Peripheral Contributions to Vestibular Migraine: A CSF-inner Ear Perspective

To the EditorI read the meta-analysis by Vosbeek et al. with great interest. Their synthesis shows that canal paresis on caloric testing and abnormal horizontal vHIT (with corrective saccades) occur far more often in Ménière’s disease (MD) than in vestibular migraine (VM), supporting the practical use of these peripheral tests in MD–VM differentiation. However, I am concerned that an interpretative drift toward “VM as a purely central disorder and peripheral findings as incidental” may take root. The pooled data indicate frequency differences, not absence, of peripheral involvement in VM1. VM pathophysiology is not settled. The classic review by Furman, Marcus, and Balaban frames VM as a disorder of central vestibular network modulation (brainstem monoaminergic nuclei and thalamo-cortical circuits) and emphasizes that mechanisms remain incomplete. That framework guides, but does not exclude, peripheral contributions2. A substantial experimental literature shows tight pressure coupling between CSF and perilymph via the cochlear aqueduct: CSF pressure steps transmit to perilymph with minimal delay in animals, and translational observations corroborate rapid inner-ear pressure changes after posture or ICP shifts. This CSF-to-perilymph pathway is well reviewed by Salt and Hirose and demonstrated by Carlborg and by Böhmer3–5. Clinically, small low-frequency air-bone gaps (≈5–15 dB at 250–500 Hz; occasionally at 4 kHz)—often with normal acoustic reflexes—are recognized in hydrops and have long been attributed to pressure-related oval-window mechanics (reduced stapes footplate mobility/altered impedance), low-frequency air-bone gaps (LFABG). Temporal-bone and experimental data support pressure-linked mechanisms underlying these small conductive components6. Although described most clearly in MD/ endolymphatic hydrops the mechanism is not disease-exclusive and offers a testable explanation for what we and others observe in a subset of VM patients with aural fullness At the bedside, many VM patients are female (30s–50 s) with overweight/obesity, have aural fullness and LFABG as above, and coexisting BPPV that responds to canalith repositioning. BPPV–migraine comorbidity is documented and suggests increased otoconial instability or altered otolith control in migraine biology. We also encounter atypical positional nystagmus (eg, persistent geotropic rotary nystagmus) that is often labeled “central,” yet may reflect peripheral otolith–canal interactions superimposed on central gain changes7. Otolith–velocity-storage coupling strengthens this link. Velocity storage (a brainstem–cerebellar integrator) is explicitly modulated by otolith cues and visual context; foundational work localizes and models this network8. VM cohorts demonstrate heightened self-motion sensitivity and frequency-dependent abnormalities paralleling velocity-storage dynamics, consistent with central–peripheral interplay rather than a purely cortical lesion9. Finally, IIH-spectrum overlap provides a unifying pressure link. Case-level and cohort observations show that IIH without papilledema can present with VM-like vestibular symptoms; given CSF-perilymph coupling, ICP fluctuations plausibly modulate labyrinthine mechanics and otolith function in susceptible patients. Our own experience includes VM-phenotype patients with venous outflow abnormalities/IIHWOP features, reinforcing this interface10. In interpreting Vosbeek and colleagues, I agree that caloric and vHIT abnormalities are less frequent in VM than in MD and therefore help differentiate the two. But the presence of such abnormalities in a non-trivial minority of VM patients should not be dismissed as coincidence. I propose a dual-site model: VM as a disorder of central network modulation that is susceptible to peripheral perturbations—including pressure-coupled perilymph changes and otolith dysregulation—in subsets of patients. This model aligns with (i) CSF-perilymph literature, (ii) pressure-linked oval-window mechanics, (iii) BPPV comorbidity, and (iv) IIH-spectrum associations1–10. Future work should prospectively pair caloric/vHIT with otolith metrics (SVV and/or VEMPs), rotational-chair/velocity-storage analyses, and ICP-sensitive proxies (posture, venous outflow imaging) to quantify central–peripheral coupling.