89: Immune Profiling in Trigeminal Neuralgia: Altered Cytokine/Chemokine Signatures in CSF But Not Serum

Topic: Basic Science
Subtopic: Pain category (ICD-11), Chronic primary headache, , , Neuroimmunology, , , , , ,

Background and Aims: Trigeminal neuralgia (TN) is a debilitating neuropathic pain disorder traditionally attributed to neurovascular compression; however, this mechanism does not fully explain its clinical heterogeneity or persistent pain in a subset of patients. Increasing evidence implicates central neuroinflammatory processes in neuropathic pain, yet immune profiles in the cerebrospinal fluid (CSF) and serum of patients with TN remain poorly characterized. This exploratory study aimed to identify potential neuroimmune biomarkers by comparing CSF and serum immune mediator profiles in patients with TN.

Methods: We conducted a single-center cross-sectional study including 14 patients with TN, all classified as classical TN, and 19 non-pain controls. The TN group reported severe pain at enrollment (median numerical rating scale score 8). CSF samples were obtained from 14 TN patients and 10 controls, while serum samples were available from 10 TN patients and 9 controls. Concentrations of 48 immune mediators, including cytokines, chemokines, and growth factors, were quantified using a Luminex multiplex immunoassay platform. Group comparisons were performed using Mann-Whitney U tests with false discovery rate correction for multiple comparisons.

Results: Patients with TN reported severe pain (median numerical rating scale score 8), whereas controls reported no pain. Demographic characteristics, including age, sex and body mass index, were comparable between groups. Compared with controls, CSF from TN patients showed significantly elevated levels of multiple pro-inflammatory cytokines and chemokines, including TNF-α, IL-1β, IL-6, IL-8, IL-17, IFN-γ, CCL5, CXCL12, and macrophage migration inhibitory factor (MIF) (all false discovery rate-adjusted p < 0.05). In contrast, vascular endothelial growth factor (VEGF) concentrations were significantly reduced in the CSF of TN patients. No corresponding inflammatory alterations were observed in serum samples.

Conclusions: The compartment-specific dissociation between CSF and serum immune profiles supports the involvement of localized central neuroimmune mechanisms in TN. These findings identify CSF mediators as promising candidate biomarkers for mechanistic patient stratification and may guide the development of targeted neuroimmune therapies.

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Presenting Author: ziwei liu
Submitting Author: ziwei liu

Senior Author: tong liu

IASP 2026 Global Year theme of Neuropathic Pain: Yes