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Saccadic Velocity Studies in Patients with Endocrine Ocular Disease
SACCADIC VELOCITY STUDIES IN PATIENTS WITH E N D O C R I N E OCULAR DISEASE H E N R Y S. M E T Z ,
M.D.
San Francisco, California
Limited elevation of one or both eyes, often accompanied by exophthalmos and eyelid retraction, is the most common motility defect seen in patients with thy roid eye disease. 1 Goldstein 2 suggested that a paralytic superior rectus muscle in patients with thyroid disease was respon sible for the hypotropia and limited ele vation. In 1943, Dunnington and Berke 3 de scribed a number of patients with exoph thalmos caused by chronic orbital myositis. These patients probably had thyroid eye disease and the traction test was used to differentiate a paralytic superior rectus muscle from inferior restrictions as the etiology of limited ocular elevation. The positive test results in all of these patients suggested that limited elevation was not caused by weakness of the superior rectus muscle. Breinin 4 described an ocular electromyographic pattern of paresis of innerva tion in the congestive stage of thyroid eye disease. H e believed that damage to the extraocular muscles results from orbital swelling in a toxic neuropathy. Miller, 5 in an ocular electromyographic study of pa tients with endocrine eye disease, indicat ed that tracings obtained from the superi or rectus muscle were normal. Saccadic velocity measurements in pa tients with paretic or paralytic extraocular muscles have indicated slowing of the saccadic eye movements proportional to the degree of extraocular muscle weak-
ness. 6 , 7 Utilizing saccadic velocity mea surements, we studied 15 patients with thyroid eye disease to determine the role of extraocular muscle weakness in the etiology of limited ocular rotation. S U B J E C T S AND M E T H O D S
All 15 patients were in the noncongestive, stable stage of endocrine ophthalmopathy and had a positive forced duction test in either the vertical or horizon tal direction, or both. Studies were per formed before extraocular muscle sur gery. Two patients had no deviation in pri mary gaze. Of the 13 remaining patients, 12 had a vertical deviation averaging 26 prism diopters (range, 5 to 75 prism diop ters). Seven of these patients had only a vertical deviation, while five patients also had esotropia averaging 17 prism diopters (range, 4 to 40 prism diopters). One pa tient, without a vertical deviation, had 15 prism diopters of esotropia alone. There were no patients with exotropia. All 15 patients had limitation of u p ward gaze, ranging from mild to very severe (Fig. 1), while ten patients also had some limitation of horizontal gaze, which was generally mild (Fig. 2). Downgaze was slightly limited in two patients. Saccadic velocity measurements were made by electro-oculography. 8 Saccades were generated by voluntary movements of 40 degrees. Because of the limited range of vertical movement, saccades were made in the area where the eye was free to move and the measured eye was From the Smith-Kettlewell Institute of Visual Sciences, San Francisco, California. This study was used for fixation. supported in part by National Institutes of Health Vertical eye movements were recorded grants EY 1585 and EY 0727, and in part by the by placing miniature skin electrodes cen Smith-Kettlewell Eye Research Foundation. Reprint requests to Henry S. Metz, M.D., 2232 trally on the lower eyelid and brow, and Webster St., San Francisco, CA 94115. an indifferent electrode temporal to the 695
696
AMERICAN JOURNAL OF OPHTHALMOLOGY
NOVEMBER, 1977
A Beckman type RS dynograph with modified, rectilinear ink writers, dyno graph amplifier type 462, preamplifier type 461 B, direct nystagmus coupler type 9859, and nystagmus velocity coupler type 9841 were used for electrooculography recordings. The eye position channel had a band width from 0 to 10 Hz. The gain was 0.6 mV/cm. The veloci ty channel had a band width of 2.2 to 10 Hz with a gain of 5 μν/cm. Ocular electromyography of the verti cal recti was performed in two patients, and one patient had active force genera tion testing9 of the superior rectus mus cle. RESULTS
Fig. 1 (Metz). Endocrine ophthalmopathy with bilateral limitation of upgaze (top), small right hypertropia and bilateral upper eyelid retraction and proptosis (center), and full range of downward rota tion bilaterally (bottom).
lateral canthus. Horizontal eye move ments in the same eye were measured separately by placing electrodes at the medial and lateral canthus, and the indif ferent electrode on the brow.
