Endoscopic Orbital And Optic Nerve

Otolaryngol Clin N Am 39 (2006) 943–958

Endoscopic Orbital and Optic Nerve Decompression Steven D. Pletcher, MDa, Raj Sindwani, MD, FACS, FRCSb, Ralph Metson, MDc,d,* a

Department of Otolaryngology–Head and Neck Surgery, University of California, San Francisco, San Francisco, CA, USA b Department of Otolaryngology–Head and Neck Surgery, Saint Louis University School of Medicine, Saint Louis, MO, USA c Department of Otology and Laryngology, Harvard Medical School, Boston, MA, USA d Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, MA, USA

For more than 100 years, surgical decompression of the orbit has been used to treat the severe proptosis and optic neuropathy associated with Graves’ disease. Although decompression techniques involving removal each of the four walls of the orbit have been described [1–4], the WalshOgura decompression [5] described in the 1950s was favored by most otolaryngologists. This operation uses the familiar Caldwell-Luc approach to remove the inferior and medial orbital walls, allowing the enlarged orbital fat and muscles to decompress into the ethmoid and maxillary sinus cavities. Soon after the introduction of transnasal endoscopic sinus surgery in the mid 1980s, surgeons began to experiment with endoscopic orbital surgery. Endoscopic orbital decompression was first described by Kennedy [6] and Michel [7] in the early 1990s. Enhanced visualization of key anatomic landmarks allowed for safe and thorough decompression of the entire medial orbital wall, as well as the medial portion of the orbital floor. This improved visualization is most notable in the region of the orbital apex, a critical area of decompression in patients with optic neuropathy. These advantages have allowed the endoscopic approach to replace the Walsh-Ogura procedure as the technique of choice for orbital decompression. The benefits of endoscopic instrumentation for orbital decompression can be similarly applied when operating in the vicinity of the optic nerve. Decompression of the optic nerve involves complete removal of the bone * Corresponding author: Zero Emerson Place, Suite 2D, Boston, MA 02114. E-mail address: [email protected] (R. Metson). 0030-6665/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.otc.2006.06.003

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that forms the medial wall of the optic canal. Although the indications for and surgical techniques of orbital decompression are fairly well established, controversy exists regarding both the indications and extent of surgery necessary for optic nerve decompression.

Graves’ orbitopathy (dysthyroid orbitopathy) Graves’ disease is an autoimmune disorder that affects primarily the thyroid and the orbit. Thyroid manifestations are characterized by the production of autoantibodies to the TSH receptor with subsequent hyperstimulation and resultant hyperthyroidism. The thyroid manifestations of Graves’ disease an be treated with thyroid-suppressive medications, radiation (I131), or surgery. The orbital manifestations of Graves’ disease, known as dysthyroid orbitopathy, also represent an autoimmune process although the exact antibody target remains unclear. Inflammation associated with infiltration of T-cells and deposition of glycosaminoglycan results in enlargement of orbital fat and extraocular muscles. This increase in volume of contents within the confines of the rigid bony orbit results in increased pressure and resultant proptosis, or compression of the optic nerve. The degree of proptosis does not correlate with the overall severity of disease, as patients with poor compliance of the orbital septum may not experience significant proptosis but can have severe compression at the orbital apex and develop optic neuropathy. The orbital and thyroid manifestations of Graves’ disease follow distinct and independent clinical courses. Clinical manifestations of dysthyroid orbitopathy range from mild findings such as tearing, photophobia, and conjunctival injection to significant proptosis, diplopia, exposure keratopathy, and visual loss from optic neuropathy. The clinical course of Graves’ orbitopathy can be divided into the acute phase, characterized by active inflammation, which lasts 6 to 18 months and the chronic phase, characterized by fibrosis with stabilization of proptosis. It is preferable to perform orbital decompression during the chronic phase.

Medical treatment of dysthyroid orbitopathy Local measures such as lubrication, eyelid taping, and patching for patients with dryness and diplopia represent initial conservative treatment approaches. More aggressive treatments include the use of systemic corticosteroids and orbital radiation. Both of these treatments appear to be most effective during the acute phase of the disease. Systemic corticosteroid treatment usually results in marked improvement, but the symptoms generally recur following discontinuation of steroid treatment. Because of the deleterious side effects of long-term corticosteroid use, steroid treatment

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are often used as a temporizing measure or in conjunction with surgical decompression. The use of orbital radiation is controversial, and its efficacy has been challenged by two recent randomized prospective trials [8,9].

