The John Pratt-Johnson Annual Lecture
Restrictive Strabismus: Diagnosis and Management Michael Flanders, M.D., F.R.C.S.C.
ABSTRACT Introduction: Restrictive strabismus is a type of ocular misalignment with limitation of motility caused by intrinsic or extrinsic mechanical forces. The clinical spectrum of either purely or partially restrictive strabismus is very broad. Most cases are of congenital, traumatic, endocrine, post-paralytic or myopathic origin. The surgical treatment strategies are designed to correct abnormal head posture, to eliminate diplopia in primary and functional positions of gaze and to enhance aesthetic and psychosocial aspects of a patient’s life. Purpose: The objective of this paper is to present a clinical approach to the diagnosis and evaluation of patients with restrictive strabismus and to propose a logical surgical approach to the correction of this type of ocular misalignment. Patients and Methods: As representative of the broad spectrum of restrictive strabismus problems, twelve cases are presented and the preoperative and postoperative clinical finding are illustrated with photographs. Conclusion: The clinical spectrum of either purely or partially restrictive strabismus is very broad. The clinical evaluation of patients with this problem must include a careful and detailed history, which is crucial to establishing the diagnosis and must also explore the patient’s concerns. Analysis of fixation, head posture, and ocular alignment require both traditional and special examination techniques. Patient and surgeon expectations must be synchronized preoperatively. A variety of surgical strategies can be applied to improve head posture, eliminate diplopia, and improve cosmesis.
INTRODUCTION Restrictive strabismus is a type of ocular misalignment with limitation of motility From the Department of Ophthalmology, McGill University, Montreal, Quebec, Canada. Requests for reprints should be addressed to: Michael Flanders, M.D., F.R.C.S.C., Department of Ophthalmology, McGill University, 4095 Tupper Street, Westmount, Quebec H3Z 3E5, Canada; e-mail: [email protected] Presented at The Canadian Orthoptic Society annual meeting in Montreal, Quebec, Canada, June 17th, 2013.
caused by intrinsic or extrinsic mechanical forces. The clinical spectrum of either purely or partially restrictive strabismus is very broad. Most cases are of congenital, traumatic, endocrine, post-paralytic, or myopathic origin. The objective of this paper is to present a clinical approach to the diagnosis and evaluation of these patients and to use this approach to explore this exciting subject of restrictive strabismus. The surgical treatment strategies are designed to correct abnormal head posture, to eliminate diplopia in primary
© 2014 Board of Regents of the University of Wisconsin System, American Orthoptic Journal, Volume 64, 2014, ISSN 0065-955X, E-ISSN 1553-4448
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and functional positions of gaze, and to enhance aesthetic and psychosocial aspects of a patient’s life. CLINICAL ASSESSMENT History The history is an essential part of the evaluation because it establishes the etiology, dates the onset, clarifies the degree of functional and / or psychosocial difficulty, and explores the expectations of the patient. The onset of diplopia or ocular misalignment may be congenital or acquired and can be further clarified by examining the family album or reviewing the family history. A previous history of ocular or orbitofacial trauma, thyroid orbitopathy, or previous neurological or neurosurgical problems provides useful information. Characterizing the diplopia (horizontal, vertical, oblique, or torsional), and relating it to a compensatory head posture allows for a focused approach to the orthoptic examination. Examination Concepts and Techniques Certain concepts are helpful in understanding and examining the patient with restrictive strabismus. “Fixation duress” occurs when the fixating eye generates extra motor input against a restrictive or paralytic force in order to maintain the eye in its desired position of gaze. This extra input is transferred to the yoke muscle of the fellow eye in accordance with Hering’s law of equal innervation of yoked muscles. It also explains the concept of primary and secondary deviation which is seen in patients with paralytic strabismus. Patients with restrictive strabismus adopt abnormal head positions not only to eliminate diplopia or to achieve single binocular vision. They are sometimes obliged to position their head in order to align a re-
American Orthoptic Journal
