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Purpose: To report infraorbital nerve dysfunction after laser in situ keratomileusis., Design: Observational case report., Methods: Neuro-ophthalmologic examination with brain and orbital magnetic resonance imaging (MRI) and orbital computed tomography (CT)., Results: During laser in situ keratomileusis, two healthy women, aged 42 and 46 years, experienced acute onset of sharp ipsilateral cheek pain. Both cases occurred during manipulation of the eyelid speculum. Postoperatively, ipsilateral numbness and tingling or pain of the upper cheek was reported, and examination showed decreased sensation in the distribution of the infraorbital nerve. In both cases, brain and orbit MRI and orbit CT were normal. Both patients were managed medically. In one patient, mild symptoms persisted 1 year postoperatively, and in the second patient, moderate discomfort persisted 8 months postoperatively., Conclusion: Infraorbital nerve palsy is a potential complication of laser in situ keratomileusis. Symptoms improve but may persist.

Purpose: We examined a 28-year-old woman who developed incongruous binasal and bitemporal visual field defects one week after having a febrile gastroenteritis characterized by severe diarrhea while traveling in Mexico., Methods: The patient was treated with intravenous methylprednisolone sodium succinate, 1 g daily for three days, followed by an eight-week course of oral prednisone., Results: Neuroradiologic examination demonstrated bilaterally increased signal intensity within the lateral geniculate bodies. Cerebrospinal fluid analysis disclosed isolated protein increase., Conclusion: Severe diarrhea may be associated with an aseptic bilateral lateral geniculitis resulting in hourglass-shaped visual fields. Corticosteroid therapy may provide mild improvement.

Purpose: Severe vistral acuity loss associated with pseudotumor cerebri is usually caused by chronic optic disk edema or a retinal abnormality., Methods: We treated a women, with known pseudotumor cerebri treated with a lumboperitoneal shunt, who developed acute pallied optic disk swelling and visual acuity of R.E.: no light perception and L.E.: 20/70 in association with lumboperitoneal shunt failure. There were no contributory retinal lesions., Results: The patient underwent optic nerve sheath fenestration and lumboperitoneal shunt revision. Visual acuity improved to 20/20 in both eyes. The papilledema resolved., Conclusion: The severe sudden visual loss was attributed to axoplasmic stasis and optic nerve ischemia associated with a sudden rise in intracranial pressure.

Purpose/methods: Orthoclone OKT3 is a monoclonal murine IgG immunoglobulin used to treat acute cellular rejection of allografted organs. Aseptic meningitis and meningoencephalopathy are known adverse side effects from the drug. OKT3 caused additional ophthalmologic and neurologic complications in an 18-year-old woman who was treated for transplanted kidney graft rejection. Papilledema and bilateral abduction deficits developed., Results/conclusions: Results of magnetic resonance imaging and magnetic resonance angiography were unremarkable. Lumbar puncture disclosed increased intracranial pressure and sterile meningeal inflammation. Most of the symptoms resolved by one week after discontinuation of OKT3. Ophthalmologists and neurologists should be aware that optic disk swelling and abducens palsies can be associated with OKT3 when used in the treatment of transplanted kidney graft rejection.

We treated four patients who had acute, severe visual loss associated with pseudotumor cerebri with intravenous methylprednisolone (250 mg four times per day) for five days followed by an oral taper, in combination with acetazolamide and ranitidine. In addition to high-grade disk edema, one patient had serous detachment of both maculas and lipid deposition, one had a unilateral macular star, and one had a monocular branch retinal artery occlusion. These three patients experienced rapid and lasting improvement in visual acuity, visual field, papilledema, and symptoms. Vision of the fourth patient did not improve, requiring optic nerve sheath fenestration for chronic papilledema. Transient acne developed in one patient. This regimen is a safe, effective treatment of acute, severe visual loss associated with florid papilledema of pseudotumor cerebri. Lack of immediate improvement is an indication for optic nerve sheath decompression.

We treated two patients with Crohn's disease and one patient with ulcerative colitis who developed headache, papilledema, and intracranial hypertension (pseudotumor cerebri) during corticosteroid withdrawal. One had four separate episodes with corticosteroid withdrawal, which suggested a causal relationship. This association between pseudotumor cerebri and corticosteroid withdrawal has been documented in children, but is rare in adults with inflammatory bowel disease.

