Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia

Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia

The search is on for a third pain descriptor for chronic pain that is more appropriate for the large group of people whose pain is not associated with tissue damage (i.e. “nociceptive pain”) or with demonstrable nerve damage (i.e. “neuropathic pain”).

A recent article in the prestigious journal PAIN outlines the need for such a third descriptor and suggests the following candidates: “nociplastic”, “algopathic” and “nocipathic” [Kosek et al. 2016].

It is important to recognise that these descriptors are not diagnoses, just as “pain” itself is not a diagnosis. However they are intended to imply underlying neurophysiological mechanisms.

But another candidate has recently appeared upon the scene – “centralized pain” [Clauw 2014]. In this context, centralized refers to “central nervous system origins or amplification of pain”. Given that pain as an experience always originates from within the nervous system, and that pain is not a “thing” that can amplify itself, this proposition does not make sense.

The term “centralized” can refer only to an anatomical location within the central nervous system. Not only does the word itself not imply a mechanism but also it creates potential for confusion with conditions such as “central post-stroke pain” (which is technically “neuropathic”) and quite different from the phenomena that underlie Fibromyalgia.

Therefore “centralized” has no legitimate place as a descriptor for pain.

 

John Quintner & Milton Cohen

 

References:

Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555,

Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain 2016; 157(7): 132-186.

FIBROMYALGIA AND THE SARNO CONNECTION

Have you struggled with chronic pain or another medically unexplained symptom for a long time? Have you tried everything to alleviate your pain, but nothing worked? Have you had doctors tell you they “just can’t find anything wrong?”

Then you may have Tension Myositis Syndrome (TMS). TMS is a condition that causes real physical symptoms that are not due to pathological or structural abnormalities and are not explained by diagnostic tests. In TMS, symptoms are caused by psychological stress.

http://www.tmswiki.org/ppd/An_Introduction_to_Tension_Myositis_Syndrome_(TMS)

Introduction

People with fibromyalgia who are desperate for pain relief might well be tempted to read on to find out more about Tension Myositis Syndrome (TMS). At face value it does appear to be a genuine medical condition. But when they delve into its origins, there may be some unwelcome surprises.

Tension Myositis Syndrome, also known as Tension Myoneural Syndrome and Mind Body Syndrome, was originally described in 1981 by Dr John Sarno, a retired professor of Clinical Rehabilitation Medicine at New York University School of Medicine, and attending physician at the Howard A. Rusk Institute of Rehabilitation Medicine at New York University Medical Center.

This article will trace the development of Dr Sarno’s ideas over the past four decades and will show how he and his followers have tackled the vexed problem of the relationship between mind and body by inventing a psychologically based condition (TMS) together with an imagined musculoskeletal lesion. As an aside, their strategy bears more than a passing resemblance to that of those who pioneered the now discredited concept of the “myofascial trigger point”.

What is TMS?

According to Sarno (1998) TMS is “a benign (though painful) physiologic aberration of soft tissue (not the spine) and it is caused by an emotional process.” He suggests that this process is the result of “specific, common emotional situations”. The various soft tissues that can be affected in this peculiar disorder include muscles, nerves, tendons and ligaments (Sarno, 1998).

As Coen and Sarno (1989) explained:

“Of approximately 4000 patients with neck, shoulder and back pain seen by physiatrist author (JES) over 15 years, over 95% were diagnosed as having TMS. What stands out most from our clinical material are the contributions of tension and chronic character defences to musculoskeletal symptoms, and then the uses made of pain (for dependency, defence of narcissistic preoccupation with the pain, for punishment, and to express anger against caretakers (internal and external).

We emphasise the relative ease of helping patients out of their back pain syndrome … Empathic explanation of the role of anxiety and defensive states in causing back pain, together with reassurance that this is a reversible self-limited process, usually leads to recovery.

The capacity to tolerate one’s affective life seems, in effect, to preclude the back pain syndrome. We believe that the more able patients are to tolerate what they feel, including their anxiety, vigilance, mistrust, anger and depressive feelings, the less troubled they will be by back pain.”

To further confuse the issue of nomenclature, Sarno proposed that TMS syndrome be relabelled “the mind body syndrome,” which includes the musculoskeletal disorder now referred to as “musculoskeletal mind-body syndrome (MMS), as well as a large variety of other psychophysiologic conditions involving other systems (Rashbaum & Sarno, 2003).

What is the postulated mechanism?

Physical symptoms are said to occur when the unconscious mind senses that repression of emotions may fail and an “emotional eruption” is imminent. The conflict is between “the reasonable, intelligent, moral, conscious mind and the childish, primitive archaic mind that continues to have a strong influence on the unconscious” (Rashbaum & Sarno, 2003).

Repressed unconscious emotions (e.g. rage) can trigger abnormal autonomic nervous system activity, apparently resulting in mild ischaemia (i.e. lack of blood supply) and mild oxygen deprivation that can adversely affect muscles, nerves & tendons. These changes in physiology are supposedly manifested by muscle pain, nerve pain, tendon pain, paraesthesias (“pins and needles”) and muscle weakness.

There is of course no scientific evidence whatsoever to support these wild guesses.

TMS & fibromyalgia

Sarno (1998) decided to characterize fibromyalgia as a severe form of “musculoskeletal mind-body syndrome” with multiple ischemic foci involving muscle, nerve, and tendon. Rashbaum and Sarno (2003) chided the American College of Rheumatology (ACR) because although the diagnosis required the identification of 11 of a potential 18 tender points in the trunk, arms, and legs, it did not make the connection between the emotions and clinical findings.”

Resorting to psychoanalytic theory, Sarno made the connection by proposing that fibromyalgia was caused by “the psychosomatic avoidance of psychic conflict.” He even gave the pain a purpose, which was “to distract attention from frightening, threatening emotions and to prevent their conscious expression.” Fibromyalgia therefore signified the person’s abject failure to resolve his or her own psychic conflict:

Physical symptoms occur when the mind senses that repression of emotions may fail and an emotional eruption is imminent. The conflict is between the reasonable, intelligent, moral, conscious mind and the childish, primitive archaic mind that continues to have a strong influence on the unconscious.

Current status of Sarno’s ideas

Schechter et al. (2007) published outcomes of a “mind-body” treatment offered to a convenience sample of 51 patients with persistent low back pain and a diagnosis of TMS (note that Sarno is referenced in relation to making this diagnosis). The primary goal of this program was “to raise patient awareness of how emotional issues, including repressed emotions, affect their physical pain” by counseling and educating patients on “how psychological factors can manifest as physical pain” and learn to begin “thinking psychologically,” instead of “structurally,” about their pain.

The authors conceded the many limitations of this study, with financial and logistical constraints forcing them to conduct a case series study instead of a randomized clinical trial. The authors’ lack of specific criteria for a diagnosis of TMS and their inability to precisely standardize the program for all patients makes interpretation of this paper impossible.

However, Dr Howard Schubiner and his co-workers are others who continue to advocate John Sarno’s ideas. As he informs those who visit his blog site:

Your body is producing pain because it’s manifesting unresolved stress, possibly from your childhood, or from stressful events in your adulthood, or from your present circumstances, and as a result of your personality traits (which affects how you respond to stress and how much pressure you tend to put upon yourself).

http://mind-body-blog.blogspot.com.au/2008/02/mindbody-syndrome-tension-myositis.html

In a more recent publication, Lumley et al. (2015) have restated these views:

We view the key pathological process in both unresolved trauma and internal conflict to be the avoidance or suppression of one’s primary or adaptive emotions, which then activates neural pathways that trigger, augment, or maintain pain and other symptoms.

In the meantime, Hsu et al. (2010) reported the results of a randomized controlled trial of Dr Schubiner’s program of intervention – Affective Self-Awareness (ASA) – developed at Providence Hospital.

Without going into details, the 24 of the 45 participants who attended Dr Schubiner’s three 2 hour small group sessions over three weeks and had read one of Dr Sarno’s standardized texts (Sarno, 1998) reported less pain and improved physical functioning compared to those in the 21 wait-listed control group. Members of the latter group were “free to engage in any interventions on their own, as recommended by their providers …”

It comes as no surprise that the authors reported:

Individuals with fibromyalgia in this study appeared to accept the central message of the intervention: that the experience of pain in fibromyalgia is real, that fibromyalgia pain is processed in the central nervous system, that unrelated emotional experiences can initiate and perpetuate physical symptoms, and that the mind-body link can be tapped to empower individuals with fibromyalgia to more effectively diminish pain and associated symptoms.

The authors conceded that they had no idea as to the mechanisms responsible for the benefits of the ASA intervention. But at least they did acknowledge the possible contribution of various contextual factors.

The pivotal research question posed by Schubiner et al. (2012) is to “determine if targeting unresolved stress and emotions offers an advance in the treatment of chronic non-structural pain.”

Hsu et al (2010) do intend to conduct a larger study that will “not only assess the efficacy of this type of intervention in comparison to an active control group, but will allow for assessment of mediating and moderating variables to help determine mechanisms of action and subgroups of patients that respond best to this intervention.”

There can be no doubt that this formidable (and impossible?) task will continue to tantalize future generations of researchers who have embraced Dr Sarno’s ideas.

