Non-functioning pituitary adenoma may lead to blindness and causes visual impairment in 58% of cases and, more rarely, ocular motor disorder. Patients are slow to become aware of their visual dysfunction, vision in one eye compensating the deficit in the other. Assessment of visual function, comprising visual acuity and visual field evaluation and fundus examination, should be performed regularly according to the severity of impairment. Optic nerve optical coherence tomography (OCT) can quantify optic atrophy reproducibly, and is of prognostic value for postoperative visual recovery. Diplopia most often involves decompensation of heterophoria, visual field fusion being hampered by the visual field defect; such diplopia without ocular motor deficit is known as "hemifield slide". Diplopia associated with ocular motor palsy is caused by tumoral invasion of the cavernous sinus (IIIrd, IVth or VIth nerve palsy); in large impairment, restricted eye movement is easily observed; milder palsies require neuro-ophthalmologic assessment and/or Lancaster test. Pituitary apoplexy induces ocular motor impairment in 70% of cases, strongly guiding diagnosis. Visual impairment is associated in 75% of cases. The degree of neuro-ophthalmologic (visual and ocular motor) impairment is one of the main criteria guiding treatment of pituitary apoplexy (conservative medical and/or surgical treatment) and follow-up.
A 40-year-old man developed a Horner syndrome as part of a dorsolateral medullary brainstem infarction. Thirty-six hours after the onset of the stroke, topical instillation of 0.5% apraclonidine produced reversal of anisocoria. This is the first case in which apraclonidine testing has been applied to a patient with a Horner syndrome caused by a lesion in the first segment of the oculosympathetic pathway and the shortest reported interval between clinical manifestations of the lesion and apraclonidine-induced reversal of anisocoria. A review of all reported cases of apraclonidine testing in Horner syndrome suggests that this is a promising diagnostic adjunct that must be validated in larger studies.
OBJECTIVE To report the clinical features and treatment outcomes of patients with peripapillary choroidal neovascular membrane (CNVM) secondary to idiopathic intracranial hypertension (IIH). METHODS Retrospective, multicenter chart review of patients diagnosed with peripapillary CNVM in the course of the treatment and follow-up of IIH. RESULTS Records were reviewed from 7 different institutions between 2006 and 2016. Ten patients (13 eyes) with a diagnosis of IIH and at least 3 months of follow-up developed CNVM. Three of the total 10 patients developed bilateral CNVM. The mean time from the diagnosis of IIH to CNVM diagnosis was 41 months. Mean follow-up period was 8 months after diagnosis of CNVM. All patients were treated with acetazolamide for IIH. Seven eyes were observed, and 6 eyes were given anti-vascular endothelial growth factor (anti-VEGF) injections, including bevacizumab, ranibizumab, and aflibercept. All CNVMs regressed with subretinal fibrosis, and visual acuity improved in most patients. Papilledema resolved in only 1 eye, while the other 12 eyes had persistent papilledema at last follow-up. CONCLUSIONS Peripapillary CNVM, a rare complication of IIH, often resolves spontaneously with treatment of IIH. In vision-threatening and/or persistent cases, intravitreal anti-VEGF treatment may be a safe and effective therapeutic option.
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