A case of pain, motor impairment, and swelling of the arm after acute herpes zoster infection

Förster, Matti; Umnus, Astrid; Siebrecht, Dieter; Baron, Ralf; Wasner, Gunnar

doi:10.1016/j.pain.2012.08.005

Cited by 11 publications

(8 citation statements)

References 22 publications

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“…Interestingly, GBS is more frequent after certain viral and bacterial infections, for example, cytomegalovirus and Campylobacter jejuni , presumably due to the cross-reactivity of disease-fighting antibodies with neuronal cell proteins [5, 43]. Limited clinical evidence suggests a similar postinfectious (or postimmunization) preponderance of CRPS cases [12, 49, 57, 63]. In the case of paraneoplastic neuropathies, autoimmunity involving anti-Hu and anti-CV2/CRIMP5 antibodies have been linked to sensory changes involving pain [31].…”

Section: Discussionmentioning

confidence: 99%

Autoimmunity contributes to nociceptive sensitization in a mouse model of complex regional pain syndrome

Guo

Shi

et al. 2014

Pain

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Complex regional pain syndrome (CRPS) is a painful, disabling, chronic condition whose etiology remains poorly understood. The recent suggestion that immunological mechanisms may underlie CRPS provides an entirely novel framework in which to study the condition and consider new approaches to treatment. Using a murine fracture/cast model of CRPS, we studied the effects of B-cell depletion using anti-CD20 antibodies or by performing experiments in genetically B-cell-deficient (µMT) mice. We observed that mice treated with anti-CD20 developed attenuated vascular and nociceptive CRPS-like changes after tibial fracture and 3 weeks of cast immobilization. In mice with established CRPS-like changes, the depletion of CD-20+ cells slowly reversed nociceptive sensitization. Correspondingly, µMT mice, deficient in producing immunoglobulin M (IgM), failed to fully develop CRPS-like changes after fracture and casting. Depletion of CD20+ cells had no detectable effects on nociceptive sensitization in a model of postoperative incisional pain, however. Immunohistochemical experiments showed that CD20+ cells accumulate near the healing fracture but few such cells collect in skin or sciatic nerves. On the other hand, IgM-containing immune complexes were deposited in skin and sciatic nerve after fracture in wild-type, but not in µMT fracture/cast, mice. Additional experiments demonstrated that complement system activation and deposition of membrane attack complexes were partially blocked by anti-CD20+ treatment. Collectively, our results suggest that CD20-positive B cells produce antibodies that ultimately support the CRPS-like changes in the murine fracture/cast model. Therapies directed at reducing B-cell activity may be of use in treating patients with CRPS.

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Section: Discussionmentioning

confidence: 99%

Autoimmunity contributes to nociceptive sensitization in a mouse model of complex regional pain syndrome

Guo

Shi

et al. 2014

Pain

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“…One core feature is painful mono-or oligo-post-traumatic neuropathy in 1 extremity [31]. Ninety percent of cases are triggered by trauma (sprains/strains, fractures, iatrogenic), and some of the nontraumatic cases follow known or suspected focal nerve lesions, for example infarction, entrapment, and shingles [32,33]. Complex regional pain syndrome (CRPS) is definitionally distinguished from post-traumatic neuralgia by additional visible signs, specifically "edema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain" [34] (Fig.…”

Section: Complex Regional Pain Syndromementioning

confidence: 99%

Immunotherapy Prospects for Painful Small-fiber Sensory Neuropathies and Ganglionopathies

Oaklander

2016

Neurotherapeutics

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The best-known peripheral neuropathies are those affecting the large, myelinated motor and sensory fibers. These have well-established immunological causes and therapies. Far less is known about the somatic and autonomic "small fibers"; the unmyelinated C-fibers, thinly myelinated A-deltas, and postganglionic sympathetics. The small fibers sense pain and itch, innervate internal organs and tissues, and modulate the inflammatory and immune responses. Symptoms of small-fiber neuropathy include chronic pain and itch, sensory impairment, edema, and skin color, temperature, and sweating changes. Small-fiber polyneuropathy (SFPN) also causes cardiovascular, gastrointestinal, and urological symptoms, the neurologic origin of which often remains unrecognized. Routine electrodiagnostic study does not detect SFPN, so skin biopsies immunolabeled to reveal axons are recommended for diagnostic confirmation. Preliminary evidence suggests that dysimmunity causes some cases of small-fiber neuropathy. Several autoimmune diseases, including Sjögren and celiac, are associated with painful small-fiber ganglionopathy and distal axonopathy, and some patients with "idiopathic" SFPN have evidence of organ-specific dysimmunity, including serological markers. Dysimmune SFPN first came into focus in children and teenagers as they lack other risk factors, for example diabetes or toxic exposures. In them, the rudimentary evidence suggests humoral rather than cellular mechanisms and complement consumption. Preliminary evidence supports efficacy of corticosteroids and immunoglobulins in carefully selected children and adult patients. This paper reviews the evidence of immune causality and the limited data regarding immunotherapy for small-fiberpredominant ganglionitis, regional neuropathy (complex regional pain syndrome), and distal SFPN. These demonstrate the need to develop case definitions and outcome metrics to improve diagnosis, enable prospective trials, and dissect the mechanisms of small-fiber neuropathy.

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“…Some viral infections including hepatitis C, herpes zoster, leprosy, human immunodeficiency virus, and parvovirus B19 have been associated with CRPS in the literature (5)(6)(7)12,13). But the exact pathogenesis of how the infection initiates CRPS is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Most common predisposing factor of CRPS type 1 is reported as trauma (1,2). Infectious diseases such as hepatitis C, herpes zoster, and leprosy are able to cause CRPS type 1 (5)(6)(7). Although, some cases CRPS type 1 cases associated with hepatitis B vaccination, there is no clear evidence on the relationship between CRPS type 1 and hepatitis B infection (8).…”

Section: Introductionmentioning

confidence: 99%

Can hepatitis B infection be a risk factor for Complex Regional Pain Syndrome Type 1?

Kozanoğlu¹

2020

Erciyes Med J

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A case of pain, motor impairment, and swelling of the arm after acute herpes zoster infection

Cited by 11 publications

References 22 publications

Autoimmunity contributes to nociceptive sensitization in a mouse model of complex regional pain syndrome

Autoimmunity contributes to nociceptive sensitization in a mouse model of complex regional pain syndrome

Immunotherapy Prospects for Painful Small-fiber Sensory Neuropathies and Ganglionopathies

Can hepatitis B infection be a risk factor for Complex Regional Pain Syndrome Type 1?

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