By John Quintner & Milton Cohen
Over forty years ago John Bonica  first made the proposal to accord disease status to chronic pain. He regarded intractable pain as “a destructive force that often imposes severe emotional, physical, economic, and sociological stresses on the patient as well as his family as well as on society.”
Nearly 30 years later, Siddall & Cousins  outlined a detailed case in favour of Bonica’s proposition. They recited the knowledge to that date on the pathophysiology of nociception, including central sensitization, which they termed “a host of pathological changes” that in turn constitute a “pain pathology.”
As they correctly noted:
“People [experiencing pain] often report mood disturbances, including irritability, helplessness, and depression. More complex cognitive responses can also develop, such as loss of belief in the ability to perform tasks and fear avoidance. These in turn can result in loss of employment, breakdown of family relationships, and loss of community status.”
Siddall & Cousins  then went on to assert that these changes are “pathologies” that are “dependent on and unique to the presence of pain,” termed by them “secondary pathologies.”
They also invoked, as the “tertiary pathology” of pain, “factors such as genetic makeup, level of spinal inhibition, psychological status and the societal litigation system.” They argued that these, in toto, justify considering pain as “an environmental disease.”
In response, Cohen et al.  argued against this proposition:
“To what extent does the theory of pain-as-a-disease offer an explanation of pain? The proponents of this thesis argue not only that pain is a disease defined by a unique pathology but also that pain functions as a causative agent: “Pain activates brain structures”; “these pathologies . . . are . . . dependent on . . . the presence of pain”; “persistent pain does give rise to its own secondary pathology” [Siddall & Cousins 2004].
But the lived experience of pain is too complex and pervasive to be reducible to a ‘thing’ that can cause itself. This argument confuses pain-as-an-experience, pain-as-a-symptom, pain-as-a-pathological- entity, and pain-as-a-cause-of-pathology.
By blurring the lines of cause and effect and of antecedent and consequent, taken together with the failure to propose an acceptable name for this disease other than the morally charged maldynia [Quintner et al. 2011], this proclamation ultimately constitutes the philosophical error captured by Wittgenstein  in his aphorism #114: One thinks that one is tracing the outline of the thing’s nature over and over again, and one is merely tracing round the frame through which we look at it. The claim that pain is a disease is thus passed off as an assertion of certainty but only because that is demanded by the frame of reasoning through which it was conceived.”
The continuing debate
Clauw et al.  have recently reactivated this important issue. They suggest reframing chronic pain both as “a biopsychosocial disease”. (Conclusion p.9) and a “maladaptive neuropathological disease state.” (p.4, col. 1) However, in so doing they seem not to understand that “biopsychosocial” is a conceptual framework, and not an explanatory model of disease. The observed peripheral and central nervous system changes seen in “novel experimental and neuroimaging techniques” that might support the view of a “maladaptive” disease state are not referenced.
Essentially Clauw et al.  recapitulate (but fail to acknowledge) the arguments of Siddall and Cousins :
“The development and persistence of pain involve three major pain pathways, which may act independently or in combination (i.e. nociceptive, neuropathic, and central sensitization). Various risk/vulnerability factors, such as fear, anxiety/depression, and sleep disorders, as well as resilience/ protective factors, such as social support, coping skills, and self-efficacy, interact with patients’ neurobiology to modulate their experience of pain and related outcomes.”
Comment: Note that their use of the term “pain pathways” is inaccurate; the correct term is nociceptive pathways. However the terms nociceptive, neuropathic, and central sensitization – the last officially termed “nociplastic” by the IASP are descriptors from which broad mechanisms – but not pathways – can be inferred.
“In 2015, the National Institutes of Health  introduced the concept of ‘chronic overlapping pain conditions’ in recognition of the high rates of co-prevalence among a cluster of chronic pain disorders, particularly in women, including fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, interstitial cystitis, vulvodynia, endometriosis, chronic migraine and tension-type headache, CLBP, and temporomandibular disorders. The implications of chronic overlapping pain conditions in terms of diagnosis, classification, and management are the subject of recent review and ongoing research [Maixner et al. 2016].” (p.3, col. 2) Although chronic pain remains incompletely understood and difficult to define, it is increasingly perceived as a disease entity in itself” (p.1 col 2)
Comment: So, the “disease” (singular) of chronic pain is not only “difficult to define” but also actually comprises “overlapping pain conditions” (which, no doubt, are also difficult to define). But how can that be, if this disease is “characterized by unique pathological modifications of the central and peripheral nervous system”? (p.1 col 2 & Conclusion) Does this mean that the biology of, say, endometriosis and TMD is fundamentally the same? If so, the argument of Clauw et al. is anti-biopsychosocial and a reversion to biomedical, viz, that “central sensitization is the “unique” pathology. However the correct term in this context would be “central sensitization of nociception”.
“Centralized sensitization (sic) is thought to be the predominant mechanism in numerous clinical pain conditions, including, perhaps most notably, the phantom limb pain that develops in some amputees after surgery [Li et al. 2015]. This phenomenon also appears to be an important contributor to fibromyalgia, temporomandibular joint disease, chronic fatigue syndrome, chronic pelvic pain syndromes (e.g. interstitial cystitis, irritable bowel syndrome, vulvodynia, and chronic prostatitis), headache, and endometriosis [Eller-Smith et al. 2018]. The latter central pain conditions often coexist and share certain other CNS-related clinical symptoms, including widespread pain, fatigue, and mood, cognitive, and/or sleep problems. Moreover, chronic pain conditions characterized by central sensitization are frequently diagnosed in patients with other types of persistent pain, including nociceptive spine pain, RA, and OA [Brummett et al. 2013; Yunus 2012]”. (p.3, col 2)
Comment: Again, does this mean that the biology of, say, “failed back surgery syndrome” is the same as that of “interstitial cystitis”? If so, then this “disease” of chronic pain is indeed protean in its manifestations – as indeed is an entity labelled “fibromyalgia”. But then not only are we back in a tautology but also all we would need for diagnosis of the disease is a questionnaire.
The argument put forward by Clauw et al.  in favour of the proposition that chronic pain is a disease entity is not new and contains the same epistemological flaws as earlier iterations. Primary among these, the proponents of chronic pain-as-a-disease speak of pain as a “thing” with agentive properties, thus contradicting the definition of “pain” as an experience.
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