Foundation
The vestibulo-ocular circuit
Every eye sign in this chapter is a failure mode of the same circuit — from the hair cell at one end to the extraocular muscle at the other. Understand the wiring and the signs almost localise themselves.
From hair cell to eye muscle
When the head turns, the fluid inside the ear's three loops (the semicircular canals) sloshes and bends tiny hair cells. The brain reads this as movement and instantly moves the eyes the opposite way, so the world stays still on the retina. That reflex is the vestibulo-ocular reflex.
Two more sensors — the utricle and saccule — detect gravity and head tilt. Together with the canals they tell the brain which way is up, where the body is, and how the eyes should sit. When the wiring between these sensors and the eye muscles breaks, the eyes drift, misalign, or jerk — and we see vertigo's ocular signs.
Angular head acceleration deflects cupulae in the three orthogonally arranged semicircular canals; linear acceleration and tilt deflect otolith maculae in the utricle and saccule. Hair-cell signals travel via the vestibular nerve to the vestibular nuclei in the dorsal pontomedullary tegmentum, then through the medial longitudinal fasciculusto the abducens, trochlear, and oculomotor nuclei.4
Cerebellar input — particularly the flocculus, paraflocculus, and nodulus/uvula — calibrates the VOR's gain and time-constant and enables fixation suppression and smooth pursuit. The classical Zee studies of floccular ablation in primates quantified this role.3 The head impulse test directly probes horizontal-canal VOR integrity.1
Beyond the brainstem the system projects to the thalamus and to multimodal cortical vestibular areas — including the parieto-insular vestibular cortex and temporo-parietal junction — that subserve motion perception, graviception, and spatial orientation. Lesions here cause vertigo with disorientation and subtle ocular misalignments without obvious brainstem signs.2
Localising the lesion follows the wiring: a peripheral disorder (labyrinth or vestibular nerve) gives unidirectional, fixation-suppressed nystagmus without other neuro-ophthalmic signs; an MLF lesion gives an INO; a midline cerebellar lesion gives gaze-evoked or downbeat nystagmus and saccadic pursuit. The diagrammatic localiser below pins each sign to its most likely region.5
VOR intact — as the head yaws, the eyes counter-rotate by an equal and opposite amount, holding the target on the fovea.