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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 (QST), 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). QST 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, QST did not detect or predict neuropathic pain. Gene expression of peptidylglycine α-amidating monooxygenase was higher in NL patients compared to 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 to NL-0 (p<0.05), and interleukin-1ß was higher, but IL-10 lower in NL-1 patients compared to 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 pro-inflammatory pattern.