Conclusion

It is indeed unfortunate that Dr Sarno’s outdated theories, which were always highly speculative and heavily influenced by insupportable psychoanalytic theory, continue to influence some clinicians in their approach to patients with fibromyalgia. Their laudable aim may have been to close the mind-body split but in effect they have only succeeded in widening the gap and, in so doing, have inadvertently shifted the blame for their pain onto their patients.

References:

Coen SJ, Sarno JE. Psychosomatic avoidance of conflict in back pain. J Am Acad Psychoanal 1989; 17(3): 359-376.

Hsu MC, Schubiner H, Lumley MA, et al. Sustained pain reduction through affective self-awareness in fibromyalgia: a randomized controlled trial. J Gen Intern Med 2010; 25 (10): 1064-1070.

Lumley MA, Schubiner H, Carty JN, Ziadni MS. Beyond traumatic events and chronic low back pain: assessment and treatment implications of avoided emotional experiences. Pain 2015; 156; 565–566.

Rashbaum IG, Sarno JE. Psychosomatic concepts in chronic pain. Arch Phys Med Rehabil 2003; 84 (Suppl. 1): S76-S80.

Sarno JE. The mind-body prescription: healing the body, healing the pain. New York: Warner Books, 1998.

Schechter D, Smith AP, Beck J, et al. Outcomes of a mind-body treatment program for chronic back pain with no distinct structural pathology – a case series of patients diagnosed and treated as tension myositis syndrome. Altern Ther Health Med. 2007; 13(5): 26-35.

Schubiner H, Burger A, Lumley M. P02.147. Emotions matter: sustained reductions in chronic non-structural pain after a brief, manualized emotional processing program. BMC Complement Alt Med 2012; 12 (Suppl 1): P203.

 

 

TO KILL A MYOFASCIAL TRIGGER POINT

“Remember it’s a sin to kill a mockingbird.” That was the only time I ever heard Atticus say it was a sin to do something, and I asked Miss Maudie about it. “Your father’s right,” she said. “Mockingbirds don’t do one thing but make music for us to enjoy … but sing their hearts out for us. That’s why it is a sin to kill a mockingbird.”

The late Harper Lee struck an intense moral chord in the USA with her acclaimed novel – To Kill a Mockingbird (1960).

But does the innocent mockingbird have anything in common with the “myofascial trigger point (MTrP)”? Is it a sin to kill a MTrP?

There are physical therapists who firmly believe that MTrPs can cause considerable harm to people:

Myofascial TrPs are a preventable cause of musculoskeletal pain, they cause dysfunctions, such as blurry vision, erectile dysfunction, balance disturbance and dizziness, irritable bowel, diarrhea, vomiting, voice disturbances, and loss of fine motor control. They can cause colic in babies or contribute to falls in the elderly–and in the rest of us [Starlanyl & Sharkey, 2013].

Furthermore, in their eyes the potential havoc that MTrPs can wreak extends even to fibromyalgia (aka chronic widespread pain).

In their recent book Starlanyl and Sharkey (2013) make this promise to their readers:

“You will discover how TrPs can cause or maintain fibromyalgia and why the ability to control the TrPs directly affects the control of FM symptoms … the key to controlling trigger points is identifying and controlling perpetuating factors.”

Accordingly, Starlanyl and Sharkey (2013) see fit to issue a stern warning to those individuals who are unfortunate enough to harbour MTrPs:

If the perpetuating factors are not brought under control, satellite TrPs can develop in muscles that overwork trying to compensate for the TrP-weakened ones, or in muscles in the referral zone. Once primary TrPs develop satellite TrPs in other body areas, life, and treatment, becomes more complex. The satellites themselves can develop more satellites involving more of the body. Trigger points can cause body-wide pain.

On close examination, these perpetuating factors, of which the list is exceedingly lengthy, turn out to have only been figments of the fertile imagination of the original proponents of the MTrP theory [Travell & Simons, 1983].

The belief that MTrPs can be “controlled” has spawned a worldwide industry of therapists eager to kill (“deactivate”) them by various drastic methods, which include needling, compression, and manual release.

On her website Starlanyl (2014) advises therapists to proceed cautiously, as follows:

“Use the least invasive option for therapy, with the understanding that most treatment options may activate more TrPs and cause a temporary increase in pain. Toxins and waste materials trapped in the myofascia (sic) must be processed by the body and be eliminated, and that can only proceed so fast. It takes a while for the Gordian knot to unravel, and the process is not fun for the patient.

Starlanyl (2014) describes: “… a cadre of patients with too many TrPs to count, in multiple levels in multiple muscles. They have chronic myofascial pain (CMP). The muscles may be so tight and swollen that you can’t see them move beneath the skin, and the pain levels escalate. These patients may have had multiple surgeries and procedures. There may have been multiple traumas. There may be a wide variety of perpetuating factors.”

When the preferred treatment fails to kill the MTrP(s), the blame then shifts from the therapist to the pain sufferer, who without any shadow of doubt must harbour one or more of these so-called perpetuating factors.

It may be a sin to kill a mocking-bird – but has any one ever seen a “dead” MTrP, let alone be able to identify and describe its true nature? No doubt there are some who would see it as sinful should therapists not try to “kill” as many MTrPs as possible in their attempts to alleviate human suffering. However the published research on outcomes for “treating trigger points” suggests that they are not easy to kill [Cohen & Quintner, 2008; Quintner et al., 2015].

Could this apparent resistance to destruction be explained by their very non-existence? Unless and until this is appreciated, the MTrP will continue to mock its followers.

 

John Quintner

 

References:

Cohen ML, Quintner JL. The horse is dead: let myofascial pain syndrome rest in peace [letter]. Pain Medicine 2008; 9: 464-465.

Quintner J, Bove G, Cohen M. A critical evaluation of the “trigger point” phenomenon. Rheumatology 2015; 54: 392-399.

Starlanyl DJ, Sharkey J. Healing through trigger point therapy: a guide to fibromyalgia, myofascial pain and dysfunction. Berkeley, California: North Atlantic Books, 2013.

Starlanyl D. Fibromyalgia and trigger points for care providers, 2014. Available at: http://www.fmcmpd.org/physinfo.htm Accessed 13th May 2016.

Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual. Baltimore: Williams and Wilkins, 1983.

LA DOULOU (Provençal word for pain)

Many patients with fibromyalgia are desperately seeking out non-drug measures to relieve their pain and improve their quality of life. This article was inspired by the struggles of one of France’s most eminent 19th century writers against his unfortunate predicament. His eloquent words will resonate with all who suffer chronic pain. — John Quintner

LA DOULOU (Provençal word for pain)

I only know one thing, and that is to shout to my children ‘long live Life!’.

But it’s so hard to do, when I am ripped apart by pain.”

From his anecdotal journal entries (translated by Julian Barnes), we can get an idea of how the French novelist, playwright and poet Alphonse Daudet [1840-1897] addressed his extremely painful neurosyphilitic condition i.e., tabes dorsalis. Its manifestations are due to degeneration of the posterior columns and nerve roots of the spinal cord. In today’s parlance, such pain would be described as neuropathic.

Fortunately, syphilis (in all its manifestations) is curable with antibiotics and now rarely seen. But there are many other medical conditions, such as fibromyalgia and complex regional pain syndrome (CRPS), which can be associated with severe pain that is poorly controlled by the currently available medications.

I asked my colleague Melanie Galbraith, physiotherapist, to comment from the point of view of a pain sufferer upon Daudet’s methods for obtaining pain relief. Melanie experiences intractable cervical radicular (neuropathic) pain.

With the permission of Professor Abraham Olivier* the following excerpts have been transcribed directly from his book “Being in Pain” (2007):

  1. By means of imagination

Daudet: “It’s hilarious, this land of neurotics, filled with shouting, trumpet calls, sirens.”

From such passages, which refer to the people he meets at thermal stations within various health spas, it is apparent that he describes the land of pain in terms of fantasy, of theatre, of tragedy.

I argued (Chapters 4 and 5) that imagination can change a bodily state like pain into an unreal object, even while it remains a bodily state. In this way imagination can make pain vanish behind a mask. We cannot place ourselves into a space of fantasy without any pain, for we remain beings embedded in bodies. But our bodies can change our states of pain by projecting in the place of the land of pain a space of fantasy. Indeed, according to Daudet, this has the effect of a morphine injection (p. 175).

Melanie: “meets at thermal spas” – Heat – it’s a very under-utilised form of treatment for chronic pain. Sometimes when my pain is at a high level I’ll imagine being at the beach on a hot, summer’s day and scrunching the warm, white beach sand between my toes.

Daudet’s use of imagination as a strategy for pain management is supported by recent research, which has found encouraging but inconclusive evidence that guided imagery can alleviate both muscular and non-muscular pain (Posadzki & Ernst, 2011; Posadzki et al, 2012)

Of course, there is a limit to imaginative projection. Theatre is not endless and as the music fades away the pain will return. But the same goes for morphine. Why not try fantasy instead? … But again, it is one thing to use fantasy as an additional tool to physiological therapy, another to integrate it as a primordial means to treat pain. I advocate the latter. Daudet demonstrates the power of this approach: it is like a morphine injection.

