April 1968
Volume 7, Issue 2
Free
Articles  |   April 1968
Pathology of the Optic Nerve in Experimental Acute Glaucoma
Author Affiliations
  • PETER W. LAMPERT
    Armed Forces Institute of Pathology and the Veterans Administration Central Laboratory for Anatomic Pathology and Research, AFIP Washington, D.C.
  • MARTIN H. VOGEL
    Armed Forces Institute of Pathology and the Veterans Administration Central Laboratory for Anatomic Pathology and Research, AFIP Washington, D.C.
  • LORENZ E. ZIMMERMAN
    Armed Forces Institute of Pathology and the Veterans Administration Central Laboratory for Anatomic Pathology and Research, AFIP Washington, D.C.
Investigative Ophthalmology & Visual Science April 1968, Vol.7, 199-213. doi:
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      PETER W. LAMPERT, MARTIN H. VOGEL, LORENZ E. ZIMMERMAN; Pathology of the Optic Nerve in Experimental Acute Glaucoma . Invest. Ophthalmol. Vis. Sci. 1968;7(2):199-213.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

The pathology of the optic nerve resulting from experimental acute glaucoma was studied by electron microscopy in owl monkeys (Aotus trivirgatus). Two distinct stages in the evolution of the pathological changes were recognized. The first stage consisted of widespread axonal changes with or without focal areas of necrosis. The axons showed severe hydropic swellings and/or reactive axonal enlargements filled with mitochondria, dense bodies, vesicles, and membranous whorls. The hydropic degeneration of the axons accounted for the vacuolar changes seen by light microscopy in severely affected nerves. No enlargement of extracellular spaces and no penetration of vitreous could be demonstrated at this stage. The second phase, developing several days after onset of glaucoma, began with the cystic transformation of necrotic tissue beneath the internal limiting membrane, causing its dissolution or rupture in focal areas. Vitreous, together with injected electron-dense markers (Thorotrast or India ink), was forced through these gaps into the damaged nerve, producing cavernous extracellular spaces. The degenerated axons and other debris were removed by phagocytes.The origin of at least some of these cells from hematogenous monocytes is discussed and illustrated.

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