Feasibility and efficacy of endoscopic transorbital optic canal decompression for meningiomas causing compressive optic neuropathy.

OBJECTIVE

The endoscopic transorbital approach (ETOA) and transorbital anterior clinoidectomy have been suggested as novel procedures through which to reach the superolateral compartments of the orbit, allowing optic canal decompression. However, there is limited literature describing the technical details and surgical outcomes of these procedures. In this study, the authors aimed to analyze the feasibility and efficacy of endoscopic transorbital decompression of the optic canal through anterior clinoidectomy for compressive optic neuropathic lesions.

METHODS

Between 2016 and 2022, the authors performed ETOA for compressive optic neuropathic lesions in 14 patients. All these patients underwent transorbital anterior clinoidectomy through the surgically defined "intraorbital clinoidal triangle," which is composed of the roof of the superior orbital fissure, the medial margin of the optic canal, the medial border of the superior orbital fissure, and the optic strut. Demographic data, tumor characteristics, pre- and postoperative imaging, pre- and postoperative visual examinations, and surgical outcomes were retrospectively reviewed.

RESULTS

The mean age at the time of ETOA was 53.3 years (range 41-64 years), and the mean follow-up was 16.8 months (range 6.7-51.4 months). The inclusion criterion in this study was having a meningioma (14 patients). In the preoperative visual function examination, 7 patients with a meningioma showed progressive visual impairment. After endoscopic transorbital optic canal decompression, visual function improved in 5 patients, remained unchanged in 8 patients, and worsened in 1 patient. No new-onset neurological deficit was associated with ETOA and anterior clinoidectomy in any patients.

CONCLUSIONS

Endoscopic transorbital decompression of the optic canal with extradural anterior clinoidectomy is a safe and feasible technique that avoids significant injury to the clinoidal internal carotid artery and surrounding neurovascular structures.