Sign · 2
INO, skew deviation & the ocular tilt reaction
When the eyes don't move as a pair, the brainstem is the suspect. Three related signs — INO, skew deviation, and the full ocular tilt reaction — are almost always central, and each pin-points a different part of the circuit.
Internuclear ophthalmoplegia
On looking to one side, both eyes should turn together. With internuclear ophthalmoplegia one eye fails to turn inwards (towards the nose) while the other goes outwards (towards the temple) and jerks. The lesion sits on a small white-matter tract called the medial longitudinal fasciculus, and a quick way to confirm it is that the patient can still cross their eyes to look at the tip of their nose (convergence is preserved).
The MLF carries interneurons from the abducens nucleus to the contralateral medial-rectus subnucleus of the oculomotor nucleus. On attempted horizontal gaze, the eye ipsilateral to the lesion fails to adduct while the contralateral eye abducts normally with a dissociated abducting nystagmus. Convergence is spared because the medial-rectus subnucleus also receives a supranuclear input that bypasses the MLF.
INO is essentially central. In the young it is multiple sclerosis (often bilateral — BINO);1 in the older patient it is most often a paramedian pontine or midbrain infarct. The pattern of accompanying torsional-vertical nystagmus mirrors the affected MLF level.2
Subtle INO — a small adduction lag without overt failure — is easily missed at the bedside; video-oculography can capture it. Look explicitly for associated brainstem signs (dysarthria, limb ataxia, hemiparesis) and for the one-and-a-half syndrome when the lesion extends to involve the adjacent PPRF or abducens nucleus. An INO with vertigo in any age group mandates MRI with diffusion-weighted sequences.
A left-sided MLF lesion. Horizontal gaze to the right: the left eye should adduct but lags — the medial-rectus drive from the contralateral abducens interneurons is cut. The right (abducting) eye reaches gaze fully but jerks with dissociated nystagmus. Convergence is spared because its supranuclear input bypasses the MLF.
Skew deviation and the ocular tilt reaction
Your inner ear contains a built-in level — the otolith organs — that tell the brain which way is up. When one side's signal is lost, the eyes can drift to different heights (skew deviation), the eyes rotate slightly inside their sockets (ocular torsion), and the head may tilt — all toward the side of the lesion. Together they are the ocular tilt reaction.
The graviceptive (otolith-ocular) pathway runs from the utricle, through the vestibular nuclei, up the MLF, and across the interstitial nucleus of Cajal in the midbrain. Unilateral interruption gives the OTR triad, with the lesioned-side eye sitting lower (hypotropic) on alternate cover testing. Halmagyi and colleagues described the OTR with peripheral vestibular lesions four decades ago,3 but the great majority of clinically encountered OTR sits centrally.
The “T” of HINTS — the test of skew — is the bedside marker. A vertical refixation on alternate cover-uncover testing in an acute vertigo patient is highly specific for a central cause, more so than early DWI-MRI.4,5
Small skews are easy to miss; the alternate cover test must be performed deliberately, with the patient fixating distance and the examiner watching for a vertical refixation as cover swaps. Maddox-rod or double-Maddox-rod quantification captures ocular torsion; the subjective visual vertical tilts with the graviceptive imbalance and can be tested with a bucket. The full OTR with vertigo localises to dorsal pons, lateral medulla, or paramedian thalamus and warrants urgent imaging.
- Head tilt toward the left
- Conjugate ocular torsion toward the left
- Skew — left eye hypotropic (lower)
The full ocular tilt reaction — head tilt, ocular torsion and skew — all run toward the lesion side, reflecting unilateral disruption of the otolith-ocular (graviceptive) pathway. The fovea-disc axis rotates with the torsion; alternate cover testing reveals the vertical skew.