After transsphenoidal resection of a pituitary (or other) tumor, the remaining intrasellar cavity, and sphenoid sinus are usually packed with exogenous fat or muscle to prevent cerebrospinal leak and prolapse of the optic chiasm into an empty sella. We treated two patients in whom chiasmal compression occurred postoperatively because of packing of fat. In one patient, the expected visual improvement in the postoperative period was suboptimal. The subsequent removal of fat resulted in total visual recovery. In the other patient, chiasmal compression persisted from intrasellar fat and residual tumor. Iatrogenic compression of the optic nerves or chiasm should be considered in all patients in whom visual recovery is incomplete.

Clinical data and fundus fluorescein angiograms were analyzed from 35 patients with acute (onset less than four weeks) anterior ischemic optic neuropathy. Nineteen of the 35 patients (54%) had nonarteritic disease, and 16 patients (46%) had giant cell arteritis confirmed by biopsy. Patients with arteritis had higher erythrocyte sedimentation rates, larger cup/disk ratios, and delayed fluorescein dye appearance and choroidal filling times. Three additional patients with cranial arteritis confirmed by biopsy, but without visual loss, had angiographic characteristics similar to patients with arteritic ischemic neuropathy. We consider fluorescein angiography a valuable diagnostic adjunct in identifying patients with giant cell arteritis.

Hodgkin's disease is a rare cause of infiltrative optic neuropathy, which typically evolves late in the disease course. We managed an unusual case of isolated optic neuropathy in a 21-year-old man occurring during clinical remission from Hodgkin's disease. Radiotherapy and treatment with high-dose systemic corticosteroids resulted in dramatic improvement in vision. Even without other evidence of recurrent disease, acute-onset optic neuropathy in a patient with a history of a lymphoproliferative disorder should raise the question of a reemergence of the malignancy.

Three patients with delayed radiation optic neuropathy after radiation therapy for parasellar neoplasms underwent magnetic resonance imaging. The affected optic nerves and chiasms showed enlargement and focal gadopentetate dimeglumine enhancement. The magnetic resonance imaging technique effectively detected and defined anterior visual pathway changes of radionecrosis and excluded the clinical possibility of visual loss because of tumor recurrence.

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.

A 40-year-old white woman had slowly progressive unilateral loss of visual acuity and increasing proptosis during an eight-year period. Ophthalmoscopy and fluorescein angiography revealed chronic disk edema and optociliary shunt vessels in the right eye. Polytomography showed an enlarged right optic canal. Cerebral arteriography demonstrated a dumbbell-shaped tumor blush in the right juxtasellar region and a diffuse tumor blush in the right orbit. Right frontal craniotomy and orbital exploration showed a cranio-orbital junction (spheno-orbital) meningioma that invaded the sclera and peripapillary choroid. Anomalous optociliary veins were demonstrated histologically at the optic disk.

We performed visual contrast sensitivity testing with Regan's low-contrast letter charts on 30 patients with optic neuropathies and good Snellen visual acuity. Results of this testing were compared with color vision and the presence of an afferent pupillary defect. Regan's low-contrast letter charts were found to be 93% sensitive for detecting subtle optic neuropathies, with the apparent false-negative findings being readily explainable. Color vision testing was abnormal in only 49% of eyes with known optic neuropathies.

A 24-year-old woman developed bilateral blindness after recovery from coma secondary to acute intermittent porphyria. Gradual return of vision in the right eye with a permanent unilateral visual field defect and optic atrophy followed. We believe the pathophysiologic mechanism was spasm of the vessels supplying the optic disk leading to ischemia and infarction of the optic nerve.

Two patients had paresis of the trochlear nerve contralateral to the site of lesions in the brainstem. Both patients had ipsilateral blepharoptosis and miosis suggesting oculosympathetic paresis from involvement of the descending sympathetic tract, adjacent to the fourth cranial nerve nucleus and its fascicles, in the caudal mesencephalon. Cerebral antiography documented an arteriovenous malformation of the brainstem in Case 1. Magnetic resonance imaging disclosed a lesion of high signal intensity on T2-weighted images involving the dorsal mesencephalon in Case 2. Involvement of the superior cerebellar peduncle produced ipsilateral dysmetria and ataxia. Lesions involving the fourth cranial nerve nucleus or its fascicles, before decussation in the superior medullary velum, and adjacent sympathetic fibers may produce an ipsilateral Horner's syndrome and contralateral superior oblique muscle paresis.

Three patients with multiple sclerosis (women 20, 24, and 30 years old) had demyelinative plaques that produced homonymous hemianopsia. These lesions were identified by computed tomography which showed the plaques as hypodense areas. All patients with homonymous hemianopsia should undergo computed tomography; if a hypodense or enhancing lesion is identified, the diagnosis of multiple sclerosis must be considered.

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.

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.

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.