Ericson H, Abu Hamdeh S, Freyhult E, et al. - In view of the observation that all cases of trigeminal neuralgia (TN) can not be explained by a neurovascular conflict, and TN can exist without a neurovascular contact, researchers examined if aberrant inflammatory mechanisms are involved in the pathophysiology of TN. They assessed lumbar cerebrospinal fluid from patients with TN (n = 27) before and after microvascular decompression and from individuals without TN to analyze the levels of 92 protein biomarkers related to inflammation using Proximity Extension Assay technology. Following surgery, they observed a reduction in immunological protein levels in the cerebrospinal fluid from patients with TN towards levels observed in healthy controls. Two proteins—TRAIL and TNF-β—appeared to be of particular interest for TN. Thus, in TN, inflammatory activity may represent one relevant mechanism.