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.
The Orbital Apex
Composed of seven different bones, the orbit encompasses the eye, extraocular muscles, nerves, blood vessels, fat, and much of the lacrimal apparatus. The periorbita encases the extraconal space, which consists mostly of orbital fat. Located within the fascia of the extraocular muscles, the intraconal space contains the muscles, optic nerve, and ophthalmic artery. Situated at the intersection of the cranium and face, the orbit contains multiple intricate orifices that convey a vast network of neurovascular elements. The orbit communicates with the middle cranial fossa via the optic canal and superior orbital fissure, the infratemporal fossa and the pterygopalatine fossa via the inferior orbital fissure, the nasal cavity via the anterior and occasionally the posterior ethmoidal foramen, the inferior meatus of the nose via the nasolacrimal canal, and the face via the infraorbital and supraorbital foramen.
The orbital apex, positioned at the posterior aspect of the pyramid-shaped orbit, exists at the craniofacial junction linking the orbit and anterior ventral skull base. Situated in the medial portion of the apex, the optic canal is neighbored laterally by the superior orbital fissure. These two channels are separated by a thin osseous wall known as the optic strut. The inferior orbital fissure lies in the inferolateral aspect of the apex, located between the lateral wall and floor of the orbit. The annulus of Zinn, another elemental landmark of the orbital apex, remains the site of attachment for the extraocular muscles. This fibrous thickening is the least expandable portion of the optic sheath and is usually located at the narrowest part of the optic canal.
The Optic Nerve and Its Canal
Unlike other peripheral nerves, the optic nerve is a direct extension of the brain and has three meningeal layers as well as subarachnoid space containing CSF. There are four segments of the optic nerve: intracranial, intracanalicular, intraorbital, and intraocular. Once intraorbital, the dura of the optic nerve splits to form an outer layer, contributing to the periorbital, and an inner layer, which merges with the arachnoid. The intracanalicular optic nerve shares the optic canal with the ophthalmic artery, typically located inferomedially to the nerve, making it highly susceptible to injury from a midline approach. The optic canal is bounded medially by the body of the sphenoid bone, superiorly by the anterior root of the lesser wing of the sphenoid, and inferolaterally by the optic strut. The anterior clinoid process forms the lateral margins of the optic canal. Attached to this process is the falciform ligament, a dural fold that extends over the optic nerve to attach to the tuberculum sellae.
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.
Each patient considered for optic nerve decompression should undergo a thorough and complete ophthalmologic physical examination, including fundoscopic evaluation, measurement of intraocular pressure, visual field testing, visual acuity testing, and color vision testing as the perception of red is lost first. If the patient is unable to cooperate or unconscious, monitoring of visual evoked potentials is of high value. Other causes of vision loss should be ruled out before proceeding with the procedure.
Preoperative radiographic imaging should include fine-cut computed tomographic (CT) scans of the sinuses and orbits to evaluate the anatomy and extent of optic canal compression. This imaging modality offers information on the ethmoid and sphenoid sinus pneumatization and septation. Additionally, a fine-cut CT scan reveals dehiscence of the carotid artery. CT scans are also valuable in assessing bone density and thickness, noteworthy details in cases of spheno-orbital meningiomas or fibrous dysplasia. Review of coronal and axial magnetic resonance images (MRI) should follow to analyze the soft tissue contents of the orbital apex. Beyond traditional MRI sequences (T1- and T2-weighted), three-dimensional time-of-flight high-resolution sequences may be considered, as these demonstrate the relationship between the optic nerve, the ophthalmic artery, and underlying compressive pathologies. Intraoperative navigation systems, coupling CT and MRI data, ensure identification of critical structures and anatomic landmarks, increasing the surgeon’s ability to perform complete decompression and/or resection.
The relation of the lesion to the optic nerve should be considered. The superolateral and lateral aspects of the optic canal are relatively inaccessible from this inferomedial approach. Furthermore, the ability to perform safe exposure and resection with the endoscopic endonasal approach is limited when the dural attachment of tumors extends beyond the lateral aspect of the optic canal and along the orbital roof and anterior clinoid process. Under these circumstances, complete lesion resection cannot be reasonably obtained. If findings of lateral optic canal extension or vascular encasement are demonstrated on preoperative imaging, a transcranial approach is preferable.