Melanie: It would be great – but … when my pain is at a maximum, it’s as if your ‘beach scene’ has been overtaken by a violent storm with booming thunder, torrential rain and blinding lightning. Added to this, vicious waves are crashing against the ‘sea wall’ and threatening to ‘burst the dam’.

  1. By means of relocation

Daudet: “One ought to go to different baths each season”

On the one hand, Daudet turns the thermal station into a place of fantasy. On the other hand, he thinks a literal change of space to be as important as positing an imaginative space.

This illustrates once more that space is not, as traditionally thought, some place (a container or extension) belonging to the external environment, but the perspective we adopt toward our environment.

This may be taken as a useful therapeutic insight – we may even label it as space therapy: moving away as a means of removing pain, that is, changing our perspective as a means to change the quality of pain.

But if it would help, then anyone can find a means to travel. If not by plane or car or boat, then our feet, or at the end our fantasy may carry us to places that harbour new perspectives (p. 176)

Melanie: If only Medicare would fund a ‘week away’! Whilst working in the UK I saw many, many patients whose pain improved or disappeared altogether when they were away somewhere that was warm and ‘stress-free’! I’m convinced we could save a mountain of health dollars if doctors could ‘prescribe a holiday’! It’s much cheaper (and likely MUCH more effective!) than a range of ‘interventions’ such as spinal injections, drugs and surgery.

  1. By means of compassion

Returning from a sojourn at a thermal station could cast patients into desolation. This could mean extreme loneliness even to someone in a caring family.

Daudet conjures up a dialogue between two ataxic patients to demonstrate this desolation, but also to suggest compassion as a means to counter it. One patient is a bachelor, the other a family father. They discuss whether it is better to be alone while suffering or not.

The family father argues that it is better to be alone: firstly, because it is a terrible weight on a household to have someone around whose pain drags on for years. Furthermore, it adds to your own suffering to see how the pain, which always appears new to you, becomes familiar and wearisome to others. Moreover, the responsibility of taking care of your family while in pain increases your burden. Finally, family life has taught him to keep his pain to himself rather than to show it, but not showing it is a big constraint.

The bachelor counters quite sharply and forcefully: the lack of someone who cares adds to the loneliness the pain brings about, yet it is important to care for others, for your family, instead. Eventually caring for them helps you to get away from yourself, which in turn supports them in caring for you. Compassionately taking another or another’s perspective could thus be an effective means to step out of one’s misery. In this sense compassion entails a liberating perspective (p. 177).

Melanie: This is the classic situation of “the grass is always greener on the other side of the fence.” As I was alone (not in a relationship) when my chronic pain started, I often thought: “how nice it would be to have someone to care for me”. At other times, especially when pain is high, I think: “thank goodness I can shut myself away”. It’s a relief to not feel like a burden on someone else, but I didn’t choose this life situation for myself so surely I have as much “right” as the next person to have a fulfilling relationship with a significant other?

  1. By means of consultation

This does not so much refer to meetings with doctors as to discussions with fellow-patients. Such talks often consisted in the exchange of advice.

To be clear, Daudet knew how to be self-critical about such advice: “Patients giving one another advice: ‘This is what you have to do.’ ‘But does it work?’ ‘No.’ ‘Are you any better?’ ‘No.” ‘So why are you giving me advice?’ Lunacy.”

But Daudet did give advice … to those who are weak; Daudet recommended that they treat pain as an unwanted guest to whom no special attention should be accorded. Daily life should be continued as normally as possible … this advice has a strong underpinning once we see pain as bodily perception … as a change of perspective changes the quality of pain, it is certainly possible to adopt a perspective to drive out the unwanted guest … Daudet’s advice for those who do not scare too easily is that they should dare to examine their pain carefully … the question is: how can the body remove its pain by means of thinking? Once we rephrase the question, we are much closer to the possibility of realizing the power of the bodily axis our perception pivots on (p. 177).

Melanie: If I disclose my own pain problem, my patients appear to appreciate the fact that a health professional “understands what they are going through”. Despite pain being a “unique experience” – personal to the individual, I’ve found patients seem to let go their defenses when they know I’m “one of them”. Sometimes, I’ve found it’s the ONLY thing that will ‘get them on board’ and try some new strategies for managing their pain.

*Abraham Olivier is Professor and Head of the Department of Philosophy at the University of Fort Hare. In addition to this he is Co-Founder and Co-Chair of the Centre for Phenomenology in South Africa (http://saphenomenology.wordpress.com/). He was Editor of the South African Journal of Philosophy and secretary of the Southern African Philosophical Society (PSSA). Olivier obtained his PhD from the University of Tübingen and has held lecturing and research posts at the Universities of Tübingen, Stellenbosch, Hamburg and Padua. He is the author of Being in Pain as well as numerous international peer-reviewed articles.

References:

Daudet A. In the Land of Pain. Transl. Barnes J. New York: Alfred A Knopf, 2003.

Olivier A. Being in Pain. Frankfurt am Main: Peter Lang, 2007: 161-200.

Posadzski P, Ernst E. Guided imagery for musculoskeletal pain: a systematic review of randomized clinical trials. Clin J Pain 2011; 27: 648-653.

Posadzki P, Lewandowski W, Terry R, et al. Guided imagery for non-musculoskeletal pain. J Pain Symptom Manage 2012; 44: 95-104.

Some Discussions on Pain, Clinician and Patients …

CLINICIAN DISCOURSE WITH PERSISTENT PAIN SUFFERERS

Horst Ruthrof, FICI, FAHA, is Emeritus Professor in English and Philosophy at Murdoch University, Perth, Western Australia.

Annotations by John Quintner & Melanie Galbraith

These notes were prepared by Emeritus Professor Horst Ruthrof following a conversation (over wine) with John Quintner, retired rheumatologist, and Melanie Galbraith, physiotherapist, that took place on Friday 29th January 2016. John and Melanie have annotated them for the benefit of the broad readership of Fibromyalgia Perplex. Where necessary, they have drawn upon definitions from ‘The Philosopher’s Toolkit’ (2nd ed. 2010) by Baggini and Fosl.

Introduction

We believe that all clinicians who regularly engage with people who experience persistent pain, fibromyalgia being an example par excellence, will need to learn a “new” language in order to more meaningfully and ethically engage with them. Fortuitously, the philosophers who have pioneered the field of phenomenology have already given us the valuable language tools that we as clinicians really need.

Notes as taken by Horst Ruthrof (annotations appear in italics)

They (these notes) are amended by additional considerations, on what might be relevant to and useful for your search for an appropriate approach to a ‘third space’ narrative about the relation between clinician and sufferers of persistent pain.

The ‘third space,’ which is also known as the ‘intersubjective space,’ is a concept that can best be understood by watching how children play together. They agree to construct and then share a world for whatever purpose their play requires. When people decide to go to a concert, when they are listening attentively to the music they are all in the same (third) space. In the same way, clinicians and their patients can agree to share a ‘third space’ where all relevant issues can be raised and discussed.

Science and normativity

Beginning with a broad perspective, a distinction that appears to me to be relevant to the characterization of the two domains of the clinician, on the one hand, and of persistent pain sufferers, on the other, is that between a scientific focus and one informed by normativity.

The former can be classified traditionally as committed to the data of empirically observable evidence systematized via the testing of hypotheses and procedures of deduction and induction.

This is the essence of the scientific method upon which modern medicine is so reliant.

Normativity, in contrast, can be regarded as a summary bag containing all the sort of things that science, as science, is not designed to deal with, such as ethical, aesthetic, religious, and political values, as well as ideological dispositions. While in social practice the two domains always overlap, the principles that inform each are plainly different. It seems to me that it is the clash of those principles that make medicine an ethically highly complex arena of human endeavour.

This clash also explains why so many sufferers of persistent pain are perplexed and disappointed when their clinicians appear to be deaf to some of these important issues in their lives.

The social expectations about clinicians appear to be that they are trained primarily to apply scientific principles to the injured human body in order to return it to functional health. Persistent pain throws a big spanner in this social mechanism.

According to your descriptions, the strong case of chronic pain is typically not curable, in which case the fundamental assumption of the clinician’s task is misguided from the outset. For hardly any of our basic scientific principles appear to be relevant. For example, deduction in the strict sense is not available in this sort of medical practice since the patient is never a closed system where all data are observable for verification.

Deduction is the form of reasoning one sees acted out in classical detective fiction where all the suspects are gathered together in the drawing room awaiting the analysis of the brilliant detective. A successful deductive argument is one where if the premises are true, then the conclusion is definitely true and the murderer is revealed to one and all.

Even the process of induction by which a patient could be regarded as an open-ended system, allowing for ever more information and hence an ongoing process of falsification and corroboration of hypotheses, does not look promising. The reason for this appears to lie in the difficulties of establishing a data set that could be elicited reliably from the patient.

Often, induction involves reasoning from a limited number of observations to wider, probable generalisations. For instance, from a series of observations that a woman walks her dog by the market at 8am on Monday, it seems valid to infer that next Monday she will do the same, or that, in general, the woman walks her dog by the market every Monday. That next Monday the woman walks by the market merely adds to the series of observations, it does not prove she will walk by the market every Monday.

In the absence, then, of standard inductive procedures the clinician seems to be less in the position of a scientist as in that of the interpreter of a complex and perhaps even hermetic (i.e. closed or sealed) work of art. In which case, abduction rather than deduction or induction would be an appropriate tool of analysis, interpretation, and healing procedure.

