Thyroid Eye Disease: Optic Neuropathy and Orbital Decompression
Andrew Jacob Victores, M.D.
Masayoshi Takashima, M.D., F.A.C.S., F.A.A.O.A.
From the Bobby R. Alford Department of Otolaryngology - Head and Neck Surgery, Baylor College of Medicine, Houston, Texas (A.V., M.T.)
Thyroid eye disease (TED) includes a number of orbital complications that arise as a result of thyroid autoimmune disease, most commonly related to Graves disease. TED can lead to both cosmetic disfigurement and functional deficits, including exophthalmos, diplopia, and vision loss. Perhaps the most feared manifestation of TED is optic neuropathy. Optic neuropathy is usually diagnosed by a combination of clinical and radiologic findings and can be managed by medical or surgical intervention. Most current treatment algorithms for this condition utilize either oral or intravenous corticosteroids as a first-line therapy with surgical orbital decompression reserved for recalcitrant disease. Orbital decompression can also help address other manifestations of thyroid eye disease, including diplopia, ocular surface damage, proptosis, lid retraction, chemosis, lid edema, and fat prolapse. A variety of techniques for orbital decompression have been described, although few studies have compared these techniques. The objective of the present chapter is to provide an overview of optic neuropathy and orbital decompression in TED and review relevant literature.
Thyroid eye disease (TED) is an orbital condition that has a strong association with thyroid autoimmune diseases. Most cases of TED are associated with Graves disease, however the condition has also been linked with other thyroid diseases such as Hashimoto thyroiditis. Between 25-50% of patients with Graves disease exhibit clinical features of TED, making it the most common extrathyroidal manifestation of Graves disease (Gillespie 2012, Bahn 1993). TED can present with both cosmetic disfigurement and functional deficits, including exophthalmos, diplopia, and vision loss.
Hyperthyroidism in Graves disease has a relatively well-understood pathogenesis. Thyroid stimulating hormone (TSH) is a hormone secreted by the pituitary and functions to bind to thyrotropin receptors on the thyroid gland and stimulate thyroid hormone production. Hyperthyroidism in Graves disease results from overstimulation of these receptors by thyrotropin-receptor antibodies. Although still controversial, it appears that Graves-associated orbitopathy may be a result of a different process. Genetic and environmental factors have both been implicated in the pathogenesis of the disease (Gillespie 2012, Brix 2001, Brix 2000). Studies suggest that antibodies, other than thyrotropin-receptor antibodies, may have a direct effect on orbital cells leading to the clinical expression of the disease (Bahn 1993, Atkinson 1984, Shillinglaw 1968). Given the inconclusive pathogenesis of the disease, no directed therapy has been formulated.
TED has both an active, progressive phase and a stable phase. During the active phase, orbital inflammation drives enlargement of the extraocular muscles (EOM) and orbital fat (Gillespie 2012, Sorisky 1996). Unfortunately, disease activity can be difficult to determine. Some tools, such as the Clinical Activity Score (CAS), have been devised to more consistently predict the active disease state and response to treatment (Mourits 1989, Mourits 1997). Improved means of evaluating TED activity remains a critical objective of the European Group on Graves Orbitopathy (EUGOGO) and the International Thyroid Eye Disease Society (ITEDS) (Bartalena 2008, Douglas 2009).
Most patients with TED have mild symptoms that spontaneously resolve. Moreover, many of these symptoms can be managed medically. However, the disease can progress to more severe complications such as vision loss from optic neuropathy or require invasive intervention by way of surgical decompression.
Perhaps the most feared complication of thyroid eye disease is optic neuropathy. Without treatment, 30% of patients with dysthyroid optic neuropathy (DON) will develop permanent vision loss (Fichter 2012, Char 1997). Fortunately, optic neuropathy in TED is relatively rare, affecting up to 5% of patients in most studies (Prummel 2003, Otto 1996, Bahn 1992). Risk factors associated with DON include older age, diabetes mellitus, and smoking (Fichter 2012, Eckstein 2003, Kalmann 1999, Bartley 1996).
Dysthyroid optic neuropathy is thought to arise from expanding orbital contents, primarily being enlarged extraocular muscles, which crowd the orbital apex and compress the optic nerve or its vasculature. The anatomy of the orbital apex includes the confluence of extraocular muscles and their insertion into the annulus of Zinn, a tendinous ring that encircles the optic nerve (Alford 2013). The increase in soft-tissue volume in the orbital apex causes direct compression and stretch of the optic nerve leading to vision loss.
