Inferior oblique myectomy for postoperative limitation of elevation in abduction

Abstract

Antielevation syndrome is commonly described following anteriorization of the inferior oblique muscle. A similar phenomenon may occur following inferior oblique muscle recession, creating a distinct strabismus pattern in the setting of cranial trochlear nerve palsy. We report 3 adult patients, 69-72 years of age, who presented at the Stanford Byers Eye Institute with a similar strabismus pattern—limited elevation in abduction following previous inferior oblique muscle recession for congenital/long-standing trochlear nerve palsy. All 3 patients had a small hypertropia in primary gaze with ipsilateral inferior oblique overaction, limited elevation in abduction, and inferotemporal conjunctival scars. Two patients had a V-pattern strabismus. Following myectomy of the previously recessed inferior oblique muscle, elevation in abduction improved, and symptoms resolved in all 3 patients.

Case 1

A 71-year-old pseudophakic woman presented with recurrent double vision of 3 years’ duration. Twelve years prior, she had vertical diplopia due to a right trochlear nerve palsy that was treated surgically with inferior oblique muscle recession. On examination, her visual acuity was 20/30 in the right eye and 20/40 in the left eye. Stereoacuity was 100 arcsec. Sensorimotor examination (Figure 1) demonstrated a right hypertropia worse in right head tilt, right eye overelevation in adduction, a supraduction deficit in abduction of the right eye, and 15° of extorsion by Double Maddox rod testing. Based on these findings, a right inferior oblique myectomy was performed. Intraoperatively, exaggerated traction testing of the right eye demonstrated the inferior oblique “bump,” with mild restriction. Exploration of the inferior oblique muscle revealed it to be inserted 4 mm posterior to insertion of the inferior rectus muscle (10.5 mm from the limbus). There were no residual nonrecessed muscle fibers or fat adhesions. A 5 mm myectomy was performed after which repeated exaggerated traction testing was negative. Two months later, her vertical diplopia had resolved, as did the overelevation in adduction and supraduction deficit in abduction (Figure 1).

FIG 1.

Pre- (A) and postoperative (B) strabismus measurements in case 1. All numerical values represent strabismus deviations in prism diopters unless otherwise indicated. DMR, double Maddox rod; HT, hypertropia; H(T), intermittent hypertropia; L-, left; R-, right; X, exophoria.

Case 2

A 69-year-old man presented for recurrent vertical diplopia following an unknown strabismus surgery on the left eye 35 years prior. Motor examination demonstrated a left hypertropia with right hypertropia in upgaze due to severely restricted elevation of the left eye in abduction and overelevation in adduction of the left eye, a V-pattern exotropia, and a right head tilt with chin up posture (Figure 2). Visual acuity was 20/20 in the right eye and 20/25 in the left eye. Stereoacuity was 40 arcsec, with the right head tilt. Intraoperatively, exaggerated traction testing demonstrated mild restriction to elevation. The inferior oblique was found inserted 4.5 mm posterior to the insertion of the inferior rectus muscle (11 mm posterior to the limbus). After confirming no fat adhesions or residual muscle fibers, the inferior oblique was myectomized 5 mm, and repeated exaggerated traction testing was negative. Tenon’s layer was sutured to ensure that the inferior oblique would not reattach anteriorly. Four days after surgery, he demonstrated significant improvement of elevation in abduction of the left eye and single vision, with a mild intermittent vertical tropia (Figure 2). He had a significantly improved right head tilt. Improvements were sustained 5 months later.

FIG 2.

Pre- (A) and postoperative (B) strabismus measurements in case 2. All numerical values represent strabismus deviations in prism diopters unless otherwise indicated. DMR, double Maddox rod; HT, hypertropia; H(T), intermittent hypertropia; L-, left; R-, right; XT, manifest exotropia; X(T), intermittently manifest exotropia.

Case 3

A 72-year-old woman presented with an established diagnosis of a right trochlear nerve palsy managed with an inferior oblique recession 6 years prior by an outside provider. Her previous surgery led to temporary resolution of vertical diplopia. Visual acuity was 20/25 in the right eye and 20/20 in the left eye, with mild hyperopia. She had minimal stereoacuity: 3,552 arcsec (+fly). Her strabismus pattern consisted of an intermittent right hypertropia, better in right than left gaze, right eye overelevation in adduction, supraduction deficit in abduction of the right eye, and a V-pattern esotropia (Figure 3), for which she underwent a right 5 mm inferior oblique myectomy and left inferior rectus muscle recession.

