- Email: [email protected]
Cure by Fiat?
Ò
Letters to the Editor / PAIN 154 (2013) 2234–2238 [9] Suzan E, Midbari A, Treister R, Haddad M, Pud D, Eisenberg E. Oxycodone alters temporal summation but not conditioned pain modulation: preclinical findings and possible relations to mechanisms of opioid analgesia. PAINÒ 2013;154:1413–8. [10] Tesarz J, Gerhardt A, Schommer K, Treede RD, Eich W. Alterations in endogenous pain modulation in endurance athletes: an experimental study using quantitative sensory testing and the cold-pressor task. PAINÒ 2013;154:1022–9.
⇑
Wolfgang Freund Department of Diagnostic and Interventional Radiology, University Hospitals Ulm, Albert-Einstein-Allee 23, Ulm 89081, Germany Tel.: +49 73 138 5651. E-mail address: [email protected] (W. Freund) Uwe H. Schuetz Department of Diagnostic and Interventional Radiology, University Hospitals Ulm, Albert-Einstein-Allee 23, Ulm 89081, Germany Outpatient Rehabilitation Centre, University Hospitals Ulm, Pfarrer-Weiß-Weg 10, 89077 Ulm, Germany Frank Weber Department of Neurology, German Armed Forces Hospital, Oberer Eselsberg 40, 89081 Ulm, Germany Frank Birklein Department of Neurology, University Medical Centre Mainz, Langenbeckstraße 1, 55131 Mainz, Germany q
DOI of original article: http://dx.doi.org/10.1016/j.pain.2013.03.014 0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.07.014
Whiplash disorder—is definition?
it
a
valid
disease
To the Editor, The authors of a recent article published in PAIN report that a more extended therapy including exposure desensitization in whiplash-associated disorders was superior to an informational booklet alone because fear was more effectively reduced [7]. The importance of the fear-avoidance model in whiplash-associated disorders is underlined by the commentary of Meulders and Vlaeyen [6]. This assessment reflects a treatment-oriented perspective. It is evident that consideration of the patient’s fears regarding neck pain after a whiplash injury will improve the treatment results. However, the results do not clarify whether the treatment is truly necessary or ensues from civil legal disputes between individuals involved in traffic accidents. Grade I and II whiplash injuries describe neck pain after rearend collision without signs of structural damage. The long history of the whiplash disorder has taught us several things. Whiplashlike symptoms may occur if rear-end collision was simulated by accident-like play-back noise when sitting in a car [3], functional treatment and continuing pre-injury activities are better than immobilization [1,2], multimodal therapy is not superior to pharmaceutical treatment [4], usual care and simple advice are better than active management consultations and physiotherapy packages [5], treatment results are worse if outstanding liability claims exist [10], and reports of pain decrease substantially when liability claims do not exist [8]. In other words, we are dealing with a socially and legally defined pain condition that is exacerbated by patients’ expectations and medical overtreatment. Despite the importance of treatment
2235
optimization (in some individual cases), it appears more important to question the meaningfulness of the disease definition [9]. There is substantial evidence indicating that this definition is not valid. References [1] Borchgrevink GE, Kaasa A, McDonagh D, Stile TC, Haraldseth O, Lereim I. Acute treatment of whiplash neck sprain injuries. A randomized trial of treatment during the first 14 days after a car accident. Spine 1998;23:25–31 (Phila Pa 1976). [2] Cassidy JD, Carroll LJ, Côté P, Frank J. Does multidisciplinary rehabilitation benefit whiplash recovery? Results of a population-based incidence cohort study. Spine 2007;32:126–31 (Phila Pa 1976). [3] Castro WH, Schilgen M, Meyer S, Weber M, Peuker C, Wörtler K. Eur Spine J 1997;6:366–75. [4] Jull G, Kenardy J, Hendrikz J, Cohen M, Sterling M. Management of acute whiplash: A randomized controlled trial of multidisciplinary stratified treatments. PAINÒ 2013;154:1798–1806. [5] Lamb SE, Gates S, Williams MA, Williamson EM, Mt-Isa S, Withers EJ, Castelnuovo E, Smith J, Ashby D, Cooke MW, Petrou S. Underwood MR; Managing Injuries of the Neck Trial (MINT) Study Team. Emergency department treatments and physiotherapy for acute whiplash: a pragmatic, two-step, randomised controlled trial. Lancet 2013;381:546–56. [6] Meulders A, Vlaeyen JWS. Fear reduction in subacute whiplash-associated disorders: the royal road to recovery? PAINÒ 2013;154:330–1. [7] Robinson JP, Theodore BR, Dansie EJ, Wilson HD, Turk DC. The role of fear of movement in subacute whiplash disorders grades I and II. PAINÒ 2013;154:393–401. [8] Schrader H, Obelieniene D, Bovim G, Surkiene D, Mickeviciene D, Miseviciene I, Sand T. Natural evolution of late whiplash syndrome out side the medicolegal context. Lancet 1996;347:1207–11. [9] Schrader H, Stovner LJ, Eisenmenger W. Doubtful nosological validity of the chronic whiplash syndrome [in German]. Orthopäde 2012;41:147–52. [10] Sterling M, Hendrikz J, Kenardy J. Similar factors predict disability and posttraumatic stress disorder trajectories after whiplash injury. PAINÒ 2011;152:1272–8.
