"Squint & Pediatric Ophthalmology" — Practice

Question 1

A 2-year-old appears to have crossed eyes. The corneal light reflex is central in both eyes and there is no movement on cover testing. Diagnosis?

Accepted Answer

C

Question 2

What is the primary action of the superior oblique?

Accepted Answer

B

Question 3

A 3-year-old has convergent squint. Cycloplegic refraction shows plus 5 dioptres in each eye. Best initial treatment?

Accepted Answer

B

Question 4

A 5-year-old has moderate amblyopia and the family cannot achieve six hours of patching. What does the evidence support?

Accepted Answer

B

Question 5

A 4-month-old has watering and mucoid discharge, no photophobia, and a clear cornea of normal size. Management?

Accepted Answer

B

Question 6

Why does the same misalignment cause diplopia in an adult and amblyopia in a child?

Accepted Answer

Because the two cortices respond differently to conflicting input, and the difference is a matter of plasticity.

When the eyes are misaligned, the same object falls on non-corresponding retinal points, and the brain receives two images of the world that cannot be fused. Something has to give.

The mature cortex has fixed connections. It cannot suppress one eye's input selectively, so it presents both images to consciousness and the patient sees double. This is unpleasant and often disabling, but the eyes themselves remain fully functional, and if the misalignment is corrected the diplopia disappears immediately.

The immature cortex is still allocating territory between the two eyes, and that allocation is competitive and use-dependent. Faced with conflicting input, it suppresses one eye's signal actively at the cortical level. The double image disappears, which is why children do not complain.

The cost is that the suppressed eye stops driving cortical development. Its ocular dominance columns fail to consolidate, binocular cells are lost, and after the critical period closes the deficit is permanent regardless of how well the eye is subsequently aligned or focused.

The clinical corollary is uncomfortable. Absence of symptoms in a child with a squint is not reassurance but evidence that suppression is already occurring, and the longer it operates the less recoverable the loss.

This also explains why alternating squint is relatively benign, since the child suppresses each eye in turn and both continue to develop, and why constant unilateral squint is the pattern that blinds.

Question 7

Explain why glasses can cure accommodative esotropia, and why cycloplegia is essential to detect it.

Accepted Answer

Because accommodation and convergence are yoked, so a refractive problem is being converted into a motor one.

A hypermetropic eye focuses light behind the retina, and the child must accommodate continuously to bring the image forward and see clearly. Children can do this easily, since accommodative amplitude is enormous in the first decade, which is why a hypermetropic child usually has normal acuity.

Accommodation, convergence and miosis form the near reflex and are driven together. Sustained accommodative effort therefore produces sustained convergence drive, and if the child's fusional divergence cannot overcome it, the eyes turn inward.

Correcting the hypermetropia with spectacles removes the accommodative demand. With no accommodation required, no convergence is generated, and the eyes align. This is one of very few situations in medicine where a pair of glasses is a curative rather than a palliative treatment.

Cycloplegia is essential because that same powerful accommodation conceals the diagnosis. During ordinary refraction a child will accommodate through a plus lens, neutralising it, so several dioptres of hypermetropia can be missed entirely. Cycloplegic drops paralyse the ciliary muscle and reveal the true refractive state.

Missing this has real consequences. A child whose accommodative esotropia is not identified may be listed for surgery to correct a deviation that spectacles would abolish, and operating on it risks overcorrection once the accommodative component is later treated.

A related variant is high accommodation-to-convergence ratio esotropia, in which the deviation is greater at near than at distance, and bifocals reduce the accommodative demand for near work specifically.

Question 8

Why is axial length the outcome that matters in myopia control, and what does the current evidence support?

Accepted Answer

Because the harm of myopia comes from the physical dimensions of the eye rather than from the refractive error itself.

Myopia in children is overwhelmingly axial, meaning the eye is too long rather than the cornea or lens being too powerful. Spectacles or contact lenses correct the resulting refractive error completely, so a highly myopic child can have perfect corrected acuity while remaining at substantially raised lifetime risk.

That risk follows from elongation. A longer globe means the retina is stretched over a larger area, which thins it, predisposes to lattice degeneration and retinal breaks, and raises the risk of rhegmatogenous detachment. It also stretches the posterior pole, producing myopic maculopathy with lacquer cracks, choroidal neovascularisation and atrophy, and it is associated with a higher incidence of open angle glaucoma.

None of that is altered by correcting the refraction, which is why trials of myopia control report axial elongation as a primary outcome and why slowing elongation, not improving vision, is the therapeutic aim.

Two interventions have evidence. Time outdoors reduces the onset of myopia, and the effect appears related to light intensity rather than to viewing distance, so the advice is to be outdoors rather than to read less.

Low-concentration atropine slows progression once myopia is established. The LAMP study compared 0.05, 0.025 and 0.01 percent against placebo and found a concentration-dependent effect: at one year, 0.05 percent reduced spherical equivalent progression by 67 percent and axial elongation by 51 percent, against 27 and 12 percent for 0.01 percent. The 0.05 percent concentration remained the most effective at three and five years with minimal rebound on stopping.

Question 9

A child has limited abduction of the left eye. On adduction, the left globe retracts and the palpebral fissure narrows. What is the diagnosis and why does neuroimaging add nothing?

Accepted Answer

Duane retraction syndrome, and imaging adds nothing because the abnormality is a congenital miswiring rather than an acquired lesion.

The abducens nucleus fails to develop, so the lateral rectus receives no sixth nerve supply. Instead it is innervated aberrantly by a branch of the third nerve that normally supplies the medial rectus.

The consequences follow directly. On attempted abduction the lateral rectus receives no appropriate signal and the eye does not move outward, which is what makes it resemble a sixth nerve palsy.

On attempted adduction, the shared third nerve branch fires both the medial rectus and the aberrantly innervated lateral rectus simultaneously. The two horizontal recti pull against each other, and because their combined force is directed backwards along the axis of the globe, the eye is drawn into the orbit. Retraction narrows the palpebral fissure, and that combination is pathognomonic.

A true sixth nerve palsy shows none of this, because the lateral rectus is simply weak and there is no co-contraction.

Imaging is unnecessary because the condition is present from birth, non-progressive, and explained entirely by the aberrant innervation. An acquired sixth nerve palsy in a child would require imaging, since it may indicate raised intracranial pressure or a pontine lesion, which is precisely why distinguishing the two matters.

Many children with Duane syndrome adopt a compensatory face turn to place the eyes in a position where they are aligned, and surgery is considered mainly to reduce that head posture rather than to restore abduction, which cannot be achieved.

Practice — "Squint & Pediatric Ophthalmology"

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