FIG 3.

Pre- (A) and postoperative (B) strabismus measurements in case 3. All numerical values represent strabismus deviations in prism diopters unless otherwise indicated. DMR, double Maddox Rod; E, esophoria; ET, esotropia; HT, hypertropia; H(T), intermittent hypertropia; L-, left; R-, right.

Intraoperative findings included an inferior oblique bump on exaggerated traction testing. The inferior oblique was found inserted posterior to the inferior rectus muscle insertion; its quantitative position was not recorded. No residual fibers or fat adhesions were present, and repeated exaggerated traction testing demonstrated no restriction. The contralateral inferior rectus muscle was also recessed 4 mm on an adjustable suture. Four days after surgery, the vertical deviation, supraduction deficit in abduction, and overelevation in adduction resolved (Figure 3), and these improvements persisted at 5 months’ follow-up.

Discussion

Antielevation syndrome (AES) is defined as an ocular elevation deficit most prominent in abduction. It classically occurs secondary to inferior oblique anterior transposition for dissociated vertical deviation.¹ Repositioning the inferior oblique muscle anterior to the inferior rectus muscle insertion creates an oppositional vector to supraduction, causing restricted elevation.¹ The degree of antielevation correlates to the degree of anteriorization relative to the inferior rectus insertion.^1,2 Other potential mechanisms include surgically induced extorsion and postoperative establishment of a new effective origin relative to the neurovascular bundle.^3,4 These same mechanisms likely play a role in AES following inferior oblique recession.

AES is less commonly reported following Parks’ definition of inferior oblique recession.⁵ Many techniques that are commonly defined as inferior oblique recession do involve some level of anteriorization relative to the equator and original inferior oblique insertion, which may be contributory. Niyaz and colleagues⁶ describes AES in 2 of 23 patients (9%) following unilateral inferior oblique recession for trochlear nerve palsy treatment. They suggested that incomplete dissection of the inferior oblique muscle from surrounding tissues may be contributory. For congenital trochlear nerve palsy, Kim and colleagues⁴ found that 6 of 7 patients (86%) developed AES following unilateral inferior oblique recession on average 5.5 mm posterior to the inferior rectus insertion (ie, along the calculated equator for each patient); 4 had clear apparent contralateral inferior oblique overaction, presumably due to postoperative restriction of the operated eye. None of the 7 patients with inferior oblique recession 10 mm posterior to the lateral corner of the inferior rectus insertion (ie, 14 mm inferior oblique recession) developed AES, although 3 showed minimal apparent contralateral inferior oblique overaction. Our observations provide examples of the strabismus pattern that may result from this previously described phenomenon.

We describe a distinct strabismus pattern resulting from previous recession of inferior oblique muscles. All 3 cases demonstrated residual secondary inferior oblique overaction and AES, both of which resolved following myectomy of the previously recessed inferior oblique muscle. A preoperative V pattern also resolved in cases 2 and 3. The inferior oblique muscle was invariably found at least 4 mm posterior to the temporal pole of inferior rectus muscle insertion. No additional inferior oblique muscle fibers were found that had potentially been neglected during initial surgery. There were no significant adhesions to fibrofatty tissue or inferior rectus muscle. In hindsight, primary inferior oblique myectomy in our patients might have resulted in better long-term outcomes from their initial surgeries, given less risk of postoperative AES and reports of similar surgical success rates.⁷ These cases demonstrate that resolution of limitation to elevation in abduction may be achieved with an inferior oblique myectomy, obviating the need to perform a more complex recession of an anteriorly displaced inferior oblique insertion.

Two patients were initially evaluated by other strabismus surgeons who proposed an inferior rectus recession (case 1) and superior oblique tuck (case 3). By instead exploring the suspected previously recessed inferior oblique muscle based on preoperative strabismus patterns, the pathology was directly addressed, and the patients were spared surgery on additional muscles.

Our findings are limited by our small sample size, incomplete 9-gaze position measurements, and lack of clinical photographs. Full measurements would help to further distinguish this pattern from others, such as the inverted Brown pattern (ie, superior oblique underaction in adduction without inferior oblique overaction due to a tight inferior oblique muscle),⁸ although both etiologies can be treated with inferior oblique myectomy.