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Show Letters to the Editor Idiopathic Intracranial Hypertension Without Papilledema With Improvement in Visual Field Defect Following Optic Nerve Sheath Fenestration: Comment I Downloaded from http://journals.lww.com/jneuro-ophthalmology by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdgGj2MwlZLeI= on 05/04/2022 read with interest the recent article in JNO by ScofieldKaplan et al (1). Although I appreciate the difficulties authors faced in taking care of this patient, I am struck by the lack of objective evidence of visual dysfunction in this case where, literally, every intervention possible has been used (optic nerve sheath fenestration, dural sinus stenting, and now the patient is waiting for a CSF diversion procedure). Authors acknowledge the high prevalence of functional visual field loss in patients with idiopathic intracranial hypertention (IIH), and in fact, the visual fields in this patient do look nonphysiologic exhibiting very symmetric concentric constriction. Authors state that “. . . confrontational visual fields did not suggest a nonphysiologic defect” but that is not a confirmation that these fields represented organic pathology. Although authors postulate that the optic nerve swelling involved retrobulbar compartment of both optic nerves only and did not involve the optic nerve head, to my knowledge, none of the patients who were previously reported to have IIH without papilledema had central or peripheral visual loss (2,3). We also know that patients with severe IIH who have decreased central vision and severe visual field loss at presentation (which by itself is uncommon in IIH), such as the patient described in this article, will almost invariably develop varying degrees of optic nerve pallor and thinning of ganglion cell layer of the macular complex (not reported here) after the resolution of papilledema. If ganglion cell analysis of the macular complex was performed and was normal, the objective causes of optic nerve dysfunction here can be ruled out as even if increased intracranial pressure involved only the retrobulbar component of the optic nerves, it would have caused obvious loss of the ganglion cells in the macular complex, especially with the Idiopathic Intracranial Hypertension Without Papilledema With Improvement in Visual Field Defect Following Optic Nerve Sheath Fenestration: Response W e read with interest the letter from Dr. Margolin concerning our article “Idiopathic intracranial hypertension without papilledema with improvement in visual field following optic nerve sheath fenestration” (1). In reply, we wish to focus on the main point stressed in Letters to the Editor: J Neuro-Ophthalmol 2021; 41: 135-140 degree of the visual compromise this patient was reporting on subjective testing (central acuities and peripheral visual fields). On another note, measurements of opening pressure on lumbar puncture (LP) are prone to error especially when LP is not performed in lateral decubitus position as was the case here. I believe it is important to comment on this case because the obvious take home message otherwise is that any patient with severe headaches, despite the absence of papilledema is at risk of visual loss and requires further investigations and treatment, which I do not believe is the case. Although it is possible that this patient had intracranial hypertension (they did have indirect imaging sings of increased intracranial pressure and had increased opening pressure on several LPs), there was no objective evidence of visual dysfunction such as optic nerve head pallor, presence of relative afferent pupillary defect or thinning of retinal nerve fiber layer, and/or ganglion cell layer on ocular coherence tomography. Thus, it is very difficult to believe that the subjective findings here (decreased acuities and constricted visual fields) were real. Edward Margolin, MD Department of Ophthalmology and Vision Sciences and Department of Medicine, University of Toronto, Toronto, Canada The author reports no conflicts of interest. REFERENCES 1. Scofield-Kaplan SM, Patel K, Jones FR Jr, Hogan RN. Idiopathic intracranial hypertension without papilledema with improvement in visual field defect following optic nerve sheath fenestration. J Neuroophthalmol. 2021;41:e31–e33. 2. Hoffmann J, Mollan SP, Paemeleire K, Lampl C, Jensen RH, Sinclair AJ. European headache federation guideline on idiopathic intracranial hypertension. J Headache Pain. 2018;19:93. 3. Sengupta S, Eckstein C, Collins T. The dilemma of diagnosing idiopathic intracranial hypertension without papilledema in patients with chronic migraine. JAMA Neurol. 2019;76:1001– 1002. his letter, which is the lack of objective evidence of visual dysfunction. In the previous publications regarding idiopathic intracranial hypertension without papilledema (IIHWOP), the overwhelming majority have normal visual fields with few having nasal defects or nonphysiologic visual fields (2,3). In a previous study, a nonphysiologic visual field was reported if on tangent screen testing, the 3-m visual field was inside the 1-m visual field (2). Although we do not have tangent screen results for our patient, we performed confrontation visual fields at numerous distances, which did not show similar or worse constriction when confrontation 135 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
