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ARTICLES: T. Eberle, B. Doganci, H. H. Krämer, C. Geber, M. Fechir, W. Magerl, and F. Birklein Warm and cold complex regional pain syndromes: Differences beyond skin temperature? Neurology 2009; 72: 505-512 [Abstract] [Full text] [PDF]

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Warm and cold complex regional pain syndromes: Differences beyond skin temperature?

Almar W.A. Bruggeman, Margreet H. Oerlemans, Jan Paul M. Frölke   (9 June 2009)

Reply from the authors

Tatiana Eberle, Frank Birklein   (9 June 2009)

Warm and cold complex regional pain syndromes: Differences beyond skin temperature? 9 June 2009
Almar W.A. Bruggeman, UMC St Radboud Postbox 9101 6500 HB Nijmegen The Netherlands, Margreet H. Oerlemans, Jan Paul M. Frölke Send Correspondence to journal: Re: Warm and cold complex regional pain syndromes: Differences beyond skin temperature? a.bruggeman{at}chir.umcn.nl Almar W.A. Bruggeman, et al.	Eberle et al. investigated the difference between patients with primarily warm and cold complex regional pain syndrome (CRPS). [1] In this study, 25% of the patients were excluded due to inconsistent findings at CRPS onset. To further validate this classification, a reassessment of 80% of the 50 patients was done 6 weeks later and warm and cold switch was not observed. We prospectively investigated 26 patients (19 women, 7 men) with acute CRPS—according to Bruehl/IASP criteria—3-12 months after the trigger event. Patients confirmed that their affected limb felt warmer, colder, or indistinct compared to the unaffected limb. Measurements of skin temperature were routinely measured with an infrared thermometer (GENIUS™ Covidien, Mansfield MA) according to an established method. [2] During a 12-week followup, patients’ skin temperatures were measured using an advanced infrared thermometer (DermaTemp™ Exergen, Newton MA). Each patient visited six times with at least one week between visits. In our measurement protocol, there were 13 different measurement sites distally on each limb, resulting in 26 sites per patient. On each site, the temperature was measured twice, averaged, and then the 13 averages were averaged again. The two temperature averages between affected and unaffected side were then compared during each visit. Of 26 patients included in our study, 15 (58%) presented with unclear or inconsistent signs and symptoms of warm or cold CRPS. The remaining 11 patients included 7 patients presenting with cold CRPS who had a mean temperature of -1,8 °C (SD 1,34) and 4 patients with warm CRPS with a mean temperature of +1,4 °C (SD 0,90) compared to the unaffected extremity. During follow-up, two patients out of eleven who had experienced either warm or cold CRPS switched from warm to cold CRPS or vice versa. The other nine did not switch during the follow-up period. In contrast with the Eberle et al.’s results, we suggest that patients with primarily warm or cold CRPS only exist in a minority of patients (30% instead of 75%). Small subgroups can be identified using any diagnostic tool from Bruehl et al.’s criteria. [3] It is unlikely that warm or cold CRPS imply different pathophysiology. We consider any objective difference in skin temperature as vasomotor instability in the diagnostic assessment of patients suspected of CRPS. Therefore, temperature measurements are an important tool. References 1. Eberle T, Doganci B, Krämer HH et al. Warm and cold complex regional pain syndromes: differences beyond skin temperature? Neurology 2009;72:505-512. 2. Oerlemans HM, Graff MJ, Dijkstra-Hekkink JB, de Boo T, Goris RJ, Oostendorp RA. Reliability and normal values for measuring the skin temperature of the hand with an infrared tympanic thermometer: a pilot study. J Hand Ther 1999;12:284-290. 3. Bruehl S, Harden RN, Galer BS, et al. External validation of IASP diagnostic criteria for Complex Regional Pain Syndrome and proposed research diagnostic criteria. Pain 1999;81:147–154. Disclosure: The authors report no disclosures.
Reply from the authors 9 June 2009
Tatiana Eberle, Johannes Gutenberg University Mainz Heidelberg, Germany, Frank Birklein Send Correspondence to journal: Re: Reply from the authors eberlet{at}uni-mainz.de Tatiana Eberle, et al.	Bruggeman et al. concluded that only 30-40% of their patients—in contrast to 75% in our investigation—could be classified as “warm” or “cold” (11/26) depending on repeatedly assessed skin temperature. If the patients were classified once, a minority of their patients (2/11) switched from warm to cold and vice versa. The authors concluded that warm and cold skin might be the result of vasomotor instability but that it was not indicative of distinct CRPS pathophysiology. These findings seem to conflict with our conclusion yet this may not be the case. In a recent study employing long-term ambulatory skin temperature measurement, Krumova et al. repeatedly showed that acute CRPS patients mainly present with “warm” skin turning into “indifferent” or “cold” when CRPS lasts longer. [4] Our patients might be more acute and more homogeneous (21 +/- 3 wks CRPS duration). Further understanding CRPS pathophysiology will likely negate imprecise neurological denominations like vasomotor instability. There are peripheral cytokine, peptides, and nociceptor changes that may indicate inflammatory symptoms. [5] There are also CNS changes becoming more apparent during the course of CRPS. [6] One consequence of CNS changes is pathological cross-modality sympathetic activation (i.e., during motor imagery). [7] Alternatively, cold skin has been explained by endothelial dysfunction. [8] In CRPS, these pathomechanisms might coincide leading to alternating vasodilation and vasoconstriction (vasomotor instability) as we discussed. [1] This may indicate that skin temperature could provide a clue to individual CRPS pathophysiology. We agree with Bruggeman et al. that skin temperature difference alone is insufficient to explain the different CRPS facets. Nevertheless, it is easy to assess, which makes it an important tool for CRPS differentiation and diagnosis. [4]. References 4. Krumova EK, Frettloh J, Klauenberg S, Richter H, Wasner G, Maier C. Long-term skin temperature measurements - A practical diagnostic tool in complex regional pain syndrome. Pain 2008;140:8-22. 5. Birklein F, Kingery WS. Complex regional pain syndrome: A loss of inhibition? Pain 2009; 142:177-178. 6. Maihöfner C, Handwerker HO, Neundorfer B, Birklein F. Cortical reorganization during recovery from complex regional pain syndrome. Neurology 2004;63:693-701. 7. Moseley GL, Zalucki N, Birklein F, Marinus J, van Hilten JJ, Luomajoki H. Thinking about movement hurts: the effect of motor imagery on pain and swelling in people with chronic arm pain. Arthritis Rheum. 2008;59:623-631. 8. Groeneweg JG, Huygen FJ, Heijmans-Antonissen C, Niehof S, Zijlstra FJ. Increased endothelin-1 and diminished nitric oxide levels in blister fluids of patients with intermediate cold type complex regional pain syndrome type 1. BMC.Musculoskelet.Disord. 2006;7:91. Disclosures The original study was Supported by the German Research Foundation, DFG Bi 579/1 and Bi 579/4 to F.B., and by the Bundesministerium für Bildung und Forschung (DFNS; Grant: 01EM0506). Dr. Birklein received honoraria from serving on the scientific advisory boards of Lilly, Germany, UCB and Pfizer Fibromyalgia, Germany. He received honoraria for presentations from Lilly, UCB, Pfizer, Grünenthal and NeuroUpdate, he is a field editor of the European Journal of Pain, and member of the editorial boards of Neurology, Pain medicine and The Open Neurology Journal. Dr. Eberle reports no disclosures.