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Comment on, Pain elicited by blunt pressure: neurobiological basis and clinical relevance. Treede et al., (Pain 98 (2002) 235)
Pain 104 (2003) 711–716 www.elsevier.com/locate/pain
Letters to the Editor
Comment on, Pain elicited by blunt pressure: neurobiological basis and clinical relevance. Treede et al., (Pain 98 (2002) 235) The Topical Review article by Treede et al. [2002] cannot go unchallenged, thus escaping critical review. The article evidently has been written from the point of view of the experimental physiologist rather than that of the clinician. This does not excuse the confusion in its presentation, the circularity of its arguments and its failure to address its explicit purpose, to link basic neurobiological insights to the clinical situation. Our criticism turns on two major themes emerging from the article: the uncritical acceptance of the existence of discrete clinical syndromes characterised by sensitivity to pressure and the circular argument which results from loose and confusing connotations of hyperalgesia. “Myofascial pain can be distinguished from FM (fibromyalgia), but both conditions may occur in the same patient” (p. 236). If so, how could one make the distinction? What is the difference between the phenomenon of a ‘trigger point’ and that of a ‘tender point’? In the only study of its type in the literature, a group of ‘experts’ in fibromyalgia and myofascial pain could not distinguish between them (Wolfe et al., 1992). Both types of ‘points’ are examples of mechanical hyperalgesia: why would one need even to postulate that they are different phenomena? On several occasions in the article, localised tenderness is stated as indicating peripheral sensitisation or central sensitisation or alteration in descending pathways. These three options include all possibilities: how are clinicians expected to gain insight from this tautological proposition? “Exaggerated pain sensitivity to mechanical stimuli is also a hallmark of other hyperalgesia syndromes, including primary and secondary hyperalgesia following injury, postoperative pain and neuropathic pain.” (p. 237). Translated, this formulation may mean that hyperalgesia is a marker of hyperalgesic syndromes. Not only does this constitute circular reasoning but also it conflates the experimental physiological phenomena of ‘primary’ and ‘secondary’ hyperalgesia with clinical hyperalgesia. In reiterating the circular argument, the authors fail to resolve
this confusion: “Enhanced pain sensitivity to blunt pressure is attributed to hyperalgesia of deep tissues…” (p. 238). Logic dictates that the term ‘hyperalgesia’ cannot denote both the clinical phenomenon of ‘tenderness’ or ‘exaggerated’ or ‘enhanced pain (sic) sensitivity’ and its explanation or inferred mechanism. Hyperalgesia cannot have been caused by itself. The authors write, “[T]enderness to blunt pressure may be due to peripheral sensitization of primary afferents or to central sensitization, e.g in the spinal cord.” (p. 237) (the tautology again) and later, “[H]yperalgesia to blunt mechanical stimuli appears to be based on peripheral sensitization of C-fibre nociceptors” which is “confined to a site of tissue injury” (p. 237). What about the tenderness to blunt stimuli in normal tissue? By contrast, “[H]yperalgesia to punctate mechanical stimuli appears to be based on central sensitisation to A-fibre nociceptor input” (p. 237), whereas “Pain to light touch …appears to be mediated by central sensitisation to… non-nociceptive A betafibre afferents” (p. 238). Surely the difference between painful responses to light touch, to punctate pressure or to blunt pressure is a function of the applied pressure (force per unit area). In that case, the ranking of those stimuli in terms of increasing ‘pressure’ is light touch, blunt pressure, punctate pressure. Why then should the responses to the least and the most potent of these stimuli be determined by central sensitization but the response to the intermediate stimulus be mediated by peripheral sensitization? This conundrum exemplifies the difference between the experimental laboratory where hyperalgesia may be induced by controlled nociception (e.g. nerve damage or injection of capsaicin) and the clinic where the challenge is to deduce the nociceptive process. When confronted with a patient who is experiencing mechanical hypersensitivity to light touch, blunt pressure or punctate pressure in a region of pain which to all intents and purposes is normal tissue, surely the clinician is justified in considering that this is analogous to a region of ‘secondary hyperalgesia’. If so, the logical inference, on the basis of current concepts in the neurobiology of nociception, is that central sensitisation of nociception has occurred.