Marcus Schiltenwolf Nicholas A. Beckmann Department of Pain Management, University of Heidelberg, Schlierbacher Landstraße 200a, Heidelberg 69118, Germany Tel.: +49 62 219 66389; fax: +49 62 219 66389. E-mail addresses: [email protected] (M. Schiltenwolf), [email protected] (N.A. Beckmann) 0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.06.047
Cure by Fiat?
To the Editor, We appreciate the comments on our manuscript regarding the role of fear in whiplash-associated disorders (WADs) [8] provided by Drs. Schiltenwolf and Beckman. Although they make several points in their letter, it appears that their primary theses are that: (1) the case definition of WAD used in our study is not valid, and (2) the treatment patients in our study received might not be truly necessary. Drs. Schiltenwolf and Beckman invoke three pieces of evidence that could be viewed as supporting their initial thesis. First, they opine that there is typically no conclusive evidence of structural damage to the neck in patients with Grade I and Grade II WAD. Second, they allude to one study that found that some individuals reported neck pain after being subjected to simulated motor vehi-
2236
Ò
Letters to the Editor / PAIN 154 (2013) 2234–2238
cle collisions (MVCs) that did not put biomechanical stress on their necks [4]. Finally, they seem to be relying on the results of a paper reporting that in Lithuania, a country where financial compensation for MVC-related neck pain was not present, chronic WAD symptoms were no more prevalent among individuals who had sustained MVCs than among control subjects who had not been involved in MVCs [9]. We agree with Drs. Schiltenwolf and Beckman that there is no structural abnormality or other clear-cut biomarker in individuals with Grade I or II WAD [6,7,10]. This does create ambiguity, and sets the stage for misattribution or frank deception by individuals who have sustained MVCs. We also agree that a variety of psychological factors (eg, preinjury anxiety or tendency toward somatization [4]) and social factors (eg, financial compensation for injuries in MVCs [1,3]) can influence the prevalence of WAD and the responses of patients to treatment for WAD. These factors make it clear that a simple biomedical model that postulates straightforward linkages among injury stimulus, tissue damage, pain experience, pain reports to health professionals, and response to treatment is vastly oversimplified. We contend that this can be said of all health conditions and is the basis of the biopsychosocial model that emphasizes the relative contributions of psychosocial and behavioral factors as well as anatomy and physiology in all disease states eg, [5,11]. Apparently Drs. Schiltenwolf and Beckman believe that nonbiological contributors to WAD are so overwhelming that case definition of WAD [10] is invalid. But they do not offer any alternative term to apply to individuals who report neck pain after an MVC, and do not discuss the implications of dispensing with the term WAD. We assume that they accept the fact that some individuals report WAD symptoms and attribute them to an MVC. If research is to be conducted with these individuals, we believe that there needs to be a case definition that basically includes a stimulus (eg, an MVC) and a set of responses (primarily neck pain and headache). If the term WAD is to be purged from our lexicon, we would simply need to invent an alternative term to characterize these individuals. Thus, we believe that our understanding of WAD is not benefitted by eliminating the term from use. It should be noted that the factors that make WAD ambiguous— absence of a clear biomarker and presence of psychosocial influences—are also found in a wide variety of other pain disorders, including mechanical low back pain, fibromyalgia, and interstitial cystitis. Should the terms designating these disorders also be expunged from our vocabulary? If we followed this path, it would be very difficult to conduct research on many chronic pain disorders, or for health care providers to communicate with each other about subgroups of chronic pain patients. We believe it is much better to retain the terms we now have to describe WAD and other potentially ambiguous pain syndromes, but to recognize that the symptoms reported by patients who meet case definitions for these syndromes are affected by complex mixtures of biological, psychological, and social factors. Drs. Schiltenwolf and Beckman also question whether the treatments described in our paper are truly necessary. They do not clarify their rationale for their assertion. There are a few possibilities. One is that the treatments are unnecessary because patients’ symptoms will resolve uneventfully without treatment. Unfortunately, this does not appear to be the case. For the patients included in our study, symptoms had not resolved at up to 3 months after onset. Other evidence to date suggests that approximately 50% of individuals with WADs will continue to have significant symptoms 1 year after injury [2]. A second possibility is that the treatments we provided should not be offered because they are not effective. Our data refute this. Finally, Drs. Schiltenwolf and Beckman might assert that treatment directed toward WAD is mis-
guided because WAD does not exist. As discussed earlier, we reject this nihilistic view. In summary, we believe that we need a term to describe individuals with neck pain and related symptoms after MVCs, even as we recognize that their symptoms are influenced by multiple factors. Also, although we recognize that health care providers might make excessive use of diagnostic imaging and overtreat WAD patients, we believe that it is reasonable to provide ‘‘fearful’’ WAD patients with treatment that helps them cope with their symptoms and overcome their fears. Such treatment may be as simple as providing information as to the natural course and positive prognosis for the majority of patients, as was included in the information booklet that was provided to all patients in our study; however, for those whose symptoms persist, further intervention may be required.