Vertical saccades were measured in 19 eyes of 14 patients. Upward saccades av eraged 260 degrees per second (range, 190 to 330 degrees per second), while down ward saccades averaged 241 degrees per second (range, 160 to 320 degrees per second) (Fig. 3). In normal subjects in our laboratory, vertical saccades average 250 degrees per second, with a range of 200 to 300 degrees per second. Upward saccades are slightly more rapid than downward saccades, which may be caused by an upper eyelid artifact. This tracing is simi lar to that obtained in a normal subject (Fig. 4). When the extent of the saccade came close to the full extent of ocular move ment, a "tailing-off" of the movement occurred (Fig. 5). Saccadic velocity was reduced near the end of the movement.
Fig. 2 (Metz), Endocrine ophthalmopathy with limitation of abduction both to the right (right) and left (left).
VOL. 84, NO. 5
SACCADES IN E N D O C R I N E
OPHTHALMOPATHY
697
I sec
40<
300V seC u
i sec
T Fig. 3 (Metz). Electro-oculography of vertical saccades from 20 degrees up to 20 degrees down in a patient with endocrine ophthalmopathy. Upper trace represents eye position, lower trace represents velocity. Upward saccades (U) and downward saccades (D) are both rapid (280 degrees per second upward and 250 degrees per second downward).
Horizontal saccades were measured in ten eyes of eight patients. Abduction saccades averaged 252 degrees per second (range, 160 to 320 degrees per second), while adduction saccades averaged 266 degrees per second (range, 200 to 330 degrees per second). We usually found no difference between abduction and adduc tion saccadic velocity in normal subjects. Results of ocular electromyography of the vertical rectus muscles were normal in two patients. Active force generation of the superior rectus muscle of another pa tient was also within normal limits. DISCUSSION
Kroll and Kuwabara10 indicated that the extraocular muscles were firm, rubbery, and enlarged in dysthyroid ocular myopathy. Histologically, interstitial edema was found, as well as round cell infiltration. Falconer and Alexander11 reported some
lOO^sec fy**»tyM\s*W*#l
Fig. 4 (Metz). Electro-oculography of vertical saccades in a normal subject, 10 degrees up and 10 degrees down. Upward and downward saccades are rapid and equal in velocity (250 degrees per second).
cases with degenerative changes of the muscle fibers followed by increased fi brous tissue replacement of degenerated muscle fibers. Kroll and Kuwabara10 reported marked resistance to passive stretching, most prominent in the inferior and medial rec ti. Jampolsky12 indicated that these mus cles were normal by direct inspection, but retracted markedly when severed from the globe. Pratt-Johnson13 stated that confusion may arise between an inferior restriction syndrome and a superior rectus palsy in dysthyroid ocular disease, particularly when the forced duction test is not obviously positive. The Hess chart mim ics exactly the picture of a true paresis of the superior rectus muscle. Several electromyography studies have
698
_h_
AMERICAN JOURNAL OF OPHTHALMOLOGY
_h I see h_
300ZSM
Fig. 5 (Metz). Electro-oculography of vertical saccades from 20 degrees up to 20 degrees down. This patient with endocrine ophthalmopathy could bring her eye to 20 degrees up only with maximal effort, and upgaze was limited to 10 to 12 degrees without maximum effort. Downward saccades (D) were rapid (200 degrees per second). Upward saccades were initially rapid (230 degrees per second for the first 35 degrees of movement), and considerably slower for the last 5 degrees (40 degrees per second, see arrow).