Complete ophthalmologic evaluation is critical to recognize and confirm the diagnosis of DON. No single finding has been shown to be completely sensitive making definitive diagnosis challenging. DON is typically diagnosed when evidence of apical crowding or optic nerve stretching is noted on orbital imaging with clinical signs of optic neuropathy in the absence of another explanation for visual loss (Curro 2014). The clinical manifestations of DON include loss of visual acuity, decreased color vision, visual field defects, relative afferent pupillary defect, and optic disk swelling. A prospective study by the European Group on Graves Orbitopathy (EUGOGO) determined that altered color perception, optic disc swelling, and evidence of optic nerve compression on imaging were the most useful findings for the diagnosis of DON (McKeag 2007). This group also found that patients with DON frequently lack severe proptosis or orbital inflammation. Normal visual acuity also does not preclude the diagnosis. Most visual field defects in DON present as central scotoma (Kennedy 1990, Warren 1989, Trobe 1978, Calcaterra 1986). Approximately half of patients demonstrate optic disc swelling (McKeag 2007). High-resolution imaging is a critical component of the evaluation of optic neuropathy. The imaging technique of choice for DON is computed tomography or MRI. Another diagnostic tool is visual evoked potentials (VEPs). Patients with optic neuropathy characteristically demonstrate increased latency or reduction of amplitude on VEPs. Some studies suggest that VEPs have high diagnostic specificity and have supported their use as an adjunct in the diagnosis and the monitoring of dysthyroid optic neuropathy (McKeag 2007, Tsaloumas 1994, Neigel 1988).
The diagnosis of DON warrants urgent treatment to prevent potentially permanent vision loss. A variety of treatment strategies have been described for DON including oral or intravenous corticosteroids, surgical decompression, and orbital radiation (Kauh 2014, Bartella 2000, Wiersinga 1988, Trobe 1978, Wiersanga 2002). Most current treatment strategies initially use high-dose corticosteroids as a first-line therapy for optic neuropathy and reserve decompression surgery for persistent defects. Orbital radiation is occasionally used as an adjunct to corticosteroids (Bartalena 2008). Predictors of unresponsiveness to corticosteroids include the presence of optic disc swelling at diagnosis and persistent active disease after two weeks of treatment (Curro 2014). Both the intravenous (IV) and the oral route of corticosteroid administration have demonstrated efficacy in treating DON. Currently, there appears to be some regional disparity with the selection of IV or oral route. A survey of physicians in Europe and Latin America suggests that clinicians in these regions prefer IV corticosteroids as a first-line regimen for DON (Perros 2006, Ramos 2008). The use of IV corticosteroids is also supported by the EUGOGO as described in their Consensus Statement for the treatment of DON (Bartella 2008). In contrast, a similar survey conducted with ophthalmologists primarily in the United States suggested that oral corticosteroids were slightly preferred over IV corticosteroids (Perumal 2014). Unfortunately, both IV and oral high-dose corticosteroids can have significant side effects including weight gain, hypertension, diabetes mellitus, acute liver failure, and even death (Wakelkamp 2005, Marino 2004). If no significant improvement is evident within 1 to 2 weeks of initiating corticosteroid treatment, surgical decompression should be considered.
Some practitioners prefer to perform early decompression surgery, citing significant rates of visual improvement. Studies have shown up to 76-90% of patients with optic neuropathy have improved visual function after surgical decompression (Wakelkamp 2005, Mourits 1990, Garrity 1993, Soares-Welch 2003). Lipski et al. found that all patients in their study demonstrated improvement in vision after orbital decompression, supporting the importance of early decompression (Lipski 2011, Clauser 2012). However, one randomized controlled study by Wakelkamp et al. compared the efficacy of each, corticosteroids and orbital decompression, as a first-line treatment (Wakelkamp 2005). Over half of the patients receiving corticosteroids as first-line intervention did not require surgical decompression (Wakelkamp 2005). In addition, over three-fourths of the patients receiving surgical decompression as a first-line measure ultimately required additional treatment with methylprednisolone. The study concluded that immediate surgery did not improve patient outcomes, suggesting that corticosteroids should be considered as the first-line treatment.