Acknowledgements The study in the original article was funded by the National Institutes of Health (National Institute of Arthritis and Musculoskeletal and Skin Diseases, R01AR47298). The authors declare no conflicts of interest.
References [1] Carroll LJ, Holm LW, Hogg-Johnson S. Course and prognostic factors for neck pain in whiplash-associated disorders (WAD): results of the bone and joint decade 2000–2010 task force on neck pain and its associated disorders. Spine 2008;33:S83–92. [2] Carroll LJ, Holm LW, Hogg-Johnson S, Cassidy JD, Haldeman S, Nordin M, Hurwitz EL, Carragee EJ, van der Velde G, Peloso PM, Guzman J. Course and prognostic factors for neck pain in whiplash-associated disorders (WAD): results of the bone and joint decade 2000–2010 task force on neck pain and its associated disorders. J Manipulative Physiol Ther 2009;32:S97–S107. [3] Cassidy JD, Carroll LJ, Côté P, Lemstra M, Berglund A, Nygren A. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000;342:1179–86. [4] Castro WH, Meyer SJ, Becke ME, Nentwig CG, Hein MF, Ercan BI, Thomann S, Wessels U, Du Chesne AE. No stress—no whiplash? Prevalence of ‘‘whiplash’’ symptoms following exposure to a placebo rear-end collision. Int J Legal Med 2001;114:316–22. [5] Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull 2007;133:581–624. [6] Li Q, Shen H, Li M. Magnetic resonance imaging signal changes of alar and transverse ligaments not correlated with whiplash-associated disorders: a meta-analysis of case-control studies. Eur Spine J 2013;22:14–20. [7] Matsumoto M, Okada E, Ichihara D, Chiba K, Toyama Y, Fujiwara H, Momoshima S, Nishiwaki Y, Hashimoto T, Inoue T, Watanabe M, Takahata T. Prospective ten-year follow-up study comparing patients with whiplashassociated disorders and asymptomatic subjects using magnetic resonance imaging. Spine 2010;35:1684–90. [8] Robinson JP, Theodore BR, Dansie EJ, Wilson HD, Turk DC. The fear of movement in subacute whiplash-associated disorders grades I and II. PAINÒ 2013;154:393–401. [9] Schrader H, Obelieniene D, Bovim G, Surkiene D, Mickeviciene D, Miseviciene I, Sand T. Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet 1996;347:1207–11. [10] Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, Zeiss E. Scientific monograph of the quebec task force on whiplashassociated disorders: redefining ‘‘whiplash’’ and its management. Spine 1995;20:1S–73S. [11] Turk DC, Swanson KS, Wilson HD. The biopsychosocial model of pain and pain management. In: Ebert M, Kerns RD, editors. Behavioral and pharmacological pain management. New York: Cambridge University Press; 2011. p. 16–43.