shown a myopathie pattern in the ex traocular muscles with normal recruitment. 5 · 1 2 , 1 4 - 1 6 However, there some re ports still describing paresis of extraocular muscles with dysthyroid myopa thy. 2 · 10 Our saccadic velocity measurements are within normal limits, suggesting an absence of extraocular muscle paresis in patients in the noncongestive stage of endocrine ophthalmopathy. These findings, combined with a positive forced duction test, implicate mechanical re striction as the cause of limited ocular rotations and strabismus. Jensen, 17 using ocular electromyography, suggested that limited ocular motility in endocrine ophthalmoplegia is not caused by myopathy, but by mechanical immobilization. Re lease of these surgical restrictions im
NOVEMBER, 1977
proves the range of ocular movements and reduces or eliminates strabismus. 18 In the absence of ocular muscle paresis or paralysis, large recession-resection proce dures or muscle transposition surgery are not required to achieve satisfactory re sults. The saccades demonstrated in Figures 3 and 5 show a slight undershoot, with a small corrective saccade to reach the fixa tion point. This has been seen in normal subjects and is not considered significant with regard to endocrine ophthalmopa thy. When saccades were made toward the limit of the range of ocular rotation, a decrease in velocity was noted. This may be caused by restriction of the antagonist muscle. The restriction can be stretched out by the force of the saccade, but does not release completely, thus slowing the saccadic movement at its end. We have seen this pattern in other patients with orbital or extraocular muscle restrictions. T h e pattern slowing becomes apparent only as the eye movement approaches its limit. It is different from paresis of an extraocular muscle, where the entire movement is slow. 6,7 The velocity tracing depicts both the positive and negative acceleration of the eye movement. Figure 5 (velocity tracing) suggests that the positive acceleration is normal, while the negative acceleration (deceleration) is reduced. If the superior rectus muscle were paretic, both positive and negative acceleration would be slowed. Since this is not the case, reduc tion of only the negative acceleration represents the effect of inferior restric tion. SUMMARY
We measured either vertical or horizon tal saccadic eye movements, or both of 15 patients with noncongestive, endocrine ophthalmopathy. All velocity measure-
VOL. 84, NO. 5
SACCADES IN ENDOCRINE OPHTHALMOPATHY
ments were within the normal range, suggesting the absence of paresis of an extraocular muscle. Results of ocular electromyography in two patients, and active force generation studies in one patient were also within normal limits. These findings and the positive forced duction test suggest a mechanical, restric tive etiology for limitation of ocular movements and strabismus in patients with endocrine ophthalmopathy. REFERENCES 1. Burian, H. M., and von Noorden, G. K.: Binoc ular Vision and Ocular Motility. St. Louis, C. V. Mosby, 1974, p. 378. 2. Goldstein, J.: Paresis of superior rectus muscle associated with thyroid dysfunction. Arch. Ophthalmol. 72:5, 1964. 3. Dunnington, J. H., and Berke, R. N.: Exophthalmos due to chronic orbital myositis. Arch. Ophthalmol. 30:4, 1943. 4. Breinin, G. M.: New aspects of ophthalmoneurologic diagnosis. Arch. Ophthalmol. 58:375, 1957. 5. Miller, J. E., Van Heuven, W., and Ward, R.: Surgical correction of hypotropia associated with thyroid dysfunction. Arch. Ophthalmol. 74:509, 1965. 6. Metz, H. S., Scott, A. B., O'Meara, D. M., and Stewart, H. L.: Ocular saccades in lateral rectus palsy. Arch. Ophthalmol. 84:453, 1970.
699
7. Metz, H. S.: Third nerve palsy. Saccadic veloc ity studies. Ann. Ophthalmol. 5:526, 1973. 8. Metz, H. S., Scott, W. E., Madson, E., and Scott, A. B.: Saccadic velocity and active force studies in blowout fractures of the orbit. Am. J. Ophthalmol. 78:665, 1974. 9. Scott, A. B.: Active force tests in lateral rectus paralysis. Arch. Ophthalmol. 85:397, 1971. 10. Kroll, A. J., and Kuwabara, T.: Dysthyroid ocular myopathy. Arch. Ophthalmol. 76:244, 1966. 11. Falconer, M. A., and Alexander, W. S.: Exper iences with malignant exophthalmos. Relationships of condition to thyrotoxicosis and to the pituitary thyrotropic hormone. Br. J. Ophthalmol. 35:253, 1951. 12. Jampolsky, A.: What can electromyography do for the ophthalmologist? Invest. Ophthalmol. 9:570, 1970. 13. Pratt-Johnson, J., and Drance, S. M.: Surgical treatment of dysthyroid restriction syndromes. Can. J. Ophthalmol. 7:405, 1972. 14. Magora, A., Chaco, J., and Zauberman, H.: An electromyographic investigation of ophthalmoplegia in thyrotoxicosis. Arch. Ophthalmol. 79:170, 1968. 15. Biodi, F.: Ophthalmology of Graves' disease. In Dabexies, O. H., Pinschmidt, N. W., Caplan, H. (eds.): Symposium on Surgery of the Orbit and Adnexae. St. Louis, C. V. Mosby, 1974, p. 104. 16. Schultz, R. O., Van Allen, M. W., and Biodi, F. C.: Endocrine ophthalmoplegia. Arch. Ophthal mol. 63:217, 1960. 17. Jensen, S. F.: Endocrine ophthalmoplegia. Acta Ophthalmol. 49:679, 1971. 18. Schimek, R. A.: Surgical management of ocu lar complications of Graves' disease. Arch. Ophthal mol. 87:655, 1972.
