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A Retrospective Review of 26 Cases of Dysthyroid Optic Neuropathy
A R E T R O S P E C T I V E R E V I E W O F 26 CASES O F DYSTHYROID OPTIC NEUROPATHY GREGORY J. PANZO, M.D., AND ROBERT L. TOMSAK, M.D. Chveland, Ohio
Sixteen patients (14 women and two men) with dysthyroid optic neuropathy (26 involved eyes) were treated with either oral corticosteroids, orbital irradiation, surgical orbital decompression, combined corticosteroids and irradiation, or combined corticosteroids and surgi cal decompression. Thirteen of 16 eyes responded favorably to corticosteroid therapy but eight of the 13 relapsed upon discontinuation of treatment. Two of four eyes responded to irradiation initially but later relapsed. The response to orbital decompression was almost uniformly beneficial (eight of nine eyes responded) and lasting in all. Combined modes of therapy offered no additional advantage. Accepted treatments for dysthyroid optic neuropathy include systemic corti costeroids, orbital irradiation, and surgi cal decompression of the orbit. We retro spectively analyzed cases of dysthyroid optic neuropathy treated here between 1972 and 1982. SUBJECTS AND METHODS
The study included 16 patients (26 eyes) affected by dysthyroid optic neu ropathy. All the involved eyes demon strated optic nerve dysfunction and the characteristic external signs of ocular dysthyroidism. Optic nerve dysfunction was documented by examination of visual acuity, visual fields, pupils, and color vision. We excluded patients with other conditions that might have accounted for visual impairment (opaque media, maculopathy, and the like). The patients ranged in age from 26 to
Accepted for publication May 11, 1983. From the Department of Ophthalmology, Cleve land Clinic Foundation, Cleveland, Ohio. Reprint requests to Robert L. Tomsak, M.D., Department of Ophthalmology, 9500 Euclid Ave., Cleveland, OH 44106. 190
69 years (mean age, 51 years). Fourteen of the 16 patients were female. At the time dysthyroid optic neuropathy was diagnosed, 11 patients were euthyroid, four were hyperthyroid, and one was hypothyroid. All eyes were exophthal mic, 24 had soft tissue changes, and 21 demonstrated extraocular muscle in volvement. Mild, optically insignificant corneal changes were noted in 13 eyes. By Werner's 1 classification, four eyes had severe ophthalmopathy and the remain ing 22 demonstrated mild to moderate ophthalmopathy. All affected eyes had decreased central visual acuities or visual field defects, or both. Central scotomas, inferior altitudinal and arcuate defects, generalized con striction, and paracentral scotomas were demonstrated by Goldmann perimetry. Ten eyes had afferent pupillary defects. Abnormal color vision was demonstrated by AOH-R-R pseudoisochromatic plates in nine of 15 tested eyes. Sixteen of 26 eyes had ophthalmoscopically normal optic disks. All patients were treated. Treatment consisted of oral prednisone, orbital irra diation, surgical decompression, concur-
© AMERICAN JOURNAL OF OPHTHALMOLOGY 96:190-194, 1983
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DYSTHYROID OPTIC NEUROPATHY
rent corticosteroids and irradiation, or concurrent corticosteroids and orbital de compression. Response to therapy was evaluated for each form of treatment as well as for the entire group. We defined a successful response as improvement of two or more lines of visual acuity or a visual acuity of 20/20 with improvement of visual fields to normal within eight weeks of therapy. RESULTS
Corticosteroids—Sixteen eyes (11 pa tients) were treated with high doses of oral prednisone (Fig. 1). The patients' ages ranged from 29 to 60 years (mean age, 52 years). Dosage was 80 to 100 mg daily. The patients received a maximum dosage for a mean of 11 days after which the dosage was gradually decreased. Total days of corticosteroid therapy ranged from 14 to 51 days with a mean of 32 days. Thirteen eyes (nine patients) initially improved with treatment (Table 1). Three eyes remained unchanged. There was no instance of deterioration during therapy.
