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Journal of Neuro-Ophthalmology:
doi: 10.1097/WNO.0b013e3181d6f208
Letters to the Editor

Progressive Optic Neuropathy in Idiopathic Intracranial Hypertension After Optic Nerve Sheath Fenestration

Killer, Hanspeter E MD; Jaggi, Gregor P MD; Miller, Neil R MD

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Department of Ophthalmology, Kantonsspital Aarau, Aarau, Switzerland Eye Institute, University of Basel, Basel, Switzerland, Department of Ophthalmology, Kantonsspital Aarau, Aarau, Switzerland, Wilmer Ophthalmological Institute, Johns Hopkins Hospital, Baltimore, Maryland killer@ksa.ch

No financial or other conflicts of interest to be declared.

We read with interest the article by Wilkes and Siatkowski (1) and believe that it raises several important questions concerning the pathophysiology of papilledema. Their patient had idiopathic intracranial hypertension and underwent optic nerve sheath fenestration (ONSF) because of progressive visual loss, loss of color vision, and worsening visual field defects. The patient's visual parameters initially improved after surgery, including the development of spontaneous venous pulsations (SVP), but visual sensory function subsequently deteriorated again despite normal-appearing optic discs and persistent SVPs, suggesting normal intracranial pressure (ICP). A ventriculoperitoneal shunt was placed without effect on progressive visual loss.

Because the subarachnoid space (SAS) of the optic nerve (ON) contains numerous trabeculae and septa (2), it is probably incorrect to consider the SAS of the ON as one continuous cerebrospinal fluid (CSF) space that allows free flow of fluid throughout. Although an ONSF appears to be able to reduce ICP (evidenced in this case by the resolution of optic disc swelling and the appearance of SVPs), it is possible that some SAS compartments still exist that contain toxic substances in the trapped CSF. In a recent study, we found a deleterious effect of lipocalin-like prostaglandin D synthase, a substance that appears to be increased in the SAS of the ON in patients with papilledema (HE Killer, MD, unpublished data), on cultured astrocytes (3). The case reported by Wilkes and Siatkowski emphasizes that the pathophysiology of papilledema may be far more complicated than we used to believe (4). The use of more sophisticated imaging techniques, such as computed tomographic cisternography, provides a dynamic view of CSF flow and ultimately may be helpful in determining the optimum treatment for patients with worsening visual function in the setting of severe papilledema.

Hanspeter E. Killer, MD

Department of Ophthalmology, Kantonsspital Aarau, Aarau, Switzerland Eye Institute, University of Basel, Basel, Switzerland killer@ksa.ch

Gregor P. Jaggi, MD

Department of Ophthalmology, Kantonsspital Aarau, Aarau, Switzerland

Neil R. Miller, MD

Wilmer Ophthalmological Institute, Johns Hopkins Hospital, Baltimore, Maryland

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REFERENCES

1. Wilkes BN, Siatkowski RM. Progressive optic neuropathy in idiopathic intracranial hypertension after optic nerve sheath fenestration. J Neuroophthalmol. 2009;29:281-283.

2. Killer HE, Laeng HR, Flammer J, Groscurth P. Architecture of arachnoid trabeculae, pillars, and septa in the subarachnoid space of the human optic nerve: anatomy and clinical considerations. Br J Ophthalmol. 2003;87:777-781.

3. Xin X, Huber A, Meyer P, Flammer J, Neutzner A, Miller NR, Killer HE. L-PGDS (betatrace protein) inhibits astrocyte proliferation and mitochondrial ATP production in vitro. J Mol Neurosci. 2009;39:366-371.

4. Killer HE, Jaggi GP, Miller NR. Papilledema revisited: is its pathophysiology really understood? Clin Experiment Ophthalmol. 2009;37:444-447.

© 2010 Lippincott Williams & Wilkins, Inc.

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