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Ryngloma thou8h there D1iiY be ireu of cystic or necrotic change and/or hemorrhage. Cavernous sinus compression or invasion may occur. In pmeots praeotins with ~s insipidus, the brighl spot may be absent. Mlaoadenomas typically show delayed and d«retued en~uutammr on clynamlc O'lnlopblry1'411ollllf • Epidemiofo&y. Acmunl for 21D SX of primary intracranial tumors. There Is no gender predominance. Bimodal age distribution with a peak at <20 yean or age and a semod peak at 50 years. Fig. noldal surgery with gross mtal median Dl the mass.
U:klng (G~roM). Bllml'lll aptlc nerve sheath meningioma. l)iQgnosis Optic glioma F1f. I;Ddal mass centered In the eJqJeCted loc;rtion af the optlt dlliiSm, compilllble with an optk glioma. Rg. 17 Mone superforly, tile mass hilS a moll! lnftftrallng ;~ppear ance as It extends posterolatel'illly along tile expected course of boti1 optic tram (Cit70WS). llaml • Epfdemlolof;y. enWe predo~ ~sod aiM witb NF-1. M with NP-1. • Clirric:al ~ V1s\W dysfunction, b:ypothalamic dY$fwv:tion. allc $)'11drome.
Retinal d~chment. Fluid collects between the sensory retina and the retinal pigment epithelium. • Amaurosis fugrJx. Sudden onset of transient monocular blindness usually from a small fibrin en~bolus. • Retinitis pigmentosa. Begins in childhood and adolescence, male preponderance. Autosomal recessive (AR) or autosomal dominant (AD) inheritance on chromosome 3. Degeneration of all retinal layers (neuroepithelium and pigment epithelium) with foveal sparing. Starts with impairment of twilight vision (nJII:IIllopia) progressing to blindness.