Most patients with TED will not require surgical intervention. Only 5% of patients undergo surgery in the first year after diagnosis and up to 20% by 10 years (Fichter 2012, Bartley 1996). However, medical therapy can fail and patients can have persistent complaints. The purpose of surgical intervention is to address functional deficits by reducing diplopia, reversing ocular surface damage, or reversing vision loss, as well as reduction in disfiguring proptosis, lid retraction, chemosis, lid edema, and fat prolapse.
Orbital decompression usually serves as the first and primary rehabilitative surgery for TED. This can be achieved by removal of the orbital walls, which opens the orbital space into the adjacent paranasal sinuses, thereby increasing the orbital volume. The congested orbital contents then expand into the additional spaces, decreasing intraorbital pressure (Fig. 1). Orbital decompression has been shown to decrease retrobulbar pressure by 8-12 mmHg (Otto 1996). In addition, removal of orbital fat can decrease the volume of the orbital contents. As part of the pre-operative evaluation for orbital decompression, clinicians should typically obtain a high-resolution computed tomography (CT) scan of the orbits and paranasal sinuses. CT imaging helps to delineate bony anatomy and surrounding structures as well as serves as a potential tool for intraoperative surgical navigation.
There are both acute and delayed indications for orbital decompression in thyroid eye disease. The indications for acute surgical decompression include optic neuropathy, globe subluxation, and corneal ulceration (Mourits 1990, Clauser 2001, Clauser 2012). A planned, delayed surgical decompression can be considered for patients requiring rehabilitation for diplopia, proptosis, or cosmetic reasons. In these patients, the decompression usually is delayed at least six months to allow the orbitopathy to become inactive (Bartalena 2008).
A variety of techniques for orbital decompression have been described over the years (Clauser 2009, Keating 1999). Each of these techniques removes one or more of the four orbital walls. Early attempts at decompression generally removed a single orbital wall. In 1911, Dollinger et al. first described orbital decompression surgery (Dollinger 1911). He reported a lateral wall technique that achieved minimal decompression. In 1931, Naffziger described a transcoronal approach that allowed for superior decompression of the orbital contents into the anterior cranial fossa (Naffziger 1931). In 1930, Hirsch and Urbanek described removal of the orbital floor, which was followed by Sewall in 1936 with a report of removal of the medial orbital wall (Hirsch 1930, Sewall 1936). Later, these techniques would be combined to remove multiple orbital walls concurrently. In 1957, Walsh-Ogura reported his technique of orbital decompression using a combination of medial wall and orbital floor removal through an extension of the Caldwell-Luc approach (Walsh 1957). Over a decade later, a three-wall decompression would be described by Tessier and a four-wall decompression described by Kennerdell and Maroon (Tessier 1969, Kennerdell 1982). With the advent of endoscopic techniques in sinus surgery, Kennedy introduced an endoscopic transnasal approach to orbital decompression (Kennedy 1990). This approach has become widely accepted by otolaryngologists in recent years, largely replacing the Walsh-Ogura technique. Transfacial, minimal access approaches have also been devised and used either alone or in conjunction with other approaches. These techniques include the transpalpebral, transcaruncular, and lateral canthotomy approaches.
Few randomized controlled trials have been performed to compare surgical techniques for orbital decompression (Boboridis 2011). As a result, no single surgical technique has been convincingly shown to be superior (Alford 2013, Eckstein 2012, Boboridis 2011, Leong 2009). The best approach appears to be a tailored one, in which patient specific anatomic and clinical findings are used to guide selection of the appropriate surgery. In particular, efforts should be made to select a procedure that will be effective while minimizing the potential for complications.
Proptosis is a common manifestation of thyroid eye disease and indication for surgical decompression. The severity of proptosis can be objectively quantified using a Hertel exophthalmometer. Researchers have used these objective measurements to determine the average reduction in proptosis from various decompression procedures. Many of these studies compared two wall and three wall decompression techniques. Not surprisingly, the reduction in proptosis appears to be greater as more walls of the orbit are decompressed (Mourits 2009). Two-wall techniques typically decompress the medial wall along with either the lateral wall or the orbital floor. Three-wall decompression is usually performed by a combination of external and endonasal approaches. Most studies suggest that the two-wall technique reduces proptosis by approximately 4 mm whereas the three-wall decompression further reduces proptosis up to 7.4 mm (Chu 2009 O, Cansiz 2006, Graham 2003). Orbital fat removal can also contribute to improvement in proptosis when used in combination with these techniques (Leong 2009). By better understanding the expected improvement in proptosis, surgeons can better formulate the surgical approach and devise treatment algorithms for proptosis in TED (Clauser 2009).