VISION BEFORE TREATMENT
Fig. 1 (Panro and Tomsak). Dysthyroid optic neu ropathy response to oral prednisone therapy.
191
Maximum response occurred within 14 to 40 days (mean, 24 days). A lasting remission was achieved in five eyes (three patients) with follow-up peri ods of five to 12 months. Clinical relapse occurred in eight eyes (six patients) with in four to 72 days (mean, 33 days) of discontinuation of therapy (Table 1). Two relapsing eyes (one patient) responded to four separate courses of corticosteroids (three relapses) before achieving a lasting remission for a follow-up period of three years. All of the remaining eyes that relapsed later underwent surgical decom pression. Irradiation—Four eyes (three patients) were treated with orbital irradiation (Fig. 2). Their ages ranged from 45 to 54 years (mean age, 50 years). Treatment consisted of 1,600 to 2,000 rads in eight to ten daily divided doses (200 rads/dose) through lateral ports to the orbital apices. Two eyes (two patients) remained un changed. One patient with bilateral dys thyroid optic neuropathy responded suc cessfully within 27 days of beginning therapy, but both eyes relapsed on the 38th day after the final radiation treat ment (Table 1). Orbital decompression—Nine eyes (seven patients) underwent surgical de compression transantrally in the manner described by Ogura and Lacente 2 (Fig. 3). Their ages ranged from 35 to 58 years (mean age, 52 years). Two eyes had decompression as the primary treatment. Four had relapsed after responding to corticosteroid therapy. Three had failed to respond to either corticosteroids or irradiation. Eight of the nine eyes im proved. There were no relapses during an average follow-up period of 14 months (Table 1). Oral corticosteroids with irradiation— Three eyes (two patients) were treated with concurrent corticosteroids and irra diation (Table 2). Their ages were 35 and 55 years. All eyes initially responded, but
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AUGUST, 1983
TABLE 1 RESPONSE TO SINGLE METHOD OF TREATMENT
Response
Corticosteroids
Treatment Irradiation
Decompression
No. of eyes Improved Unchanged Worsened Relapse after initial response No. responding No. relapsing Time to relapse (days) Mean Range
16 13 3 0
4 2 2 0
9 8 1 0
13 8
2 2
8 0
33 4 to 72
38 38
— —
later relapsed and underwent surgical decompression. Oral corticosteroids with orbital decompression—Four eyes (three pa tients) were treated with concurrent cor ticosteroids and surgical decompression (Table 2). Their ages ranged from 43 to 69 years (mean age, 57 years). Three orbits were decompressed transantrally, and one orbit was decompressed by a Kronlein procedure. Two of the four eyes improved. Both of these were done by the transantral approach. One eye re lapsed. The one eye decompressed by a Kronlein procedure showed no change. Vision deteriorated in one patient who underwent transantral decompression.
20/100 or worse, six had final visual acui ties of counting fingers to no light percep tion. In our series, four of 26 eyes had final visual acuities of 20/100 or less and none had a final visual acuity worse than 20/400. Twenty of 26 eyes had final visual acuities of 20/40 or better. Trobe, Glaser, and Laflamme 7 found that only two of 29 eyes had final visual
DISCUSSION
The natural course of untreated dysthyroid optic neuropathy has been evalu ated in a combined total of 29 affected eyes.3"6 Of the untreated eyes in these studies, 18 had final visual acuities of 20/40 or better but nine had final visual acuities of 20/100 or worse. This suggest ed that although spontaneous remission and a favorable outcome are common, nearly one fourth of the described pa tients were severely visually impaired. Of the nine patients with visual acuities of
VISION BEFORE TREATMENT
Fig. 2 (Eanzo and Tomsak). Dysthyroid optic neu ropathy response to orbital irradiation.
