The ophthalmoscopic manifestations of increased intracranial pressure have stimulated much clinical and experimental investigation during the past century. Türk1 in 1853, was the first to describe retinal venous engorgement in brain tumor. It remained however, for Von Graefe2 to elaborate and describe completely the condition of papilledema. He deserves due credit for emphasizing that the earliest and most reliable manifestation of increased intracranial pressure is distension of the retinal veins. It seemed most logical that this ophthalmoscopic finding was a reflection of venous stasis, and in 1860 he advanced the theory that with increased intracranial pressure there was a concomitant rise in intracranial venous pressure. Increased venous pressure within the dural sinuses would lead to stasis and would result in a rise in venous pressure in the cavernous sinus and, in a retrograde fashion, in the orbital veins and central retinal vein.Sesemann,3 in 1869, demonstrated
HEDGES TR, WEINSTEIN JD, CRYSTLE CD. Orbital Vascular Response to Acutely Increased Intracranial Pressure in the Rhesus Monkey. Arch Ophthalmol. 1964;71(2):226–237. doi:10.1001/archopht.1964.00970010242018
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