Synopsis
Distinguish internuclear disconnection, nuclear and infranuclear ocular-motor palsy, and supranuclear gaze disorders from the pattern of saccades, pursuit, vestibulo-ocular responses and accompanying brainstem signs.
- Horizontal conjugate gaze requires coordinated activity between the pontine horizontal gaze centre, ipsilateral sixth-nerve nucleus and the contralateral third-nerve medial rectus subnucleus linked by the medial longitudinal fasciculus.
- Internuclear ophthalmoplegia causes impaired adduction of the eye on the side of the medial longitudinal fasciculus lesion with abducting nystagmus of the other eye during horizontal gaze.
- Convergence may be preserved in a classic posterior internuclear lesion, but variable convergence neither proves nor excludes the diagnosis and depends on lesion extent and examination technique.
- Bilateral internuclear ophthalmoplegia in a younger adult suggests demyelination, while sudden unilateral disease in an older adult suggests brainstem ischaemia; neither age rule is absolute.
- One-and-a-half syndrome combines an ipsilateral horizontal gaze palsy with internuclear ophthalmoplegia, leaving only abduction of the contralateral eye for horizontal voluntary gaze.
- One-and-a-half syndrome plus an ipsilateral lower motor neurone facial palsy is often called eight-and-a-half syndrome and localises a compact dorsal pontine lesion.
- A supranuclear gaze palsy may improve with the vestibulo-ocular reflex, whereas a nuclear or infranuclear palsy generally restricts both voluntary and reflex movement; only test the reflex safely and when neck movement is appropriate.
- A cerebral hemispheric destructive lesion often drives the eyes toward the lesion and away from the weak limbs; an irritative seizure focus may drive gaze away, but patterns vary and must be integrated with consciousness and imaging.
- Vertical gaze centres lie in the rostral midbrain. Upgaze or downgaze limitation with lid, pupil, convergence or consciousness changes raises midbrain, hydrocephalic, degenerative or drug causes.
- Differentiate binocular diplopia from oscillopsia and blur, record the direction of maximal separation and inspect alignment, pupils and lids before repeating fast pursuit or saccade manoeuvres.
- Myasthenia can mimic almost any painless ocular-motor palsy but does not cause an internuclear tract lesion; variability, fatigable ptosis and inconsistent anatomy support junctional testing.
- MRI can miss a very small early brainstem infarct, so persistent coherent signs and vascular tempo require stroke-specialist review despite unrevealing first imaging.
Key red flags
Adduction failure on one side with abducting nystagmus of the fellow eye during horizontal gaze supports an ipsilateral medial longitudinal fasciculus lesion, often ischaemic when onset is abrupt.
An ipsilateral horizontal gaze palsy plus ipsilateral INO permits only contralateral-eye abduction for horizontal voluntary gaze and localises to the pontine gaze centre or sixth nucleus plus adjacent MLF.
Upgaze palsy, convergence–retraction movements, light–near pupillary dissociation and lid retraction points to the dorsal rostral midbrain and warrants assessment for hydrocephalus, mass, demyelination or vascular disease.
Acute conjugate gaze preference with contralateral face-arm weakness, aphasia or neglect supports a cerebral hemispheric lesion. Deviation and ability to cross midline should be recorded before reperfusion treatment.
Variable ophthalmoplegia and ptosis changing with effort or time, without a stable tract pattern, can reflect myasthenia. Pupils and sensation remain normal, but bulbar and respiratory risk must be assessed.
Vertical ocular misalignment from imbalance in central otolith pathways can accompany brainstem or cerebellar disease and may change with gaze or head position; sudden skew within acute vestibular syndrome is a central warning.
Investigation priorities
Define conjugacy, direction, speed, range and nystagmus to separate internuclear, gaze-centre, nerve and junctional patterns.
Management branches
A conjugate gaze abnormality or internuclear pattern starts abruptly, especially with vertigo, ataxia, dysarthria, weakness or sensory change.
- Establish last known well, perform ABCDE and glucose and document pupils, eye positions, horizontal and vertical range, nystagmus, face, bulbar function, limbs, sensation and coordination.
- Contact the stroke service for urgent CT, vascular imaging and MRI planning; do not dismiss disabling diplopia because FAST is negative or non-contrast CT appears normal.
- Follow specialist reperfusion, swallowing and observation decisions and repeat the ocular-motor map after treatment or deterioration to identify evolving brainstem involvement.