VOL. 96, NO. 2
I
DYSTHYROID OPTIC NEUROPATHY
O 8 O O 8
£
S § | àà
M
a ~ BEFORE TREATMENT VISION
Fig. 3 (Panzo and Tomsak). Dysthyroid optic neu ropathy response to surgical orbital decompression.
acuities of 20/100 or worse with therapy. Therefore, therapeutic intervention does appear to exert a beneficial effect by reducing the ultimate severity of visual loss. Oral systemic corticosteroid therapy led to a beneficial response in ten of ten patients studied by Day and Carrol.8 Six of eight patients described by Brown and associates9 and ten of 21 eyes described by Trobe, Glaser, and Laflamme7 also
TABLE 2 RESPONSE TO COMBINED THERAPY
Response No. of eyes Improved Unchanged Worsened Relapsed
Treatment Corticosteroids Corticosteroids and and Irradiation Decompression 3 3 0 0 3
Transantral decompression. t Kronlein procedure.
4 2* lf
1* 1*
193
improved with corticosteroids alone. In our series, 13 of 16 eyes responded favor ably to oral prednisone. Although successful response to corti costeroid therapy occurred frequently in our patients, eight of the 13 corticosteroid-responsive eyes relapsed. This was a much higher incidence than that reported by Trobe, Glaser, and Laflamme7 (three of ten eyes) and was more consistent with the relapse fre quencies (42%9 and 100%10 reported by others treating congestive ophthalmopathy. Two of our patients responded to repeated courses of corticosteroids, and one patient achieved a lasting remission in both eyes only after a fourth separate course of therapy. This suggested that alternative treatments may not be abso lutely necessary after corticosteroid re lapse. A repeat course of corticosteroids should be considered. Two of four eyes receiving orbital irra diation alone responded transiently to therapy. This was consistent with data published by Trobe, Glaser, and Laflamme7 (six of 12 eyes responded) and less favorable than that reported by Ravin, Sisson, and Knapp.11 All three eyes in patients who received concurrent oral corticosteroids and orbit al irradiation responded successfully, but all suffered relapses. Although our num bers were small, irradiation did not seem to be highly effective or lasting. The response to surgical decompres sion in our series was almost uniformly beneficial. Eight of nine eyes responded favorably to transantral decompression and none relapsed. This was somewhat more favorable than results published by Trobe, Glaser, and Laflamme7 (six of nine responded) and was consistent with re ports of successful decompression by Gorman and associates12 (17 of 18 eyes responded) and by Linberg and Ander son13 (six of seven eyes responded). All but two eyes in the series of Trobe,
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Glaser, and Laflamme7 were decom pressed by Kronlein procedures with or without orbital floor fracture. Gorman and associates12 treated one half of their cases transantrally and the other half transfrontally. Linberg and Anderson13 used transorbital decompression, which combines decompression of the medial wall and floor through a lateral orbital approach. Interestingly, Riley14 reported that only 50% of eyes decompressed with Kronlein procedures for dysthyroid optic neuropathy had a successful response. Decompression by Kronlein methods may be less favorable than transantral, transfrontal, or transorbital decompres sion. Of those who responded to therapy in our series, all did so maximally within one month of the onset of treatment. There were no clinical differences in the degree of ophthalmopathy between responders and nonresponders. The mean number of lines of improvement in visual acuity was similar in all treatment groups. A relapse was common after discontin uation of therapy in the corticosteroidtreated and irradiation-treated groups within one month of completion of therapy. There was a slight variation in duration of therapy within the corticosteroid-treated group, but no significant dif ference existed between eyes with and without relapses.