Endoscopic orbital decompression The endoscopic technique allows for unmatched visualization of critical anatomic regions including the skull base and orbital apex and avoids external or sublabial incisions. The entire medial orbital wall as well as the medial portion of the orbital floor is removed with endoscopic decompression (Fig. 1). Technique The patient is positioned in the supine position, and topical vasoconstriction is achieved with topical oxymetazoline (0.05%) pledgets. The eyes are maintained within surgical field, protected with scleral shields. Imageguidance systems may be used at the surgeons discretion. Local injection of lidocaine 1% with 1:100,000 epinephrine is administered along the lateral nasal wall in the region of the maxillary line (a bony eminence that extends from the anterior attachment of the middle turbinate to the root of the inferior turbinate). Surgery begins with an incision just posterior to the maxillary line. The uncinate process is medialized and removed, exposing the natural ostium of the maxillary sinus. With orbital decompression it is important to widely open the maxillary sinus to achieve adequate access to the orbital floor and prevent blockage of the ostium from orbital fat, which protrudes following decompression. Enlargement is performed primarily in a posterior direction as extension of the antrostomy too far anteriorly risks of damage to the

Fig. 1. Bone removed during endoscopic orbital decompression includes the medial orbital wall and the medial aspect of the orbital floor.

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nasolacrimal duct. Using a 30 degree endoscope, the wide antrostomy should allow easy visualization of the infraorbital nerve as it courses along the floor of the orbit. An endoscopic sphenoethmoidectomy is performed in standard fashion. We advocate removal of the middle turbinate during orbital decompression to optimize exposure of the medial orbital wall and facilitate postoperative cleaning. An image guidance system may be used at this point to confirm removal of all ethmoid cells along the medial orbital wall, and to ensure complete dissection to the sphenoid face and posterior skull base. The skeletonized medial orbital wall is then carefully penetrated in a controlled fashion with a spoon curette or other blunt instrument. It should be noted that once the lamina is transgressed, orbital fat should not be visible, as long as the underlying periorbital fascia is left intact. The thin bone of the lamina papyracea is elevated while preserving the underlying periorbita. Bone fragments are removed using Blakesly forceps (Fig. 2). Bone removal proceeds superiorly toward the ethmoid roof, inferiorly to the orbital floor, and anteriorly to the maxillary line. Bone in the region of the frontal recess is left intact; if bone is removed from this region, herniated fat may obstruct drainage of the frontal sinus. As dissection proceeds posteriorly, thick bone is encountered in the region of the orbital apex within 2 mm of the sphenoid face. This bone corresponds to the annulus of Zinn, from which the extraocular muscles originate and through which the optic nerve passes. This landmark represents the posterior limit of a standard decompression. For patients with optic neuropathy, experienced surgeons may consider continuing the decompression posteriorly into the sphenoid sinus; however, the benefits of incorporating

Fig. 2. Once the medial orbital wall has been exposed, Blakesly forceps are used to remove fragments of the lamina papyracea.

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and optic nerve decompression into standard orbital decompression are unclear, and may lead to inadvertent injury to the nerve. Removal of the orbital floor can be technically challenging, depending on its thickness. Only that portion of the floor that is medial to the infraorbital nerve is removed. A spoon curette is used to engage the orbital floor at its medial extent and down-fracture the bone (Fig. 3). The bone of the orbital floor is thicker than that of the medial orbital wall, and significant force may be required for this maneuver. If the spoon curette is not sturdy enough for this portion of the procedure the heavier mastoid curette may be used. The bone may fracture in one large piece, typically with a natural cleavage plane at the canal of the infraorbital nerve, or, more frequently, it fractures into several small pieces. A 30-degree endoscope and angled forceps may facilitate bone removal while preserving the infraorbital canal as the lateral limit of dissection. Once the lamina papyracea and medial orbital floor have been removed, the periorbita is fully exposed. A sickle knife is then used to open this fascial layer. Care must be taken to avoid ‘‘burying’’ the tip of the sickle knife and potentially injuring the underlying orbital contents such as the medial rectus muscle. The periorbital incision should be initiated at the posterior limit of decompression (just anterior to the sphenoid face) and brought anteriorly so that prolapsing fat does not obscure visualization. Parallel incisions are performed along the ethmoid roof and orbital floor. To minimize the risk of postoperative diplopia, a 10 mm-wide sling of fascia overlying the medial rectus muscle may be preserved while the remainder of the periorbita is removed using angled Blakesley forceps (Fig. 4) [10]. In patients with optic neuropathy, the fascial sling technique is not used to allow maximal

