| OCR Text |
Show Journal of Neuro- Ophthalmology 35( 3): 142- 146, 1995, © 1995 Lippincott- Raven Publishers, Philadelphia The Treatment of Superior Oblique Myokymia Utilizing the Harada- Ito Procedure Gregory S. Kosmorsky, D. O., Brian D. Ellis, M. D., Nick Fogt, O. D., and R. John Leigh, M. D. A woman with superior oblique myokymia ( SOM) was cured of her condition by performing a Harada- Ito procedure. This procedure involves transposing the anterior portion of the superior oblique tendon, which is responsible for cyclorotation, nasally to create an effective weakening of the anterior portion of the tendon instead of temporal displacement utilized for superior oblique paresis. We measured the patient's eye movements before and after surgery, using the magnetic search coil technique, and confirmed that ( 1) the SOM was abolished and ( 2) vertical eye movements, including saccades, were unaffected. Key Words: Superior oblique myokymia- Harada- Ito procedure. Manuscript received March 28, 1994; revision accepted July 7, 1994. From the Department of Ophthalmology, Cleveland Clinic Foundation ( G. S. K.); Optometry Service, Department of Neurology ( N. F.), Veterans Affairs Medical Center; Case Western Reserve University ( R. J. L.), Cleveland, Ohio, and West Virginia University, Robert C. Byrd Health Sciences Center ( B. D. E.); U. S. A. This work was supported by USPHS grant EY06717 ( to Dr. Leigh), the Department of Veterans Affairs, and the Evenor Armington Fund. Address correspondence and reprint requests to Dr. Gregory S. Kosmorsky, Department of Ophthalmology A- 31, Cleveland Clinic Foundation, 1 Clinic Center, Cleveland, OH 44195- 5024. Superior oblique myokymia is a disorder in which periodic contraction of the superior oblique muscle produces symptoms of intermittent movement of the visual environment. These movements can be in the vertical or torsional planes or in both planes simultaneously. These movements are usually quite subtle and require a good history and a careful slit lamp examination to diagnose. Although these movements are subtle, their effects are quite disconcerting to the patient. There are no dependable treatments for SOM, although individual patients have responded to a number of drugs that include carbamazepine, baclofen, beta blockers ( given systemically or topically), or benzodiazepines ( 1- 5). These medications may have significant untoward side effects sometimes necessitating their withdrawal. The use of prisms to reduce symptoms has been advocated by other authors ( 6,7). Even if these therapies are well tolerated their ameliorating effects may not be permanent and require either switching medications or resorting to surgery. The surgical therapy for SOM has been limited to tenectomy that creates a complete superior oblique palsy. This induced palsy requires concomitant myectomy or recession of the inferior oblique as well as occasionally the contralateral inferior rectus ( 8- 10). Following these surgeries, the patient can seldom achieve single binocular vision in all fields of gaze, although they are relieved of these symptoms and can compensate quite well. We utilized one of the variants of the Harada- Ito procedure that creates an effective weakening of the anterior portion of the tendon and used it to eliminate SOM while leaving ocular motility intact. CASE REPORT A 38- year- old Caucasian woman first presented to the Cleveland Clinic on April 15, 1992, with a 142 HARADA- 1T0 PROCEDURE IN SOM 143 1- year history of episodic " quaking" of her right eye. This phenomenon was made worse by stressful situations, and, although she could control it with concentration, she could not do this for long periods of time. These episodes would occur at a rate of approximately 3- 4 Hz when present. She denied any vertical imbalance in the visual environment but did note that things would " tilt." She had no significant past medical history except for thyromegaly with normal thyroid