AUGUST, 1983
REFERENCES 1. Werner, S. C : Classification of eye changes of Graves' disease. Am. J. Ophthalmol. 68:646, 1969. 2. Ogura, J. H., and Lacente, F. E.: Surgical results of orbital decompression for malignant exoph thalmos. Laryngoscope 84:637, 1974. 3. Ingersheimer, J. : Visual changes in progressive exophthalmos. Arch. Ophthalmol. 53:94, 1955. 4. Hedges, T. R., and Scheie, H. G.: Visual field defects in exophthalmos associated with thyroid dis ease. Arch. Ophthalmol. 54:885, 1955. 5. Henderson, J. W.: Optic neuropathy of exoph thalmic goiter (Graves' disease). Arch. Ophthalmol. 59:471, 1958. 6. Day, R. M., and Carrol, F. D.: Optic nerve involvement associated with thyroid dysfunction. Arch. Ophthalmol. 67:289, 1962. 7. Trobe, J. D., Glaser, J. S., and Laflamme, P.: Dysthyroid optic neuropathy. Arch. Ophthalmol. 96:1199, 1978. 8. Day, R. M., and Carrol, F. D.: Corticosteroids in the treatment of optic nerve involvement associat ed with thyroid dysfunction. Arch. Ophthalmol. 79:279, 1968. 9. Brown, J., Coburn, J. W., Wigod, R. A., Hiss, J. M., Jr., and Dowling, J. T.: Adrenal steroid thera py of severe infiltrative ophthalmopathy of Graves' disease. Am. J. Med. 34:786, 1963. 10. Medical Research Council Panel: Cortisone in exophthalmos. Report on a therapeutic trial of corti sone and corticotrophin (ACTH) in exophthalmos and exophthalmic ophthalmoplegia. Lancet 1:6, 1955. 11. Ravin, J. G., Sisson, J. C , and Knapp, W. T.: Orbital radiation for the ocular changes of Graves' disease. Am. J. Ophthalmol. 79:285, 1975. 12. Gorman, C A . , Desanto, L. W., MacCarty, C. S., and Riley, F. C : Optic neuropathy of Graves' disease. Treatment by transantral or transfrontal orbital decompression. N. Engl. J. Med. 290:70, 1974. 13. Linberg, J. V., and Anderson, R. L.: Transor bital decompression. Indications and results. Arch. Ophthalmol. 99:113, 1981. 14. Riley, F. C : Surgical management of ophthal mopathy in Graves' disease. Mayo Clin. Proc. 47:986, 1972.
Sixteen patients (14 women and two men) with dysthyroid optic neuropathy (26 involved eyes) were treated with either oral corticosteroids, orbital irradiation, surgical orbital decompression, combined corticosteroids and irradiation, or combined corticosteroids and surgi cal decompression. Thirteen of 16 eyes responded favorably to corticosteroid therapy but eight of the 13 relapsed upon discontinuation of treatment. Two of four eyes responded to irradiation initially but later relapsed. The response to orbital decompression was almost uniformly beneficial (eight of nine eyes responded) and lasting in all. Combined modes of therapy offered no additional advantage. Accepted treatments for dysthyroid optic neuropathy include systemic corti costeroids, orbital irradiation, and surgi cal decompression of the orbit. We retro spectively analyzed cases of dysthyroid optic neuropathy treated here between 1972 and 1982. SUBJECTS AND METHODS
The study included 16 patients (26 eyes) affected by dysthyroid optic neu ropathy. All the involved eyes demon strated optic nerve dysfunction and the characteristic external signs of ocular dysthyroidism. Optic nerve dysfunction was documented by examination of visual acuity, visual fields, pupils, and color vision. We excluded patients with other conditions that might have accounted for visual impairment (opaque media, maculopathy, and the like). The patients ranged in age from 26 to
Accepted for publication May 11, 1983. From the Department of Ophthalmology, Cleve land Clinic Foundation, Cleveland, Ohio. Reprint requests to Robert L. Tomsak, M.D., Department of Ophthalmology, 9500 Euclid Ave., Cleveland, OH 44106. 190
69 years (mean age, 51 years). Fourteen of the 16 patients were female. At the time dysthyroid optic neuropathy was diagnosed, 11 patients were euthyroid, four were hyperthyroid, and one was hypothyroid. All eyes were exophthal mic, 24 had soft tissue changes, and 21 demonstrated extraocular muscle in volvement. Mild, optically insignificant corneal changes were noted in 13 eyes. By Werner's 1 classification, four eyes had severe ophthalmopathy and the remain ing 22 demonstrated mild to moderate ophthalmopathy. All affected eyes had decreased central visual acuities or visual field defects, or both. Central scotomas, inferior altitudinal and arcuate defects, generalized con striction, and paracentral scotomas were demonstrated by Goldmann perimetry. Ten eyes had afferent pupillary defects. Abnormal color vision was demonstrated by AOH-R-R pseudoisochromatic plates in nine of 15 tested eyes. Sixteen of 26 eyes had ophthalmoscopically normal optic disks. All patients were treated. Treatment consisted of oral prednisone, orbital irra diation, surgical decompression, concur-
