Visual field defects Flashcards
how are visual field defects examined for?
visual fields to confrontation testing-use hatpin with red (can determine blind spot-can assess if enlarged e.g. optic disc swelling e.g. papilloedema-raised ICP) or white head (for peripheral vision)
check visual acuity 1st to ensure pt can see the pin
would also want to check pupils, look for RAPD, examine fundus, and consider neurological examination. can also use Amsler grid.
quantitative tests=static and kinetic perimetry
where is the lesion located to result in a visual field defect?
anywhere along the optic pathway from the retina to the occipital cortex
causes of central visual field loss?
ARMD optic neuropathy optic neuritis macular hole-identifiable with ophthalmoscopy-red circle apparent in region of macula as viewing underlying choroid, and OCT-gap in retina*, treated with surgery cone dystrophies drugs e.g. chloroquine
causes of peripheral visual field loss?
glaucoma retinal detachment retinitis pigmentosa chorioretinitis pituitary adenoma stroke
hx to ascertain in visual field loss?
onset-rapid onset of a homonymous hemianopia favours stroke over a SOL
what part of the visual field is missing?
is it 1 or both eyes?-patient may think only 1 eye if defect worse in this eye than the other so must check vision of other eye with other eye closed
what does the visual defect look like?
look for features of asymptomatic loss e.g. bumping into things, problems driving-car damage?, assoc. neurological or ophthalmic symptoms?
what is a scotoma?
type of visual field defect surrounded by normal visual field
e.g. upper arcuate scotoma in chronic simple glaucoma (primary open angle), or central scotoma in AMD and macular oedema
causes of optic disc swelling, producing an enlarged blind spot?
papilloedema-raised ICP
SOLs of optic nerve head e.g. sarcoidosis infiltration
papillitis-optic neuritis affecting optic nerve head
malignant HTN
ischaemic optic neuropathy
central retinal vein occlusion-sudden marked visual loss, tortuous veins, gross retinal haemorrhage
what does the Amsler grid assess with respect to the visual field?
the central 10 degrees of the visual field
used in assessment for AMD such as progression from dry AMD to wet AMD
causes to consider of field defecit in 1 eye?
so lesion before the optic chiasm
optic nerve damage tends to produce central, asymmetrical unilateral defect e.g. optic neuritis, optic atrophy, glaucoma, trauma.
what do lesions in the anterior visual cortex cause?
contralateral homonymous hemianopia with macular sparing e.g. posterior cerebral artery occlusion.
what visual field defect might blunt trauma to the occiput produce?
a congruous homonymous macular defect due to macular cortex lesion
what is optic neuritis?
inflammation or demyelination of optic nerve
if just head affected then termed papillitis
and if nerve affected more posteriorly with no disc swelling, then termed retrobulbar neuritis.
presentation of optic neuritis?
acute visual loss that may progress over a few days and then slowly improve
ocular pain, espec. on eye movement in retrobulbar neuritis as rectus contraction pulls on sheath of optic nerve
may be preceding hx of viral illness, or other neurological symptoms suggestive of MS-weakness, paraesthesia, loss of sensation*
can be photopsia (light flashes), uhtoff’s phenomenon-increased symptoms with raised body temp., pulfrich’s phenomenon-altered perception of direction of movement, fatigue.
signs: reduced visual acuity
reduced colour vision (dyschromatopsia), red desaturation
RAPD as reduced optic nerve conduction, may not be apparent if bilateral optic neuritis
central scotoma on field testing, altitudinal field defects-upper or lower part of field lost, and arcuate defects
normal disc if retrobulbar inflammation, swollen if papillitis (optic nerve head inflamed)
management of patient with optic neuritis?
MRI-identify plaques of demyelination
steroids e.g. methylprednisolone to speed up visual recovery?-slow over several wks, although often not quite as good as before attack, rpt episodes may cause optic atrophy and decline in vision, rarely vision may not recover.
MS investigation-MRI, lumbar puncture-myelin basic protein, oligoclonal bands, elevated IgG index and synthesis rate
? use of beta interferon in patients with acute demyelinating optic neuritis to delay onset of MS, but many even with abnormal MRI will not develop MS, tment not completely effective and visual prognosis good even if MS develops.
how does ischaemic optic neuropathy develop?
compromisation of posterior ciliary vessels, due to vaso-occlusive or vasculitic arteriole disease, which supply anterior optic nerve so it becomes ischaemic.
usual cause of blindness in GCA?
ischaemic optic neuropathy
can also be central artery of retina occlusion if affected secondarily to ophthalmic artery arteritis.
visual field defect in ischaemic optic neuropathy e.g. pt with GCA?
altitudinal scotoma-absence of lower or upper half of the visual field
investigations in patient with non-arteritic ischaemic optic neuropathy?
FBC-exclude anaemia
ESR and CRP-GCA check
BP
blood glucose
DM and HTN assoc. with ischaemic optic neuropathy
symptoms of retinitis pigementosa?
often start in childhood with impaired night vision (nyctalopia) or dark adaptation
progressive loss of peripheral vision-causing tendency to trip over things, if central vision loss tends to occur later
symptoms commonly present between 10 and 30 yrs, leber’s amaurosis-children can become severely sight impaired in 1st 6mnths of life
signs of retinitis pigmentosa?
retina-black or dark brown star shaped concentrations of pigmentation
assoc. ocular problems: myopia
subcapsular cataract
vitreous changes-posterior vitreous detachment
keratoconus
open angle glaucoma
what systemic conditions might retinitis pigmentosa be a feature of?
usher’s syndrome-hearing loss, responsible for 50% of combined deafblindness
other conditions assoc. with hearing loss-alport’s syndrome, waardenburg’s syndrome
most critical diagnostic test in retinitis pigmentosa?
electroretinogram-provides objective function of rods and cones across the retina, typically showing marked reduction in signals from both, rods predominating.
management of retinitis pigmentosa?
aim to slow degenerative process, provide low vision aids and psychological support
r/f to low vision specialist
advice on sight impaired registration
regular screening and tment by eye specialist of complications e.g. cataract, glaucoma and cystoid macular oedema
sunglasses
genetic counselling
DVLA informing and DVLA Estermann visual field test
?drug role e.g. beta carotene, lutein, acetazolamide, steroids-if anti-retinal Abs.
causes of optic neuritis
acute demyelinating and MS
ischaemic optic neuropathy e.g. GCA
inflammatory-behcets, sarcoidosis, SLE, neuromyelitis optica-devic’s syndrome, post-infection, post-vaccination
infection-TB. syphilis, orbital cellulitis, VSV, mumps, rubella, glandular fever
vit B12 deficiency
drugs-ethambutol, amiodarone
optic neuritis in children-viral infection is a common cause
Triad of funds signs in retinitis pigmentosa?
Arteriolar attenuation
Retinal bone-spicule pigmentation
Waxy disc pallor
