The disorder
Pathophysiology & mechanisms
No single lesion explains vestibular migraine. The best current model has the migraine machinery itself — not the inner ear — driving the vertigo, through networks that link pain and balance.
A network disorder, not an ear lesion
In migraine, the brain becomes temporarily over-excitable and over-sensitive to normal signals. In vestibular migraine, that same process spills into the brain’s balance pathways, producing dizziness or spinning. The inner ear is usually structurally normal — the problem is in how the brain is processing balance during an attack.
The leading model invokes the trigeminovascular system and cortical spreading depression — the substrates of migraine pain and aura — together with reciprocal connections between brainstem migraine generators and the central vestibular network (vestibular nuclei, thalamus, and multisensory cortex).1 Released neuropeptides, including CGRP, and central sensitisation are thought to modulate vestibular processing.
VM is best conceived as a channelopathy-influenced network disorder: heritable thresholds, shared neurotransmitter systems (serotonergic, CGRP-ergic), and bidirectional vestibulo-trigeminal connections. This explains the clinical hallmark that most confuses trainees — the vertigo and headache need not be time-locked — and the absence of progressive end-organ damage on long-term follow-up.3
Cortical spreading depression
The proposed substrate of aura — a slow wave of depolarisation crossing the cortex, trailed by suppression — also activates the trigeminovascular system, tying the cortical event to migraine pain and, in VM, to vestibular processing.1
Why headache and vertigo decouple
Because the vestibular symptoms arise from central network activation rather than from the headache pain pathway directly, the two can occur together, separately, or years apart. The Bárány criteria reflect this — they require a migraine link, not a headache during every attack.2 Many patients, especially midlife women, develop the vertigo only after their headaches have waned — scrub the age below to see the decoupling.
What stays normal
Unlike Ménière’s disease, VM does not cause progressive low-frequency sensorineural hearing loss; the audiogram remains essentially stable over years.3 Interictal examination is usually normal, though subtle central oculomotor signs or persistent motion sensitivity may be found — a point we return to in clinical features.
Key points
- VM is a network disorder of the migraine machinery, not an inner-ear lesion.
- Trigeminovascular activation, cortical spreading depression and central sensitisation are the proposed substrates.
- Central activation of vestibular pathways explains why vertigo and headache decouple in time.
- No progressive end-organ (cochlear) damage — a key contrast with Ménière’s.