Fig. 3. A spoon curette is used to down-fracture the medial portion of the orbital floor.

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Fig. 4. Following bony decompression, a sickle knife is used to incise the periorbita. In patients without optic neuropathy, a sling of fascia may be preserved overlying the medial rectus muscle to minimize postoperative diplopia.

decompression. A ball-tipped probe and sickle knife may be used to identify and incise remaining fibrous bands that often course superficially between lobules of orbital fat. Upon completion of the procedure, a generous prolapse of fat into the opened ethmoid and maxillary cavities should be observed (Fig. 5). The globe may be blotted to encourage maximal fat herniation and confirm a decrease in retropulsive resistance. Depending on the clinical scenario and desired degree of decompression, a subsequent lateral decompression may be performed through an external approach. When performed immediately following medial decompression, the orbital contents are easily retracted in a medial direction, allowing for excellent exposure of the lateral bony wall. Bilateral decompressions may be performed concurrently or in a staged procedure. Nasal packing is avoided to ensure maximal decompression and avoid compression of exposed orbital contents. The patient is discharged the morning after surgery with a prescription for oral antistaphylococcal antibiotics and instructions to begin twice daily nasal saline irrigations. At the first postoperative visit 1 week following surgery, crusts and debris are cleaned from the surgical site under endoscopic guidance. For patients with severe comorbidities, a strong preference for local anesthesia, or in whom surgery is being performed on an only seeing eye, decompression may be performed under local anesthesia with sedation [11]. This approach allows the surgeon to monitor the patient’s vision throughout the procedure. Sedation may be achieved with an intravenous bolus of propofol (0.4–0.8 mg/kg) before injection of local anesthesia, followed by an infusion of 75 to 95 mg/kg during the procedure. Local anesthesia is

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Fig. 5. Following decompression, orbital fat protrudes into the ethmoid and maxillary spaces (A). With the ortbital sling technique, a strip of periorbita remains to support the medial rectus muscle and minimize postoperative diplopia (B).

administered initially with 4% cocaine pledgets followed by injection of lidocaine 1% with 1:100,000 epinephrine. Patients may report discomfort during removal of the lamina papyracea. This sensation may be relieved by infiltration of a small amount of additional anesthetic solution along the medial orbital wall. Results The goals of orbital decompression vary depending upon the indication for the procedure. In patients with compressive optic neuropathy,