While deduction works uncontroversially in closed systems, and induction caters well for an extended series of observed phenomena, abduction is the norm in interpretation when individual phenomena require the construction of a meaningful whole that is not specified.

Abduction is a process of reasoning used to decide which explanation of a given phenomenon we should select. Here is an example: A man is found in a cabin in a remote forest, with all the doors and windows locked from the inside, hanging dead from a noose. A suicide note in the man’s handwriting lies on the table nearby. What would best explain this set of facts? Was it an open and shut case of suicide or are there other possible explanations? This is the stuff of murder mysteries!

Much of human communication works on this wobbly principle, which seems to me to be central to the difficulties in the interpretative task confronted by the clinician facing a persistent pain sufferer.

Clinician-patient discourse

Viewing the topic from the narrower perspective of the kind of discourse that typically operates in exchanges between clinician and patient, two polarities suggest themselves: the medical master narrative versus a narrative informed primarily by patient needs.

While this division is hardly ever so clearly visible in actual practice, it is useful for analytically sorting the principles that underpin them.

In this theoretical opposition, three standard forms of discourse are involved, the objective discourse of factuality (science), subjective discourse (personal expressiveness), and the intersubjective discursive negotiation of meaning (social discourse).

Science deals with facts or established knowledge and medical science is no exception. Traditionally, personal beliefs and attitudes do not fall within its province. But this knowledge is not helpful to the person with chronic widespread pain who does not have a detectable lesion to explain the ongoing pain.

Medical master discourses impose messages on patients, while patient needs can be revealed only by the intersubjective negotiation of the subjective expressions between them and their clinicians.

Edmund Husserl developed a number of phenomenological insights for the characterization of what is occurring in this kind of negotiation. First, we perform acts of “introjection”, that is, tentative mental projections of the likely states of mind of persons we are communicating with, (Logical Investigations, 1900/01), followed by acts of “apresentation,” constructions of absent scenarios by way of extrapolating from observable evidence (Cartesian Meditations, 1930), which leads to intersubjective reciprocity in the social discourse of the lifeworld (Crisis, 1936).

Edmund Husserl [1859-1938] was a German philosopher associated with one of the most important philosophical revolutions of recent times. His deep influence has extended to the overall field of disciplines, which we call the humanities – psychology, sociology etc. He founded the field of study known as phenomenology (see Kockelmans, 1994).

Philosopher Thomas Nagel famously mused over the question ‘What is it like to be a bat?’ Phenomenology, by contrast, might be thought of as the project of discerning what it’s like and how it’s possible to be a human being (Baggini & Fosl, 2010: p.211).

Husserl’s phenomenological insights have recently been endorsed by empirical research conducted by Michael Tomasello, American primate and child language acquisition expert working at the Max Planck Institute at the Leipzig zoo. He talks of ‘intention-reading’ as a necessary component of early language ontogenesis (Tomasello 2006; Tomasello & Carpenter, 2007).

‘Intention reading’ is the proposition that children (and adults) acquire a mastery of language through social interaction. ‘Ontogenesis’ refers to the origin and development of an individual.

Typical examples of the medical master narrative would be the bio-behavioural story of chronic pain as conditioned response; the biomedical narrative reducing the patient to a mere organism in the hands of a techno-scientific apparatus; the brain-centred (homuncular) narrative; the stress response-survival narrative; the egotistic clinician narrative, where social standing and career goals overshadow patient needs; the ironic-sarcastic discourse, which though superficially friendly barely conceals the clinician’s contempt for the patient’s explanatory story; and, above all others, the stigmatizing narrative by which the patient is declared an immoral malade imaginaire. When considering the needs of persistent pain sufferers, all such narratives can be counted amongst unethical options for medical practice.

The homunculus refers to the idea of a “little man” inside the brain who is making decisions and generating pain.

The French playwright and actor Moliere [1622-1673] wrote ‘Malade Imaginaire’ (The Imaginary Invalid) in 1673. It concerns a hypochondriac who lives in fear of death and doctors.

What then would a discursive strategy look like that is aware of and sensitive to the needs of patients who suffer from serious chronic pain?

‘Discursive’ implies that the conversation would move from topic to topic without any order being imposed by either party.

First, what appears to be required on the part of the clinician is a conscious shift from a science dominated position to one that allows medical practice to be informed by the demands of normativity, the domain of human values. Specifically, the clinicians need to shift their professional attitude from medically curing a body to existential, pastoral care for a person. The conscious shift from focusing on a body to harkening to a person has significant, practical implications. One of which is a change of emphasis in the observation of the Hippocratic Oath (to prevent it from becoming hypocritical) towards the emotional well being of the patient.

In this context, ‘existential’ includes all matters relating to one’s existence.

The Hippocratic Oath binds new physicians to the ethos and profession of medicine, while the Western tradition of scientific medicine traces its roots to the Hippocratic writings that still shape the values of contemporary western medicine in relation to the obligations placed on clinicians to their patients and their colleagues (Bulger & Barbato 2000).

Another basic principle here appears to be a fundamental asymmetry of authority. We must ask, according to Michel Foucault (1972), who is speaking, under what conditions, with what sort of authority, and from what kind of institutional setting?

Michel Foucault [1926-1984] was an influential French philosopher who critically examined the origins and development of ideas of knowledge, punishment, madness and sexuality. His book ‘The Birth of the Clinic: An Archaeology of Medical Perception’ has become a classic in the history of human sciences.

In the clinical situation, the clinician always has the greater authority, leaving the patient in the inferior position of utterance. Even the most sensitive and sympathetic approach to patient needs cannot eliminate this asymmetry. Therefore it needs to be acknowledged by the clinician and built into the interpretive process. A similar, theoretically relevant point about discourse is made by Jean-Francois Lyotard (1989) via his theorization of the differend, a discursive injustice resulting from inequality in speech situations.

Jean-Francois Lyotard [1924-1998] was a French philosopher, sociologist and literary theorist, who developed the concept of ‘differend’ as a powerful analytical tool. For example, in the legal world, the ‘differend’ relates to the case where the means to argue is taken away from the plaintiff or when adjudication of a dispute is conducted only in the language of one party.

Fundamental too is the establishment of trust between clinician and patient, to be initiated and sustained by the medical expert. The establishment of mutual trust in itself is a complex process, in which felicity conditions play an important role (Cf. John Langshaw Austin, 1962; Paul Grice, 1989).

In this case, the most important of the felicity conditions is sincerity. The sincerity condition specifies that the clinician must have the requisite thoughts, feelings and intentions to successfully undertake this important task of establishing trust.

Likewise important are a genuine interest in the patient as a person by the facilitation of a genuine dialogue (cf. the principle of dialogism in the work of Michael Bahktin (1963, 1992) with a goal towards directing patients towards coming to terms with their fundamental existential situation.

From a dialogical standpoint, listening is the capacity to share what makes someone’s story worth telling and worth hearing. This is in contrast to a monologic discourse, which pretends to be the ultimate word, is finalized and deaf to the other’s response.

Patients require gentle guidance to reveal their deepest fears and learn to accept their condition without falling into despair. Persistent pain, not unlike terminal illness, can be regarded as ‘limit situations’ or ‘boundary situations’ in the sense in which they were theorized by Karl Jaspers (1954).

Karl Jaspers [1883-1969] was a German-Swiss psychiatrist who later became a leading philosopher. ‘Boundary situations’ are those that cause us to be aware of our own weakness and helplessness. These situations are usually unalterable.

Against this background, and taking practicalities of time constraints and other limitations into account, the clinician should be able to achieve a satisfactory ‘validation’ of the patient narrative in the sense of being able to accept patient utterance as felicitous and truthful.

Sad to say, as the demand for medical diagnostic skills has increased, as has the influence of insurers and systems of managed care, (Bieber et al. 2007) the precarious balance between available clinical resources – reducible to time and money – and the possibility of individual patient benefit has been tilted towards ever shortening consultation times.

The term ‘validate’ is being used here in relation to its Latin root ‘validus’ – to strengthen. It highlights an ethical obligation for the clinician, which is to “strengthen” the person in pain.

References:

Austin JL. How to Do Things with Words. In: Urmson JO, Sbisā M (eds). Clarendon Press, Oxford, 1962.

Baggini J, Fosl PS. The Philosopher’s Toolkit. 2nd ed. Chichester: Wiley-Blackwell, 2010.

Bakhtin M (1963) Problems of Dostoyevsky’s Poetics. Moscow: Khudozhestvennaja literatura. English edition: Emerson C (1984) Minneapolis: University of Minnesota Press, Minnesota.

Bakhtin M. The Dialogic Imagination: Four Essays. Austin: University of Texas Press, 1992.

Bieber C, Müller KG, Blumenstiel K, et al. Long-term effects of a shared decision-making intervention on physician-patient interaction and outcome in fibromyalgia: A qualitative and quantitative 1 year follow-up of a randomized controlled trial. Patient Educ Couns 2006; 63: 357-366.

Bulger RJ, Barbato AL. On the Hippocratic source of Western medical practice. Hastings Center Report 2000; 30(4): S4-S7.

Foucault M. The Archaeology of Knowledge. London: Tavistok, 1986.

