Optic nerve and visual field examinations

smaller discs or smaller cupping than eyes with open angles. However, to our knowledge, there was only one study which compared optic disc area in eyes with angle closure with those in normal eyes or eyes with open angle glaucoma: Sihota et al. reported that disc area in eyes with chronic angle-closure glaucoma had smaller disc area (2.62 mm2) than eyes with open-angle glaucoma (2.77 mm2) but disc area in normal eyes was still smaller (2.38 mm2).23 Moreover, there is a lack of clinical studies on physiological cupping of the optic disc of eyes with primary angle closure before developing glaucomatous damage or their fellow eyes.

Acquired changes in the optic disc

Acquired changes in the optic disc and surrounding tissues following acute or chronic increase in intraocular pressure have been intensively studied. As an early histological study described in the text by Duke-Elder,24 the pathological changes in the optic nerve occurred within the first few weeks of an attack of primary angle closure as follows: 24 hours after the onset, the nerve head shows neither papilledema nor cupping, but acute hydropic degeneration of nerve fibers is seen with and just after the lamina cribrosa. The papilledema appears mildly at the third day and apparently at the sixth day after the onset. Deep cupping of the optic disc became evident and the nerve showed commencing cavernous degeneration. In these same cases, the changes in the retinal ganglion cells were minimal at least in the first week after the onset. As significant changes found in human eyes with secondary angle-closure glaucoma, thinner lamina cribrosa, deeper and wider optic cup, finer peripapillary scleral ring, and thinner choroidal vascular bed were reported. Pathological changes were studied also in experimental monkey eyes in which intraocular pressure was acutely increased. More recently, morphometric changes in the optic disc or retinal nerve fiber layers in monkey eyes of experimental glaucoma were studied using confocal scanning laser tomogra- phy33-40 or scanning laser polarimetry.35,41,42 One experimental study using monkey eyes36 showed the time-course changes in the optic nerve head morphology after the acute intraocular pressure rise: intraocular pressure was increased to about 40 mmHg after laser trabeculoplasty and gradually reduced to about 30 mmHg during the following three months; cup volume measured with confocal scanning laser tomography gradually increased and retinal nerve fiber layer thickness evaluated with scanning laser polarimetry gradually decreased during the first month after the laser procedure.

As an early study in the 1970s, Douglas et al. reported the changes in the optic disc of eyes following unilateral acute-angle-closure glaucoma or with unilateral chronic angle-closure glaucoma.43 In their report, none of 18 acute, but five of 11 chronic angle-closure patients, showed asymmetry of cupping, while pallor was seen in seven of the acute and nine of the chronic patients, suggesting that disc pallor should be a dominant change compared to enlargement of the cupping in eyes following acute angle-closure. Recent years, a lot of clinical studies regarding the optic disc in angle-closure glaucoma have been released from Asian countries. Yang et al.44 reviewed 103 patients with 23 acute and 80 chronic primary angleclosure glaucoma and found that concentric steep enlargement of the cupping in 99 (96%) of the eyes, while focal notcing of the neuroretinal rim was seen in only three (3%) eyes. And, both alpha and beta zones of parapapillary atrophy were more frequent in angle-closure glaucoma eyes compared to normal controls.44 Shen et

al.45 reported that cut-to-disc ratio significantly increased from 0.56 to 0.59 from the second week to the sixth week after the acute angle-closure attack episode and the neuroretinal rim loss was more evident in the superotemporal and inferotemporal portions of the optic disc, although they did not mention which of general or focal enlargement of the cupping was more common. Uhm et al.46 compared the optic disc appearance between acute angle-closure eyes and chronic angle-closure eyes: abnormal disc findings, such as abnormal shaped rim width, bared circumlinear vessel, vessel bayoneting, and zone beta of parapapillary atrophy, were more commonly found in eyes with chronic angle-closure glaucoma than acute one. Thus, in acute angle-closure glaucoma eyes, the changes in optic disc morphology including neuroretinal rim loss and enlargement of the cupping are not necessarily common, while pallor is a dominant finding in the optic disc. On the other hand, intrapapillary changes similar to those in eyes with primary open-angle glaucoma were more often observed in eyes with chronic angle-closure glaucoma.

