Ophthalmology – Knowledge Test
1. Define the following terms: anisocoria, nystagmus, amblyopia, homonymous hemianopia
i. Anisocoria – unequal pupil size. May be physiological, pathological (e.g. CN lesion), mechanical (e.g. post-trauma), or pharmacological (e.g. use of mydriatic or miotic eyedrops) ii. Nystagmus – repetivie, involuntary, rhythmic jerking of the eyes, may be horizontal, vertical, or rotational. Defined by the direction of movement of the ‘fast phase’ of movement. Physiological at the extremes of gaze, but can be a sign of a wide number of central, vestibular, and peripheral pathologies iii. Amblyopia – ‘lazy eye’, typically childhood onset. Visual information from the eye is incorrectly processed by the brain, and over time, the other eye is favoured. May be due to strabismus, refractive error, or disruption to signal e.g. congenital cataract iv. Homonymous hemianopia – visual field loss on the same side of both eyes, please see diagram above. Caused by lesions to the contralateral visual pathway between the optic tract and the occipital visual cortex
2. What are the main types of strabismus (squint)?
i. Strabismus – when eyes don’t point in the same direction. May be paralytic or non-paralytic, determine by assessing eye movements as above ii. -Phorias are latent squints, i.e. only present when binocular vision is disrupted iii. -Tropias are manifest squints, i.e. present when using binocular vision iv. Squints may be eso- (inwards), exo- (outwards), hyper- (upwards), hypo- (downwards), cyclo- (rotational), or a combination of any of the above v. These are detected using the cover test (-tropias) and alternating-cover test (-phorias), or Hirschberg corneal reflex if these are not possible (e.g. in young children)
3. What are the ocular manifestations of cranial nerve lesions?
i. CNII – decreased vision. May be field loss, or diminished acuity/colour vision depending on cause. Unilateral CNII damage – loss of direct but intact consensual pupillary light reflex on the affected side ii. CNIII – diplopia, strabismus (‘down and out’), ptosis, mydriasis. ‘Medical’ lesions e.g. microvascular disease ay spare pupil, as autonomic pupillary fibres run on the outside of the nerve; ‘surgical’ lesions e.g. aneurysms compress these as well. Unilateral CNIII damage – loss of ipsilateral constriction but contralateral eye’s consensual reflex is intact iii. CNIV – diplopia, strabismus (‘up and in’). Longest intracranial course, but smallest nerve, and the only nerve to exit from the dorsal aspect of the brainstem iv. CNVI – diplopia, strabismus (‘in’). Note: may be false localising sign due to tractional injury
4. What are some causes of a relative afferent pupillary defect (RAPD)?
i. A.k.a. Marcus Gunn pupil ii. Causes include multiple sclerosis, optic neuropathies (e.g. glaucoma), or severe retinal pathology iii. Detected by swinging light test
5. What are some causes of a ptosis?
i. Congenital – usually due to levator palpebrae muscle defect ii. Acquired – most commonly due to age-related weakness of the levator aponeurosis iii. Pathological causes include Horner’s syndrome, CNIII pathology, Muller’s muscle damage, or ocular trauma iv. Assess fatiguability – fatigable ptosis (worse in the evening or after light exercise) is a common presentation of myasthenia gravis