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Objective: To determine the efficacy of optic nerve sheath fenestration in eyes with the progressive form of common anterior ischemic optic neuropathy. This investigation complements a previously reported initial series of 26 similar patients., Patients and Methods: Optic nerve sheath fenestrations were performed in 21 eyes for treatment of common (nonarteritic) ischemic optic neuropathy with documented progressive deterioration of visual function. All patients underwent thorough preoperative and postoperative ocular evaluations by the Neuro-Ophthalmology Service at the Bascom Palmer Eye Institute, Miami, Fla., Results: During a mean follow-up of 22.5 weeks (range, 3 to 104 weeks), results were as follows: visual acuity increased by 2 or more lines on the Snellen chart in two eyes (9.5%; the combined improvement rate for the two series was 14.9%); visual acuity decreased by 2 more lines in two eyes (9.5%)., Conclusions: Data from this series of 21 surgical procedures indicate no beneficial effect on visual morbidity in cases of common ischemic optic neuropathy and confirm the generally poor visual outcome implied from the results of optic nerve sheath decompression in our initial series. Based on this experience with a total of 47 eyes, we have discontinued optic nerve sheath decompression as a form of therapy for ischemic optic neuropathy.

Pulseless disease (PD) is a rare disorder in which inflammation of the aorta and its major branches leads to stenosis or occlusion of these arteries. It mainly affects young Oriental women, who suffer chronic ischemic injury to tissues of the brain, orbits, upper limbs, myocardium, and kidneys. The ophthalmologic features of pulseless disease tend to be late manifestations, and can include ischemia of the retina, choroid, and anterior segment. The inflammatory process may be reversed in early stages with systemic corticosteroids, but, more frequently, significant arterial stenosis necessitates arterial bypass surgery. A 59-year-old Caucasian woman with stenosis of all four major cervical arteries presented with recurrent blurred vision, syncope, mental obtundation, and a remarkable funduscopic appearance due to bilateral orbital hypoperfusion. Her acute symptoms improved slightly on high-dose systemic corticosteroids, and then resolved completely following arterial bypass surgery.

Optic nerve sheath fenestration was performed in 26 eyes for treatment of the progressive type of common (nonarteritic) anterior ischemic optic neuropathy. During a mean follow-up period of 21 weeks (range, 6 to 52 weeks), results were as follows: visual acuity increased by two or more lines on the Snellen chart in 7 eyes; visual acuity decreased by two or more lines in four eyes; some regression of visual field defects occurred in six eyes, including two eyes in which acuity also improved. These results, attributed to surgical decompression, do not exceed the spontaneous recovery rates reported in the literature pertaining to nonarteritic anterior ischemic optic neuropathy and fail to substantiate the sanguine visual outcome in recently reported series of patients undergoing optic nerve sheath decompression.

Four patients with typical anterior ischemic optic neuropathy experienced progressive deterioration of visual function, to acuity levels of finger-counting in two eyes, 20/400 in one, and 20/50 in the fourth. All subsequently enjoyed significant spontaneous recovery of vision to 20/60, 20/60, 20/40, and 20/25, respectively. No previous reports have documented the details of such improvement in the progressive form of anterior ischemic optic neuropathy. The natural history of this common optic nerve disorder is reconsidered in light of these observations. The potential for spontaneous recovery should be taken into account in the interpretation of visual outcome in medical or surgical therapeutic trials for progressive anterior ischemic optic neuropathy.

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.

The etiology of anterior ischemic optic neuropathy (AION), when not associated with giant cell arteritis, is usually unknown. Clinical, pathologic, and experimental studies have not determined a cause. The optic disc appearance in both the involved and normal fellow eye was studied in 51 patients with acute nonarteritic AION. The number of discs (both involved and fellow) without a physiologic cup was significantly greater than would be expected from normal population studies. The etiology of nonarteritic AION may be related to the anatomic configuration of the optic nerve.

Anterior ischaemic optic neuropathy is characterised by a sudden, painless loss of vision, optic disc oedema, and nerve fibre bundle visual field defects. It may be associated with giant cell arteritis but is usually idiopathic. Although subsequent involvement of the second eye is common, more than one episode in the same eye is extremely rare. Four patients with recurrent anterior ischaemic optic neuropathy in the same eye are described.

Of 196 patients with anterior ischemic optic neuropathy, 169 had the nonarteritic form and 27 had the arteritic type. Visual acuities were 20/40 or better in 83 of 184 eyes with nonarteritic anterior ischemic optic neuropathy but only eight of 45 eyes with the arteritic type. We found systemic disease associations for hypertension and diabetes mellitus only for patients with nonarteritic anterior ischemic optic neuropathy who were between 45 and 64 years of age. After a mean follow-up period of five years, 92 nonarteritic patients showed no changes in the first affected eye; there was eventual involvement of the second eye in 20 patients.

Twenty-two patients with ischemic chiasmal syndrome (ICS) have been examined by means of magnification angiography and polytomographic encephalography. The causes of ICS may be divided into 5 categories: (1) mechanical compression of the chiasm by ectatic redundant anterior cerebral arteries, (2) atherosclerotic vascular occlusions, (3) optochiasmal arachnoidal fibrosis, (4) various forms of arteritis especially giant cell (cranial) arteritis, and (5) post-partum pituitary necrosis associated with ICS. The most common cause of ICS appears to be optochiasmal arachnoiditis which occasionally developed some time after a craniotomy and radiation therapy for pituitary or other juxta-sellar tumors; similar fibrotic change may develop following steroid treatment of granulomatous lesions.