M.D.
San Francisco, California
Limited elevation of one or both eyes, often accompanied by exophthalmos and eyelid retraction, is the most common motility defect seen in patients with thy roid eye disease. 1 Goldstein 2 suggested that a paralytic superior rectus muscle in patients with thyroid disease was respon sible for the hypotropia and limited ele vation. In 1943, Dunnington and Berke 3 de scribed a number of patients with exoph thalmos caused by chronic orbital myositis. These patients probably had thyroid eye disease and the traction test was used to differentiate a paralytic superior rectus muscle from inferior restrictions as the etiology of limited ocular elevation. The positive test results in all of these patients suggested that limited elevation was not caused by weakness of the superior rectus muscle. Breinin 4 described an ocular electromyographic pattern of paresis of innerva tion in the congestive stage of thyroid eye disease. H e believed that damage to the extraocular muscles results from orbital swelling in a toxic neuropathy. Miller, 5 in an ocular electromyographic study of pa tients with endocrine eye disease, indicat ed that tracings obtained from the superi or rectus muscle were normal. Saccadic velocity measurements in pa tients with paretic or paralytic extraocular muscles have indicated slowing of the saccadic eye movements proportional to the degree of extraocular muscle weak-
ness. 6 , 7 Utilizing saccadic velocity mea surements, we studied 15 patients with thyroid eye disease to determine the role of extraocular muscle weakness in the etiology of limited ocular rotation. S U B J E C T S AND M E T H O D S
All 15 patients were in the noncongestive, stable stage of endocrine ophthalmopathy and had a positive forced duction test in either the vertical or horizon tal direction, or both. Studies were per formed before extraocular muscle sur gery. Two patients had no deviation in pri mary gaze. Of the 13 remaining patients, 12 had a vertical deviation averaging 26 prism diopters (range, 5 to 75 prism diop ters). Seven of these patients had only a vertical deviation, while five patients also had esotropia averaging 17 prism diopters (range, 4 to 40 prism diopters). One pa tient, without a vertical deviation, had 15 prism diopters of esotropia alone. There were no patients with exotropia. All 15 patients had limitation of u p ward gaze, ranging from mild to very severe (Fig. 1), while ten patients also had some limitation of horizontal gaze, which was generally mild (Fig. 2). Downgaze was slightly limited in two patients. Saccadic velocity measurements were made by electro-oculography. 8 Saccades were generated by voluntary movements of 40 degrees. Because of the limited range of vertical movement, saccades were made in the area where the eye was free to move and the measured eye was From the Smith-Kettlewell Institute of Visual Sciences, San Francisco, California. This study was used for fixation. supported in part by National Institutes of Health Vertical eye movements were recorded grants EY 1585 and EY 0727, and in part by the by placing miniature skin electrodes cen Smith-Kettlewell Eye Research Foundation. Reprint requests to Henry S. Metz, M.D., 2232 trally on the lower eyelid and brow, and Webster St., San Francisco, CA 94115. an indifferent electrode temporal to the 695
696
AMERICAN JOURNAL OF OPHTHALMOLOGY
NOVEMBER, 1977
A Beckman type RS dynograph with modified, rectilinear ink writers, dyno graph amplifier type 462, preamplifier type 461 B, direct nystagmus coupler type 9859, and nystagmus velocity coupler type 9841 were used for electrooculography recordings. The eye position channel had a band width from 0 to 10 Hz. The gain was 0.6 mV/cm. The veloci ty channel had a band width of 2.2 to 10 Hz with a gain of 5 μν/cm. Ocular electromyography of the verti cal recti was performed in two patients, and one patient had active force genera tion testing9 of the superior rectus mus cle. RESULTS
Fig. 1 (Metz). Endocrine ophthalmopathy with bilateral limitation of upgaze (top), small right hypertropia and bilateral upper eyelid retraction and proptosis (center), and full range of downward rota tion bilaterally (bottom).
lateral canthus. Horizontal eye move ments in the same eye were measured separately by placing electrodes at the medial and lateral canthus, and the indif ferent electrode on the brow.