stricted eye with its object of regard. If both eyes are restricted in their movements and cannot physically move into primary position, it may be necessary to measure the misalignment of each eye relative to head position by introducing enough prism in front of each eye separately to allow the head to rotate into primary position. When performing the prism-and-cover test, the corrective prism should always be placed before the restricted eye so that it will be able to remain in its deviated position behind the prism and will not be subject to “fixation duress.” Prism and cover test measurements at distance and near, in up-gaze and down-gaze and in the cardinal positions of gaze should be performed. Incomitance is a consistent feature of restrictive strabismus and will become evident during the course of the examination. Alignment and Motility Examination of ocular motility involves several techniques. Versions (binocular eye movements) demonstrate the presence of an incomitant deviation and quantify the function of individual muscles in their functional fields of gaze. Ductions (monocular eye movements) can help differentiate between paretic or restrictive limitation of movement. A paretic muscle will produce a better duction than a restricted muscle. Rapid saccades indicate normal agonist muscle function whereas slow saccades indicate paresis. Muscle-Force-Generation-Test measures the function of the agonist muscle by feeling the pull of the muscle against a forceps that is grasping the eye and preventing its displacement in the direction of the agonist contraction. This test should correlate with the results of the saccadic velocity test. The Forced-Duction-Test signals the presence of a restrictive force. The eye is grasped with a forceps, the patients looks in a direction away from the restrictive element, and the eye is forcibly rotated in that direction. The degree of resistance to rotation defines
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the amount of restrictive element present. Finally, a prism adaptation test can be done in the office to provide a surgical simulation of what is performed in the operating room. Patterns of Restriction Patterns of restriction can be organized into different categories based on the direction of restriction as follows: An abduction deficit could be seen in patients with infantile esotropia, Duane type I, sixth nerve palsy, and thyroid orbitopathy; adduction deficit in third nerve palsy and “tight” lateral rectus syndrome; elevation deficit in orbital floor fracture, thyroid orbitopathy, monocular elevation deficit, congenital inferior rectus fibrosis, and Brown syndrome; depression deficit in thyroid orbitopathy and inferior rectus palsy; combined horizontal and vertical deficit in thyroid orbitopathy. Associated Findings Associated findings will provide clues to the etiology and pathogenesis of the problem. Lid malposition such as ptosis and retraction should be documented. The presence of palpebral fissure narrowing as well as exophthalmos or enophthalmos should be noted. The pupils should be examined. Conjunctival scarring should be observed. Informed Consent Informed consent involves much discussion to achieve the goal of synchronizing patient and surgeon expectations. Topics to be discussed include perceived postoperative changes and improvements in head position, double vision, ocular alignment, lid changes, and aesthetics. Possible need for secondary surgery or for postoperative glasses and / or prisms should be included in the discussion.
individual case studies and by using the examination techniques illustrated above. A small “x” has been placed on many of the photographs to indicated the location of a restrictive element or a restricted muscle. Postoperative results will be presented and the rationale for the surgical strategies will be explained. Restrictive strabismus can become evident in infancy and is presumed to be of congenital origin. Brown syndrome, congenital fibrosis of the extraocular muscles, Duane syndrome, and monocular elevation deficit are examples. The first case shows a patient with Brown syndrome as well as intermittent exotropia.1, 2 He had a marked chin-up position and a moderate head turn to the right (Figure 1A). There was a marked limitation of elevation in adduction of the left eye. The forced duction test was positive. A left superior oblique tenotomy and bilateral lateral rectus recessions were performed. Postoperatively, primary position ocular alignment has been restored, elevation in adduction of the left eye is significantly improved, and the head posture is normal (Figure 1B). Congenital fibrosis of the extraocular
FIGURE 1A: Preoperative Brown Syndrome and intermittent exotropia. (Photos courtesy of author.)
ILLUSTRATIVE CASES The clinical spectrum of restrictive strabismus will now be illustrated by using
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FIGURE 1B: Postoperative left superior oblique tenotomy with chicken suture and bilateral lateral rectus recession. (Photos courtesy of author.)
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FIGURE 2B: Postoperative bilateral inferior rectus recession 8 mm and bilateral facia lata sling. Improved ptosis and head position and reduced hypotropia. Poor elevation and decreased depression. (Photos courtesy of author.) FIGURE 2A: Twenty-two month old baby girl with congenital fibrosis of the extraocular muscles: Preoperative marked chin-up position, severe ptosis, brow elevation, marked bilateral hypotropia, and variable esotropia. Bilateral elevation deficit greater than depression deficit. (Photo courtesy of author.)
