ArticleThe journal of headache and pain2026
Posterior insular cortex hyperactivation drives vestibular migraine and comorbid anxiety.
Article in The journal of headache and pain, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundVestibular migraine, a debilitating disorder characterized by recurrent episodes of headache and vertigo, is frequently comorbid with persistent anxiety and depression. The neural mechanisms that integrate these disparate sensory and affective symptoms remain elusive.
findingsHere, we combined clinical characterization with a translational mouse model to identify the posterior insular cortex (pIC) as a critical hub driving the pathophysiology of vestibular migraine. In patients, anxiety and depression scores remained elevated interictally, suggesting a trait-like affective disturbance. Using a validated mouse model combining nitroglycerin (NTG) administration and rotarod vestibular stimulation, which recapitulates vestibular migraine-like phenotypes (hyperalgesia, balance deficits, and anxiety-like behaviors), we observed hyperactivity within the pIC. This region responded to both nociceptive and vestibular challenges. Chemogenetic inhibition of the pIC reversed hyperalgesia and vestibular-motor deficits. Notably, while acute inhibition did not affect anxiety-like behaviors, chronic inhibition produced a full rescue, including the affective component, paralleling the clinical persistence of mood symptoms. Conversely, chronic chemogenetic activation of the pIC was sufficient to promote all core phenotypes under a subthreshold NTG regimen combined with rotarod vestibular stimulus. Furthermore, systemic administration of the NMDA receptor antagonist memantine alleviated vestibular migraine-like symptoms and normalized pIC hyperactivity.
conclusionsOur results establish pIC hyperactivation as a causal neural substrate that converges nociceptive, vestibular, and affective processing in vestibular migraine, and identify pIC suppression as a promising therapeutic strategy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.