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restoration of visual deficits is the key outcome, while in patients with corneal exposure or severe proptosis, ocular recession may be the primary end point. The reported incidence of improvement following endoscopic orbital decompression for Graves’ orbitopathy ranges from 22% to 89% [6,12,13]. This wide variation in results reflects the diverse patient populations and definitions of improvement. Postoperative deterioration of visual acuity occurs in less than 5% of patients [7,12,13]. Ocular recession as a result of endoscopic decompression alone averages 3.5 mm (range 2–12 mm). The addition of concurrent lateral decompression to the endoscopic procedure provides an additional 2 mm of globe recession [13]. Complications Diplopia is not an uncommon occurrence following orbital decompression with 15% to 63% of postoperative patients reporting new-onset diplopia or worsening of preexisting symptoms [7,11,13–16]. This complication is believed to be a result of a change in the vector of pull of the extraocular muscles. Decompressive surgery rarely alleviates preexisting diplopia. Patients who have diplopia following decompressive surgery often require strabismus surgery for correction. All patients should be informed of the possibility of postoperative double vision, as well as the potential need for further surgical intervention if this persists. Several methods to decrease postoperative diplopia have been reported. Multiple authors have described the preservation of a strut of inferomedial bone between the decompressed floor and medial wall [12,17]. When this strut is maintained, however, it is technically difficult to remove the orbital floor through a purely endoscopic technique. The maintenance of a facial sling in the region of the medial rectus has also been demonstrated to decrease the incidence of postoperative diplopia [10]. This technique provides similar support as the medial strut technique, but allows for endoscopic access to decompress the medial orbital floor. The concept of a balanced decompression (concurrent medial and lateral decompression) has also been suggested as a means to decrease postoperative diplopia [14,18,19]. When operating for compressive optic neuropathy, techniques designed to limit diplopia may also limit the extent of decompression, and postoperative diplopia is often accepted as a concession to improved visual acuity. Postoperative bleeding following decompression is best managed through endoscopic identification and direct cauterization of the bleeding site. Nasal packing is generally not used to avoid pressure on the exposed orbital apex and optic nerve. Postoperative infection is minimized through the use of postoperative antibiotics with staphylococcal coverage. A large maxillary antrostomy and limited bone removal in the frontal recess region minimize the risk of developing postoperative sinusitis. Epiphora may develop if the maxillary antrostomy is extended too far anteriorly with transection of the nasolacrimal duct. This complication is treated with an endoscopic

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dacryocystorhinostomy. Leakage of cerebrospinal fluid and blindness are very rare complications that have been reported following nonendoscopic decompression techniques. Optic nerve decompression Historically the most common, and perhaps most controversial, indication for optic nerve decompression has been traumatic optic neuropathy (TON). The efficacy of decompression in this setting remains unclear. Endoscopic and nonendoscopic techniques of optic nerve decompression have also been used for a variety of nontraumatic causes of compressive optic neuropathy such as benign tumors and inflammatory or fibroosseus lesions [20]. It is in these patients with nontraumatic, compressive optic neuropathy that endoscopic optic nerve decompression appears to be most successful. Controversy regarding the treatment of TON exists because the two mainstays of therapy, corticosteroids and surgical decompression, have not shown definitive clinical benefit when compared with observation alone [14,21]. To address this issue the International Optic Nerve Trauma Study (IONTS) was undertaken. The initial goal of a randomized, controlled trial was abandoned when patient recruitment was insufficient to support this study design. Thus, a comparative nonrandomized interventional study with concurrent treatment groups was performed with 127 patients [14]. No clear benefit was found for either corticosteroid therapy or surgical optic canal decompression. The authors discussed numerous published uncontrolled studies, and their overall recommendation based on the IONTS and their literature review was that treatment should be determined on an individual patient basis. Several retrospective studies subsequent to the IONTS have suggested improvement in visual acuity with optic nerve decompression following failure of visual improvement with steroids [22–24]. The uncontrolled nature of these studies, however, must be taken into account when considering surgical decompression for traumatic optic neuropathy. Surgical anatomy The optic nerve may be divided into three segments: the intraorbital, the intracanalicular, and the intracranial segment. Optic nerve decompression aims to relieve compressive forces within the intracanalicular portion of the nerve. The canal of the optic nerve is formed by the two struts of the lesser wing of the sphenoid and carries both the optic nerve and the ophthalmic artery. At the orbital apex is the fibrous annulus of Zinn. Pathophysiology Compression on the optic nerve may result from neoplastic, inflammatory, or traumatic processes. Initial theories of vascular compromise from