Vertical saccades were measured in 19 eyes of 14 patients. Upward saccades av eraged 260 degrees per second (range, 190 to 330 degrees per second), while down ward saccades averaged 241 degrees per second (range, 160 to 320 degrees per second) (Fig. 3). In normal subjects in our laboratory, vertical saccades average 250 degrees per second, with a range of 200 to 300 degrees per second. Upward saccades are slightly more rapid than downward saccades, which may be caused by an upper eyelid artifact. This tracing is simi lar to that obtained in a normal subject (Fig. 4). When the extent of the saccade came close to the full extent of ocular move ment, a "tailing-off" of the movement occurred (Fig. 5). Saccadic velocity was reduced near the end of the movement.
Fig. 2 (Metz), Endocrine ophthalmopathy with limitation of abduction both to the right (right) and left (left).
VOL. 84, NO. 5
SACCADES IN E N D O C R I N E
OPHTHALMOPATHY
697
I sec
40<
300V seC u
i sec
T Fig. 3 (Metz). Electro-oculography of vertical saccades from 20 degrees up to 20 degrees down in a patient with endocrine ophthalmopathy. Upper trace represents eye position, lower trace represents velocity. Upward saccades (U) and downward saccades (D) are both rapid (280 degrees per second upward and 250 degrees per second downward).
Horizontal saccades were measured in ten eyes of eight patients. Abduction saccades averaged 252 degrees per second (range, 160 to 320 degrees per second), while adduction saccades averaged 266 degrees per second (range, 200 to 330 degrees per second). We usually found no difference between abduction and adduc tion saccadic velocity in normal subjects. Results of ocular electromyography of the vertical rectus muscles were normal in two patients. Active force generation of the superior rectus muscle of another pa tient was also within normal limits. DISCUSSION
Kroll and Kuwabara10 indicated that the extraocular muscles were firm, rubbery, and enlarged in dysthyroid ocular myopathy. Histologically, interstitial edema was found, as well as round cell infiltration. Falconer and Alexander11 reported some
lOO^sec fy**»tyM\s*W*#l
Fig. 4 (Metz). Electro-oculography of vertical saccades in a normal subject, 10 degrees up and 10 degrees down. Upward and downward saccades are rapid and equal in velocity (250 degrees per second).
cases with degenerative changes of the muscle fibers followed by increased fi brous tissue replacement of degenerated muscle fibers. Kroll and Kuwabara10 reported marked resistance to passive stretching, most prominent in the inferior and medial rec ti. Jampolsky12 indicated that these mus cles were normal by direct inspection, but retracted markedly when severed from the globe. Pratt-Johnson13 stated that confusion may arise between an inferior restriction syndrome and a superior rectus palsy in dysthyroid ocular disease, particularly when the forced duction test is not obviously positive. The Hess chart mim ics exactly the picture of a true paresis of the superior rectus muscle. Several electromyography studies have
698
_h_
AMERICAN JOURNAL OF OPHTHALMOLOGY
_h I see h_
300ZSM
Fig. 5 (Metz). Electro-oculography of vertical saccades from 20 degrees up to 20 degrees down. This patient with endocrine ophthalmopathy could bring her eye to 20 degrees up only with maximal effort, and upgaze was limited to 10 to 12 degrees without maximum effort. Downward saccades (D) were rapid (200 degrees per second). Upward saccades were initially rapid (230 degrees per second for the first 35 degrees of movement), and considerably slower for the last 5 degrees (40 degrees per second, see arrow).
