Neuro-Ophthalmologic Monitoring in the Management of Increased Intracranial Pressure From Leaking Arachnoid Cysts.

BACKGROUND: Intracranial arachnoid cysts are common incidental imaging findings. They may rarely rupture, leading to the development of subdural hygromas and high intracranial pressure (ICP). Neurosurgical intervention has been advocated in the past, but recent evidence indicates that most cases resolve spontaneously. The role of neuro-ophthalmologic monitoring in identifying the few cases that have persisting vision-threatening papilledema that justifies intervention has not been emphasized. METHODS: Retrospective review of 4 cases of leaking arachnoid cysts drawn from the files of the University of Michigan Medical Center (Michigan Medicine) between 2007 and 2018. RESULTS: In 1 case, surgery was avoidable as papilledema resolved over time despite lingering imaging features of mass effect. In 3 cases, papilledema persisted with the threat of permanent vision loss, prompting neurosurgical intervention. In one of those cases, the fluid collection was thinly but extensively spread across both hemispheres without brain shift; yet, papilledema was pronounced. Emergent evacuation led to rapid resolution of papilledema and encephalopathy, but with residual optic nerve damage. CONCLUSIONS: Because constitutional symptoms and even imaging are not always reliable indicators of high ICP in leaking arachnoid cysts, neuro-ophthalmologic monitoring of papilledema is valuable in identifying the cases when neurosurgical intervention is necessary.

Management of Peripapillary Choroidal Neovascular Membrane in Patients With Idiopathic Intracranial Hypertension.

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.

Neuro-ophthalmologic exploration in non-functioning pituitary adenoma.

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.

Bilateral fungal endophthalmitis masquerading as multifocal chorioretinitis.

PURPOSE: Spontaneous healing of ocular Candida infection is extremely rare, and early clinical manifestations may be misleading. This report explicates how to make the appropriate diagnosis when facing atypical presentation of the disease. METHODS AND PATIENTS: Case report. RESULTS: A 36-year-old woman presented with bilateral chorioretinitis. Intravenous drug abuse was not suspected, and a diagnosis of multifocal chorioretinitis was made. Oral corticosteroid treatment was started. Three months later, all previously seen lesions had healed on the right eye but had increased on the left with development of severe endophthalmitis. Microbiologic analysis of scalp pustules yielded Candida albicans. She underwent vitrectomy, intravitreous amphotericin B injection, and systemic fluconazole treatment. The uveitis responded well to this treatment regiment, but subsequent development of macular edema and retinal detachment in the left eye limited the final visual acuity to 20/200. Visual acuity remained 20/20 on the right without any evidence of inflammation. CONCLUSION: This case demonstrates a broad range of potential outcomes after Candida endophthalmitis in the same patient, from very rare healing without antifungal treatment in one eye to severe panuveitis in the other eye. The delayed diagnosis in this case led to the inappropriate treatment with corticosteroids alone and delayed antifungal treatment. Early differentiation of Candida chorioretinitis from multifocal chorioretinitis is critical to final visual outcome.

Positive apraclonidine test 36 hours after acute onset of horner syndrome in dorsolateral pontomedullary stroke.

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.