Vascular aspects in the pathogenesis of optic neuropathy in primary angle-closure glaucoma

As mentioned above, pale appearance of the neuroretinal rim and optic disc edema are characteristic findings for eyes during or following acute angle-closure attack. Frequently seen disc pallor suggests a role of vascular insufficiency in pathogenesis of optic neuropathy following acutely elevated intraocular pressure due to angle-closure attack. Vascular occlusion, as well as hydropic degeneration of the optic disc tissue24 and axonal swelling from blockage of axoplasmic transport,47,48 is thought to play a role in developing optic disc edema. A study using color Doppler ultrasonography showed that blood velocity in retrobulbar arteries was lower in eyes with elevated intraocular pressure due to angle-closure in comparison to eyes with normalized pressure following angle-closure attack or to normal control eyes.49 The same authors also reported that blood velocity in the retrobulbar arteries was significantly decreased in chronic angle-closure eyes with normally controlled intraocular pressure than in age-matched healthy eyes.50 Reduced choroidal thickness with marked decrease in choroidal vessel diameter25 may also suggest possible association between blood flow and development of optic neuropathy in angle-closure glaucoma.

Parapapillary atrophy is as usual known to relate to primary open-angle glaucoma: parapapillary atrophy is observed in eyes with glaucoma;51-53 glaucomatous eyes have larger parapapillary atrophy;51-55 and parapapillary atrophy is associated with the progression of glaucomatous visual field defect.56,57 It has been also reported that both alpha and beta zones of parapapillary atrophy were more frequently observed in eyes with acute or chronic primary angle-closure glaucoma than healthy eyes.44 Uchida et al., however, reported that prevalence of parapapillary atrophy was still lower in eyes with angle-closure glaucoma than in those with open-angle glaucoma.58

Visual field

Visual field in acute angle-closure glaucoma

The visual field changes are not so frequent in eyes after acute angle-closure. Longstanding or repeated elevation of intraocular pressure is necessary to develop detectable visual field loss.43,59,60 Douglas et al. reported that 11 (61%) of 18 eyes following acute angle-closure had no abnormal visual field, while ten (91%) of 11 eyes with chronic angle-closure showed apparent visual field changes.43 Bonomi et al. showed that abnormal visual fields were found in 19 (86%) of 22 eyes one or two days after acute angle-closure attack, while only 12 (55%) of the same 22 eyes showed field defects one month following the attack.59 Thus, visual field defects will not remain in about half of the eyes after acute angle closure attack. Recently, however, thinning of the retinal nerve fiber layer in the inferior region evaluated with optical coherence tomography was observed even in eyes after a single acute angle closure attack with normal visual field,61 suggesting that functional damage in such eyes should exist but it should be below the detectable level with the currently used perimetric techniques.

During acute angle closure attack, the condition of vision is such that reliable visual field testing is impossible. According to the study of Bonomi et al.,59 in eyes one or two days after acute angle closure attack, the most frequent abnormality found in visual field was general depression especially in the upper nasal quadrants; and severity of visual field defects was significantly correlated with maximum level of intraocular pressure during the attack and with the duration of the attack. Irregular depression of all isopters and enlargement of the blind spot, and widening of the angioscotoma, arcuate scotoma, and cecocentral scotoma can be listed as visual field changes during or just after acute angle closure attack.

Visual field in chronic angle-closure glaucoma

As to chronic angle-closure glaucoma, Lau et al.62 made detailed analysis of the patterns of visual field defects. They found that the superior and inferior nasal area was most commonly damaged in the early stage of chronic angle-closure glaucoma and the superior arcuate area was being involved with the deterioration of visual field damage. In comparison with primary open-angle glaucoma, visual filed damage of chronic angle-closure glaucoma shows more generalized pattern63 and the severity and speed of progression are more closely associated with the level of intraocular pressure.64,65 Gazzard et al.66 showed that the tendency that the superior hemifield is more severely affected than the inferior was less pronounced in angle-closure glaucoma than in open-angle glaucoma. Severity of visual field loss in chronic angle-closure glaucoma is also correlated with the extent of peripheral anterior synechia.67

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