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external compression with resultant injury to the optic nerve have been largely discarded. Manual compression resulting in conduction block and focal demyelination from compression are the favored pathophysiologic explanations for compressive optic neuropathy. Rapid recovery following decompression results from relief of the manual compression block while a delayed recovery may occur over a period of weeks to months as a result of remyelination [25]. Traumatic optic neuropathy may be divided into two categories: indirect and direct. Direct TON results from a penetrating injury with projectiles or other sharp objects. In these cases the intraorbital portion of the optic nerve is generally injured and decompression is not recommended. Indirect TON results from blunt trauma to the head. This injury can occur with or without associated fractures of the orbital canal. The pathophysiology of visual loss in these cases is frequently unclear, and may include intraneural edema, hematoma, shearing injury to the microvasculature or axons, altered cerebrospinal fluid circulation, and interruption of direct axonal transport. If there is evidence of complete disruption of the optic nerve, decompression is not indicated, as the optic nerve will not recover from such injury. In cases where edema, hematoma, or moderate bony compression is suggested, however, decompression may be considered. Evaluation and treatment Compressive optic neuropathy may have an insidious onset resulting in delayed diagnosis. Patients’ initial symptoms are often vague including mild blurry or ‘‘fuzzy’’ vision without significant loss of visual acuity and with normal fundoscopic examination. More rigorous examination often reveals variable, limited visual field defects, a decrease in color vision, and an afferent papillary defect on the affected side. Unfortunately, these symptoms may go unnoticed until the more advanced stages of compression result in decreased visual acuity. Thus, careful ophthalmologic examination is essential in discovering early signs of compression and, if abnormal, should be evaluated with an MRI scan. Once a compressive optic neuropathy is diagnosed, surgical decompression is considered based upon the pathology and extent of the compressive lesion. Systemic corticosteroids frequently provide temporary improvement and may be considered while awaiting definitive treatment. Patients with suspected TON generally have sustained significant blunt force trauma and should be evaluated by a trauma team for evidence of multisystem injury. As soon as TON is suspected, examination by an ophthalmologist is mandatory. Visual acuity should be determined as soon as possible and closely monitored. Patients should be tested for an afferent pupillary defect, which may be the only sign of TON in unconscious patients. If possible, formal visual field testing and color vision testing should be performed as abnormalities of color and peripheral vision typically precede

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decreased visual acuity in the progression of optic neuropathy. Evaluation of ocular pressure and fundoscopic exam may also yield important information. A fine cut CT scan through the orbit and optic canal should be obtained to look for fractures and bone displacement in the orbital apex. Observation and treatment with corticosteroids are both reasonable medical approaches to traumatic optic neuropathy. Steroid dosing is controversial, and in the IONTS steroid dosing did not correlate with clinical outcome. Frequently a loading dose of methylprednisone (30 mg/kg bolus) followed by a continuous infusion of 5.4 mg/kg/h is given for 48 hours. This regimen is based upon studies of spinal cord injury. Endoscopic optic nerve decompression Traditional surgical approaches for optic nerve decompression include transorbital, extranasal transethmoid, transantral, intranasal microscopic, and craniotomy approaches. Endonasal endoscopic decompression of the optic nerve offers many advantages over these approaches, including excellent visualization, preservation of olfaction, rapid recovery time, a lack of external scars, and less operative stress in patients who may be suffering from multisystem trauma. Technique Patients are prepared for surgery in a similar manner to those undergoing orbital decompression. A standard sphenoethmoidectomy is performed. The sphenoid face is widely opened and the bulge of the optic canal is identified along the lateral wall of the sphenoid sinus, superior to the carotid artery. In some patients, the optic canal may be initially identified in a posterior ethmoid or Onodi cell, which can be seen on preoperative CT scan [26]. Identification and opening of the Onodi cell is important to provide adequate surgical exposure and allow full access to the optic canal. Following exposure of the medial orbital wall, a spoon curette is used to fracture the lamina papyracea approximately 1 cm anterior to the optic canal. The lamina is then carefully removed in a posterior direction to expose the annulus of Zinn and the optic canal. Care must be taken to avoid penetration of the periorbita, as subsequent herniation of orbital fat will obscure the surgical field. As the optic canal is approached, the thin lamina will be replaced with the thick bone of the lesser wing of the sphenoid. This bone must be thinned before removal. A long-handled drill with a diamond burr is used to methodically thin the medial wall of the optic canal (Fig. 6). While drilling, care must be taken to prevent contact of the drill bit with the prominence of the carotid artery, which is located just inferior and posterior to the optic nerve. Care should also be taken to avoid excess generation of heat while drilling this bone as thermal damage to the optic nerve may result. After the bone is appropriately thinned, a microcurette

