Endoscopic Optic Nerve Decompression: Intracanalicular Portion

Optic Nerve Decompression

The Evolution of Optic Nerve Decompression

Although endoscopic transnasal surgery has become a widely used method for optic nerve decompression, its emergence would not be conceivable without technological advances in modern endoscopic surgery. Improvements in optics, instrumentation, and image-guided surgical navigation have transformed the approach to the optic nerve from an open craniotomy to the minimally invasive methodology of today. Historically, the route to the optic canal encompassed transcranial approaches (pterional, supraorbital, orbitozygomatic, and so on), which require both brain retraction and manipulation of critical neurovascular structures. Other surgical approaches that have been described include a medial approach by external ethmoidectomy or an inferomedial approach via a transantral transethmoidal route. The current purely endoscopic endonasal extended transsphenoidal approach provides a direct midline trajectory and immediate access to the base of both optic nerves, allowing for 270-degree decompression and bimanual microsurgical resection of associated pathology.

Since 1998, patients have benefited from the advantages of the endoscopic transnasal approach. These advantages include lack of external incisions, early extradural decompression of both optic nerves, preservation of olfaction, superior visualization of the infrachiasmatic perforators, and access to the inferomedial aspect of the optic nerve, a site often involved in neoplastic extension. In addition, a recent meta-analysis reported greater visual outcomes with the transnasal approach compared with the transcranial, with postoperative visual improvement in 75% and 58.4% of patients, respectively. The endoscopic transnasal approach is often criticized for higher rates of cerebrospinal fluid (CSF) leak compared with the transcranial approach. However, recent advancements in techniques for the coverage of skull base defects have provided a valuable solution: a vascularized pedicle nasoseptal flap offers robust tissue for coverage of skull base defects and has been shown to significantly reduce the CSF leak rate to 5.4%. Although this procedure is characterized by low invasiveness and wide exposure, endoscopic transnasal optic nerve decompression remains a procedure that is not yet practiced universally, a fact likely related to the close proximity of critical neurovascular structures localized in this portion of the skull.

Anatomy

Surrounding Structures

Optic nerve decompression remains a formidable challenge because of this structure’s intimate involvement with critical neurovascular structures, such as the optic apparatus and the anterior cerebral artery complex and associated perforators. The paranasal sinuses provide surgical access to the optic canal without compromising critical surrounding structures and subsequent functionality. The ethmoid sinus, bounded by the middle and superior turbinates, anterior skull base, and lamina papyracea, can be traversed to access the sphenoid sinus. The optic nerve impression can be found within the superolateral aspect of the sphenoid sinus, with the bulge of the internal carotid artery located just inferior ( Fig. 21.1 ). The lateral opticocarotid recess (OCR), a critical landmark representing the pneumanization of the optic strut of the anterior clinoid process, is located at the 10-o’clock and the 2-o’clock points laterally to the sellar floor ( Fig. 21.1 ). It should be noted that there is wide variability in sphenoid sinus pneumatization, and knowledge of a patient’s distinctive anatomy is essential when planning for optic nerve decompression.

In about 10% of cases, the optic nerve travels through a sphenoidethmoidal cell, also known as an Onodi cell, which is a posterior ethmoid cell that has pneumatized superolaterally to the sphenoid sinus ( Fig. 21.2 ). The prevalence of Onodi cells among a cohort of patients has been cited as high as 65.3%. This provides an opportunity for potential injury of the nerve if the appropriate attention is not given to identifying the nerve before entering the sphenoid sinus.

Pathology Involving the Optic Nerve: Indications and Contraindications for Decompression

A variety of insults can inflict injury on the optic nerve, ranging from traumatic etiologies to neoplasia. Furthermore, each disease process has the capability to inflict injury on the optic nerve through a variety of mechanisms, including ischemia, compression, demyelination, and tumor invasion. Although many of the mechanisms that cause optic neuropathy are irremediable, compressive insults are potentially reversible with timely surgical management.

Traumatic optic neuropathy (TON), a consequence of blunt head trauma, is a well-described cause of optic neuropathy. TON results in indirect injury to the optic nerve via increased intracranial pressure and vascular ischemia. Nontraumatic optic neuropathy is a less common disorder encompassing several etiologies, including endocrine orbitopathy, idiopathic intracranial hypertension, bone dysplasia, and infectious insults. These processes result in direct or indirect mechanical compression of the optic nerve or its vascular supply, resulting in atrophy.

In addition to the previously mentioned etiologies, surgical decompression of the optic nerve is useful in the resection of intracranial and extracranial tumors that invade the territory of the optic canal. Optic nerve decompression is indicated for both primary compressive processes, such as intraorbital tumors, or as a preliminary step in the pursuit to resect deeper pathology, such as pituitary adenomas. The endoscopic endonasal approach has been shown to treat lesions of the sellar and parasellar regions, such as meningiomas, pituitary adenomas, craniopharyngiomas, and sinonasal malignancies. Meningiomas commonly occur in this anatomically complex region, with anterior skull base meningiomas representing 40% of all intracranial meningiomas, and of these, 25% are tuberculum sellae tumors. These tumors are often characterized by extension into the optic canals, displacing the optic chiasm backward and the optic nerves superolaterally. Intracanalicular tumor extension typically occurs on the inferomedial side of the optic canal, a position difficult to visualize from an ipsilateral anterolateral approach but readily accessible by an endoscopic endonasal approach. This particular pathology highlights the benefits of wide exposure when working within the sellar region, especially within the optic canal, in regard to both the preservation of vision and avoidance of tumor recurrence.

In general, conservative management consisting of medical therapy should precede consideration of surgical decompression when appropriate. However, if there is no evidence of improvement, or if visual acuity deteriorates with the tapering of medical therapy, surgery should be performed. Optic nerve decompression is a well-known therapeutic concept that is indicated for the pathologic conditions of traumatic optic neuropathy, Graves ophthalmopathy associated with optic neuropathy, vision loss secondary to idiopathic intracranial hypertension (pseudotumor cerebri), fibro-osseous lesions, and the neoplasms mentioned previously. Considerable controversy exists regarding decompression for TON, particularly because of the high rate of spontaneous resolution without surgical intervention. The superiority of medical, surgical, or combination therapy remains a focus of current research endeavors. A recent meta-analysis by Dhaliwal, Sowerby, and Rotenberg reported that endoscopic decompression for treatment of TON resulted in improved visual outcomes compared with medical therapy or observation alone.

Contraindications for optic nerve decompression involve irreversible visual deficits resulting from complete disruption or atrophy of the nerve and/or chiasm before decompression. Another contraindication, specific to this procedure, is the presence of a carotid-cavernous fistula. As with all surgeries, other life-threatening problems or medical comorbidities making this surgical procedure hazardous will result in a lack of candidacy for surgical decompression.