Rim Loss Research Articles

Clinical Disc Biometry in Early Glaucoma

To assess the potential of a clinical method of optic disc measurement in the detection of early neuroretinal rim loss in glaucoma. A method of disc biometry based on indirect ophthalmoscopy was used to estimate disc and neuroretinal rim areas in 81 ocular hypertensive eyes of 43 patients and in 28 fellow eyes with normal visual fields of patients with unilateral visual field loss from primary open-angle glaucoma. The results were compared with those from age-matched visually normal patients. Neuroretinal rim area was significantly smaller in both hypertensive and fellow eye groups compared with controls (P < 0.0001; P = 0.0009). Disc area also was smaller in both groups (P = 0.0034; P = 0.046); however, this was inadequate to explain the differences in rim area, which, when corrected for disc size, were still highly significant (P < 0.0001; P = 0.0001). The differences in neuroretinal rim area observed are likely to indicate that a proportion of the eyes studied had suffered a reduction of neuroretinal rim area, which was measurable by this method at a stage before the development of demonstrable visual field loss.

Intraocular pressure-related pattern of optic disc cupping in adult glaucoma patients.

The pattern of glaucomatous optic disc cupping was investigated in 67 eyes of 67 primary open-angle glaucoma patients with early-to-moderate visual field loss and a wide range of intraocular pressure. We determined the position of the deepest point of the optic disc cup using the Rodenstock Analyzer. This position correlated significantly with intraocular pressure: the deepest point tended to be located below the center of the optic disc at high intraocular pressure and above the center at low intraocular pressure. There was no significant correlation between the position of the deepest cup point along the horizontal axis and intraocular pressure. The position of the deepest point of the cup also correlated significantly with the severity of glaucoma, albeit less strongly than with intraocular pressure: it tended to be in the inferior portion of the disc at an early stage of glaucoma and in the superior portion of the disc at a more advanced stage of glaucoma. Therefore, the inferior portion of the optic nerve head appears to be most yielding to changes of intraocular pressure. These findings are consistent with histologic evidence of the least connective tissue support in the inferoperipheral region of the lamina cribrosa and with greater prevalence of inferior rim loss and corresponding superior visual field defects in early to moderately advanced primary open-angle glaucoma patients.

Glaucomatous Parapapillary Atrophy

Glaucomatous optic nerve damage is typically associated with intrapapillary changes, such as neuroretinal rim loss. In this study, parapapillary chorioretinal atrophy was evaluated in 691 normal eyes, 1081 glaucomatous eyes, and 31 eyes with ocular hypertension. It was significantly larger and occurred more often in the glaucomatous eyes (parapapillary atrophy area, 1.07 +/- 0.83 mm2) (mean +/- SD) than in the normal eyes (0.55 +/- 0.64 mm2) or in the eyes with ocular hypertension (0.55 +/- 0.37 mm2). These differences were significant also for eyes with moderate glaucomatous damage (0.86 +/- 0.62 mm2). Parapapillary chorioretinal atrophy was associated with shallow glaucomatous cupping, diffuse nerve fiber loss, a marked tessellated fundus, and only moderately elevated intraocular pressure. It increased with a decreasing neuroretinal rim area. It showed a spatial correlation to neuroretinal rim loss inside the optic disc. In unilateral glaucoma, it was larger in the affected eye than in the unaffected eye. Parapapillary chorioretinal atrophy is associated with glaucoma.

Dark adaptation in glaucomatous and nonglaucomatous optic nerve atrophy

Optic nerve damage is associated with impairment of psychophysical functions. We measured dark adaptation in 21 eyes of 14 normal subjects, 35 eyes of 19 patients with primary open-angle glaucoma, and 7 eyes of 4 patients with nonglaucomatous descending optic nerve atrophy. In the normal subjects light thresholds and time of the shoulder in the dark adaptation curve increased significantly with age. In eyes with glaucomatous or nonglaucomatous optic nerve damage light sensitivity was lower than in normal eyes of age-matched control groups. Rod light sensitivity was significantly (P less than 0.05) correlated with neuroretinal rim loss, parapapillary chorioretinal atrophy, and relative afferent pupillary defects. We conclude that velocity and degree of dark adaptation decrease with increasing age. Patients with glaucomatous and nonglaucomatous optic nerve atrophy show decreased light sensitivity especially in the rod part of dark adaptation worsening with advancing optic nerve damage.

Comparison of Optic Disc Features in Low-Tension and Typical Open-Angle Glaucoma

This study was undertaken to identify features of optic nerve head architecture that might explain, in part, why ganglion cell loss occurs in patients with low-tension glaucoma. We compared retrospectively the disc photographs of 25 patients with low-tension glaucoma with those of 26 control patients with typical open-angle glaucoma. No differences were observed in any of the following features: pore length, shape, or size variation; cup/disc and disc/arteriole ratio; clock positions of total rim loss; central retinal vessel entry site; rim pallor; number of rim-crossing vessels; and presence or absence of peripapillary nerve fiber layer hemorrhages, optic pits, and central retinal vessel canals. An hour-glass appearance of connective tissue bundles within the scleral lamina cribrosa, however, was present statistically less often in patients with low-tension glaucoma (p = 0.007). We speculate that the microscopic arrangement of fiber bundles within the lamina cribrosa may play an etiologic role in the pathogenesis of low-tension glaucoma.