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Discuss Night Blindness!

Discuss Night Blindness!



Discuss Night Blindness! - Dr James Beatty

Discuss Night Blindness! - Dr James Beatty



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    Discuss Night Blindness! Discuss Night Blindness! Presentation Transcript

    • Discuss Night Blindness!Discuss Night Blindness! J.Beatty
    • OverviewOverview Physiology Tests Classification: – Normal physiological response – Acquired – Congenital Focus on vitamin A and R.P.
    • PhysiologyPhysiology -Exposure to strong light decreases visual sensitivity, but increases visual acuity/discrimination and temporal acuity/discrimination. -Exposure to dark increases light sensitivity, but decreases visual acuity and temporal acuity.
    • -Mechanisms of adaptation are: Pupil: change in size, very rapid response. Rods and cones: duplex theory of vision (with increased retinal illumination , vision changes from a rod to cone dominated system), slow response. Photopigment: rhodopsin regeneration in the dark, slow response. Automated gain control: very rapid response Cellular mechanisms: photoreceptors, bipolar cells, ganglion cells. Very rapid response.
    • TestsTests Goldman-weekes adaptometry: The patient is adapted to a standard light, which is than turned off and the patient is then presented with test stimuli. The lowest perceivable intensity is then recorded against time.
    • ClassificationClassification Normal physiological response: When moving from a bright to a dark room. Initial blindness followed by good discrimination by 10 mins (cones), and max adaptation by 10 to 20 min (rods).
    • Acquired causes: -Pathological myopia: ? chorioretinal atrophy -Undercorrected myopia: ? abberations -Early prebyopia: ? decreased accommodation in the dark -Vitamin A deficiency: necessary for making photopigments/rhodopsin. Causes = inadequate diet, malabsorption, alchoholism, cirrhosis, ? measels and pregnancy. Marked night blindness, numerous small yellow- white, well demarcated spots deep in the retina seen peripherally. Also dry eye, Bitot spots and Xerophthalmia.
    • -Zinc deficiency (needed for vit A metabolism) -Advanced glaucoma and other causes of severe optic atrophy. -Diffuse opacification of the media: cataract, vitreous opacities, ect. -Hysteria or malingering. -End stage syphalitic neuroretinitis. -Cancer-related retinopathy. -Drugs. Isotretinoin (used in acne), ?others.
    • Congenital causes: Congenital stationary night blindness: normal fundus: -AD types: Nougart type, decreased rod and cone ERG. Riggs type, normal cone ERG. -AR or XL congenital nyctalopia with myopia. abnormal fundus -Oguchi disease: 2-12 hrs to attain normal dark- adapted rod thresholds. - Fundus albipunctatus: multipal yellow-white spots, sparing the fovea, erg and eog abn, but revert to normal on prolonged dark adapration.
    • -Gyrate atrophy: AR, high levels of ornithine, multipal sharply defined areas of chorioretinal atrophy separated by pigment margins. -Choroideremia: XL recessive, diffuse RPE and choroidal atrophy throughout the fundus. -Vitreoretinal dystrophies: esp Goldmann- Favre disease
    • Retinitis Pigmentosa Prevalence: 1:5000 Inheritence: Isolated, Autosomal dominant (mild), Autosomal recessive (severe), X-linked (most severe). Clinical: Nyctalopia, arteriolar attenuation, RP sine pigmentosa, Retinitis puncta albescens, Bone spicules, unmasking of choroidal vessels, maculopathy, vitreous changes, waxy disc.
    • Erg: first reduced scotopic and combined, later photopic. Eog: subnormal. Dark adaptometry: prolonged. Colour vision: normal. Perimetry: annular mid peripheral scotoma, progress to small central field. FA: diffuse hyper (unmasking) and areas of hypo (masking by bone spicules).
    • Prognosis: poor , 25% maintain good reading VA, most pts less than 20yrs have VA > 6/60, by 50 yrs most have VA < 6/60. Ocular associations: post. sub cap. Cataract, open angle glaucoma, myopia, keratokonus, vitreous changes, optic disc drusen. Atypical RP: Sector RP, pericentral RP (along the arcades), RP with exudative vasculopathy (coats like appearance in periphery)
    •  Systemic associations:  -Bassen-kornzweig syndrome: due to B- lipoproteinaemia deficiency. Ataxia, acanthocytosis in blood, ophthalmoplegia, ptosis. Treat with Vit E)  -Refsum disease: AR inborn error of metabolism with increased phytanic acid in serum, multiple CNS abn, retina more salt and pepper like)  -Usher syndrome: AR, 5% of all profound deafness in children and half of all blind and deaf.  -Kearns-Sayer syndrome: mitochondrial DNA deletions. Atypical RP with central clumping.  -Bardet-Biedel syndrome: mental handicap, polydactyly, obesity and hypogenitalism.