Search

Oculomotor nerve paresis, ocular hypotony, anterior segment ischemia, and the ocular ischemic syndrome are uncommon manifestations of giant cell arteritis. Four patients with these findings had giant cell arteritis documented by temporal artery biopsy. Cerebral angiography or ultrasonography, or both, performed in three patients, excluded hemodynamically significant stenosis of the internal carotid artery as the cause of ocular ischemia and cerebral aneurysms as the cause of oculomotor nerve paresis. Corticosteroid treatment, administered to three patients, resulted in resolution of the oculomotor deficits and the clinical signs of ocular ischemia, although the visual acuity in one patient improved from 20/400 to 20/60. Giant cell arteritis should.be considered in the differential diagnosis of the ocular ischemic syndrome.

Anatomic features unique to periocular tissues alter the clinical appearance of angioedema, making it difficult to distinguish from cellulitis and other inflammatory conditions. Two patients had prominent periocular manifestations of chronic angioedema with necrotizing vasculitis, a systemic disease often associated with multiorgan involvement. The diagnosis was established by exclusion of other inflammatory disorders and confirmed by biopsy. The scarcity of reports in the ophthalmic literature on chronic angioedema of the eyelids may be caused by its underrecognition. The distinction between chronic angioedema and typical angioedema or urticaria is important because of differences in their diagnostic evaluation, treatment, and prognosis.

We studied four patients with HIV-associated optic neuropathies. One had syphilitic optic perineuritis, which responded promptly and completely to penicillin therapy. The second had cytomegalovirus papillitis and visual acuity subsequently deteriorated to no light perception. The third showed varicella zoster optic neuritis, which improved after intravenous acyclovir treatment. The fourth patient developed cryptococcal retrobulbar neuritis and died shortly thereafter. Optic neuropathy was among the initial symptoms of HIV infection in two of the four cases.

Intracranial hypertension with papilledema occurred in two patients receiving danazol therapy for either cyclic neutropenia or immune hemolytic anemia. Results of clinical, laboratory, and neuroradiologic studies showed no apparent cause for the condition in Case 1 and the papilledema resolved one month after discontinuing danazol. Carotid angiography in Case 2 demonstrated cerebral venous sinus thrombosis; the papilledema showed gradual improvement after cessation of danazol. An additional seven cases of pseudotumor cerebri presumed secondary to danazol therapy have been reported to the Food and Drug Administration. The papilledema resolved in all seven cases soon after discontinuing danazol. A drug-induced complication should be suspected, and alternative therapy sought, in patients who develop intracranial hypertension associated with administration of danazol.

Ocular motility manifestations of focal brainstem dysfunction were the initial clinical features in three patients with human immunodeficiency virus (HIV) infection. These included conjugate gaze palsy with ipsilateral facial paresis, bilateral abducens palsy and a gaze paresis, and homolateral internuclear ophthalmoplegia and abducens nerve paresis. Two patients had focal brainstem lesions as evidenced on neuroimaging. The third showed concurrent infection with Treponema pallidum.

We reviewed the records of 38 consecutive patients who had persistent binocular diplopia after cataract surgery. The patients were divided into ten categories based on the suspected conditions underlying the diplopia. Of 16 patients who underwent strabismus surgery, five achieved the therapeutic goal of single binocular vision in the primary and reading position, and four attained this with prismatic or botulinum toxin therapy in addition to surgery. Seven patients continued to have diplopia despite strabismus surgery and adjunctive therapy. Even small residual deviations were often intolerable, because of highly diminished fusional amplitudes.

Presumed accidental corneal exposure to Hibiclens (chlorhexidine 4% and detergent) in two patients resulted in severe and permanent corneal opacification. We investigated the corneal toxicity of Hibiclens by gross, biomicroscopic, and histopathologic studies of rabbit eyes exposed to Hibiclens for varying time intervals ranging from five to 15 minutes. Severe, irreversible, and progressive corneal damage resulted in all eyes studied.

We examined three patients who developed optic neuropathies while undergoing chronic hemodialysis. One patient developed severe bilateral deterioration of vision, but recovered totally four weeks after discontinuing deferoxamine chelation therapy. Another patient had bilateral visual loss associated with chronic papilledema of idiopathic increased intracranial pressure. A third showed atypically severe consecutive anterior ischemic optic neuropathy. The latter two patients showed little improvement with high-dose intravenous methylprednisolone therapy combined with more vigorous hemodialysis. These cases, in addition to those previously described, underscore the heterogeneity of optic nerve disease in patients with uremia.