Grice P. Studies in the Way of Words. Oxford: Clarendon Press, 1989.

Jaspers K. Way to Wisdom: An Introduction to Philosophy. Manheim R (trans). New Haven: Yale University Press, 1954: 7.

Kockelmans JJ. Edmund Husserl’s Phenomenology. Lafayette, Indiana: Purdue University Press, 1994.

Lyotard J-F. The Differend: Phrases in Dispute. Bennington G & Massumi B (trans). Manchester: Manchester University Press, 1988.

Tomasello M. Why Don’t Apes Point? In: N. J. Enfield & S. C. Levinson (eds.), Roots of Human Sociality: Culture, Cognition and Interaction. Oxford & New York: Berg, 2006: 506-524.

Tomasello M, Carpenter M. Shared Intentionality. Developmental Science 2007;10 (1):121-125.

 

 

VISCERAL MANIPULATION: THE REDISCOVERY OF GLÉNARD’S DISEASE?

What is visceral manipulation?

Over the last three decades, French osteopath Jean-Pierre Barral has pioneered the practice of “visceral manipulation” as a distinct branch of osteopathy.

According to Barral’s estimates: “In a single day, your internal organs move 30,000 times” and “Your liver alone travels 600 meters. But when one organ cannot move in harmony with its viscera due to abnormal tone, adhesions or displacement, it works against the body’s other organ’s and muscular, membranous, fascial and osseous structures” [Skari, 2001].

His key insight was that each internal bodily organ has a capacity to cause spinal pain, whereas conventional osteopathic thinking had assumed the opposite:

“At the time nobody was talking about manipulating organs but I kept seeing patients with aches and pains that I could relieve simply by kneading their organs” [Skari, 2001].

In the March 2013 issue of Osteopathy Today, Barral outlined his approach to diagnosis:

“I use a lot of listening which means you put your hands on the body and your hand is attracted to the tissues which have a density or express a tension and then it is up to your medical knowledge to know what kind of tissue you have found. It is to let the body express itself.”

As to the question of diagnosis, Barral claimed to be able to locate areas of “stress” in the body by palpating the associated (thermal) energy.

The therapeutic approach is then to coax “traumatised” or malfunctioning organs (e.g. kidneys, liver, stomach and other soft tissues) back to their natural movement by applying soft pressure to the respective abdominal, thoracic and urogenital areas:

“The goal is to help the body’s normal forces remove abnormal effects, whatever their sources. Those effects can be global, encompassing many areas of bodily function. These gentle manipulations can potentially improve the functioning of individual organs, the systems the organs function within, and the structural integrity of the entire body.”

https://barralinstitute.com.au/courses/what-is-visceral-manipulation/

In relation to fibromyalgia, visceral manipulation is included in the list of manual therapy techniques that are said to possess the extraordinary capacity to “help to calm down the autonomic nervous system, decrease inflammation in soft tissue, release adhesions of the organs, and calm down irritation of the spinal cord.”

http://www.breakthroughsinhealing.com/tag/fibromyalgia/

Historical antecedents

There are at least three threads in the history of Medicine that can be teased out to uncover the origins of some of the remarkable ideas behind visceral manipulation.

1. Glénard’s disease

The idea that a wandering uterus could cause health problems is an ancient one, and is allied to that of mischief being caused by other “wandering organs” [Desvoeux, 1752].

During the 19th century there was a body of authoritative surgical opinion that excessively movable abdominal organs could be held responsible for abdominal pain and for even more widespread symptoms [Treves, 1896; Daly, 1996].

Some thought that descent of the stomach could result in neurasthenia, the 19th century counterpart of fibromyalgia and chronic fatigue syndrome. Gastropexy (fixation of the stomach) was deemed to be an effective and safe procedure [Daly, 1996].

Colenard, a French physician practicing in Lyons, was the first to describe, in a paper published in 1885, the condition of enteroptosis, or falling of the viscera, due to relaxation of their supporting ligaments [Lund, 1897].

Frantz Glénard (1848-1920), a French physician who for health reasons left Paris to live at Vichy, wrote a number of papers on the subject of visceroptosis (“sinking of abdominal viscera”) [Glénard, 1899].

He devised a simple test wherein the examiner, standing behind the patient, places his arms around the patient so that his hands meet in front of the patient’s abdomen; he squeezes and raises the viscera and then allows them to fall suddenly. If the patient feels relieved by the raising pressure and experiences distress upon release, the condition is probably one of visceroptosis.

2. The Irish stroker

Valentine Greatrakes [1628-1666] was a soldier who served as a lieutenant in the ranks of Cromwell’s army. By harnessing the popular belief in the efficacy of “the king’s touch” – the belief that illness could be cured by the touch of a divinely inspired leader – he is said to have practiced a lay form of psychotherapy [Alexander & Selesnick, 1967].

Greatrakes became known as the “Irish stroker” when, after the beheading of Charles I in 1649, it was widely believed that the healing power of the king’s touch had been passed on to him and that through this method he could cast out evil spirits causing disease. Thousands of patients came to be touched by him, and “his barns and outhouses were crammed with innumerable specimens of suffering humanity [Laurence, 1910].”

3. Mesmerism

Franz Anton Mesmer [1734-1815], who had studied medicine in Vienna, claimed that he too could cure, initially by using a horseshoe magnet and later on by simply touching his patient with his bare hand.

Mesmer and his followers believed that obstacles to the free flow of this fluid caused illness, and that skilled healers or “sensitives” could remove these obstructions by making passes over the patient’s body with their hands.

Mesmer thought he had discovered a specific magnetic force in humans and that this force could be transferred through the laying on of hands [Lanska & Lanska, 2007].

Like many other therapists of all times, Mesmer was unable to appreciate that his successes were due, not to his non-existent magnetic force, but to powerful suggestion [Ackerknecht, 1968].

Conclusion

When assessing the place of visceral manipulation as a form of therapy, perhaps the words of Ecclesiastes 1:9 still ring true:

“What has been will be again, what has been done will be done again, there is nothing new under the sun.”

References:

Ackerknecht EH. A Short History of Medicine. New York: The Ronald Press Company, 1968: 208-209.

Alexander FG, Selesnick ST. The History of Psychiatry. London: George Allen and Unwin Ltd., 1967: 71-88.

Daly A. Fantasy Surgery 1880-1930: with special reference to Sir William Arbuthnot Lane. Clio Medica 38/The Wellcome Institute Series in the History of Medicine. Amsterdam: Editions Rodopi B.V 1996.

Desvoeux V. The Compendious Library: or, Literary Journal Revived. For November and December, 1751. Dublin: S. Powell, 1752.

Glénard F. Les Ptoses Viscérales: Diagnostic et Nosographie.  Paris: Ancienne Libraire Gemmer Balliere & Co., 1899.

Lanska DJ, Lanska JT. Franz Anton Mesmer and the rise and fall of animal magnetism: dramatic cures, controversy and ultimately a triumph for the Scientific Medicine. In: Whitaker H, Smith CUM, Finger S. Brain, Mind and Medicine. New York: Springer Science, 2007: 301-320.

Laurence RM. Primitive Psychotherapy and Quackery. Boston: Houghton Mifflin, 1910: 255.

Lund FB. Enteroptosis. Boston Med Surg J 1897; 1(8): 7-11.

Skari T. Has your liver been liberated? Time 2001; 157 (15): 64.

Treves F. The treatment of Glenard’s disease by abdominal section. Brit Med J 1896; i: 1-4.

Fibromyalgia Meets Craniosacral Therapy

Fibromyalgia
The current criteria for making the diagnosis of fibromyalgia are based upon the scoring obtained from two subjective measures, the Widespread Pain Index and the Symptom Severity Scale, the results of which are then combined [Wolfe et al, 2010]. Fibromyalgia is therefore neither a distinct syndrome nor a specific disease, which is now being understood as an indication of polysymptomatic distress [Wolfe et al. 2013].

Complementary and Alternative Medicine
Practitioners who operate under the umbrella of Complementary and Alternative Medicine (CAM) have exploited this diagnostic uncertainty, as evidenced by a recent systematic overview of such therapies, which are utilized by many patients with fibromyalgia [Lauche et al., 2015].

Although some of the interventions appeared to be beneficial, in others the outcomes were either inconsistent or inconclusive. The investigators remarked upon the “methodological flaws limiting definite conclusions about their efficacy and safety” [Lauche et al., 2015].

Somewhat surprisingly, craniosacral therapy (CST) was not included in the systematic overview. However, this form of therapy is being confidently offered around the world to patients with fibromyalgia. [For example, see: http://www.fibromyalgia-symptoms.org/fibromyalgia_craniosacral.html]

The origins of craniosacral Therapy (CST)
CST is an approach that appears to have been modeled upon the remarkable theories of 18th century Swedish philosopher and scientist, Emanuel Swedenborg [Tubbs et al. 2011]. Because of his many prescient insights about the brain and nervous system, Swedenborg has been recognized as a neuroscientist who was well ahead of his time [Gross, 2009], and has been accorded a prominent place in the history of neurology [McHenry, 1969].

He gave an accurate account of the importance of the cerebral cortex as the seat of the higher psychical functions and was the first to suggest somatotopic organization of the motor cortex, as well as the importance and function of the pituitary gland (which he termed the “arch gland”).