Surgical decompression also serves an important role in the management of vision loss in TED. Optic neuropathy and corneal ulceration both are rare complications of TED that cause vision loss. A variety of surgical techniques have been described to address these problems. Unfortunately, interpretation of the findings is particularly difficult due to the heterogeneous populations and study designs found in the literature. In recent years, endoscopic transnasal techniques have emerged as promising and safe approaches that allow for complete bone removal along the orbital apex and optic canal (Fig. 2). Techniques that combine the endoscopic approach with transantral or transfacial approaches have also shown favorable improvement in visual acuity (Leong 2009).
Surgery is certainly not without its risks. The overall complication rate of orbital decompression for TED was 9.3% in one systematic review (Leong 2009). Some of the studies included in this review did not report complications, suggesting that the actual rate could be higher. Surgically-induced diplopia or strabismus is relatively common, reported in up to one-third of orbital decompression procedures (Mainville 2014). This complication is thought to result from change in the vector pull of the extraocular muscles (Metson 2006). Balanced decompression of the medial and lateral walls with orbital floor preservation can help to reduce this complication (Unal 2003, Graham 2003). Other techniques to reduce surgically-induced diplopia include preservation of an inferomedial strut of bone and maintenance of a facial sling in the region of the medial rectus (Metson 2002, Schaefer 2003, Goldberg 1992). In some cases, surgically-induced diplopia can be avoided altogether. One such situation is in the subset of patients with dysthyroid optic neuropathy and no pre-operative diplopia. These patients can be managed with a targeted decompression of the orbital apex using an endoscopic transnasal approach as demonstrated by Chu et al (Chu 2009). Their study found that visual acuity was improved or stabilized in all five patients receiving urgent selective orbital apex decompression and no patient developed post-operative diplopia. The small number of studies and sample sizes in the current literature limit conclusive recommendations as to the appropriate timing or selection of patients for endoscopic orbital apex decompression. Hopefully, future studies will help to address this limitation.
Patients frequently experience some degree of periorbital ecchymosis and edema as well as parasthesia or hypoesthesia. Transient or permanent cranial nerve V2 hypoesthesia is particularly common with orbital floor decompression. A serious but much less common complication is permanent post-operative vision loss, found in less than 1% of patients (Leong 2009). Other uncommon adverse events include maxillary sinusitis, CSF leak, epiphora, and hematoma.
Surgical intervention for TED can be challenging. A multidisciplinary approach with both an ophthalmologist and an otolaryngologist is critical to successful, safe, and comprehensive surgical management of TED (Alford 2013, Gillespie 2012, Boboridis 2011).
1. Atkinson S, Holcombe M, Kendall-Taylor P. Ophthalmopathic immunoglobulin in patients with Graves' ophthalmopathy. Lancet. Aug 18 1984;2(8399):374-376.
2. Bahn RS. Graves' ophthalmopathy. N. Engl. J. Med. Feb 25 2010;362(8):726-738.
3. Bahn RS, Bartley GB, Gorman CA. Emergency treatment of Graves' ophthalmopathy. Baillieres Clin. Endocrinol. Metab. Jan 1992;6(1):95-105.
4. Bahn RS, Heufelder AE. Pathogenesis of Graves' ophthalmopathy. N. Engl. J. Med. Nov 11 1993;329(20):1468-1475.
5. Bartalena L, Baldeschi L, Dickinson AJ, et al. Consensus statement of the European group on Graves' orbitopathy (EUGOGO) on management of Graves' orbitopathy. Thyroid. Mar 2008;18(3):333-346.
6. Bartalena L, Wiersinga WM, Pinchera A. Graves' ophthalmopathy: state of the art and perspectives. J. Endocrinol. Invest. Mar 2004;27(3):295-301.
7. Boboridis KG, Bunce C. Surgical orbital decompression for thyroid eye disease. The Cochrane database of systematic reviews. 2011(12):CD007630.
8. Brix TH, Hansen PS, Kyvik KO, Hegedus L. Cigarette smoking and risk of clinically overt thyroid disease: a population-based twin case-control study. Arch. Intern. Med. Mar 13 2000;160(5):661-666.