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Fig. 6. Endoscopic view of the right posterior nasal cavity following wide sphenoidotomy. The lamina papyracea has been removed to reveal periobita near the orbital apex. A diamond burr is used to thin the bone of the optic canal.

is used to fracture the thinned bone in a medial direction, away from the optic nerve (Fig. 7). Bone fragments are then removed from the decompressed nerve using blakesly forceps (Fig. 8), with resultant medial decompression of the optic nerve (Fig. 9). Controversy exists regarding the length of optic canal that should be decompressed as well as the necessity for decompression of the optic sheath. With compressive optic neuropathy secondary to neoplasms, the extent of decompression is dictated by the size and location of the neoplasm. For

Fig. 7. A microcurette is used to elevate thinned bone of the optic canal.

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Fig. 8. Blakesly forceps are used to remove bone fragments and expose the underlying optic nerve.

cases of TON and dysthyroid orbitopathy, removal of bone for a distance of 1 cm posterior to the face of the sphenoid sinus is generally thought to be sufficient [27]. Incision of the sheath has been advocated by some authors to further decompress the nerve itself; however, this maneuver may be unnecessary and risks damage to the underlying nerve fibers and ophthalmic artery as well as cerebral spinal fluid (CSF) leak, with resultant risk of meningitis. With clear

Fig. 9. The decompressed optic nerve is visible along the lateral wall of the sphenoid sinus.

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risks and an absence of data to suggest benefit for sheath decompression, we do not advocate this maneuver for most patients undergoing optic nerve decompression. Results Most patients who undergo optic nerve decompression for compressive nontraumatic optic neuropathy will have significant improvement in visual acuity. An immediate improvement in visual acuity is frequently observed, probably from relief of a mechanical conduction block. Further improvement may occur over a period of weeks to months as remyelination of the nerve leads to more efficient conduction [25]. The efficacy of optic nerve decompression in traumatic optic neuropathy is unclear. Much of the difficulty in determining the success of surgical intervention arises from the relatively high rate of spontaneous recovery from TON. Thus, well-controlled studies with significant power are required to delineate the efficacy of surgical intervention. Unfortunately, such studies have not been possible due to the rarity of this condition. In cases of nontraumatic, compressive optic neuropathy, however, the natural course of disease is not one of spontaneous resolution. Thus, it is reasonable to conclude that visual improvement following surgical decompression is a direct result of the procedure. In our recent experience of endoscopic optic nerve decompressions for nontraumatic optic neuropathy, improved visual acuity was noted following 8 of 10 decompressions. One patient required multiple decompressions due to progression of her fibrous dysplasia with recurrent impingement upon the optic nerve [20]. Complications The risk of CSF leak, meningitis, and visual loss with optic nerve decompression appears to be higher than with standard endoscopic sinus surgery or orbital decompression. Although several studies with 20 to 45 patients report no complications, the IONTS and another recent study reported several cases of CSF leak, some with associated meningitis and visual decompensation [14,23]. In the IONTS, it is unclear whether the complications occurred in patients who underwent endoscopic decompression representing less than 40% of patients in their series, or an external approach.

Summary With excellent visualization of the orbital apex and optic canal, the endoscopic transnasal approach is well suited for both orbital and optic nerve decompression. This operation is an advanced endoscopic technique, and should be performed only by surgeons experienced in endoscopic nasal surgery. Although the indications and expected results for orbital