0304-3959/03/$20.00 q 2003 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
712
Letters to the Editor
Diagrammatically, this inferential sequence is as follows: CLINICAL PHENOMENON Hypersensitivity to mechanical stimuli in clinically normal tissue
,
PHYSIOLOGICAL ANALOGUE ‘secondary hyperalgesia’
,
INFERRED MECHANISM central sensitisation
This then raises the question of confusing terminology. The authors fail to distinguish between clinical hyperalgesia and experimental hyperalgesia. The latter is tested by noxious stimuli, consistent with the IASP definition of hyperalgesia (Merskey and Bogduk, 1994). However, in clinical medicine, we do not (or certainly should not) use noxious stimuli. So the clinical phenomenon of mechanical hypersensitivity in clinically normal tissue is in fact allodynia or, strictly, ‘secondary allodynia’. The phenomenon is defined by the stimulus, not the response. We argue that so-called ‘trigger points’ and ‘tender points’ are examples of allodynia rather than of hyperalgesia and, given that they are found in clinically normal tissue, it is valid to infer that central sensitization of central nociceptive pathways to non-nociceptive information has occurred. In summary, the authors’ at times confusing presentation has helped to perpetuate the mythology that clinical syndromes characterised by mechanical ‘hyperalgesia’ can be distinguished and have obscured the valuable insight from the neurobiology of nociception of the common theme of central sensitisation. The big question to be addressed, especially from the clinical viewpoint, is what are the relative contributions of facilitated nociception and inhibited antinociception to this unifying conceptual explanatory model.
References Merskey H, Bogduk N, editors. Classification of chronic pain. Descriptions of chronic pain syndromes and definitions of pain terms, 2nd ed. Seattle, WA: IASP Press; 1994. Treede R-D, Rolke R, Andrews K, Magerl W. Pain elicited by blunt pressure: neurobiological basis and clinical relevance. Pain 2002;98: 235– 40. Wolfe F, Simons DG, Fricton J, et al. The fibromyalgia and myofascial pain syndromes: preliminary study of tender points and trigger points in patients with fibromyalgia, myofascial pain and no disease. J Rheumatol 1992;19:944–51.
M. Cohen St. Vincent’s Medical Centre, St. Vincent’s Campus, 376 Victoria Street, 2010 Sydney, Australia J. Quintner Wyllie Arthritis Centre, 6 Lemnos Street, Perth, WA 6008 Australia doi:10.1016/S0304-3959(03)00161-1
Reply to letter by Cohen and Quintner
In contrast to textbook chapters, that are supposed to represent more or less definite concepts in science, topical reviews in the journal PAIN such as our recent one on pressure pain (Treede et al., 2002) are intended to spawn a debate on the issues raised. For this reason, we are happy about the letter by Drs Cohen and Quintner, who point out that clinical syndromes characterised by enhanced painfulness to pressure stimuli at ‘trigger points’ or at ‘tender points’ are difficult to distinguish. We agree that a superficial look at the literature may lead to the conclusion that these two phenomena are different descriptions of the same entity. Even a careful literature search yields only few direct comparisons of the concepts behind trigger points in myofascial pain syndromes and tender points in fibromyalgia (e.g. Yunus et al., 1988; Schneider, 1995; Borg-Stein and Stein, 1996; Mense, 1999). The operational definitions, however, of tender points (Wolfe et al., 1990) and of trigger points (Travell and Simons, 1983) are distinct in that pressure onto trigger points may elicit both local and referred pain, whereas pressure onto tender points elicits local pain only. Universal agreement has not yet been reached on some other characteristics of trigger points (e.g. taut muscle bands, local twitch). By strictly applying these operational criteria, a few studies have tested for tender points and trigger points in the same patients. The majority of fibromyalgia patients exhibited some trigger points (Bengtsson et al., 1986; Granges and Littlejohn, 1993), but the trapezius and supraspinatus muscles which are usually tender in fibromyalgia hardly ever contained a trigger point (0 – 3%, Wolfe et al., 1992). Patients with myofascial pain exhibited some tender points, but the number of tender points was significantly less than in fibromyalgia patients and the mean tender point count did not meet the research diagnostic criteria for fibromyalgia (Wolfe et al., 1992). The majority of publications on musculoskeletal pain, however, contain only enough information to conclude that the patients studied fulfilled the research diagnostic criteria of one disease, but rarely enough information to check whether they also fulfil the diagnostic criteria of an alternative disease. More precise reporting of clinical data is essential to improve the dialogue between clinicians and basic scientists (Devor, 2003). Therefore, we join our Australian colleagues Cohen and Quintner in their appeal to clinicians, to be more critical and include both tender points and trigger points in their differential diagnosis. Only then it will become clear how different these two types of points really are. In their treatise on the mechanisms of hyperalgesia, Cohen and Quintner end with the suggestion that by analogy to secondary hyperalgesia central sensitisation may be inferred from hypersensitivity to mechanical stimuli in clinically normal tissue. We and others have suggested this
