[Early fundus changes caused by repeated small crises in the Posner-Schlossman syndrome: a model for glaucoma simplex].

In Posner-Schlossman syndrome a repeated crisis of intraocular pressure (IOP) elevation to 25-45 mmHg continues for 3-10 days. During the relapses glaucomatous damage often occurs. The IOP and its variation during the crisis are similar to those in glaucoma simplex. Therefore, the syndrome can be considered as a natural model for investigations into glaucoma simplex. By analyzing five cases of Posner-Schlossman syndrome in which the glaucomatous lesions ranged from the earliest to advanced stages, the development and progression of glaucomatous damage of the optic nerve at varying chronically elevated IOP levels became evident. The earliest evident fundus change is a nerve fiber layer defect (NFLD) in the Bjerrum tangent, and not the enlargement of the physiologic excavation. The latter does not develop before stage IV. The slit-like NFLD shows a decrease in sensitivity of 0.2-0.4 log ND unit, which is thus easily overlooked. As the disease progresses the NFLD becomes more pronounced, its width increases and it becomes wedge-shaped. Due to a considerable loss of nerve fibers at the wedge-shaped defect, a small notch which develops in the direction of NFLD is not observed until stage IV. Goldmann perimetry demonstrated a certain abnormality at stages IV-V; in addition to the wedge-shaped NFLD, diffuse thinning of the NFLD begins around the optic disk and develops into a large, concentric excavation. For identification of the most delicate NFLDs, stereo fundus photography in color with 8-fold magnification, on 6 x 6 film is recommended.