%0 Journal Article %1 Held_2019 %A Held, Melissa %A Karl, Franziska %A Vlckova, Eva %A Rajdova, Aneta %A Escolano-Lozano, Fabiola %A Stetter, Christian %A Bharti, Richa %A Förstner, Konrad U. %A Leinders, Mathias %A Dusek, Ladislav %A Birklein, Frank %A Bednarik, Josef %A Sommer, Claudia %A Üceyler, Nurcan %D 2019 %I Ovid Technologies (Wolters Kluwer Health) %J PAIN %K myown %N 10 %P 2316--2327 %R 10.1097/j.pain.0000000000001623 %T Sensory profiles and immune-related expression patterns of patients with and without neuropathic pain after peripheral nerve lesion %U https://doi.org/10.1097%2Fj.pain.0000000000001623 %V 160 %X In this multicenter cross-sectional study, we determined sensory profiles of patients with (NL-1) and without neuropathic pain (NL-0) after nerve lesion and assessed immune-related systemic gene expression. Patients and matched healthy controls filled in questionnaires and underwent neurological examination, neurophysiological studies, quantitative sensory testing, and blood withdrawal. Neuropathic pain was present in 67/95 (71%) patients (NL-1). Tactile hyperalgesia was the most prominent clinical sign in NL-1 patients (P < 0.05). Questionnaires showed an association between neuropathic pain and the presence of depression, anxiety, and catastrophizing (P < 0.05 to P < 0.01). Neuropathic pain was frequently accompanied by other chronic pain (P < 0.05). Quantitative sensory testing showed ipsilateral signs of small and large fiber impairment compared to the respective contralateral side, with elevated thermal and mechanical detection thresholds (P < 0.001 to P < 0.05) and lowered pressure pain threshold (P < 0.05). Also, more loss of function was found in patients with NL-1 compared to NL-0. Pain intensity was associated with mechanical hyperalgesia (P < 0.05 to P < 0.01). However, quantitative sensory testing did not detect or predict neuropathic pain. Gene expression of peptidylglycine α-amidating monooxygenase was higher in NL patients compared with healthy controls (NL-1, P < 0.01; NL-0, P < 0.001). Also, gene expression of tumor necrosis factor-α was higher in NL-1 patients compared with NL-0 (P < 0.05), and interleukin-1ß was higher, but IL-10 was lower in NL-1 patients compared with healthy controls (P < 0.05 each). Our study reveals that nerve lesion presents with small and large nerve fiber dysfunction, which may contribute to the presence and intensity of neuropathic pain and which is associated with a systemic proinflammatory pattern.

@article{Held_2019, abstract = {In this multicenter cross-sectional study, we determined sensory profiles of patients with (NL-1) and without neuropathic pain (NL-0) after nerve lesion and assessed immune-related systemic gene expression. Patients and matched healthy controls filled in questionnaires and underwent neurological examination, neurophysiological studies, quantitative sensory testing, and blood withdrawal. Neuropathic pain was present in 67/95 (71%) patients (NL-1). Tactile hyperalgesia was the most prominent clinical sign in NL-1 patients (P < 0.05). Questionnaires showed an association between neuropathic pain and the presence of depression, anxiety, and catastrophizing (P < 0.05 to P < 0.01). Neuropathic pain was frequently accompanied by other chronic pain (P < 0.05). Quantitative sensory testing showed ipsilateral signs of small and large fiber impairment compared to the respective contralateral side, with elevated thermal and mechanical detection thresholds (P < 0.001 to P < 0.05) and lowered pressure pain threshold (P < 0.05). Also, more loss of function was found in patients with NL-1 compared to NL-0. Pain intensity was associated with mechanical hyperalgesia (P < 0.05 to P < 0.01). However, quantitative sensory testing did not detect or predict neuropathic pain. Gene expression of peptidylglycine α-amidating monooxygenase was higher in NL patients compared with healthy controls (NL-1, P < 0.01; NL-0, P < 0.001). Also, gene expression of tumor necrosis factor-α was higher in NL-1 patients compared with NL-0 (P < 0.05), and interleukin-1ß was higher, but IL-10 was lower in NL-1 patients compared with healthy controls (P < 0.05 each). Our study reveals that nerve lesion presents with small and large nerve fiber dysfunction, which may contribute to the presence and intensity of neuropathic pain and which is associated with a systemic proinflammatory pattern.}, added-at = {2019-10-23T16:36:42.000+0200}, author = {Held, Melissa and Karl, Franziska and Vlckova, Eva and Rajdova, Aneta and Escolano-Lozano, Fabiola and Stetter, Christian and Bharti, Richa and Förstner, Konrad U. and Leinders, Mathias and Du{\v{s}}ek, Ladislav and Birklein, Frank and Bednarik, Josef and Sommer, Claudia and Ü{\c{c}}eyler, Nurcan}, biburl = {https://www.bibsonomy.org/bibtex/21d7fb5a1a6a8ee33b193a9f6a586f143/cusysmed}, doi = {10.1097/j.pain.0000000000001623}, interhash = {0e7dccae158e70442508663c0db08316}, intrahash = {1d7fb5a1a6a8ee33b193a9f6a586f143}, journal = {{PAIN}}, keywords = {myown}, month = oct, number = 10, pages = {2316--2327}, publisher = {Ovid Technologies (Wolters Kluwer Health)}, timestamp = {2019-10-23T16:53:35.000+0200}, title = {Sensory profiles and immune-related expression patterns of patients with and without neuropathic pain after peripheral nerve lesion}, url = {https://doi.org/10.1097%2Fj.pain.0000000000001623}, volume = 160, year = 2019 }