Letters to the Editor
Comment on, Pain elicited by blunt pressure: neurobiological basis and clinical relevance. Treede et al., (Pain 98 (2002) 235) The Topical Review article by Treede et al. [2002] cannot go unchallenged, thus escaping critical review. The article evidently has been written from the point of view of the experimental physiologist rather than that of the clinician. This does not excuse the confusion in its presentation, the circularity of its arguments and its failure to address its explicit purpose, to link basic neurobiological insights to the clinical situation. Our criticism turns on two major themes emerging from the article: the uncritical acceptance of the existence of discrete clinical syndromes characterised by sensitivity to pressure and the circular argument which results from loose and confusing connotations of hyperalgesia. “Myofascial pain can be distinguished from FM (fibromyalgia), but both conditions may occur in the same patient” (p. 236). If so, how could one make the distinction? What is the difference between the phenomenon of a ‘trigger point’ and that of a ‘tender point’? In the only study of its type in the literature, a group of ‘experts’ in fibromyalgia and myofascial pain could not distinguish between them (Wolfe et al., 1992). Both types of ‘points’ are examples of mechanical hyperalgesia: why would one need even to postulate that they are different phenomena? On several occasions in the article, localised tenderness is stated as indicating peripheral sensitisation or central sensitisation or alteration in descending pathways. These three options include all possibilities: how are clinicians expected to gain insight from this tautological proposition? “Exaggerated pain sensitivity to mechanical stimuli is also a hallmark of other hyperalgesia syndromes, including primary and secondary hyperalgesia following injury, postoperative pain and neuropathic pain.” (p. 237). Translated, this formulation may mean that hyperalgesia is a marker of hyperalgesic syndromes. Not only does this constitute circular reasoning but also it conflates the experimental physiological phenomena of ‘primary’ and ‘secondary’ hyperalgesia with clinical hyperalgesia. In reiterating the circular argument, the authors fail to resolve
this confusion: “Enhanced pain sensitivity to blunt pressure is attributed to hyperalgesia of deep tissues…” (p. 238). Logic dictates that the term ‘hyperalgesia’ cannot denote both the clinical phenomenon of ‘tenderness’ or ‘exaggerated’ or ‘enhanced pain (sic) sensitivity’ and its explanation or inferred mechanism. Hyperalgesia cannot have been caused by itself. The authors write, “[T]enderness to blunt pressure may be due to peripheral sensitization of primary afferents or to central sensitization, e.g in the spinal cord.” (p. 237) (the tautology again) and later, “[H]yperalgesia to blunt mechanical stimuli appears to be based on peripheral sensitization of C-fibre nociceptors” which is “confined to a site of tissue injury” (p. 237). What about the tenderness to blunt stimuli in normal tissue? By contrast, “[H]yperalgesia to punctate mechanical stimuli appears to be based on central sensitisation to A-fibre nociceptor input” (p. 237), whereas “Pain to light touch …appears to be mediated by central sensitisation to… non-nociceptive A betafibre afferents” (p. 238). Surely the difference between painful responses to light touch, to punctate pressure or to blunt pressure is a function of the applied pressure (force per unit area). In that case, the ranking of those stimuli in terms of increasing ‘pressure’ is light touch, blunt pressure, punctate pressure. Why then should the responses to the least and the most potent of these stimuli be determined by central sensitization but the response to the intermediate stimulus be mediated by peripheral sensitization? This conundrum exemplifies the difference between the experimental laboratory where hyperalgesia may be induced by controlled nociception (e.g. nerve damage or injection of capsaicin) and the clinic where the challenge is to deduce the nociceptive process. When confronted with a patient who is experiencing mechanical hypersensitivity to light touch, blunt pressure or punctate pressure in a region of pain which to all intents and purposes is normal tissue, surely the clinician is justified in considering that this is analogous to a region of ‘secondary hyperalgesia’. If so, the logical inference, on the basis of current concepts in the neurobiology of nociception, is that central sensitisation of nociception has occurred.
