The disorder
Pathophysiology & anatomy
An inflamed vestibular nerve, almost always its superior division. The anatomy is not trivia — it predicts exactly which bedside and laboratory tests will be abnormal.
What inflames the nerve
The balance nerve of one ear becomes inflamed, most likely from a virus — often after a cold or other viral illness. The inflamed nerve sends faulty balance signals, so the brain thinks the head is spinning even when it is still.
The leading hypothesis is reactivation of latent herpes simplex virus type 1in the vestibular ganglion (Scarpa’s ganglion), producing inflammation and a sudden unilateral loss of vestibular tone.1 The abrupt asymmetry between the two labyrinths is what generates the vertigo and the spontaneous nystagmus.
Supporting evidence includes HSV-1 DNA and latency-associated transcripts in human vestibular ganglia and the clustering of cases — though a causal viral link remains unproven, and “neuritis” is partly a term of convenience.1 The newer term acute unilateral vestibulopathy sidesteps the aetiological claim while keeping the same clinical entity.3
Why the superior division fails
The nerve splits into a superior and an inferior division, each serving different end-organs. The superior division runs a longer, narrower bony channel and is the one usually affected — so neuritis is typically a superior vestibulopathy. Toggle the divisions to see which organs each supplies and which tests it drives:
This anatomy explains a clinically important quirk: the superior division does not supply the posterior canal, which is left intact. Dislodged otoconia can later settle in that spared canal and produce a secondary BPPV — see the BPPV chapter. For the underlying canal and otolith physiology, see Anatomy and Physiology.
When it becomes labyrinthitis
If inflammation reaches the cochlea, hearing loss and tinnitus join the vertigo — this is labyrinthitis. It may be serous (viral, the commonest), suppurative (bacterial, spreading from otitis media or meningitis — an emergency), or autoimmune. The distinction matters because suppurative labyrinthitis needs urgent antibiotics and source control, not reassurance and rehabilitation.
How the brain recovers
The peripheral deficit may never fully repair, yet most patients recover — through central vestibular compensation, in which the brain recalibrates to the asymmetry. This is why activity and vestibular rehabilitation help and why prolonged bed rest and sedatives hinder, and why the vHIT gain can stay low even in a patient who feels well.2
Key points
- Presumed reactivation of latent HSV-1 in Scarpa’s ganglion inflames the vestibular nerve.
- The superior division is usually affected — explaining the abnormal horizontal vHIT, caloric and ocular VEMP with a spared cervical VEMP.
- The spared posterior canal can later seed a secondary BPPV.
- Cochlear involvement makes it labyrinthitis; suppurative labyrinthitis is an emergency.
- Recovery is by central compensation, not peripheral repair.