Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy.
Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.
D000818:Animals; D006706:Homeostasis; D006978:Hypertension, Renovascular / Q000150:complications / Q000473:pathology*; D008253:Macaca mulatta; D008854:Microscopy, Electron; D009896:Optic Atrophy / Q000473:pathology; D009898:Optic Disk / Q000098:blood supply / Q000648:ultrastructure*; D009901:Optic Nerve Diseases / Q000209:etiology / Q000473:pathology*; D010211:Papilledema / Q000473:pathology; D012171:Retinal Vessels / Q000378:metabolism