function tests. She had no previous problems with her vision. Her ophthalmic examination was unremarkable except for obvious intorsional movements of her right eye on slit lamp examination typical for SOM. A magnetic resonance imaging ( MRI) scan failed to reveal any abnormalities. Tegretol was titrated to a level of 800 mg per day with minimal effect on her symptoms. A trial of Inderal 80- LA likewise failed to relieve her symptoms. Dilantin at a dose of 800 mg per day was discontinued as it made the patient drowsy. Therefore, on March 31, 1993, she underwent an Harada- Ito procedure and after a brief recovery period she noted no further episodes of SOM and her ocular motility remained full. She has been free of symptoms after 1 year of follow- up. SURGICAL PROCEDURE A limbal- based incision of four clock- hours was made superiorly in the right eye under local anesthesia. The superior rectus muscle was grasped with a small and then a square muscle hook. A small muscle hook was then used to grasp the superior oblique tendon and expose it temporal to the superior rectus muscle. A 6- 0 Vicryl suture was placed into the anterior portion of the superior oblique tendon, after which this portion of the tendon was cut with Wescott scissors. The tendon was then split down the longitudinal axis in order to create a free segment. This free segment of tendon was then placed 5 mm nasal to the insertion of the superior rectus muscle and 7 mm behind the limbus ( Fig. 1). The conjunctiva was then injected with 100 mg of Ancef without suturing the conjunctiva. The patient was placed on Maxitrol drops four times a day for 5 days postoperatively. METHODS Horizontal, vertical, and torsional rotations of both eyes were recorded using 6- ft magnetic field coils ( CNC Engineering, Seattle, Washington) and search coils consisting of silastic scleral annuli ( Skalar, Delft, Netherlands), as previously de- FIG. 1. The placement of the superior oblique tendon. scribed ( 11,12). The system was 98.5% linear over the operating range of ± 20 degrees in all three planes and, for the amplifier settings used, the standard deviation ( SD) of the noise of the system was less than 0.05 degrees. We measured attempted binocular fixation of a laser spot projected onto a tangent screen, and horizontal and vertical saccades in response to ± 15 degrees step displacements of the target. In addition, we measured smooth- pursuit and vestibular eye movements as previously described ( 13). Data were filtered, digitized at 200 Hz, and analyzed interactively, as previously described ( 11,14). Because of the inherent variability of torsional gaze over several seconds ( 15), and the small amplitude and velocity of the movements of SOM, we mainly used inspection of the records ( see Figs. 2 and 3), buttressed by plots of the relative amplitudes of the Fourier coefficients at frequencies from 0 to 50 Hz to detect SOM. RESULTS Prior to surgery, frequent episodes of SOM occurred; an example is shown in Fig. 2B. Note how fixation is relatively steady in the left eye, but the vertical and torsional channels show gaze instability typical of SOM ( 3,11,16,17). Fourier analysis of the torsional movements showed increased coefficients up to 50 Hz in the right eye compared with the left, typical of SOM. Also shown in Fig. 2 are some typical vertical saccades prior to surgery; / Neum- Ophthalmol, Vol. 15, No. 3, 1995 144 G. S. KOSMORSKY ET Ah. A B 1.5 LEFT EYE RIGHT EYE c TIME ( sec) D TIME ( sec) " a in o CL < LaJ > TIME ( sec) TIME ( sec) FIG. 2. ( A & B) Representative, corresponding 1- second records from the left and right eyes of the patient during a typical episode of SOM. Note how the vertical and torsional position ( arrows) of the right eye is disrupted by SOM. ( C & D) Corresponding records of some typical vertical saccades of the left and right eyes. The peak- velocity to amplitude relationship of these saccades was normal ( see fexf). Note that in this