Preparation and Patient Positioning
Because of the complex anatomy of the optic canal, a multidisciplinary team should be involved in the planning and execution of this procedure. For the endoscopic endonasal approach to the ventral skull base, the surgical team should include, but not be limited to, a skull base neurosurgeon working simultaneously with an otolaryngologist specializing in endoscopic sinus and skull base surgery. Since the introduction of endoscopes in the 1980s, the involvement of otolaryngologists in surgery of the optic canal has increased. Their expertise in endoscopic transnasal techniques is particularly valuable in cases that involve the inferomedial portion of the canal. Contrastingly, a neurosurgeon is essential in cases that involve the roof of the optic canal. Additionally, the management team should always involve an ophthalmologist, as visual assessment is critical both preoperatively and postoperatively.
After induction of general anesthesia, care should be taken to position and secure the endotracheal tube to the patient’s left, out of the way of the operating surgeon positioned on the patient’s right side. The decision to place a lumbar drain for temporary postoperative diversion of CSF varies depending on the surgeon; however, it should be noted that placement of a lumbar drain can lead to postoperative intracranial hypotension and other complications. To ensure adequate venous return, the patient should be positioned supine with the head above the heart. The head is stabilized in a three-point Mayfield head frame (Integra LifeSciences, Plainsboro, NJ) and positioned to optimize the surgeon’s comfort and ability in assessing both the nose and the deep anterior skull base: laterally bending the head gently toward the left shoulder, rotating it slightly toward the right shoulder, and extending it slightly. The draping should leave both eyes exposed in case perioperative evaluation of the globes is desired. Frameless stereotactic navigation provides continuous, three-dimensional information that facilitates both determining the extent of bone resection (sella, planum sphenoidale, tuberculum sellae, and so on) and creating the trajectory toward the optic canal and any associated pathology. Visual evoked potentials are typically used to assess for intraoperative optic nerve injury. It is preferred to maintain mean arterial pressures above 90 mm Hg to prevent optic nerve ischemia. High-dose corticosteroids are also used intraoperatively and postoperatively.
Standard antiseptic protocols should be carried out to ensure the absence of surgical site infections. Betadine solutions should not only be applied to the nose and nares, but also to any extremity sites being used for harvesting autologous fascia lata in future dura repair and reconstruction. In our practice, preparation of the nose with Betadine solution (Purdue Pharma LP, Stamford, CT) is followed by packing with oxymetazoline-soaked pledgets. Both intravenous antibiotics (preferably ampicillin/sulbactam) and 10 mg of dexamethasone are given prior to beginning the operation. Because the endoscopic endonasal approach is extra-arachnoid in nature and lacks brain retraction, anticonvulsants are not routinely administered in patients without a preexisting history of seizures.
Pearls and Potential Pitfalls
In challenging cases involving complex neoplastic extensions, a binostril technique lacking a nasal speculum allows the neurosurgeon and otolaryngologist to work simultaneously with up to three to four instruments in the field.
As recovery of visual deficits remains the primary pursued outcome of optic nerve decompression, substantial care should be taken to preserve visual function. The key to such preservation lies in minimizing direct manipulation or trauma to the optic nerve and in avoiding injury to the blood supply of the optic apparatus. Evidence suggests that the posterior portion of the optic nerve circulation is most at risk of ischemia, as it is supplied solely by the perforating dural vessels. Additionally, it is not the compression of the apical circulation that causes sufficient vasospasm of these vessels, but rather the direct handling of the vessels and the postoperative accumulation of inflammatory mediators.
Visualization is critical throughout this procedure. Early identification of the lamina papyracea with complete ethmoidectomy, wide sphenoidotomy, and, if necessary, a middle turbinectomy or middle turbinate swing procedure should be performed to provide ease in instrument placement and optimal visualization.
Owing to the accumulation of irrigant in the sphenoid sinus, a drill with simultaneous suction and irrigation can be used.
Use of preoperative CT to identify the presence of an Onodi cell is necessary. Failure to recognize an Onodi cell leaves the nerve vulnerable to injury when entering the sphenoid sinus.
Special care should be taken to keep the periorbita intact. Accidental violation of such structures results in fat prolapse and bleeding with subsequent loss of visualization.
Extreme caution must be used when incising the optic nerve sheath to avoid transecting a medially arising ophthalmic artery ( Fig. 21.3 ). The use of preoperative angiography may be invaluable for identifying the ophthalmic artery’s course and relation to the optic nerve.