Neuro-Ophthalmology — Practice

Question 1

A bitemporal hemianopia respecting the vertical midline localises the lesion to

Accepted Answer

B

Question 2

Which will produce a relative afferent pupillary defect?

Accepted Answer

C

Question 3

A 45-year-old has acute painful ptosis with the eye down and out and a dilated unreactive pupil. Next step?

Accepted Answer

B

Question 4

A 72-year-old has sudden visual loss, a chalky white swollen disc, jaw claudication and an ESR of 96. What is done first?

Accepted Answer

B

Question 5

Which favours papilloedema over papillitis?

Accepted Answer

C

Question 6

A 28-year-old has simultaneous bilateral severe optic neuritis with poor recovery. Why is this not managed as typical demyelinating disease, and what testing is required?

Accepted Answer

Because bilateral simultaneous involvement, severity and poor recovery are all atypical features, and atypical optic neuritis is now recognised as a group of distinct diseases rather than one condition.

Typical demyelinating optic neuritis is unilateral, painful, moderate in severity and recovers substantially without treatment, so observation or intravenous methylprednisolone is sufficient and the main question is the risk of multiple sclerosis.

Aquaporin-4 antibody positivity indicates neuromyelitis optica spectrum disorder. Attacks are severe, recovery is poor, and untreated relapses accumulate disability rapidly, so long-term immunosuppression is required rather than watchful waiting. The antibody is highly specific at any titre.

Myelin oligodendrocyte glycoprotein antibody disease is a third entity. It often produces marked disc swelling, recovers better than neuromyelitis optica, and relapses characteristically as steroids are withdrawn, which shapes the taper.

The 2023 MOGAD criteria require a cell-based assay and attach diagnostic weight to titre, because high-titre results carry a positive predictive value around 90 percent while low-titre results fall to roughly 53 percent and need supporting clinical and radiological features.

The practical consequence is that a young patient with severe bilateral disease should not simply be given steroids and reviewed, because the disease that most needs identifying is the one that will blind them at the next relapse.

Question 7

Explain anatomically why compression of the third nerve involves the pupil while ischaemia spares it.

Accepted Answer

Because the parasympathetic and motor fibres occupy different positions within the nerve and are supplied differently.

The pupillomotor parasympathetic fibres travel superficially, on the dorsomedial surface of the nerve, immediately beneath the epineurium. The somatic motor fibres to the extraocular muscles and levator occupy the central core.

A compressive lesion, most importantly a posterior communicating artery aneurysm, acts from outside inward. The superficial fibres are therefore the first to be affected, and pupil involvement appears early, often before the ocular motility deficit is complete.

Ischaemia works in the opposite direction. The nerve is supplied by vasa nervorum that penetrate to the core, so a microvascular occlusion, as occurs in diabetes and hypertension, produces central infarction. The superficially placed parasympathetic fibres survive because they take oxygen directly by diffusion from the surrounding cerebrospinal fluid and pial vessels.

The clinical rule that follows is asymmetric in its safety. A painful pupil-involving palsy must be imaged the same day, because the alternative diagnosis is an aneurysm that may rupture.

A pupil-sparing palsy in an older patient with vascular risk factors is usually microvascular and recovers over about three months, but it still requires review, because an incomplete palsy from an enlarging aneurysm can involve the pupil days later. Failure to recover on schedule also mandates imaging.

Question 8

A patient cannot adduct the left eye, the right eye shows nystagmus on abduction, and convergence is normal. Localise the lesion and explain each finding.

Accepted Answer

The lesion is in the left medial longitudinal fasciculus, producing a left internuclear ophthalmoplegia.

Horizontal gaze is generated by the abducens nucleus, which does two things simultaneously. It drives the ipsilateral lateral rectus directly, and it sends interneurons across the midline and up the contralateral medial longitudinal fasciculus to the medial rectus subnucleus of the third nerve nucleus. This is what yokes the two eyes together.

A lesion of the left fasciculus interrupts the signal reaching the left medial rectus subnucleus. On attempted rightward gaze, the right lateral rectus contracts normally but the left eye fails to adduct.

The abducting nystagmus in the right eye is explained by the effort involved. Because the adducting eye is not moving, the brain increases the innervational drive to achieve gaze, and the abducting eye overshoots repeatedly, producing a dissociated nystagmus.

Convergence is preserved because it is generated by a separate near-response pathway that reaches the medial rectus subnucleus without traversing the fasciculus. This is the finding that distinguishes an internuclear ophthalmoplegia from a medial rectus palsy, in which adduction fails for both gaze and convergence.

The aetiology depends on the patient. Bilateral internuclear ophthalmoplegia in a young adult suggests multiple sclerosis, while a unilateral one in an older patient with vascular risk factors suggests brainstem infarction.

If a horizontal gaze palsy to one side coexists with the internuclear lesion, the paramedian pontine reticular formation is also involved and the picture is a one-and-a-half syndrome.

Question 9

A patient on antitubercular treatment reports gradual bilateral dimming of vision over two months. What is the likely cause, what is the field defect, and why is timing critical?

Accepted Answer

Ethambutol optic neuropathy is the likely cause, and it is the toxic optic neuropathy that matters most in India because antitubercular treatment is so widely prescribed.

The presentation is characteristic of the toxic group as a whole: bilateral, symmetrical, painless and gradual, with no red eye and no pain on eye movement to draw attention to the eye.

The field defect is a centrocaecal scotoma, meaning a defect extending from fixation to the blind spot, because the papillomacular bundle is selectively affected. Loss of red-green colour discrimination appears early and often precedes measurable acuity loss, which is why colour vision testing rather than Snellen acuity is used for monitoring.

Toxicity is related to both dose and duration, and the risk is higher with renal impairment because the drug is renally cleared.

Timing is critical because the damage is potentially reversible only if the drug is stopped early. Once axonal loss is established, recovery is limited or absent, and the disc becomes pale over the following weeks. Pallor takes four to six weeks to appear, so a normal disc at presentation is entirely compatible with significant damage already sustained.

This is why baseline and periodic visual acuity and colour vision assessment are built into the treatment regimen rather than being left to symptom reporting, since a patient adapting slowly to bilateral symmetrical loss frequently does not complain until it is advanced.

The differential includes vitamin B12 deficiency and tobacco-alcohol amblyopia, which produce an indistinguishable picture and may coexist in the same patient.

Practice — Neuro-Ophthalmology

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