Swedenborg was aware of the phenomenon of pulsation of the brain [Maier, 1994] and believed that it imparted a motion to the cerebrospinal fluid [Squires, 1940]. The movements of the brain and the central nervous system were said to be reciprocal to those of the lungs i.e., when the lungs expand, the brain contracts, and vice versa. During the expansile motion of the brain cerebrospinal fluid is expressed from the IVth ventricle into the subarachnoid space.

The pumping action of the brain forced “nervous fluid” through the nerves. The spinal ganglia were thought to help propel the fluid, which was eventually returned to the spinal cord and brain by way of the meninges [McHenry, 1969].

Swedenborg attempted to explain mental events in terms of minute vibrations or “tremulations”. These, and his other important contributions to neuroscience, were only recognized when his manuscripts were discovered, translated, and published in the late 1800s.

Swedenborg’s influence
Swedenborg’s ideas seem to have influenced William Garner Sutherland (1873-1954), an American osteopathic physician, who proceeded to elaborate upon them [Scarr, 2013].

Sutherland described five components of what he called The Primary Respiratory Mechanism, an intrinsic motion that expressed itself through the entire body and was held to be a “fundamental expression of life itself.”

Agreeing with Swedenborg, Sutherland observed that the brain and spinal cord undulate rhythmically, as does the cerebrospinal fluid. Moreover, this fluid was able to move throughout the body by passing along the spinal nerve sheaths and through extra-cranial lymphatics, thereby fulfilling a nutritive function. The movements of the brain and cerebrospinal fluid also became evident in the spinal membranes as a “dynamic shifting of tension” within them.

Sutherland believed that the dura mater was held under constant tension and could transmit external forces along its length. Because of its attachment to the cranial bones, this tissue was responsible for maintaining the structural integrity of the cranium.

Thus, excessive forces applied by the dura mater to the cranium could lead to distortion of its components, which although they grew to approximate each other, remained in constant motion. The cranial sutures were thus kept open by tiny movements, estimated to be of the order of 100ths of an inch.

Sutherland’s views were at odds with the conventional thinking of anatomists, which held that the bones of the skull fused in early life. But Sutherland interpreted the fusion of certain cranial sutures to be indicative of a pathological condition, said to follow cranial traumata.

The importance given to the sacrum is due to its role in anchoring the dura mater. Motility at the level of the occiput is transmitted to the sacrum. Any trauma to the sacrum could also have an effect on the cranium (e.g. be a cause of headache).

Sutherland also believed that the body’s connective tissues are subject to a cyclic change in tension and a small amount of motion, typically 2-14 times a minute [Scarr, 2103].

In summary, the “craniosacral system” comprises the bones of the skull, the cerebrospinal fluid flowing within the spinal meninges, and the anchoring sacrum.

Upledger’s contribution
The idea of cranial bone movement and a “dural pulse” were further developed in the 1970’s through research performed by osteopath John E. Upledger (1932-2012) and his associates at the University of Michigan.

A key part of the ‘cranial’ concept is that bones of the skull remain distinct throughout life and have a rhythmic motion that is palpable as the ‘cranial rhythmic impulse’ [Scarr, 2012].

This mobility allows the CST practitioner to palpate the pulse and at the same time to gently move the cranial bones in such a way as to remove any restrictions, in order to restore bodily balance, and relieve tension in fascial tissues throughout the body. Headaches, muscles spasm, and chronic pain are said to then be able to rapidly dissipate.

In contrast to Sutherland’s Primary Respiratory Mechanism Model, Upledger suggested that the cerebrospinal fluid pressure rhythmically fluctuates according to its cycle of production and resorption. It is this “pressurestat” mechanism that drives the ventricular system of the brain to dilate and contract rhythmically—rather than “some intrinsic contractile power of the brain tissue itself” [Upledger & Vredevoogd, 1983].

Upledger’s model centered upon the presumed existence of sensory nerves and receptors positioned within human sagittal sutures that are responsive to compression and stretch, acting as a signaling system between the respective suture and the choroid plexus.

When a suture expanded, stretch receptors were activated and the production of cerebrospinal fluid (CSF) decreased. As fluid was reabsorbed into the venous system, volume and pressure of CSF reduced, activating compression receptors within the suture and signaling the choroid plexus to resume production of CSF. According to Upledger [1995]:

“The brain, in turn, rhythmically tones and relaxes the myofascial system via the motor division of the nervous system. This effect is delicate and easily inhibited by connective tissue that is restricted and not able to respond to this gentle urging of the craniosacral system via the motor system. Hence, these restrictions are easily found by the skilled therapist practicing craniosacral therapy.”

Alaquel et al. [2006] reviewed the evidence that cranial sutures do respond to mechanical loads and believed that they function as a cushion between adjacent bones. The sutures can indeed be subject to compressive stress, tensile stress, and shear stress as the underlying brain expands during development and as forces are transmitted from the masticatory muscles.

But these forces are technically difficult to measure with accuracy. Alaquel et al. [2006] considered that additional research is needed to elucidate the mechanotransduction events by which cranial sutures respond to the application of mechanical force.

Inter-rater reliability of CST
When Wirth-Pattullo and Hayes [1994] tested the claim that craniosacral therapists are able to palpate changes in cyclical movements of the cranium, they found that inter-rater reliability was unacceptable for clinical decision-making and treatment. They also wondered about the very existence of craniosacral motion and whether the evaluators in their study might have imagined such motion.

In a lengthy response, Upledger [1995] affirmed the usefulness of his “pressurestat” model and argued that other factors needed to be considered besides an assessment of the rate, amplitude, symmetry, and quality of the craniosacral rhythmical activity, as palpated using the “vault hold” on the head.

Upledger [1995] argued: “we should not allow strict adherence to the rules of experimental design to fetter human intelligence, nor should we allow it to stifle our creativity.”

He then defended his position by calling upon therapists to factor in the “wisdom of the body,” or in other words, to harness the placebo response:

“Implicit in craniosacral therapy is the concept that the patient’s own body and craniosacral system know how best to correct the problem. Our goal as therapists is to tune into that inherent wisdom and assist and facilitate its self-corrective processes.”

Controlled trials of CST in fibromyalgia
In a randomized controlled trial of a 20-week programme using a CST protocol in patients with fibromyalgia, symptoms did improve but there was no comparable control group (i.e. patients receiving another form of manual therapy) [Cástro-Sanchez et al. 2011]. The same serious design fault was evident in another study performed by the same group of researchers [Mataran-Peñarrocha et al. 2011]. The control group in each of these studies had received disconnected magnetotherapy.

The complex treatment protocol administered by the researchers was aimed at “removing the restrictive obstacle and returning the system to its natural state.” But it is noteworthy that they failed to record the nature and site of any such obstacles they encountered in members of either group.

Conclusion
From the available scientific evidence, one can only agree with the conclusion of Rogers and Witt [1997] that the opinions or beliefs of practitioners of CST do not provide sufficient reasons to support its use as an effective treatment. At the very least this appears to be the case for those with fibromyalgia.

References:

Alaquel SM, Hinton RJ, Oppenehim LA. Cellular response to force application at craniofacial sutures. Orthod Craniofacial Res 2006; 9: 111-122.

Castro-Sánchez AM, Mataran-Peñarrocha GA, Sánchez-Labraca N, et al. A randomized controlled trial investigating the effects of craniosacral therapy on pain and heart rate variability in fibromyalgia patients. Clin Rehabil 2011; 26: 25-36.

Gross CG. Three before their time: neuroscientists whose ideas were ignored by their contemporaries. Exp Brain Res 2009; 192: 321-334.

Lauche R, Cramer H, Häuser W, et al. A systematic overview of reviews for complementary and alternative therapies in the treatment of the fibromyalgia syndrome. Evid Based Complement Alternat Med 2015, Article ID 610615, 13 pages.

Maier SE, Hardy CJ, Jolesz FA. Brain and cerebrospinal fluid motion: real time quantification with M-mode MR imaging. Radiology 1994; 193: 477-483.

Mataran-Peñarrocha GA, Castro-Sánchez AM, Garcia GC, et al. Influence of Craniosacral Therapy on Anxiety, Depression and
McHenry L, Jr. Garrison’s History of Neurology, revised and enlarged. Springfield: Charles C Thomas, Publisher, 1969: 107-108.

McHenry L, Jr. Garrison’s History of Neurology, revised and enlarged. Springfield: Charles C Thomas, Publisher, 1969: 107-108.

Rogers JS, Witt PL. The controversy of cranial bone motion. JOSPT 1997; 26: 95-103.

Scarr G. Palpatory phenomena in the limbs: a proposed mechanism. Int J Osteopath Med 2013; 16; 114-120.

Squires AW. Emanuel Swedenborg and the cerebrospinbal fluid. Ann Hist Med 1940; 2: 52-53.

Tubbs RS, Riech S, Verma K, et al. Emanuel Swedenborg (1688-1772): pioneer of neuroanatomy. Childs Nerv Syst 2011; 27: 1353-1355.

Upledger JE, Vredevoogd JD. Craniosacral Therapy. Seattle: Eastland Press, 1983.

Upledger JE [Letter]. Craniosacral therapy. Phys Ther 1995; 75: 328-329.