© AMERICAN JOURNAL OF OPHTHALMOLOGY 96:190-194, 1983
VOL. 96, NO. 2
DYSTHYROID OPTIC NEUROPATHY
rent corticosteroids and irradiation, or concurrent corticosteroids and orbital de compression. Response to therapy was evaluated for each form of treatment as well as for the entire group. We defined a successful response as improvement of two or more lines of visual acuity or a visual acuity of 20/20 with improvement of visual fields to normal within eight weeks of therapy. RESULTS
Corticosteroids—Sixteen eyes (11 pa tients) were treated with high doses of oral prednisone (Fig. 1). The patients' ages ranged from 29 to 60 years (mean age, 52 years). Dosage was 80 to 100 mg daily. The patients received a maximum dosage for a mean of 11 days after which the dosage was gradually decreased. Total days of corticosteroid therapy ranged from 14 to 51 days with a mean of 32 days. Thirteen eyes (nine patients) initially improved with treatment (Table 1). Three eyes remained unchanged. There was no instance of deterioration during therapy.
VISION BEFORE TREATMENT
Fig. 1 (Panro and Tomsak). Dysthyroid optic neu ropathy response to oral prednisone therapy.
191
Maximum response occurred within 14 to 40 days (mean, 24 days). A lasting remission was achieved in five eyes (three patients) with follow-up peri ods of five to 12 months. Clinical relapse occurred in eight eyes (six patients) with in four to 72 days (mean, 33 days) of discontinuation of therapy (Table 1). Two relapsing eyes (one patient) responded to four separate courses of corticosteroids (three relapses) before achieving a lasting remission for a follow-up period of three years. All of the remaining eyes that relapsed later underwent surgical decom pression. Irradiation—Four eyes (three patients) were treated with orbital irradiation (Fig. 2). Their ages ranged from 45 to 54 years (mean age, 50 years). Treatment consisted of 1,600 to 2,000 rads in eight to ten daily divided doses (200 rads/dose) through lateral ports to the orbital apices. Two eyes (two patients) remained un changed. One patient with bilateral dys thyroid optic neuropathy responded suc cessfully within 27 days of beginning therapy, but both eyes relapsed on the 38th day after the final radiation treat ment (Table 1). Orbital decompression—Nine eyes (seven patients) underwent surgical de compression transantrally in the manner described by Ogura and Lacente 2 (Fig. 3). Their ages ranged from 35 to 58 years (mean age, 52 years). Two eyes had decompression as the primary treatment. Four had relapsed after responding to corticosteroid therapy. Three had failed to respond to either corticosteroids or irradiation. Eight of the nine eyes im proved. There were no relapses during an average follow-up period of 14 months (Table 1). Oral corticosteroids with irradiation— Three eyes (two patients) were treated with concurrent corticosteroids and irra diation (Table 2). Their ages were 35 and 55 years. All eyes initially responded, but
192
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AUGUST, 1983
TABLE 1 RESPONSE TO SINGLE METHOD OF TREATMENT
Response
Corticosteroids
Treatment Irradiation
Decompression
No. of eyes Improved Unchanged Worsened Relapse after initial response No. responding No. relapsing Time to relapse (days) Mean Range
16 13 3 0
4 2 2 0
9 8 1 0
13 8
2 2
8 0
33 4 to 72
38 38
— —
later relapsed and underwent surgical decompression. Oral corticosteroids with orbital decompression—Four eyes (three pa tients) were treated with concurrent cor ticosteroids and surgical decompression (Table 2). Their ages ranged from 43 to 69 years (mean age, 57 years). Three orbits were decompressed transantrally, and one orbit was decompressed by a Kronlein procedure. Two of the four eyes improved. Both of these were done by the transantral approach. One eye re lapsed. The one eye decompressed by a Kronlein procedure showed no change. Vision deteriorated in one patient who underwent transantral decompression.