0304-3959/03/$20.00 q 2003 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
712
Letters to the Editor
Diagrammatically, this inferential sequence is as follows: CLINICAL PHENOMENON Hypersensitivity to mechanical stimuli in clinically normal tissue
,
PHYSIOLOGICAL ANALOGUE ‘secondary hyperalgesia’
,
INFERRED MECHANISM central sensitisation
This then raises the question of confusing terminology. The authors fail to distinguish between clinical hyperalgesia and experimental hyperalgesia. The latter is tested by noxious stimuli, consistent with the IASP definition of hyperalgesia (Merskey and Bogduk, 1994). However, in clinical medicine, we do not (or certainly should not) use noxious stimuli. So the clinical phenomenon of mechanical hypersensitivity in clinically normal tissue is in fact allodynia or, strictly, ‘secondary allodynia’. The phenomenon is defined by the stimulus, not the response. We argue that so-called ‘trigger points’ and ‘tender points’ are examples of allodynia rather than of hyperalgesia and, given that they are found in clinically normal tissue, it is valid to infer that central sensitization of central nociceptive pathways to non-nociceptive information has occurred. In summary, the authors’ at times confusing presentation has helped to perpetuate the mythology that clinical syndromes characterised by mechanical ‘hyperalgesia’ can be distinguished and have obscured the valuable insight from the neurobiology of nociception of the common theme of central sensitisation. The big question to be addressed, especially from the clinical viewpoint, is what are the relative contributions of facilitated nociception and inhibited antinociception to this unifying conceptual explanatory model.
References Merskey H, Bogduk N, editors. Classification of chronic pain. Descriptions of chronic pain syndromes and definitions of pain terms, 2nd ed. Seattle, WA: IASP Press; 1994. Treede R-D, Rolke R, Andrews K, Magerl W. Pain elicited by blunt pressure: neurobiological basis and clinical relevance. Pain 2002;98: 235– 40. Wolfe F, Simons DG, Fricton J, et al. The fibromyalgia and myofascial pain syndromes: preliminary study of tender points and trigger points in patients with fibromyalgia, myofascial pain and no disease. J Rheumatol 1992;19:944–51.
M. Cohen St. Vincent’s Medical Centre, St. Vincent’s Campus, 376 Victoria Street, 2010 Sydney, Australia J. Quintner Wyllie Arthritis Centre, 6 Lemnos Street, Perth, WA 6008 Australia doi:10.1016/S0304-3959(03)00161-1
Reply to letter by Cohen and Quintner
In contrast to textbook chapters, that are supposed to represent more or less definite concepts in science, topical reviews in the journal PAIN such as our recent one on pressure pain (Treede et al., 2002) are intended to spawn a debate on the issues raised. For this reason, we are happy about the letter by Drs Cohen and Quintner, who point out that clinical syndromes characterised by enhanced painfulness to pressure stimuli at ‘trigger points’ or at ‘tender points’ are difficult to distinguish. We agree that a superficial look at the literature may lead to the conclusion that these two phenomena are different descriptions of the same entity. Even a careful literature search yields only few direct comparisons of the concepts behind trigger points in myofascial pain syndromes and tender points in fibromyalgia (e.g. Yunus et al., 1988; Schneider, 1995; Borg-Stein and Stein, 1996; Mense, 1999). The operational definitions, however, of tender points (Wolfe et al., 1990) and of trigger points (Travell and Simons, 1983) are distinct in that pressure onto trigger points may elicit both local and referred pain, whereas pressure onto tender points elicits local pain only. Universal agreement has not yet been reached on some other characteristics of trigger points (e.g. taut muscle bands, local twitch). By strictly applying these operational criteria, a few studies have tested for tender points and trigger points in the same patients. The majority of fibromyalgia patients exhibited some trigger points (Bengtsson et al., 1986; Granges and Littlejohn, 1993), but the trapezius and supraspinatus muscles which are usually tender in fibromyalgia hardly ever contained a trigger point (0 – 3%, Wolfe et al., 1992). Patients with myofascial pain exhibited some tender points, but the number of tender points was significantly less than in fibromyalgia patients and the mean tender point count did not meet the research diagnostic criteria for fibromyalgia (Wolfe et al., 1992). The majority of publications on musculoskeletal pain, however, contain only enough information to conclude that the patients studied fulfilled the research diagnostic criteria of one disease, but rarely enough information to check whether they also fulfil the diagnostic criteria of an alternative disease. More precise reporting of clinical data is essential to improve the dialogue between clinicians and basic scientists (Devor, 2003). Therefore, we join our Australian colleagues Cohen and Quintner in their appeal to clinicians, to be more critical and include both tender points and trigger points in their differential diagnosis. Only then it will become clear how different these two types of points really are. In their treatise on the mechanisms of hyperalgesia, Cohen and Quintner end with the suggestion that by analogy to secondary hyperalgesia central sensitisation may be inferred from hypersensitivity to mechanical stimuli in clinically normal tissue. We and others have suggested this