Wirth-Pattullo V, Hayes KW. Interrater reliability of craniosacral rate measurements and their relationship with subjects’ and examiners’ heart and respiratory rate measurements. Phys Ther 1994; 74: 908-916.

Wolfe F, Clauw DJ, Fitzcharles M-A, et al. The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis Care Res 2010; 62: 600-610.

Wolfe F, Brähler E, Hinz A, Häuser W. Fibromyalgia prevalence, somatic symptom reporting, and the dimensionality of polysymptomatic distress: results from a survey of the general population. Arthritis Care Res 2013; 65: 777-785.

Could Fibrositis be Making a Comeback?

Introduction

As I perused the abstracts for the upcoming 4th International Fascial Research Congress (September 2015), I came upon one that made me stop and think. It related to a half-day post-conference workshop by Kirstie Segarra – Managing Fascial Health for Individuals in Fibromyalgia:

To demonstrate clearly that managing widespread pain must include treatment of the fascia as we are structured determined systems, and to decrease pain is to invite change in the structure through the fascial matrix in order to have a correlating change in the central nervous system. In this way we restore homeostasis in the client.

Could pathology within fascia have been overlooked in the search for a peripheral source of nociception in this condition? Well, it appears that this is no longer the case.

Pathophysiological considerations

Liptan [1] hypothesized that fibromyalgia could be seen as a “bodywide fasciitis,” comparable to situations characterised by more focal fasciitis (e.g. plantar fasciitis).

The culprit appears to be chronic tension within the fascia responsible for causing micro-injuries (i.e. tears) in those with a “dysfunctional” healing response. Such a response is said to result from insufficient growth hormone release consequent upon inadequate deep sleep.

In summary, Liptan argued that: “Fascial dysfunction and inflammation may lead to widespread pain and central sensitization seen in fibromyalgia.”

She explained the tender points as possibly reflecting “areas that suffer the greatest microtrauma and mechanical stress from daily activities, and thus have higher levels of fascial inflammation.”

The main evidence put forward in support of her hypothesis derived from “recent biopsy studies [which] have found increased levels of collagen and inflammatory mediators in the fascia of fibromyalgia patients.”

But is this a novel hypothesis? In the Background section of his paper, Liptan harks back to the early 1900s when the aetiology of “muscular rheumatism” was indeed a hot topic.

Muscular rheumatism

In speculating upon the pathophysiology of low back pain, the great British neurologist, William Gowers [1904] coined the term “fibrositis” and thus championed the central role of the fascia in this condition:

In all parts it seems it seems the most susceptible to the influence we call “rheumatism” … The relation of lumbago to rheumatism would alone, make us expect to find it an affection of the fibrous tissue of the muscles, the tissue in which the spindles are situated, rather than of these alone … important proof that the malady is an affection of fibrous tissue; it may spread, and it spreads by continuity of this tissue.

Gowers postulated both focal and generalised forms of “fibrositis”:

We are thus compelled to regard lumbago in particular, and muscular rheumatism in general, as a form of inflammation of the fibrous tissue of the muscles.

The pathological findings

Ralph Stockman [1913], a Scottish pathologist, soon announced:

The essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches and as fibrous tissue is spread throughout the body the lesions may also be widely spread or may affect only a single limited area.

But after other researchers had repeatedly failed to find biopsy evidence of fibrous tissue inflammation, the “fibrositis” construct was eventually superseded by that of “fibromyalgia” [Hench, 1976] and classified in the nebulous category of non-articular rheumatism [Atkinson, 1981].

Treatment

As did Gowers, Liptan [2010] ascribed a limited role to anti-inflammatory drugs (NSAIDs and corticosteroids), which should be used only during the initial phase of injury repair.

According to Liptan [2010] “only slow and sustained pressure will effect changes in the fascial tissue” and he recommended manual therapy techniques that “don’t cause further injury and inflammation, but rather gently break apart existing fascial restrictions and adhesions to promote tissue healing.”

She wondered whether techniques said to target the fascia, which included “Rolfing” (a technique of deep tissue manipulation) and “myofascial release,” could “help define the role of fascia in producing fibromyalgia pain.”

Based upon Liptan’s hypothesis, a pilot trial was undertaken comparing Swedish massage with myofascial release therapy (MFR), each administered over 90 minutes a week for 4 consecutive weeks [Liptan et al. 2013]. The former technique utilized moderate pressure stroking of the neck, back, arms and legs, whereas MFR consisted of “prolonged assisted stretching of painful areas of soft tissue” in the same regions.

The rationale given for MFR manoeuvres is that they are designed to “break up fascial adhesions” presumed to be the consequence of tissue injuries occurring in the fascia of patients with fibromyalgia [Liptan et al. 2013]. That for Swedish massage is to increase circulation and promote general relaxation.

Although numbers were small, both forms of treatment were found to be “safe, tolerable and acceptable” with MFR producing better symptom reduction.

By contrast, the mainstay of treatment recommended by Gowers was complete rest:

Not even passive movement should be employed until it causes no pain, and then it should be most gentle. The avoidance of pain should be made the standard for all local measures.

Gowers observed that counter-irritation (cautery being the most effective form) sometimes lessens the pain, as does deep hypodermic injection of cocaine, repeated daily for 2-3 weeks.

Other treatment strategies worth trying included a Turkish bath, mild aperients and, in the most acute cases, medicinal agents such as salicylates, nitrous ether, colchicum and perchloride of mercury.

Looking ahead

Gowers conceded: “we are without any direct evidence of the real nature of these affections” but he did hope that opportunities for pathological research would be seized upon:

We cannot wonder at our ignorance, still less complain of it, for it is only quite recently that the minute structure of the sensory elements of muscle and tendon has been clearly perceived, and much of the normal structure remains obscure.

But over a century later, direct histological evidence to support the related concepts of “fibrositis” and “fascial adhesions” is still lacking.

Nonetheless, Liptan [2010] calls for the use of existing methods of in vivo microdialysis to investigate the chemical composition of fascial interstitial fluid for evidence of inflammation, as well as for evidence of activation of fibroblasts removed from fascial tissues. He did not canvass the possibility that any such inflammation might in fact be “neurogenic” [Julius & Basbaum, 2001].

As for the role of manual therapy, Liptan et al. [2013] hope that various measurement tools being developed “may provide insight into which symptom of function domains are most malleable to various types of massage intervention.”

Conclusion

To date, the search for underlying peripheral musculoskeletal pathology in fibromyalgia has not been fruitful.  Yet, a recently published book – Fascial Dysfunction: Manual Therapy Approaches (2014) – is being advertised to manual therapists with this rather astounding claim appearing in the blurb:

Fascial dysfunction is now recognized as one of the main underlying causes of musculoskeletal pain leading to impaired and reduced mobility.  [Link: http://www.amazon.com/Fascial-Dysfunction-Manual-Therapy-Approaches/dp/1909141100]

Could Gowers have been right after all? Should we now discard the term fibromyalgia and revert to his “fibrositis” model? It seems a most unlikely possibility but a critical review is urgently needed to once and for all resolve this important question.

References:

Atkinson MH. Nonarticular rheumatism. Can Fam Physician 1981; 27: 254-258.

Gowers WR. A lecture on lumbago: its lessons and analogues. Brit Med J 1904; i: 117-121.

Hench PK. Nonarticular rheumatism, 22nd rheumatism review: review of the American and English literature for the years 1973 and 1974. Arthritis Rheum 1976; 19(suppl): 1081–1089.

Julius D, Basbaum AI. Molecular mechanisms of nociception. Nature 2001; 413: 203–210.

Liptan GL. Fascia: a missing link in our understanding of the pathology of fibromyalgia. J Bodywork Mov Ther 2010; 14: 3-12.

Liptan G, Mist S, Wright C, Arzt A, Jones KD. A pilot study of myofascial release therapy compared to Swedish massage in Fibromyalgia. J Bodywork Mov Ther 2013; 17: 365-370.

Stockman R.  Discussion on fibrositis. Proc R Soc med 1913; 6: 36-39.

 

THE TRANSMUTATION OF FIBROMYALGIA

Fibromyalgia was officially recognised in 1990 when a Multicenter Criteria Committee of the American College of Rheumatology recommended the term be used as a means of classifying patients presenting with chronic widespread pain and tenderness [1].

Pain was considered to be “widespread” when it was experienced in all four quadrants of the body (i.e. on both the left and right sides and above and below the waist).

Tenderness was assessed over 18 specifically chosen tender points. When patients with widespread pain were judged by their clinician to be hypersensitive at 11 or more of these points, the diagnosis of Fibromyalgia could be applied.

Some 20 years later, the criteria for diagnosis were broadened by the introduction of a symptom severity scale score to replace the tender point count. Widespread pain remained a diagnostic criterion [2].

The clinical problem of “RSI” (repetitive strain injury)

In Australia the term “RSI” (repetitive strain injury) came to be broadly applied to all conditions characterised by neck and/or upper limb pain presenting in an occupational context.

“RSI” embraced localised conditions, such as carpal tunnel syndrome, dorsal wrist tenosynovitis, lateral epicondylitis and rotator cuff “tendonitis”, along with poorly understood conditions characterised by diffuse pain felt in the neck, pectoral girdle and arms, often accompanied by positive sensory symptoms, cramp, loss of muscle strength, and vasomotor abnormalities [3,4].

