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TNF‐alpha expression in painful and nonpainful neuropathies. (University Hospital, Basel, Switzerland) Neurology. 2001;56:1371–1377.
Author(s) -
Empl M.,
Renaud S.,
Erne B.,
Fuhr P.,
Straube A.,
SchaerenWiemers N.,
Steck A. J.
Publication year - 2001
Publication title -
pain practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 58
eISSN - 1533-2500
pISSN - 1530-7085
DOI - 10.1046/j.1533-2500.2001.1039_29.x
Subject(s) - medicine , allodynia , neurology , tumor necrosis factor alpha , cytokine , neuropathic pain , interleukin 10 , anesthesia , receptor , hyperalgesia , nociception , psychiatry
The objective of this study was to determine whether the cytokine tumor necrosis factor α (TNF‐α) acts as a pain mediator in neuropathic pain in humans. Patients with painful neuropathies showed a stronger TNF‐α immunoreactivity in myelinating Schwann cells relative to the epineurial background staining compared with patients with nonpainful neuropathy. Although there was no difference in sTNF‐RI levels between painful and nonpainful neuropathies, patients with a mechanical allodynia had elevated serums sTNF‐RI as compared to patients without allodynia. Conclude that TNF‐α expression of human Schwann cells may be up‐regulated in painful neuropathies. The elevation of sTNF‐RI in patients with centrally mediated mechanical allodynia suggests that systemic sTNF‐RI levels may influence central pain processing mechanisms.