9. Brix TH, Kyvik KO, Christensen K, Hegedus L. Evidence for a major role of heredity in Graves' disease: a population-based study of two Danish twin cohorts. J. Clin. Endocrinol. Metab. Feb 2001;86(2):930-934.
10. Chu EA, Miller NR, Lane AP. Selective endoscopic decompression of the orbital apex for dysthyroid optic neuropathy. Laryngoscope 2009;119:1236-1240.
11. Clauser LC, Tieghi R, Galie M, Franco F, Carinci F. Surgical decompression in endocrine orbitopathy. Visual evoked potential evaluation and effect on the optic nerve. J. Craniomaxillofac. Surg. Oct 2012;40(7):621-625.
12. Curro N, Covelli D, Vannucchi G, et al. Therapeutic outcomes of high-dose intravenous steroids in the treatment of dysthyroid optic neuropathy. Thyroid. May 2014;24(5):897-905.
13. Douglas RS, Tsirbas A, Gordon M, et al. Development of criteria for evaluating clinical response in thyroid eye disease using a modified Delphi technique. Arch. Ophthalmol. Sep 2009;127(9):1155-1160.
14. Garrity JA, Fatourechi V, Bergstralh EJ, et al. Results of transantral orbital decompression in 428 patients with severe Graves' ophthalmopathy. Am. J. Ophthalmol. Nov 15 1993;116(5):533-547.
15. Heufelder AE, Joba W. Cellular immunity and orbital antigens in thyroid-associated orbitopathy. Exp. Clin. Endocrinol. Diabetes. 1999;107 Suppl 5:S152-157.
16. Hodes BL, Shoch DE. Thyroid ocular myopathy. Trans. Am. Ophthalmol. Soc. 1979;77:80-103.
17. Kan E, Kan EK, Ecemis G, Colak R. Presence of thyroid-associated ophthalmopathy in Hashimoto's thyroiditis. International journal of ophthalmology. 2014;7(4):644-647.
18. Kendall-Taylor P. The pathogenesis of Graves' ophthalmopathy. Clin. Endocrinol. Metab. May 1985;14(2):331-349.
19. Kennedy DW, Goodstein ML, Miller NR, Zinreich SJ. Endoscopic transnasal orbital decompression. Arch. Otolaryngol. Head Neck Surg. Mar 1990;116(3):275-282.
20. Konishi J, Herman MM, Kriss JP. Binding of thyroglobulin and thyroglobulin-antithyroglobulin immune complex to extraocular muscle membrane. Endocrinology. Aug 1974;95(2):434-446.
21. McKeag D, Lane C, Lazarus JH, et al. Clinical features of dysthyroid optic neuropathy: a European Group on Graves' Orbitopathy (EUGOGO) survey. Br. J. Ophthalmol. Apr 2007;91(4):455-458.
22. Moore RY, Eichler VB. Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat. Brain Res. Jul 13 1972;42(1):201-206.
23. Morax S, Badelon I. [Basedow exophthalmos]. J. Fr. Ophtalmol. Oct 2009;32(8):589-599.
24. Morax S, Bok C, Chahbi M, Hurbli T. [Orbital decompression in exophthalmos due to thyroid disease. Report of 69 cases]. Ann. Chir. Plast. Esthet. Jun 1997;42(3):207-215.
25. Mourits MP, Koornneef L, Wiersinga WM, Prummel MF, Berghout A, van der Gaag R. Clinical criteria for the assessment of disease activity in Graves' ophthalmopathy: a novel approach. Br. J. Ophthalmol. Aug 1989;73(8):639-644.
26. Mourits MP, Koornneef L, Wiersinga WM, Prummel MF, Berghout A, van der Gaag R. Orbital decompression for Graves' ophthalmopathy by inferomedial, by inferomedial plus lateral, and by coronal approach. Ophthalmology. May 1990;97(5):636-641.
27. Mourits MP, Prummel MF, Wiersinga WM, Koornneef L. Clinical activity score as a guide in the management of patients with Graves' ophthalmopathy. Clin. Endocrinol. (Oxf.). Jul 1997;47(1):9-14.
28. Naffziger HC. Progressive Exophthalmos Following Thyroidectomy; Its Pathology and Treatment. Ann. Surg. Oct 1931;94(4):582-586.
29. Neigel JM, Rootman J, Belkin RI, et al. Dysthyroid optic neuropathy. The crowded orbital apex syndrome. Ophthalmology. Nov 1988;95(11):1515-1521.
