have based intervention on this finding. Pressing, application of a vapocoolant, injecting anesthetics or steroids, and combinations of these methods have staunch advocates. On the basis of controlled trials, it is clear that injection of a trigger point offers no discernible advantage over needling alone⁵⁵ and that needling or injecting has no discernible advantage over the application of a topical vapocoolant.⁵⁶ I am convinced that the patients with this illness can be even better served if tender points are ignored or, better yet, not even demonstrated.

This is not to deny that these patients are more tender when poked at the special sites designated by the ACR and elsewhere.⁵⁷ To my mind, that is part of the reason these patients feel so poorly in general. Others are convinced that it is the clue to a derangement in the patients’ neurophysiology for nociception and that this derangement may be primary in the pathophysiology disorder. These proponents argue about whether the derangements are in the central⁵⁸, ⁵⁹, ⁶⁰ or the peripheral nervous system.⁶¹,⁶² I do not find the arguments persuasive. All these psychologic observations seem to be probing behaviors that could just as easily be central neurophysiologic constructs acquired through a learning process involved in living a life of the ill as they might be primary driving forces.

I have already mentioned the community-based postal survey undertaken by the ARC Epidemiology Unit at the University of Manchester. Of 1340 adults who
replied, 13% recalled at least 1 day of widespread pain, 43% recalled regional pain, and 44% recalled no pain in the prior month. A random sample of each of these groups agreed to an interview and tender point quantification in their homes 1 year later.⁶³ The interview included three questionnaires probing general health, sleep problems, and health and fatigue, all standardized instruments. Interestingly, most recalled similar pain in the month before the interview as they described in the month before the postal survey 1 year earlier. The status of these people on the day of examination is displayed in Table 3.3. There is a correlation between tender point count and the score on each of the three instruments for the entire population and for each gender regardless of pain status (P < .001). Tender points are a correlate of distress. They are not an indicator of disease. Clearly, many people, maybe most, contend with such distress often. These individuals contend with difficult days. Some are unhappy individuals. All are casting about for some sort of solace.

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