TatianaEberle, Johannes Gutenberg University Mainz, Heidelberg, Germanyeberlet@uni-mainz.de
Frank Birklein
Submitted June 09, 2009
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.
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.