Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia.

Abstract

Trigeminal neuralgia (TN) is a chronic, debilitating facial pain disease causing stabbing pain attacks in the sensory distribution of the trigeminal nerve. The underlying pathophysiology of TN is incompletely understood, although microstructural abnormalities consistent with focal demyelination of the trigeminal nerve root have been shown in patients with TN. Studies of the cerebrospinal fluid (CSF) in patients with TN suggest an increased prevalence of inflammatory mediators, potentially implicating neuroinflammation in the pathophysiology of TN, as it has been implicated in other chronic pain conditions. This study aimed to further assess the inflammatory profile of CSF in TN. Cerebrospinal fluid was collected from 8 medically refractory patients with TN undergoing microvascular decompression surgery and 4 pain-free controls (2 with hemifacial spasm; 2 with normal pressure hydrocephalus). Cerebrospinal fluid was collected from the cerebellopontine angle cistern intraoperatively in the patients with TN. Inflammatory profiles of CSF samples were analyzed using a 71-plex cytokine and chemokine multiplex assay. Ten inflammatory markers were found to be significantly higher in TN CSF, and no analytes were significantly lower. Elevated factors can be classified into pro-inflammatory cytokines (IL-9, IL-18, and IL-33), chemokines (RANTES and ENA-78), the tumor necrosis factor superfamily (TRAIL and sCD40L), and growth factors (EGF, PDGF-AB/BB, and FGF-2). This study further supports the notion that neuroinflammation is present in TN, and that multiple molecular pathways are implicated.