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Volume 116, Issue 9, Pages 1808-1813.e1 (September 2009)


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Functional Visual Loss in Idiopathic Intracranial Hypertension

Presented at: the American Academy of Ophthalmology Annual Meeting, November 2008, Atlanta, Georgia.

Joshua J. Ney, MD1, Nicholas J. Volpe, MD12Corresponding Author Informationemail address, Grant T. Liu, MD1, Laura J. Balcer, MD, MSCE1, Mark L. Moster, MD2, Steven L. Galetta, MD1

Received 19 October 2008; received in revised form 16 March 2009; accepted 24 March 2009. published online 30 July 2009.

Objective

To identify and describe patients with idiopathic intracranial hypertension (IIH) with concurrent functional visual loss (FVL).

Design

Observational, retrospective case series.

Participants

Seventeen patients with IIH and FVL.

Methods

Clinical features were collected retrospectively. Data from 281 cases of IIH were analyzed for concurrence of FVL.

Main Outcome Measures

Occurrence of FVL diagnosed at presentation or on subsequent follow-up.

Results

Seventeen patients had FVL and IIH. Of the 17 patients with FVL and IIH, 11 (65%) had FVL on presentation, with the remaining 6 patients developing FVL after initial presentation. Two patients in this cohort had documented recurrence of their IIH. There were several common patterns of FVL. All 17 patients had functional visual fields, with 82% having tubular fields and 71% exhibiting nonphysiologic constriction on perimetry testing. Seventy-six percent of patients had nerve/field mismatch showing no atrophic disc changes. Eighty-eight percent of patients had significant psychiatric, psychosocial, or other medical comorbidities. The majority of patients were managed surgically at some point in their clinical history, with 53% having nerve decompression, shunt, or both. Three patients had optic nerve sheath fenestrations after the diagnosis of FVL.

Conclusions

Results suggest a high prevalence of FVL in IIH with a potential association with psychiatric illness and psychosocial stressors requiring careful consideration before surgical intervention.

Financial Disclosure(s)

The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Available online: May 1, 2009.

1 Departments of Neurology and Ophthalmology, Scheie Eye Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

2 Department of Neurosensory Sciences, Albert Einstein Medical Center, Philadelphia, Pennsylvania

Corresponding Author InformationCorrespondence: Nicholas J. Volpe, MD, Scheie Eye Institute, 51 North 39th Street, Philadelphia, PA 19104

 Manuscript no. 2008-1236.

 Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

PII: S0161-6420(09)00367-4

doi:10.1016/j.ophtha.2009.03.056


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