ArticleThe journal of headache and pain2025
A mouse model of classical trigeminal neuralgia via intradural compression of the trigeminal nerve.
Article in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Resting-state local brain functional synchronization after a single trigger-zone stimulation: with versus without evoked pain in classical trigeminal neuralgia patients.The journal of headache and pain · 2026Article
- Review
- Trigeminal neuralgia: from clinical challenges to molecular insights.The journal of headache and pain · 2026Review
- A modified FLIT-B model of trigeminal neuralgia reveals anterior cingulate cortex involvement in anxiety-like behavior in mice.The journal of headache and pain · 2026Article
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15 authors.
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Abstract
introductionTrigeminal neuralgia (TN) is a debilitating orofacial pain condition that adversely affects quality of life. Although heterogeneous, the most common form of TN is classical TN, characterized by paroxysmal bouts of pain in response to otherwise innocuous stimuli. It is believed that classical TN results from neurovascular compression of the trigeminal nerve. However, the underlying pathophysiology of TN is not well understood, thus limiting the development of targeted therapies. Current animal models lack translational relevance, particularly in their inability to replicate intradural nerve root compression, a core anatomic component of TN.
methodsWe developed a TN mouse model that achieves intradural nerve root compression via a retro-orbital approach confirmed by anatomic dissection and magnetic resonance imaging. To assess behavioral outcomes, we measured orofacial pain through facial wiping and interaction with a reward stimulus. Pharmacological responsiveness was tested using carbamazepine administration. Mechanistic studies included calcium imaging of trigeminal ganglia (TG), electrophysiologic recordings to measure resting membrane potential and rheobase, and immunohistochemical analysis of the TG.
resultsThe model elicited orofacial neuropathic pain, substantiated by increased facial wiping and reduced interaction with a reward stimulus, behaviors that suggest both spontaneous and evoked pain. Carbamazepine attenuated these behaviors, suggesting pharmacologic relevance to current TN treatment. Calcium imaging showed heightened spontaneous activity in the TG, and electrophysiologic recordings revealed an increased resting membrane potential and a reduced rheobase. Finally, immunohistochemical studies showed infiltration of CD45 + cells, demyelination and an increase in CGRP expression in the TG, supporting the presence of neuroinflammation after nerve root compression.
conclusionThese findings show that our approach replicates the anatomy and clinical presentation of classical TN in humans. This model may represent a new and robust platform for future mechanistic studies of TN and subsequent preclinical evaluation of therapies in mice.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.