and the following figure that upward deflections indicate eye rotations rightward, upward, or clockwise with respect to the subject. these have normal peak- velocity to amplitude relationships. For example, the first downward sac-cade in Fig. 2C and D was about 31 degrees in both eyes, and had peak velocity of 444 degrees per second in the left eye and 423 degrees per second in the right eye. After surgery, no episodes of SOM were recorded or subjectively reported; an example of the fixation characteristics is shown in Fig. 3A and B. Fourier analysis of the torsional movements showed similar coefficients in the two eyes. In addition, vertical saccadic velocities were unaffected. For example, the last downward saccades of Fig. 2C and D were about 32 degrees in both eyes, and had peak velocity of 463 degrees per second in the left eye and 461 degrees per second in the right eye. DISCUSSION In 1964, Harada and Ito described a new surgical treatment of SOM ( 18). They suggested that the superior oblique tendon was functionally divided into two separate aspects. The posterior portion of the tendon was responsible for the depressor aspect, while the anterior portion was responsible for the torsional aspect. Patients with superior oblique palsy who had a large and symptomatic torsional deviation could be successfully treated by temporally displacing the anterior portion of the tendon that created an effective strengthening of the torsional aspect with relief of the torsional symptoms. This procedure did not alter the depressor function of the tendon and therefore did / Ncuw- Ophtlwlmol, Vol. 15, No. 3, 1995 HARADA- ITO PROCEDURE IN SOM 145 T3 o 1.5 LEFT EYE 1 . 0 * WA~^ V-^ WWVVWvvvVVWVVv/ A * ' V ~ WW^^ 0.5 0.0 - 1.5 1 HOR1 VER TOR O 0- - 0.5 UJ >- L'J - 1 . 0 wW v v V w v ^ v v w w w « w w ' " » , * * w ^^ 0.0 0.2 0.4 0.6 0.8 TIME ( sec) 1.0 TIME ( sec) B D cn 00 O D_ < o or > 1.5 RIGHT EYE 1 .0 ' A^ V\ MAw/ v\ to^ MA'~ vvvwv\ w/^^ 0.5 • 1.5 HOR VER 0 . 0 wvvvv^ « ^^^ Vvv^ AV^^ A^ vvvWW^^^ A/, rw^^^ AM^ v^ v^ v^- 0.0 20 15 10 5 0 - 5 - 10 - 1 5 - 2 0 0.2 0.4 0.6 0.8 TIME ( sec) 1.0 - I "~- l I I s I / I I r1 1 1 - TIME ( sec) FIG. 3. ( A& B) Representative, corresponding 1- second records from the left and right eyes of the patient after her surgery, while she attempted steady fixation. SOM is no longer present. ( C & D) Corresponding records of some typical vertical saccades of the left and right eyes. The peak- velocity to amplitude relationship of these saccades was normal and unchanged from prior to surgery ( see text). not induce a hypertropia. They proposed that 1. Anterior partial advancement of the superior oblique results in intorsion. 2. Anterior partial recession of the superior oblique muscle results in extorsion. 3. Anterior partial advancement of the inferior oblique muscle results in extorsion. 4. Anterior partial recession of the inferior oblique muscle results in intorsion. None of these aspects alters the vertical function of these oblique muscles ( 8,19). Although the Harado- Ito procedure was effective in abolishing the SOM in our patient, vertical saccades were unaffected. It appears that the superior oblique muscle contributes little to the velocity of vertical saccades in any field of gaze, since Stathacopoulos and colleagues ( 20) showed that the velocity of vertical saccades was not reduced in patients with superior oblique palsy. The etiology of SOM is unknown ( 2,4,9,21,22), although quantitative records and electromyographic recordings from the superior oblique muscle have been interpreted as indicating neuronal damage and subsequent regeneration ( 23- 25). Experimental lesions of the trochlear nerve have demonstrated a considerable capacity for regeneration ( 25). One possibility is that mild damage to the trochlear nerve could trigger the mechanism for maintaining a constant number of axons in the nerve; some of these cases may be predisposed to SOM. Our patient had no evidence of