20/100 or worse, six had final visual acui ties of counting fingers to no light percep tion. In our series, four of 26 eyes had final visual acuities of 20/100 or less and none had a final visual acuity worse than 20/400. Twenty of 26 eyes had final visual acuities of 20/40 or better. Trobe, Glaser, and Laflamme 7 found that only two of 29 eyes had final visual
DISCUSSION
The natural course of untreated dysthyroid optic neuropathy has been evalu ated in a combined total of 29 affected eyes.3"6 Of the untreated eyes in these studies, 18 had final visual acuities of 20/40 or better but nine had final visual acuities of 20/100 or worse. This suggest ed that although spontaneous remission and a favorable outcome are common, nearly one fourth of the described pa tients were severely visually impaired. Of the nine patients with visual acuities of
VISION BEFORE TREATMENT
Fig. 2 (Eanzo and Tomsak). Dysthyroid optic neu ropathy response to orbital irradiation.
VOL. 96, NO. 2
I
DYSTHYROID OPTIC NEUROPATHY
O 8 O O 8
£
S § | àà
M
a ~ BEFORE TREATMENT VISION
Fig. 3 (Panzo and Tomsak). Dysthyroid optic neu ropathy response to surgical orbital decompression.
acuities of 20/100 or worse with therapy. Therefore, therapeutic intervention does appear to exert a beneficial effect by reducing the ultimate severity of visual loss. Oral systemic corticosteroid therapy led to a beneficial response in ten of ten patients studied by Day and Carrol.8 Six of eight patients described by Brown and associates9 and ten of 21 eyes described by Trobe, Glaser, and Laflamme7 also
TABLE 2 RESPONSE TO COMBINED THERAPY
Response No. of eyes Improved Unchanged Worsened Relapsed
Treatment Corticosteroids Corticosteroids and and Irradiation Decompression 3 3 0 0 3
Transantral decompression. t Kronlein procedure.
4 2* lf
1* 1*
193
improved with corticosteroids alone. In our series, 13 of 16 eyes responded favor ably to oral prednisone. Although successful response to corti costeroid therapy occurred frequently in our patients, eight of the 13 corticosteroid-responsive eyes relapsed. This was a much higher incidence than that reported by Trobe, Glaser, and Laflamme7 (three of ten eyes) and was more consistent with the relapse fre quencies (42%9 and 100%10 reported by others treating congestive ophthalmopathy. Two of our patients responded to repeated courses of corticosteroids, and one patient achieved a lasting remission in both eyes only after a fourth separate course of therapy. This suggested that alternative treatments may not be abso lutely necessary after corticosteroid re lapse. A repeat course of corticosteroids should be considered. Two of four eyes receiving orbital irra diation alone responded transiently to therapy. This was consistent with data published by Trobe, Glaser, and Laflamme7 (six of 12 eyes responded) and less favorable than that reported by Ravin, Sisson, and Knapp.11 All three eyes in patients who received concurrent oral corticosteroids and orbit al irradiation responded successfully, but all suffered relapses. Although our num bers were small, irradiation did not seem to be highly effective or lasting. The response to surgical decompres sion in our series was almost uniformly beneficial. Eight of nine eyes responded favorably to transantral decompression and none relapsed. This was somewhat more favorable than results published by Trobe, Glaser, and Laflamme7 (six of nine responded) and was consistent with re ports of successful decompression by Gorman and associates12 (17 of 18 eyes responded) and by Linberg and Ander son13 (six of seven eyes responded). All but two eyes in the series of Trobe,