James P. Robinson Department of Rehbilitation Medicine, University of Medicine, Seattle, United States E-mail address: [email protected] (J.P. Robinson)
Ò
Letters to the Editor / PAIN 154 (2013) 2234–2238
⇑
Dennis C. Turk Department of Anesthesiology & Pain Medicine, University of Washington, P.O. Box 356540, Seattle, WA 98195, United States ⇑ Tel.: +1 206/616 2626; fax: +1 206/543 2958. E-mail adddress: [email protected] (D.C. Turk)
0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.07.008
Does low intelligence really cause pain? The importance of measurement, methodology and implications when drawing conclusions
To the Editor: The recent publication by Gale and colleagues [1] described the first longitudinal study using a population cohort to examine the relationship between intelligence in childhood and the development of chronic widespread pain (CWP) in adulthood. Based on their findings, the authors concluded that lower intelligence in childhood is associated with an increased risk for CWP in adulthood. Research using large, population-based, longitudinal data is needed in pain research. While we commend the authors for using such a dataset, the authors’ operationalization of intelligence and interpretation of their results is of concern. The authors concluded that low childhood intelligence predates the development of and is an independent predictor of CWP in adulthood, suggesting that low intelligence may play a causal role in chronic pain in adults. This implication is further asserted in the accompanying commentary by Kingma and Rosmalen [2], wherein they commend the authors, stating ‘‘its longitudinal design enabled the researchers to study causal direction’’ (p. 2305). However, causation cannot and should not be inferred from a correlation study, even if it is a prospective correlation design. Therefore, we are concerned about the weight given to the conclusions drawn from the Gale [1] study, especially given the serious implications in the clinical and public domains. The authors’ suggestion that low intelligence is causally related to the development of chronic pain may result in individuals with low intelligence having their pain symptoms inadequately examined or inaccurately diagnosed as CWP or fibromyalgia. Conversely, the authors’ suggestion may also imply that chronic pain in adulthood is a function of low intelligence, which may lead individuals to categorize adults with chronic pain inappropriately as having low intelligence. In addition, we are also concerned about the authors’ operationalization of ‘‘intelligence’’ and their interpretation of group differences in this measure. The authors chose to operationalize intelligence as scores achieved on an 80-item test of verbal and nonverbal ability used by the National Foundation for Educational Research in the 1960s. The authors then transformed those scores into an IQ-type score with a mean of 100 and standard deviation of 15. The results of the study showed a significant difference between individuals with and without widespread pain on this constructed measure of intelligence. However, the scores obtained by both groups were extremely close to the mean of 100, with group means differing by only 3 points. Although this group difference
2237
may be statistically significant, the authors do not comment on its clinical significance. What does a 3-point difference actually mean? In modern and standardized tests of intelligence, such as the Weschler Adult Intelligence Test-IV (WAIS-IV) or the Weschler Intelligence Scale for Children-IV (WISC-IV), full-scale IQ scores ranging from 90 to 109 would all be considered to be within the average range. Even on these standardized and well-validated tests, however, the meaning of a difference of 3 points within this range would be difficult to interpret in the absence of participants’ scores on the composite measures comprising the full-scale IQ tests. For this reason, many clinicians no longer place as much emphasis on IQ scores but rather try to understand performance on intelligence tests through profile analysis, a process of comparing scores on subtests and composites in order to determine individual strengths and weaknesses [3]. A similar process could be applied to the scores obtained on the intelligence measure used in the Gale study [1], albeit with caution because the IQ scores were arbitrarily constructed and were obtained from a test that was not standardized with the same rigorous methodology as the WAIS-IV and WISC-IV. Large, population-based longitudinal studies are necessary to advance knowledge in the field of pain and should continue to be published in such highly regarded journals as PAINÒ. Although the study by Gale [1] used a dataset that has the potential to provide important new information to the field of pain research, the methodology of the study and the conclusions drawn are flawed and have serious implications for how pain is understood, both clinically and publicly. The authors of the paper and commentary ignore the fact that prospective population data are still correlational, so causal conclusions cannot be drawn from such a design. Additionally, the authors base their conclusions on a limited measure of intelligence that does not necessarily indicate a clinically meaningful difference between participants with and without pain. Strong conclusions based on this kind of design and methodology, such as those asserted in the paper and commentary, are irresponsible because of the negative implications they may have for how patients with pain are perceived by the public and treated by their health care providers.
References [1] Gale CR, Deary IJ, Cooper C, Batty GD. Intelligence in childhood and chronic widespread pain in middle age: the National Child Development Survey. PAINÒ 2012;153:2339–44. [2] Kingma EM, Rosmalen JGM. The power of longitudinal population-based studies for investigating the etiology of chronic widespread pain. PAINÒ 2012;153:2305–6. [3] Sattler JM, Dumont R, Rapport LJ. Interpreting the WISC-IV. In: Sattler JM, editor. Assessment of children: cognitive foundations. La Mesa, California: Jerome M. Sattler; 2008. p. 364–402.