multiple sclero- / Neuro- Ophthahiiol, Vol. 15, No. 3, 1995 146 G. S. KOSMORSKY ET AL. sis, which infrequently presents with SOM ( 3). Although a normal MRI scan does not eliminate multiple sclerosis as a diagnostic possibility, our patient had no other signs or symptoms of this disorder. Our patient failed to respond to multiple medications typically used for SOM, and this led us to utilize a surgical option. We do not know if this procedure will work for all patients experiencing SOM. However, we are encouraged by this initial success and present this surgical procedure as an option for the treatment of this enigmatic disorder. REFERENCES 1. Tyler RD, Ruiz RS. Propranolol in the treatment of superior oblique myokymia. Arch Ophthalmol 1990; 108: 175- 6. 2. Susac JO, Smith JL, Schatz NJ. Superior oblique myokymia. Arch Neurol 1973; 29: 432- 4. 3. Leigh RJ, Zee DS. The neurology of eye movements, 2nd Ed. Philadelphia: F. A. Davis, 1991. 4. Rosenberg ML, Glaser ] S. Superior oblique myokymia. Ann Neurol 1983; 13: 667- 9. 5. Keltner JL, Miller NR, Gittinger JW, Burde RM. The monocular shimmers: your patient isn't deluded! Surv Ophthalmol 1983; 27: 313- 16. 6. Roper- Hall G, Burde RM. Superior oblique myokymia. Am Orthop / 1978; 28: 58- 63. 7. Patterson TC, Golsch RA. Superior oblique myokymia: a prism lens approach to control. / Am Optom Assoc 1986; 57: 896- 8. 8. von Noorden GK. Clinical observations in cyclodeviations. Ophth AAO Symposium: Strabismus 1979; 86: 1451- 60. 9. Hoyt WF, Keane JR. Superior oblique myokymia: report and discussion on five cases of benign intermittent uniocu-lar microtremor. Arch Ophthalmol 1970; 84: 461- 7. 10. Palmer EA, Shults WT. Superior oblique myokymia: preliminary results of surgical treatment. / Pediatr Ophthalmol Strabismus 1984; 21: 96- 101. 11. Leigh RJ, Tomsak RL, Seidman SH, Dell'Osso LF. Superior oblique myokymia: quantitative characteristics of the eye movements in three patients. Arch Ophthalmol 1991; 109: 1710- 13. 12. Ferman L, Colliewijn H, Jansen TC, Van Den Berg AV. Human direction during voluntary head movements, evaluated with a three- dimensional scleral induction coil technique. Vision Res 1987; 27: 811- 28. 13. Grant MP, Leigh RJ, Seidman SH, et al. Comparison of predictable smooth ocular and combined eye- head tracking behavior in patients with lesions affecting the brain stem and cerebellum. Brain 1992; 115: 1323- 42. 14. Hary D, Oshio K, Flanagan SD. The ASYST software for scientific computing. Science 1987; 236: 1128- 32. 15. Ott D, Seidman SH, Leigh RJ. The stability of human eye orientation during visual fixation. Neurosci Lett 1992; 142: 183- 6. 16. Morrow MJ, Sharpe JA, Randall PJ. Superior oblique myokymia associated with a posterior fossa tumor: oculography correlation with an idiopathic case. Neurology 1990; 40: 367- 70. 17. Thurston SE, Saul RF. Superior oblique myokymia: quantitative description of the eye movement. Neurology 1991; 41: 1679- 81. 18. Harada M, Ito Y. Surgical correction of cyclotropia. jpn J Ophthalmol 1964; 8: 88- 96. 19. Metz HS, Lerner H. The adjustable Harada- Ito procedure. Arch Ophthalmol 1981; 99: 624- 6. 20. Stathacopoulos RA, Yee RD, Bateman JB. Vertical saccades in superior oblique palsy. Invest Ophthalmol Vis Sci 1991; 32: 1938- 43. 21. Duane A. Unilateral rotary nystagmus. Arn Ophthalmol Soc 1984; 11: 63- 7. 22. Lee JP. Superior oblique myokymia: a possible etiologic factor. Arch Ophthalmol 1984; 102: 1178- 9. 23. Kommerell G, Schaubele G. Superior oblique myokymia: an electromyographical analysis. Trans Ophthalmol Soc UK 1980; 100: 504- 6. 24. Komai K, Mimura O, Izaki A, et al. Superior oblique myokymia: electromyography of the extraocular muscle in superior oblique myokymia. Neuro- ophthalmol Jpn 1989; 6: 317- 21. 25. Murphy EH, Brown J, Iannuzzelli PG, Baker R. Regeneration and soma size changes following axotomy of the trochlear nerve. / Comp Neurol 1990; 292: 524- 36. / Neuro- Ophthalmol, Vol. 15, No. 3, 1995 |
