Leukocytes in Complex Regional Pain Syndrome Type I

Tan, Edward; Oyen, Wim J.G.; Goris, R.J.A.

doi:10.1007/s10753-006-9015-x

Cited by 23 publications

(12 citation statements)

References 22 publications

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“…Furthermore, elevated levels of IL-8 and sTNF-RI/II indicate an association between CRPS1 and an inflammatory process. A recent finding suggests that there is an ongoing inflammatory response in the form of increased leukocyte accumulation on the involved side (Tan et al, 2005). Another finding supporting the theory of an excessive inflammatory reaction is the increased extravasation of indium-labelled immunoglobulin as a sign of increased capillary permeability to macromolecules (Oyen et al, 1993).…”

Section: Discussionmentioning

confidence: 96%

Tumor necrosis factor‐α and interleukin‐6 are not correlated with the characteristics of Complex Regional Pain Syndrome type 1 in 66 patients

Wesseldijk

Huygen

Heijmans-Antonissen

et al. 2008

European Journal of Pain

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It was previously shown in a group of 9 patients with complex regional pain syndrome type 1 (CRPS1) that levels of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are higher in blister fluid from the involved side. We hypothesize that local inflammation is responsible for the characteristics of CRPS1. The aim of this study was to confirm the previous observation in a large group of CRPS1 patients, repeating the measurement of TNF-alpha and IL-6 in blister fluid. Furthermore, we sought to determine whether these cytokines are responsible for the characteristics of CRPS1 and characterize the relationship between cytokine levels and duration of the disease. Sixty-six patients with CRPS1 participated. Skin blisters were artificially induced for measurement of cytokines in both extremities. The following disease characteristics were assessed: pain and differences in temperature, volume, and mobility between the extremities. TNF-alpha and IL-6 levels were significantly higher in blister fluid from the involved side. However, cytokine levels did not correlate with the characteristics or duration of the disease. Our findings confirm the presence of local inflammation in a population of 66 patients in the first 2 years of CRPS1. Proinflammatory cytokines seem to be only partly involved in the pathophysiology of CRPS1, as indicated by the lack of coherence between TNF-alpha and IL-6 levels and the signs and symptoms of inflammation and disease duration. Other inflammatory mediators and mechanisms, such as central sensitization, are probably involved in the early stages of CRPS1.

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Section: Discussionmentioning

confidence: 96%

Tumor necrosis factor‐α and interleukin‐6 are not correlated with the characteristics of Complex Regional Pain Syndrome type 1 in 66 patients

Wesseldijk

Huygen

Heijmans-Antonissen

et al. 2008

European Journal of Pain

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“…This study has demonstrated an increase in the percentage of the CD14 + CD16 + monocyte subgroup in individuals afflicted with CRPS. In addition, other investigators have reported mast cell involvement [47], leucocyte accumulation in the affected extremity [48] and impaired neutrophil function [49] in patients with CRPS. Thus, further evaluation of the role the immune system plays in the pathogenesis of CRPS is warranted, and may aid in elucidating disease mechanisms as well as the development of novel therapies for its treatment.…”

Section: Discussionmentioning

confidence: 96%

Elevated blood levels of inflammatory monocytes (CD14+CD16+) in patients with complex regional pain syndrome

Ritz

Alexander

Nogusa

et al. 2011

Clinical and Experimental Immunology

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SummaryComplex regional pain syndrome (CRPS) is a chronic pain disorder. Although its pathophysiology is not completely understood, neurogenic inflammation is thought to play a significant role. Microglia and astrocytes are activated following tissue injury or inflammation and have been reported to be both necessary and sufficient for enhanced nociception. Blood-borne monocytes/ macrophages can infiltrate the central nervous system (CNS) and differentiate into microglia resulting in hypersensitivity and chronic pain. The primary aim of this study was to evaluate the proportion of the proinflammatory CD14 + CD16 + monocytes as well as plasma cytokine levels in blood from CRPS patients compared to age-and gender-matched healthy control individuals. + CD16 + monocytes became elevated prior to or after developing CRPS. In either case, the elevation of blood proinflammatoty monocytes prior to the initiating event may predispose individuals for developing the syndrome whereas the elevation of blood proinflammatory monocytes following the development of CRPS may be relevant for its maintenance. Further evaluation of the role the immune system plays in the pathogenesis of CRPS may aid in elucidating disease mechanisms as well as the development of novel therapies for its treatment.

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“…Moreover, an exaggerated expression of pro‐inflammatory cytokines in cerebrospinal fluid and even in venous blood has been determined . An enhanced migration of injected radiolabelled leukocytes and human polyclonal nonspecific immunoglobulins toward CRPS‐affected locations was shown in scintigraphic studies . Furthermore, increased intima‐media thickness of the radial and brachial artery was measured with ultrasound in CRPS‐1 affected limbs compared to the intima‐media thickness in arteries of pain‐free controls, which suggests ongoing inflammation …”

Section: Endothelial Dysfunctionmentioning

confidence: 98%

Pathophysiological Mechanisms Involved in Vasomotor Disturbances in Complex Regional Pain Syndrome and Implications for Therapy: A Review

et al. 2015

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Complex regional pain syndrome (CRPS) is characterized by continuous pain, disproportional to the initial trauma. It usually spreads to the distal parts of the affected limb. Besides continuing pain, a mix of sensory, sudo- and vasomotor disturbances, motor dysfunction, and trophic changes is responsible for physical complaints. Vasomotor disturbance is characterized by changes in skin temperature and color. In CRPS patients with a cold extremity, a decrease in blood flow can cause decreased tissue saturation and tissue acidosis, resulting in ischemic pain. The pathophysiology of vasomotor disturbances is not completely understood. Temperature asymmetry is generally assumed as a result of disturbance in the sympathetic nervous system. Vasodilating drugs and sympathetic blockade have been cornerstones of therapy in cold CRPS for years. However, only a limited part of these patients improve on this kind of therapies. Research has shown a pivotal role for inflammation in the pathophysiology of CRPS. Inflammation can result in endothelial dysfunction. Endothelial function plays an important role in the local regulation of vascular tone. Endothelial dysfunction could be another mechanism responsible for the vasomotor disturbances in cold CRPS. An important goal in the treatment of cold-type CRPS is the restoration of a normal blood flow. Consequently it is important to distinguish the underlying pathophysiological mechanisms of vasomotor disturbances. A disturbance of the sympathetic nervous system may require another type of treatment than inflammation-induced endothelial dysfunction. Diagnostic tools to distinguish these underlying pathophysiological mechanisms of vasomotor disturbances would enable a mechanism-based treatment and improve clinical outcome.

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Leukocytes in Complex Regional Pain Syndrome Type I

Abstract: We found a significantly increased accumulation of leukocytes in patients with CRPS I. This is the first study to show a possible role for leukocytes in the pathophysiology of acute CRPS I.

Cited by 23 publications

References 22 publications

Tumor necrosis factor‐α and interleukin‐6 are not correlated with the characteristics of Complex Regional Pain Syndrome type 1 in 66 patients

Tumor necrosis factor‐α and interleukin‐6 are not correlated with the characteristics of Complex Regional Pain Syndrome type 1 in 66 patients

Elevated blood levels of inflammatory monocytes (CD14+CD16+) in patients with complex regional pain syndrome

Pathophysiological Mechanisms Involved in Vasomotor Disturbances in Complex Regional Pain Syndrome and Implications for Therapy: A Review

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