30. Otto AJ, Koornneef L, Mourits MP, Deen-van Leeuwen L. Retrobulbar pressures measured during surgical decompression of the orbit. Br. J. Ophthalmol. Dec 1996;80(12):1042-1045.
31. Pliego-Maldonado A, Miranda-Ruiz R, Vargas-Aguayo A, Marin-Mendez JA, Pena-Garcia JF, Guerra-Lopez J. [Orbit decompression surgery in patients with exophthalmos caused by Graves-Basedow disease]. Gac. Med. Mex. Jan-Feb 2000;136(1):11-15.
32. Prummel MF, Bakker A, Wiersinga WM, et al. Multi-center study on the characteristics and treatment strategies of patients with Graves' orbitopathy: the first European Group on Graves' Orbitopathy experience. Eur. J. Endocrinol. May 2003;148(5):491-495.
33. Prummel MF, Mourits MP, Berghout A, et al. Prednisone and cyclosporine in the treatment of severe Graves' ophthalmopathy. N. Engl. J. Med. Nov 16 1989;321(20):1353-1359.
34. Richter DF, Stoff A, Olivari N. Transpalpebral decompression of endocrine ophthalmopathy by intraorbital fat removal (Olivari technique): experience and progression after more than 3000 operations over 20 years. Plast. Reconstr. Surg. Jul 2007;120(1):109-123.
35. Shillinglaw J, Utiger RD. Failure of retro-orbital tissue to neutralize the biological activity of the long-acting thyroid stimulator. J. Clin. Endocrinol. Metab. Jul 1968;28(7):1069-1070.
36. Soares-Welch CV, Fatourechi V, Bartley GB, et al. Optic neuropathy of Graves disease: results of transantral orbital decompression and long-term follow-up in 215 patients. Am. J. Ophthalmol. Sep 2003;136(3):433-441.
37. Trobe JD, Glaser JS, Laflamme P. Dysthyroid optic neuropathy. Clinical profile and rationale for management. Arch. Ophthalmol. Jul 1978;96(7):1199-1209.
38. Tsaloumas MD, Good PA, Burdon MA, Misson GP. Flash and pattern visual evoked potentials in the diagnosis and monitoring of dysthyroid optic neuropathy. Eye. 1994;8 ( Pt 6):638-645.
39. Wakelkamp IM, Baldeschi L, Saeed P, Mourits MP, Prummel MF, Wiersinga WM. Surgical or medical decompression as a first-line treatment of optic neuropathy in Graves' ophthalmopathy? A randomized controlled trial. Clin. Endocrinol. (Oxf.). Sep 2005;63(3):323-328.
40. Walsh TE, Ogura JH. Transantral orbital decompression for malignant exophthalmos. Laryngoscope. Jun 1957;67(6):544-568.
41. Warren JD, Spector JG, Burde R. Long-term follow-up and recent observations on 305 cases of orbital decompression for dysthyroid orbitopathy. Laryngoscope. Jan 1989;99(1):35-40.
42. Weetman AP. Graves' disease. N. Engl. J. Med. Oct 26 2000;343(17):1236-1248.
43. Werner SC. Modification of the classification of the eye changes of Graves' disease: recommendations of the Ad Hoc Committee of the American Thyroid Association. J. Clin. Endocrinol. Metab. Jan 1977;44(1):203-204.
44. Wiersinga WM, Bartalena L. Epidemiology and prevention of Graves' ophthalmopathy. Thyroid. Oct 2002;12(10):855-860.
Figure 1. Transnasal endoscopic view of medial orbital wall decompression for thyroid eye disease. A, Removal of a left lamina papyracea bone. B, Prolapse of the left periorbita into the nasal cavity following removal of the lamina papyracea.
Figure 2. Endoscopic transnasal decompression of the optic canal. A, Removal of the bony optic canal on the right side with an endoscopic drill. B, Decompression of the optic nerve sheath on the right side with a sickle knife. C, Exposed left optic nerve following a similar decompression of the left optic canal.
Send correspondence to Masayoshi Takashima, M.D., Bobby R. Alford Department of Otolaryngology - Head and Neck Surgery, Baylor College of Medicine, Smith Tower, 17th Floor, 6550 Fannin, Suite 1727, Houston, Texas 77030. E-mail: email@example.com, Phone: 713-798-3235, Fax: 713-798-507