In two articles1 a modest attempt has been made to give a more precise idea of the pathogenesis of the rise of intraocular pressure in acute glaucoma. This condition, according to my concept, does not arise primarily in the eyeball but has its origin in certain nerve structures outside the eye—the ciliary ganglion, the important diencephalic vegetative center (Karplus-Kreidl center2), at the base of the brain, in the vicinitiy of the optic chiasm and in the cortex of the brain. Mistakenly, the signs of acute and of certain kinds of chronic glaucoma were once considered to be inflammatory. Actually, the classic signs of common inflammation—arterial hyperemia, exudation and migration of white cells—cannot be demonstrated either by clinical or, to any significant degree, by histologic studies. The same holds true of the so-called inflammatory signs following thrombosis of the vena centralis retinae. If any inflammation exists in either
HESS L. PATHOGENESIS OF GLAUCOMA. Arch Ophthalmol. 1945;33(5):392–396. doi:10.1001/archopht.1945.00890170068008
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