Endoscopic Endonasal Optic Nerve Decompression for Benign Pathology of the Optic Canal

Objective: To evaluate visual outcomes and possible complications of a single institution's experience with the endoscopic endonasal approach (EEA) for optic nerve decompression for benign pathology affecting the canalicular segment of the optic nerve.

Background: Optic nerve decompression for benign pathology involving the canalicular segment of the optic nerve has traditionally been accomplished with open trans-cranial approaches. Advances in transnasal endoscopic techniques and instrumentation have enabled the EEA to be utilized in select cases.

Methods: A retrospective review of patients with intrinsic or extrinsic compression of the canalicular segment of the optic nerve that underwent an endoscopic endonasal optic nerve decompression at the University of Pittsburgh Medical Center from 2010–2013 was performed. Patients with malignant pathology, traumatic optic neuropathy, suprasellar or tuberculum meningiomas, or who underwent a concurrent trans-cranial approach were excluded. Patients underwent a spheno-ethmoidectomy and optic nerve decompression that was frequently accompanied by orbital decompression. The primary outcomes assessed included visual acuity and field testing. Visual acuity was categorized as normal (20/20) or mild (20/25 - 20/60), moderate (20/70 - 20/160), severe (20/200 - 20/400), and profound (20/500 - 20/1000) deficits. Visual field testing was evaluated relative to preoperative status.

Results: A total of 7 patients (4 female, 3 male) and 8 optic nerves were decompressed via an EEA. The mean age was 38.7 years old (range 16 - 61). Diagnoses included fibrous dysplasia (n = 4), optic nerve sheath meningioma (n = 2), and a persistent orbital apex meningioma after prior lateral sphenoid wing tumor resection (n = 1). Decreased visual acuity preoperatively (3 mild, 2 moderate, 1 profound) was noted in 6 patients while the remaining patient demonstrated an afferent pupillary defect consistent with early compressive optic neuropathy. All patients with available formal postoperative ophthalmologic examination had improvement in visual acuity with five nerves returning to normal visual acuity postoperatively (from mild [n = 4] and profound [n = 1] preoperative deficits) and 2 nerves demonstrating improvement but with a persistent mild deficit (from mild [n = 1] and moderate [n = 2] preoperative deficits). Visual field testing was ultimately improved in 2 nerves, stable in 3 nerves and was incomplete for the remaining nerves. Persistent diplopia in a single patient was the only complication noted.

Conclusion: EEA for optic nerve decompression appears to be a safe and effective treatment for patients with intrinsic or extrinsic involvement of the canalicular segment of the optic nerve by benign pathology. Further studies are required to confirm these findings as well as identify patient selection parameters for an open versus an endoscopic approach.