Kristen M. Bailey Meghan G. Schinkel Dalhousie University and IWK Health Centre, Halifax, Nova Scotia, Canada Tel.: +1 902 470 6483. E-mail address: [email protected] (K.M. Bailey)
0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.06.046
Letters to the Editor / PAIN 154 (2013) 2234–2238 [9] Suzan E, Midbari A, Treister R, Haddad M, Pud D, Eisenberg E. Oxycodone alters temporal summation but not conditioned pain modulation: preclinical findings and possible relations to mechanisms of opioid analgesia. PAINÒ 2013;154:1413–8. [10] Tesarz J, Gerhardt A, Schommer K, Treede RD, Eich W. Alterations in endogenous pain modulation in endurance athletes: an experimental study using quantitative sensory testing and the cold-pressor task. PAINÒ 2013;154:1022–9.
⇑
Wolfgang Freund Department of Diagnostic and Interventional Radiology, University Hospitals Ulm, Albert-Einstein-Allee 23, Ulm 89081, Germany Tel.: +49 73 138 5651. E-mail address: [email protected] (W. Freund) Uwe H. Schuetz Department of Diagnostic and Interventional Radiology, University Hospitals Ulm, Albert-Einstein-Allee 23, Ulm 89081, Germany Outpatient Rehabilitation Centre, University Hospitals Ulm, Pfarrer-Weiß-Weg 10, 89077 Ulm, Germany Frank Weber Department of Neurology, German Armed Forces Hospital, Oberer Eselsberg 40, 89081 Ulm, Germany Frank Birklein Department of Neurology, University Medical Centre Mainz, Langenbeckstraße 1, 55131 Mainz, Germany q
DOI of original article: http://dx.doi.org/10.1016/j.pain.2013.03.014 0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.07.014
Whiplash disorder—is definition?
it
a
valid
disease
To the Editor, The authors of a recent article published in PAIN report that a more extended therapy including exposure desensitization in whiplash-associated disorders was superior to an informational booklet alone because fear was more effectively reduced [7]. The importance of the fear-avoidance model in whiplash-associated disorders is underlined by the commentary of Meulders and Vlaeyen [6]. This assessment reflects a treatment-oriented perspective. It is evident that consideration of the patient’s fears regarding neck pain after a whiplash injury will improve the treatment results. However, the results do not clarify whether the treatment is truly necessary or ensues from civil legal disputes between individuals involved in traffic accidents. Grade I and II whiplash injuries describe neck pain after rearend collision without signs of structural damage. The long history of the whiplash disorder has taught us several things. Whiplashlike symptoms may occur if rear-end collision was simulated by accident-like play-back noise when sitting in a car [3], functional treatment and continuing pre-injury activities are better than immobilization [1,2], multimodal therapy is not superior to pharmaceutical treatment [4], usual care and simple advice are better than active management consultations and physiotherapy packages [5], treatment results are worse if outstanding liability claims exist [10], and reports of pain decrease substantially when liability claims do not exist [8]. In other words, we are dealing with a socially and legally defined pain condition that is exacerbated by patients’ expectations and medical overtreatment. Despite the importance of treatment
2235
optimization (in some individual cases), it appears more important to question the meaningfulness of the disease definition [9]. There is substantial evidence indicating that this definition is not valid. References [1] Borchgrevink GE, Kaasa A, McDonagh D, Stile TC, Haraldseth O, Lereim I. Acute treatment of whiplash neck sprain injuries. A randomized trial of treatment during the first 14 days after a car accident. Spine 1998;23:25–31 (Phila Pa 1976). [2] Cassidy JD, Carroll LJ, Côté P, Frank J. Does multidisciplinary rehabilitation benefit whiplash recovery? Results of a population-based incidence cohort study. Spine 2007;32:126–31 (Phila Pa 1976). [3] Castro WH, Schilgen M, Meyer S, Weber M, Peuker C, Wörtler K. Eur Spine J 1997;6:366–75. [4] Jull G, Kenardy J, Hendrikz J, Cohen M, Sterling M. Management of acute whiplash: A randomized controlled trial of multidisciplinary stratified treatments. PAINÒ 2013;154:1798–1806. [5] Lamb SE, Gates S, Williams MA, Williamson EM, Mt-Isa S, Withers EJ, Castelnuovo E, Smith J, Ashby D, Cooke MW, Petrou S. Underwood MR; Managing Injuries of the Neck Trial (MINT) Study Team. Emergency department treatments and physiotherapy for acute whiplash: a pragmatic, two-step, randomised controlled trial. Lancet 2013;381:546–56. [6] Meulders A, Vlaeyen JWS. Fear reduction in subacute whiplash-associated disorders: the royal road to recovery? PAINÒ 2013;154:330–1. [7] Robinson JP, Theodore BR, Dansie EJ, Wilson HD, Turk DC. The role of fear of movement in subacute whiplash disorders grades I and II. PAINÒ 2013;154:393–401. [8] Schrader H, Obelieniene D, Bovim G, Surkiene D, Mickeviciene D, Miseviciene I, Sand T. Natural evolution of late whiplash syndrome out side the medicolegal context. Lancet 1996;347:1207–11. [9] Schrader H, Stovner LJ, Eisenmenger W. Doubtful nosological validity of the chronic whiplash syndrome [in German]. Orthopäde 2012;41:147–52. [10] Sterling M, Hendrikz J, Kenardy J. Similar factors predict disability and posttraumatic stress disorder trajectories after whiplash injury. PAINÒ 2011;152:1272–8.
