Neuro-ophthalmology Flashcards
Definition of Nystagmus
Repetitive, involuntary to-and-fro eye oscillation which may be pathological or physiological
Primary congenital nystagmus, primary gaze
low amplitude pendular nystagmus that converts jerk nystagmus on side gaze
Explain Latent Nystagmus
Associated with infantile esotropia or dissociated vertical deviation
both eyes open, no nystagmus
nystagmus apparent when covering one eye or when light entering eye is reduced.
Describe classical migraine
migraine with aura that last for 20 minutes, headache is hemicranial and associated with symptoms of nausea, photophobia and phonophobia
Describe common migraine
Pounding or throbbing headache, absent of symptoms, patient often photophobic and phonophobic
Managements for migraines
Avoid food, beverages such as coffee/chocolate/cheese/alcohol, oral contraceptive pills, stress, lack of sleep, long intervals without food
Medicine for prophylaxis and acute attack
Signs of optic nerve dysfunction
Poor VA, APD, poor light brightness sensitivity, poor contrast sensitivity, dyschromatopsia, visual field defect
Primary optic atrophy pathogenesis
Occurs without swelling of ONH, may be due to lesions affecting the visual pathway from the retrolaminar portion of the optic nerve to the lateral geniculate body
Primary optic atrophy signs
pale, flat disc with clearly delineated margins.
atrophy may be diffused or sectoral
Primary optic atrophy causes
Demyelinating optic neuritis, toxic and nutritional optic neuropathy
Demyelinating optic neuritis presentation
2nd to 5th decade of life subacute monocular visual impairment with discomfort around eye, worsen with eye movement
Demyelinating optic neuritis signs
Disc is normal, temporal disc pallor indicates previous attacks, signs of optic nerve dysfunction
Demyelinating optic neuritis course
worsen up to 2 weeks then begins to improve
Demyelinating optic neuritis prognosis
VA better than 6/9 in 75%, associated with multiple sclerosis
Demyelinating optic neuritis management
refer neuro-ophthalmologist for confirmation and treatment to speed recovery
Nutritional optic neuropathy presentation
Insidious onset of progressive, bilateral, symmetrical visual impairment associated with dyschromatopsia
Nutritional optic neuropathy signs
Normal optic disc, bilateral centrocaecal scotomas
Nutritional optic neuropathy management
Refer to ophthalmologist for treatment
Secondary optic atrophy pathogenesis
Preceded by swelling of the ONH
Secondary optic atrophy signs
White/ dirty grey, slightly elevated disc, poorly delineated margin
Reduction in number of vessels
Secondary optic atrophy causes
Chronic papilloedema, Anterior ischemic optic neuropathy
Non-Arteritic Anetrior Ischaemic Optic Neuropathy pathogenesis
infarction of ONH caused by occlusion of short posterior ciliary arteries
Non-Arteritic Anterior Ischaemic Optic Neuropathy presentation
6th to 7th decade, sudden, painless mono visual loss, no forewarning of visual obscuration
Non-Arteritic Anterior Ischaemic Optic Neuropathy signs
Hyperaemic disc swelling often few peripapillary splinter shaped haemorrhages
Swelling grad. resolves, pallor after 3-6 weeks
Non-Arteritic Anterior Ischaemic Optic Neuropathy treatment
No
Arteritic Anterior Ischaemic Optic Neuropathy pathogenesis
Occlusion of posterior ciliary arteries due to giant cell arterities
Arteritic Anterior Ischaemic Optic Neuropathy presentation
8th to 9th decade, sudden profound vision loss, periocular pain, transient visual obscuration, flashing lights
Arteritic Anterior Ischaemic Optic Neuropathy signs
Severe visual loss; to light perception or worse
Strikingly pale oedematous disc
over 1-2 months, swelling gradually resolves and optic atrophy ensues
Arteritic Anterior Ischaemic Optic Neuropathy management
Refer to ophthalmologist for intravenous steroids to prevent blindness
Arteritic Anterior Ischaemic Optic Neuropathy prognosis
poor
Papilloedema pathogenesis
Swelling of ONH secondary to raised intracranial pressure
Papilloedema signs
Disc hyperaemia, elevation, indistinct margins,
Venous engorgements, peripapillary flame shaped haemorrhages, cotton wool spots
Papilloedema management
Refer to ophthalmologist urgently, suspicious of intracranial mass
Absolute afferent papillary defect characteristics
Eye complete blind, Both pupils equal in size, affected eye stimulated both no reaction, if norm eye stimulated reacts normally, near reflex is normal1
Argyll Robertson Pupil cause and signs
Caused by neurosyphilis,
Bilateral small pupils do not react to light
Near response normal
Adie pupil causes
denervation of the postganglionic supply to the sphincter pupillae and ciliary muscle
Adie pupil signs
Large regular pupil Direct light reflex: absent/sluggish Consensual light reflex: absent/sluggish Near reflex: slow contrsict, redilation Accomodation: manifest similar tonicity
Horner syndrome causes
Lesion occur anywhere on sympathetic supply, diff conditions can affect the three different sympathetic neurons.
Central
preganglionic
postganglionic
Horner syndrome signs
unilateral Mild ptosis Miosis Slight elevation of inferior eyelid Hypochromic heterochromia Reduced ipsilateral sweating normal pupillary reaction to light and near