A vigorous medical debate had taken place during the 1980s over the categorization of the sub-group of patients with diffuse pain. On the one side were those who espoused the theory of muscle overuse injury, whilst on the other side were those who argued that those with these conditions were reflecting psychological distress that was manifest as somatic symptoms [5].

However, the homogeneity of presentation of these patients implied not only a common pathophysiology but also one that could be attributed to dysfunction of the nociceptive system itself, consistent with what was then the current definition of “neuropathic” pain. This explanatory model was proposed on the basis of careful clinical observation integrated with current knowledge of mechanisms of nociception [3,6].

Fibromyalgia becomes a regional condition

The 1980s brought the dreaded “RSI” (repetition strain injury) with interaction between Fibromyalgia Syndrome and the medico-legal system [7].

One of the key proponents in Australia of fibromyalgia, Geoffrey Littlejohn, was keen to extend the construct to subsume these syndromes of less diffuse pain, which were then being called “RSI”. He and his colleagues argued that these conditions were in fact a “subset” of fibromyalgia. 

They conjectured: Mechanisms similar to those in generalised fibromyalgia are likely to operate, although to a lesser extent, in patients with primary chronic localised pain or localized fibromyalgia [8].

This reconceptualisation of “primary chronic localised pain” as “regional fibromyalgia” presumed the validity of a parent syndrome.

However this exercise was an example of the logical fallacy known as “begging the question,” and was particularly problematic when the diagnostic credibility of both conditions was being hotly contested.

In the absence of knowledge or theory regarding the pathogenesis of fibromyalgia, these authors nonetheless took a bold step to explain the pathogenesis of local pain that became regional.

To accomplish this, Littlejohn invented the concept of “simple injury to the muscle-tendon unit” but neglected to provide any pathological evidence to support the existence of such an entity:

The majority of patients with the “RSI problem” have a chronic pain syndrome, which, although it may be triggered by a simple injury to the muscle-tendon unit, is not due to persisting tissue damage of injury. Extensive investigations seeking out tissue damage will only show age-related changes which do not explain the diffuse symptoms” [9].

Thus, in summary, “RSI” is seen as a complex pathophysiological pain problem where clinical features may be approached using the paradigm of localised fibromyalgia syndrome” [9].

This step needs to be dissected in order to understand the transmutation of fibromyalgia.  A diffuse pain syndrome of unknown pathogenesis was invoked to explain “regional” or “local” apparently similar conditions of allegedly known pathogenesis.  There was never a “paradigm” of “localized fibromyalgia syndrome”; it was never proposed that (diffuse) fibromyalgia syndrome could be “triggered by a simple injury to the muscle-tendon unit”.

These assertions were and are entirely conjectural.

Medico-legal implications

Littlejohn’s next contribution was to downplay the nexus between “localised fibromyalgia syndrome” and work-related factors. This strategy was to have important implications for those with the condition who might be seeking workers’ compensation payments, particularly so in New Zealand [10].

Fibromyalgia can also occur as a syndrome of localised or regionalized pain and a low pain threshold. This situation is common after otherwise short-lived “soft tissue” injuries involving spinal areas, particularly in the context of compensation” [11].

Littlejohn defined “low pain threshold” in terms of sensitivity at the arbitrarily chosen “tender points” in fibromyalgia, which he claimed to be “characteristic regions used clinically to define pain threshold” – a circular argument – and that “sensitivity at these points is increased in pain-free subjects, but to an even greater extent in patients with fibromyalgia syndrome.”

But defining “sensitivity” in terms of the stimulus being applied is highly subjective and influenced by contextual effects and, as Littlejohn noted, this diagnostic criterion (along with widespread pain) has not been validated for medicolegal or disability purposes.

Furthermore, he did not produce evidence to support his claim that “low pain thresholds were common” after short-lived “soft tissue injuries” involving spinal areas. Yet again, conjecture was being passed off as established knowledge.

Littlejohn [12] then raised the spectre of psychogenesis:

The regional features seem to relate to local biomechanical factors around the spine, either postural or secondary to simple strains. When central sensitisation occurs it is likely that central neurophysiological factors, including psychological influences, allow for the amplification of otherwise subclinical spinal reflexes. These in turn cause regional pain, tenderness, muscle tightness and dermatographia.

The concept of “otherwise subclinical spinal reflexes” is yet another of Littlejohn’s conjectures. Furthermore, he failed to explain the mechanism(s) by which “central neurophysiological factors” could be responsible not only for their amplification but also for the various clinical phenomena.

Finally, Littlejohn [13] announced “operational” criteria for a diagnosis of localised fibromyalgia. But in fact they were Littlejohn’s own non-validated criteria [12]:

Regional pain syndromes are also referred to as localised fibromyalgia. Although no validated classification or diagnostic criteria exist for these condition, operational or clinically useful criteria have been proposed: regional pain and regional lowering of pain threshold, and the presence of sleep disturbance, fatigue, muscular stiffness and emotional distress in the absence of a primary nociceptive cause for pain.

“Using this model, regional pain syndrome appears to be on a spectrum between the simple self-limited aches and pains of everyday life and persistent musculoskeletal syndromes such as fibromyalgia.”

Littlejohn’s pronouncements are tautological: if regional pain syndrome is in fact localized fibromyalgia syndrome, then it follows that fibromyalgia is generalised regional pain syndrome.

What was achieved?

Where has this transmutation of fibromyalgia taken us? Has any light been shed on diffuse or regional pain syndromes?

Littlejohn attempted to fill gaps in our understanding of  “RSI” by interpolating his personal views on Fibromyalgia into the debate.  However all he achieved was to introduce circular arguments based on conjecture.   How did the guardians of the literature allow that to happen?

John Quintner (Physician in pain medicine and rheumatology)

Milton Cohen (Specialist pain medicine physician and rheumatologist)

References:

1. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombadier C, Goldenberg DL, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Arth Rheum 1990; 33: 160-172.

2. Wolfe F, Clauw DJ, Fitzcharles MA, Goldenberg DL, Katz RS, Mease P, et al. The American College of Rheumatology preliminary diagnostic criteria fibromyalgia and measurement of symptom severity. Arthritis Care Res 2010; 62-600-610.

3. Cohen ML, Arroyo JF, Champion CD, Browne CD. In search of the pathogenesis of refractory cervicobrachial pain syndrome. Med J Aust 1992 ; 156: 432-436.

4. Cohen ML, Arroyo JF, Champion GD. The relevance of concepts of hyperalgesia to “RSI”. In: Bammer G, ed. Working Paper No. 31. Canberra: Australian National University, 1992.

5. Quintner JL. The Australian RSI debate: stereotyping and medicine. Disabil Rehab 1995; 17(5): 256-262.

6. Quintner JL, Elvey RL. The neurogenic hypothesis of RSI. In: Bammer G, ed. Working Paper No. 24. Canberra: Australian National University, 1991.

7. Reilly P, Littlejohn GO. Fibrositis/fibromyalgia syndrome: the key to the puzzle of chronic pain. Med J Aust 1990; 226-228.

8. Granges G, Littlejohn GO. Pressure pain thresholds in pain free subjects, in patients with chronic regional pain syndrome, and in fibromyalgia syndrome. Arthritis Rheum 1993; 36: 642-646.

9. Littlejohn GO. Key issues in repetitive strain injury. J Musculoskel Pain 1995; 3(2): 25-33.

10. Rankin DB. Viewpoint: the fibromyalgia syndrome: a consensus report. NZ Med J 1999; 112: 18-19.

11. Littlejohn GO. Med J Aust 1996; 165: 387-391.

12. Littlejohn GO. Clinical update on other pain syndromes. J Musculoskeletal Pain 1996: 163-179.

13. Littlejohn GO. Fibromyalgia syndrome and disability: the neurogenic model. Med J Aust 1998; 168(8): 398-401.

 

 

ARE THEY ASKING THE RIGHT QUESTION?

The following announcement has just appeared on Myopain Seminars, one of the websites run by proponents of “dry needling”: The Federation of State Boards of Physical Therapy is working on developing a list of competencies needed for physical therapists to perform dry needling, and we would greatly appreciate your help! The Federation has developed a survey based on the Physical Therapy Practice Analysis, developed by the Federation in 2011. The survey contains a list of knowledge, skills, and activities that physical therapist have and undergo. Based on this list, the survey asks if each item is necessary to competently perform dry needling. This survey is the preliminary stage of determining the list of dry needling competencies. Although this is one of the first steps, it is critical. Please follow the link below to complete the survey. Additionally, the Federation asks that you share the survey with any colleagues or practitioners who may be performing dry needling. Please complete the survey no later than April 5, 2015. We truly appreciate your help in this endeavor! If you have any questions, please feel free to contact the Federation at any time. Link: https://survey.fsbpt.org/TakeSurvey.aspx?SurveyID=m80049l Before such a survey is undertaken, the really important question that needs to be asked and urgently addressed by the Federation is whether the currently available scientific evidence supports a continuation of the popular practice by its constituency of “dry needling” muscles and other deep tissues. Clearly, this form of treatment is irrational and therefore the answer must be an unequivocal NO!