Marcus Schiltenwolf Nicholas A. Beckmann Department of Pain Management, University of Heidelberg, Schlierbacher Landstraße 200a, Heidelberg 69118, Germany Tel.: +49 62 219 66389; fax: +49 62 219 66389. E-mail addresses: [email protected] (M. Schiltenwolf), [email protected] (N.A. Beckmann) 0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.06.047
Cure by Fiat?
To the Editor, We appreciate the comments on our manuscript regarding the role of fear in whiplash-associated disorders (WADs) [8] provided by Drs. Schiltenwolf and Beckman. Although they make several points in their letter, it appears that their primary theses are that: (1) the case definition of WAD used in our study is not valid, and (2) the treatment patients in our study received might not be truly necessary. Drs. Schiltenwolf and Beckman invoke three pieces of evidence that could be viewed as supporting their initial thesis. First, they opine that there is typically no conclusive evidence of structural damage to the neck in patients with Grade I and Grade II WAD. Second, they allude to one study that found that some individuals reported neck pain after being subjected to simulated motor vehi-
2236
Ò
Letters to the Editor / PAIN 154 (2013) 2234–2238
cle collisions (MVCs) that did not put biomechanical stress on their necks [4]. Finally, they seem to be relying on the results of a paper reporting that in Lithuania, a country where financial compensation for MVC-related neck pain was not present, chronic WAD symptoms were no more prevalent among individuals who had sustained MVCs than among control subjects who had not been involved in MVCs [9]. We agree with Drs. Schiltenwolf and Beckman that there is no structural abnormality or other clear-cut biomarker in individuals with Grade I or II WAD [6,7,10]. This does create ambiguity, and sets the stage for misattribution or frank deception by individuals who have sustained MVCs. We also agree that a variety of psychological factors (eg, preinjury anxiety or tendency toward somatization [4]) and social factors (eg, financial compensation for injuries in MVCs [1,3]) can influence the prevalence of WAD and the responses of patients to treatment for WAD. These factors make it clear that a simple biomedical model that postulates straightforward linkages among injury stimulus, tissue damage, pain experience, pain reports to health professionals, and response to treatment is vastly oversimplified. We contend that this can be said of all health conditions and is the basis of the biopsychosocial model that emphasizes the relative contributions of psychosocial and behavioral factors as well as anatomy and physiology in all disease states eg, [5,11]. Apparently Drs. Schiltenwolf and Beckman believe that nonbiological contributors to WAD are so overwhelming that case definition of WAD [10] is invalid. But they do not offer any alternative term to apply to individuals who report neck pain after an MVC, and do not discuss the implications of dispensing with the term WAD. We assume that they accept the fact that some individuals report WAD symptoms and attribute them to an MVC. If research is to be conducted with these individuals, we believe that there needs to be a case definition that basically includes a stimulus (eg, an MVC) and a set of responses (primarily neck pain and headache). If the term WAD is to be purged from our lexicon, we would simply need to invent an alternative term to characterize these individuals. Thus, we believe that our understanding of WAD is not benefitted by eliminating the term from use. It should be noted that the factors that make WAD ambiguous— absence of a clear biomarker and presence of psychosocial influences—are also found in a wide variety of other pain disorders, including mechanical low back pain, fibromyalgia, and interstitial cystitis. Should the terms designating these disorders also be expunged from our vocabulary? If we followed this path, it would be very difficult to conduct research on many chronic pain disorders, or for health care providers to communicate with each other about subgroups of chronic pain patients. We believe it is much better to retain the terms we now have to describe WAD and other potentially ambiguous pain syndromes, but to recognize that the symptoms reported by patients who meet case definitions for these syndromes are affected by complex mixtures of biological, psychological, and social factors. Drs. Schiltenwolf and Beckman also question whether the treatments described in our paper are truly necessary. They do not clarify their rationale for their assertion. There are a few possibilities. One is that the treatments are unnecessary because patients’ symptoms will resolve uneventfully without treatment. Unfortunately, this does not appear to be the case. For the patients included in our study, symptoms had not resolved at up to 3 months after onset. Other evidence to date suggests that approximately 50% of individuals with WADs will continue to have significant symptoms 1 year after injury [2]. A second possibility is that the treatments we provided should not be offered because they are not effective. Our data refute this. Finally, Drs. Schiltenwolf and Beckman might assert that treatment directed toward WAD is mis-
guided because WAD does not exist. As discussed earlier, we reject this nihilistic view. In summary, we believe that we need a term to describe individuals with neck pain and related symptoms after MVCs, even as we recognize that their symptoms are influenced by multiple factors. Also, although we recognize that health care providers might make excessive use of diagnostic imaging and overtreat WAD patients, we believe that it is reasonable to provide ‘‘fearful’’ WAD patients with treatment that helps them cope with their symptoms and overcome their fears. Such treatment may be as simple as providing information as to the natural course and positive prognosis for the majority of patients, as was included in the information booklet that was provided to all patients in our study; however, for those whose symptoms persist, further intervention may be required.