shown a myopathie pattern in the ex traocular muscles with normal recruitment. 5 · 1 2 , 1 4 - 1 6 However, there some re ports still describing paresis of extraocular muscles with dysthyroid myopa thy. 2 · 10 Our saccadic velocity measurements are within normal limits, suggesting an absence of extraocular muscle paresis in patients in the noncongestive stage of endocrine ophthalmopathy. These findings, combined with a positive forced duction test, implicate mechanical re striction as the cause of limited ocular rotations and strabismus. Jensen, 17 using ocular electromyography, suggested that limited ocular motility in endocrine ophthalmoplegia is not caused by myopathy, but by mechanical immobilization. Re lease of these surgical restrictions im
NOVEMBER, 1977
proves the range of ocular movements and reduces or eliminates strabismus. 18 In the absence of ocular muscle paresis or paralysis, large recession-resection proce dures or muscle transposition surgery are not required to achieve satisfactory re sults. The saccades demonstrated in Figures 3 and 5 show a slight undershoot, with a small corrective saccade to reach the fixa tion point. This has been seen in normal subjects and is not considered significant with regard to endocrine ophthalmopa thy. When saccades were made toward the limit of the range of ocular rotation, a decrease in velocity was noted. This may be caused by restriction of the antagonist muscle. The restriction can be stretched out by the force of the saccade, but does not release completely, thus slowing the saccadic movement at its end. We have seen this pattern in other patients with orbital or extraocular muscle restrictions. T h e pattern slowing becomes apparent only as the eye movement approaches its limit. It is different from paresis of an extraocular muscle, where the entire movement is slow. 6,7 The velocity tracing depicts both the positive and negative acceleration of the eye movement. Figure 5 (velocity tracing) suggests that the positive acceleration is normal, while the negative acceleration (deceleration) is reduced. If the superior rectus muscle were paretic, both positive and negative acceleration would be slowed. Since this is not the case, reduc tion of only the negative acceleration represents the effect of inferior restric tion. SUMMARY
We measured either vertical or horizon tal saccadic eye movements, or both of 15 patients with noncongestive, endocrine ophthalmopathy. All velocity measure-
VOL. 84, NO. 5
SACCADES IN ENDOCRINE OPHTHALMOPATHY
ments were within the normal range, suggesting the absence of paresis of an extraocular muscle. Results of ocular electromyography in two patients, and active force generation studies in one patient were also within normal limits. These findings and the positive forced duction test suggest a mechanical, restric tive etiology for limitation of ocular movements and strabismus in patients with endocrine ophthalmopathy. REFERENCES 1. Burian, H. M., and von Noorden, G. K.: Binoc ular Vision and Ocular Motility. St. Louis, C. V. Mosby, 1974, p. 378. 2. Goldstein, J.: Paresis of superior rectus muscle associated with thyroid dysfunction. Arch. Ophthalmol. 72:5, 1964. 3. Dunnington, J. H., and Berke, R. N.: Exophthalmos due to chronic orbital myositis. Arch. Ophthalmol. 30:4, 1943. 4. Breinin, G. M.: New aspects of ophthalmoneurologic diagnosis. Arch. Ophthalmol. 58:375, 1957. 5. Miller, J. E., Van Heuven, W., and Ward, R.: Surgical correction of hypotropia associated with thyroid dysfunction. Arch. Ophthalmol. 74:509, 1965. 6. Metz, H. S., Scott, A. B., O'Meara, D. M., and Stewart, H. L.: Ocular saccades in lateral rectus palsy. Arch. Ophthalmol. 84:453, 1970.
699
7. Metz, H. S.: Third nerve palsy. Saccadic veloc ity studies. Ann. Ophthalmol. 5:526, 1973. 8. Metz, H. S., Scott, W. E., Madson, E., and Scott, A. B.: Saccadic velocity and active force studies in blowout fractures of the orbit. Am. J. Ophthalmol. 78:665, 1974. 9. Scott, A. B.: Active force tests in lateral rectus paralysis. Arch. Ophthalmol. 85:397, 1971. 10. Kroll, A. J., and Kuwabara, T.: Dysthyroid ocular myopathy. Arch. Ophthalmol. 76:244, 1966. 11. Falconer, M. A., and Alexander, W. S.: Exper iences with malignant exophthalmos. Relationships of condition to thyrotoxicosis and to the pituitary thyrotropic hormone. Br. J. Ophthalmol. 35:253, 1951. 12. Jampolsky, A.: What can electromyography do for the ophthalmologist? Invest. Ophthalmol. 9:570, 1970. 13. Pratt-Johnson, J., and Drance, S. M.: Surgical treatment of dysthyroid restriction syndromes. Can. J. Ophthalmol. 7:405, 1972. 14. Magora, A., Chaco, J., and Zauberman, H.: An electromyographic investigation of ophthalmoplegia in thyrotoxicosis. Arch. Ophthalmol. 79:170, 1968. 15. Biodi, F.: Ophthalmology of Graves' disease. In Dabexies, O. H., Pinschmidt, N. W., Caplan, H. (eds.): Symposium on Surgery of the Orbit and Adnexae. St. Louis, C. V. Mosby, 1974, p. 104. 16. Schultz, R. O., Van Allen, M. W., and Biodi, F. C.: Endocrine ophthalmoplegia. Arch. Ophthal mol. 63:217, 1960. 17. Jensen, S. F.: Endocrine ophthalmoplegia. Acta Ophthalmol. 49:679, 1971. 18. Schimek, R. A.: Surgical management of ocu lar complications of Graves' disease. Arch. Ophthal mol. 87:655, 1972.