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decompression are well established, those for optic nerve decompression continue to evolve. References [1] Kronlein R. Zur Pathologie und operativen Behandlung der Desmoid Cysten der Orbita. Beitr Klin Chir 1889;4:149–63. [2] Sewall E. Operative control of progressive exophthalmos. Arch Otolaryngol Head Neck Surg 1936;24:621–4. [3] Hirsch O. Surgical decompression of exophthalmos. Arch Otolaryngol Head Neck Surg 1950;51:325–31. [4] Naffziger HC. Progressive exophthalmos. Ann R Coll Surg Engl 1954;15:1–24. [5] Walsh TE, Ogura JH. Transantral orbital decompression for malignant exophthalmos. Laryngoscope 1957;67:544–68. [6] Kennedy DW, Goodstein ML, Miller NR, et al. Endoscopic transnasal orbital decompression. Arch Otolaryngol Head Neck Surg 1990;116:275–82. [7] Michel O, Bresgen K, Russmann W, et al. Endoscopically-controlled endonasal orbital decompression in malignant exophthalmos. Laryngorhinootologie 1991;70:656–62. [8] Gorman CA, Garrity JA, Fatourechi V, et al. A prospective, randomized, double-blind, placebo-controlled study of orbital radiotherapy for Graves’ ophthalmopathy. Ophthalmology 2001;108:1523–34. [9] Mourits MP, van Kempen-Harteveld ML, Garcia MB, et al. Radiotherapy for Graves’ orbitopathy: randomised placebo-controlled study. Lancet 2000;355:1505–9. [10] Metson R, Samaha M. Reduction of diplopia following endoscopic orbital decompression: the orbital sling technique. Laryngoscope 2002;112:1753–7. [11] Metson R, Shore JW, Gliklich RE, et al. Endoscopic orbital decompression under local anesthesia. Otolaryngol Head Neck Surg 1995;113:661–7. [12] Schaefer SD, Soliemanzadeh P, Della Rocca DA, et al. Endoscopic and transconjunctival orbital decompression for thyroid-related orbital apex compression. Laryngoscope 2003; 113:508–13. [13] Metson R, Dallow RL, Shore JW. Endoscopic orbital decompression. Laryngoscope 1994; 104:950–7. [14] Shepard KG, Levin PS, Terris DJ. Balanced orbital decompression for Graves’ ophthalmopathy. Laryngoscope 1998;108:1648–53. [15] Wright ED, Davidson J, Codere F, et al. Endoscopic orbital decompression with preservation of an inferomedial bony strut: minimization of postoperative diplopia. J Otolaryngol 1999;28:252–6. [16] Eloy P, Trussart C, Jouzdani E, et al. Transnasal endoscopic orbital decompression and Graves’ ophtalmopathy. Acta Otorhinolaryngol Belg 2000;54:165–74. [17] Goldberg RA, Shorr N, Cohen MS. The medical orbital strut in the prevention of postdecompression dystopia in dysthyroid ophthalmopathy. Ophthal Plast Reconstr Surg 1992;8:32–4. [18] Unal M, Leri F, Konuk O, et al. Balanced orbital decompression combined with fat removal in Graves’ ophthalmopathy: do we really need to remove the third wall? Ophthal Plast Reconstr Surg 2003;19:112–8. [19] Graham SM, Brown CL, Carter KD, et al. Medial and lateral orbital wall surgery for balanced decompression in thyroid eye disease. Laryngoscope 2003;113:1206–9. [20] Pletcher SD, Metson R. Endoscopic optic nerve decompression for non-traumatic optic neuropathy. American Rhinologic Society combined otolaryngologic spring meeting, Chicago, Il, 2006. [21] Cook MW, Levin LA, Joseph MP, et al. Traumatic optic neuropathy. A meta-analysis. Arch Otolaryngol Head Neck Surg 1996;122:389–92. [22] Kountakis SE, Maillard AA, El-Harazi SM, et al. Endoscopic optic nerve decompression for traumatic blindness. Otolaryngol Head Neck Surg 2000;123:34–7.

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[23] Rajiniganth MG, Gupta AK, Gupta A, et al. Traumatic optic neuropathy: visual outcome following combined therapy protocol. Arch Otolaryngol Head Neck Surg 2003;129:1203–6. [24] Li KK, Teknos TN, Lai A, et al. Traumatic optic neuropathy: result in 45 consecutive surgically treated patients. Otolaryngol Head Neck Surg 1999;120:5–11. [25] McDonald WI. The symptomatology of tumours of the anterior visual pathways. Can J Neurol Sci 1982;9:381–90. [26] Allmond L, Murr AH. Clinical problem solving: radiology. Radiology quiz case 1: opacified Onodi cell. Arch Otolaryngol Head Neck Surg 2002;128:596, 598–599. [27] Luxenberger W, Stammberger H, Jebeles JA, et al. Endoscopic optic nerve decompression: the Graz experience. Laryngoscope 1998;108:873–82.