Acknowledgements The study in the original article was funded by the National Institutes of Health (National Institute of Arthritis and Musculoskeletal and Skin Diseases, R01AR47298). The authors declare no conflicts of interest.
References [1] Carroll LJ, Holm LW, Hogg-Johnson S. Course and prognostic factors for neck pain in whiplash-associated disorders (WAD): results of the bone and joint decade 2000–2010 task force on neck pain and its associated disorders. Spine 2008;33:S83–92. [2] Carroll LJ, Holm LW, Hogg-Johnson S, Cassidy JD, Haldeman S, Nordin M, Hurwitz EL, Carragee EJ, van der Velde G, Peloso PM, Guzman J. Course and prognostic factors for neck pain in whiplash-associated disorders (WAD): results of the bone and joint decade 2000–2010 task force on neck pain and its associated disorders. J Manipulative Physiol Ther 2009;32:S97–S107. [3] Cassidy JD, Carroll LJ, Côté P, Lemstra M, Berglund A, Nygren A. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000;342:1179–86. [4] Castro WH, Meyer SJ, Becke ME, Nentwig CG, Hein MF, Ercan BI, Thomann S, Wessels U, Du Chesne AE. No stress—no whiplash? Prevalence of ‘‘whiplash’’ symptoms following exposure to a placebo rear-end collision. Int J Legal Med 2001;114:316–22. [5] Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull 2007;133:581–624. [6] Li Q, Shen H, Li M. Magnetic resonance imaging signal changes of alar and transverse ligaments not correlated with whiplash-associated disorders: a meta-analysis of case-control studies. Eur Spine J 2013;22:14–20. [7] Matsumoto M, Okada E, Ichihara D, Chiba K, Toyama Y, Fujiwara H, Momoshima S, Nishiwaki Y, Hashimoto T, Inoue T, Watanabe M, Takahata T. Prospective ten-year follow-up study comparing patients with whiplashassociated disorders and asymptomatic subjects using magnetic resonance imaging. Spine 2010;35:1684–90. [8] Robinson JP, Theodore BR, Dansie EJ, Wilson HD, Turk DC. The fear of movement in subacute whiplash-associated disorders grades I and II. PAINÒ 2013;154:393–401. [9] Schrader H, Obelieniene D, Bovim G, Surkiene D, Mickeviciene D, Miseviciene I, Sand T. Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet 1996;347:1207–11. [10] Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, Zeiss E. Scientific monograph of the quebec task force on whiplashassociated disorders: redefining ‘‘whiplash’’ and its management. Spine 1995;20:1S–73S. [11] Turk DC, Swanson KS, Wilson HD. The biopsychosocial model of pain and pain management. In: Ebert M, Kerns RD, editors. Behavioral and pharmacological pain management. New York: Cambridge University Press; 2011. p. 16–43.