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AMERICAN JOURNAL OF OPHTHALMOLOGY
Glaser, and Laflamme7 were decom pressed by Kronlein procedures with or without orbital floor fracture. Gorman and associates12 treated one half of their cases transantrally and the other half transfrontally. Linberg and Anderson13 used transorbital decompression, which combines decompression of the medial wall and floor through a lateral orbital approach. Interestingly, Riley14 reported that only 50% of eyes decompressed with Kronlein procedures for dysthyroid optic neuropathy had a successful response. Decompression by Kronlein methods may be less favorable than transantral, transfrontal, or transorbital decompres sion. Of those who responded to therapy in our series, all did so maximally within one month of the onset of treatment. There were no clinical differences in the degree of ophthalmopathy between responders and nonresponders. The mean number of lines of improvement in visual acuity was similar in all treatment groups. A relapse was common after discontin uation of therapy in the corticosteroidtreated and irradiation-treated groups within one month of completion of therapy. There was a slight variation in duration of therapy within the corticosteroid-treated group, but no significant dif ference existed between eyes with and without relapses.
AUGUST, 1983
REFERENCES 1. Werner, S. C : Classification of eye changes of Graves' disease. Am. J. Ophthalmol. 68:646, 1969. 2. Ogura, J. H., and Lacente, F. E.: Surgical results of orbital decompression for malignant exoph thalmos. Laryngoscope 84:637, 1974. 3. Ingersheimer, J. : Visual changes in progressive exophthalmos. Arch. Ophthalmol. 53:94, 1955. 4. Hedges, T. R., and Scheie, H. G.: Visual field defects in exophthalmos associated with thyroid dis ease. Arch. Ophthalmol. 54:885, 1955. 5. Henderson, J. W.: Optic neuropathy of exoph thalmic goiter (Graves' disease). Arch. Ophthalmol. 59:471, 1958. 6. Day, R. M., and Carrol, F. D.: Optic nerve involvement associated with thyroid dysfunction. Arch. Ophthalmol. 67:289, 1962. 7. Trobe, J. D., Glaser, J. S., and Laflamme, P.: Dysthyroid optic neuropathy. Arch. Ophthalmol. 96:1199, 1978. 8. Day, R. M., and Carrol, F. D.: Corticosteroids in the treatment of optic nerve involvement associat ed with thyroid dysfunction. Arch. Ophthalmol. 79:279, 1968. 9. Brown, J., Coburn, J. W., Wigod, R. A., Hiss, J. M., Jr., and Dowling, J. T.: Adrenal steroid thera py of severe infiltrative ophthalmopathy of Graves' disease. Am. J. Med. 34:786, 1963. 10. Medical Research Council Panel: Cortisone in exophthalmos. Report on a therapeutic trial of corti sone and corticotrophin (ACTH) in exophthalmos and exophthalmic ophthalmoplegia. Lancet 1:6, 1955. 11. Ravin, J. G., Sisson, J. C , and Knapp, W. T.: Orbital radiation for the ocular changes of Graves' disease. Am. J. Ophthalmol. 79:285, 1975. 12. Gorman, C A . , Desanto, L. W., MacCarty, C. S., and Riley, F. C : Optic neuropathy of Graves' disease. Treatment by transantral or transfrontal orbital decompression. N. Engl. J. Med. 290:70, 1974. 13. Linberg, J. V., and Anderson, R. L.: Transor bital decompression. Indications and results. Arch. Ophthalmol. 99:113, 1981. 14. Riley, F. C : Surgical management of ophthal mopathy in Graves' disease. Mayo Clin. Proc. 47:986, 1972.