James P. Robinson Department of Rehbilitation Medicine, University of Medicine, Seattle, United States E-mail address: [email protected] (J.P. Robinson)
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Letters to the Editor / PAIN 154 (2013) 2234–2238
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Dennis C. Turk Department of Anesthesiology & Pain Medicine, University of Washington, P.O. Box 356540, Seattle, WA 98195, United States ⇑ Tel.: +1 206/616 2626; fax: +1 206/543 2958. E-mail adddress: [email protected] (D.C. Turk)
0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.07.008
Does low intelligence really cause pain? The importance of measurement, methodology and implications when drawing conclusions
To the Editor: The recent publication by Gale and colleagues [1] described the first longitudinal study using a population cohort to examine the relationship between intelligence in childhood and the development of chronic widespread pain (CWP) in adulthood. Based on their findings, the authors concluded that lower intelligence in childhood is associated with an increased risk for CWP in adulthood. Research using large, population-based, longitudinal data is needed in pain research. While we commend the authors for using such a dataset, the authors’ operationalization of intelligence and interpretation of their results is of concern. The authors concluded that low childhood intelligence predates the development of and is an independent predictor of CWP in adulthood, suggesting that low intelligence may play a causal role in chronic pain in adults. This implication is further asserted in the accompanying commentary by Kingma and Rosmalen [2], wherein they commend the authors, stating ‘‘its longitudinal design enabled the researchers to study causal direction’’ (p. 2305). However, causation cannot and should not be inferred from a correlation study, even if it is a prospective correlation design. Therefore, we are concerned about the weight given to the conclusions drawn from the Gale [1] study, especially given the serious implications in the clinical and public domains. The authors’ suggestion that low intelligence is causally related to the development of chronic pain may result in individuals with low intelligence having their pain symptoms inadequately examined or inaccurately diagnosed as CWP or fibromyalgia. Conversely, the authors’ suggestion may also imply that chronic pain in adulthood is a function of low intelligence, which may lead individuals to categorize adults with chronic pain inappropriately as having low intelligence. In addition, we are also concerned about the authors’ operationalization of ‘‘intelligence’’ and their interpretation of group differences in this measure. The authors chose to operationalize intelligence as scores achieved on an 80-item test of verbal and nonverbal ability used by the National Foundation for Educational Research in the 1960s. The authors then transformed those scores into an IQ-type score with a mean of 100 and standard deviation of 15. The results of the study showed a significant difference between individuals with and without widespread pain on this constructed measure of intelligence. However, the scores obtained by both groups were extremely close to the mean of 100, with group means differing by only 3 points. Although this group difference
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may be statistically significant, the authors do not comment on its clinical significance. What does a 3-point difference actually mean? In modern and standardized tests of intelligence, such as the Weschler Adult Intelligence Test-IV (WAIS-IV) or the Weschler Intelligence Scale for Children-IV (WISC-IV), full-scale IQ scores ranging from 90 to 109 would all be considered to be within the average range. Even on these standardized and well-validated tests, however, the meaning of a difference of 3 points within this range would be difficult to interpret in the absence of participants’ scores on the composite measures comprising the full-scale IQ tests. For this reason, many clinicians no longer place as much emphasis on IQ scores but rather try to understand performance on intelligence tests through profile analysis, a process of comparing scores on subtests and composites in order to determine individual strengths and weaknesses [3]. A similar process could be applied to the scores obtained on the intelligence measure used in the Gale study [1], albeit with caution because the IQ scores were arbitrarily constructed and were obtained from a test that was not standardized with the same rigorous methodology as the WAIS-IV and WISC-IV. Large, population-based longitudinal studies are necessary to advance knowledge in the field of pain and should continue to be published in such highly regarded journals as PAINÒ. Although the study by Gale [1] used a dataset that has the potential to provide important new information to the field of pain research, the methodology of the study and the conclusions drawn are flawed and have serious implications for how pain is understood, both clinically and publicly. The authors of the paper and commentary ignore the fact that prospective population data are still correlational, so causal conclusions cannot be drawn from such a design. Additionally, the authors base their conclusions on a limited measure of intelligence that does not necessarily indicate a clinically meaningful difference between participants with and without pain. Strong conclusions based on this kind of design and methodology, such as those asserted in the paper and commentary, are irresponsible because of the negative implications they may have for how patients with pain are perceived by the public and treated by their health care providers.
References [1] Gale CR, Deary IJ, Cooper C, Batty GD. Intelligence in childhood and chronic widespread pain in middle age: the National Child Development Survey. PAINÒ 2012;153:2339–44. [2] Kingma EM, Rosmalen JGM. The power of longitudinal population-based studies for investigating the etiology of chronic widespread pain. PAINÒ 2012;153:2305–6. [3] Sattler JM, Dumont R, Rapport LJ. Interpreting the WISC-IV. In: Sattler JM, editor. Assessment of children: cognitive foundations. La Mesa, California: Jerome M. Sattler; 2008. p. 364–402.
Kristen M. Bailey Meghan G. Schinkel Dalhousie University and IWK Health Centre, Halifax, Nova Scotia, Canada Tel.: +1 902 470 6483. E-mail address: [email protected] (K.M. Bailey)
0304-3959/$36.00 Ó 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.pain.2013.06.046