muscles is a rare, inherited, restrictive, nonprogressive ophthalmoplegia.3 Historically, it was thought to be a primary fibrosis of the extraocular muscles. It is now considered to be a congenital cranial disinnervation defect associated with aberrant development of motor nuclei in the midbrain and pons. An example of this condition is shown in Figure 2A. The baby girl had a marked chin-up position, severe ptosis with brow elevation, marked hypotropia, and a variable esotropia. There was a marked bilateral elevation and depression defect. Large inferior rectus recessions to release the restriction in these muscles and bilateral fascia lata slings to elevate the ptotic lids reduced the hypotropia and improved head posture (Figure 2B). Duane syndrome is another congenital eye- movement disorder involving failure of the sixth cranial nerve to develop normally.4-7 There are varying degrees of abduction and adduction deficit, narrowing of the palpebral fissure with retraction of the globe on adduction, and characteris-
American Orthoptic Journal
tic up-shoots and down-shoots. Duane type I is the designated category when there is a predominance of abduction deficit, an esotropia in forced primary position, and a head turn toward the affected eye (Figure 3A). Large recessions of the medial recti, more so in the affected eye, can produce straight eyes in the primary position, normal head posture and a modest improvement in abduction, related to relieving a contracture in the medial rectus (Figure 3B). In the case of the Duane type II patient, there was a significant adduction defect, an exotropia in forced primary position, and a head turn away from the affected eye. In addition to fissure narrowing and globe retraction on adduction, there was an up-shoot and down-shoot on adduction and an associated “X” pattern. A large left lateral rectus recession produced good alignment in primary position, improved adduction (relieves a contraction in the lateral rectus muscle), restored normal head posture, diminished the globe retraction, dampened the up-shoot and down-shoot, and corrected the associated “X” pattern. Monocular elevation defect (MED) is also a type of congenital cranial disinnervation disorder.8 The elevation deficit is evident both in abduction and adduction and increases in up-gaze. A chin-up compensatory head position will be present in fusing
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FIGURE 3A: Patient with Duane type I: Preoperative moderate left head turn, left esotropia 20Δ in primary position and abduction deficit OS –4. (Photos courtesy of author.)
FIGURE 4A: Three-month-old baby with congenital elevation deficit (–6) and large left hypotropia of 45Δ. Forced duction test strongly positive. (Photos courtesy of author.)
FIGURE 3B: Postoperative left medial recession 8 mm and right medial recession 5 mm. Head straight, orthotropic in primary position, adduction OD –2, abduction OS –3. (Photos courtesy of author.)
patients. Ptosis and / or Marcus-Gunn jawwinking are variably present. The elevation deficit may be caused by an inferior rectus restriction and / or a superior rectus paresis. The patient in Figure 4A had decreased elevation and a large hypotropia of the left eye since birth. Forced duction testing demonstrated a significant contracture of the left inferior rectus. A large inferior rectus recession followed by a vertical (upward) transposition of the horizontal recti (Knapp procedure) improved the primary position alignment (Figure 4B). Periocular and orbital trauma, either accidental or iatrogenic, are frequent causes of restrictive strabismus. In the case of a blow-out fracture,9-12 a restriction to elevation is caused by entrapment of the inferior rectus muscle in a fracture site in the floor of the orbit. A restriction to depression may be related to swelling, hemorrhage, or direct injury to the inferior rectus muscle and / or secondary contracture in the ipsilateral superior rectus. The patient in Figure 5A had an elevation deficit and a chinup position associated with an entrapped
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FIGURE 4B: Postoperative: 1) left inferior recession 6 mm 2) left Knapp procedure: left hypotropia reduced to 10Δ and elevation OS improved to –3. (Photo courtesy of author.)
inferior rectus. The left hypotropia was corrected by combining a modest left inferior rectus recession (to avoid creating a down-gaze deficit), with a moderate right superior rectus recession (to enhance upgaze in the left eye by means of increasing yoke muscle activity in the left superior rectus muscle) (Figure 5B).
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FIGURE 5A: Preoperative patient with left blow-out fracture, chin-up head position and left hypotropia 20Δ, increasing to 35Δ in up-gaze and decreasing to 2Δ in down-gaze. (Photos courtesy of author.)
FIGURE 6A: Preoperative patient with “tight” lateral rectus syndrome: right exotropia 30Δ, right gaze 20Δ, left gaze 50Δ, adduction OD –3, up-shoot OD in upgaze to the left and down-shoot OD in down-gaze to the left. (Photos courtesy of author.)
FIGURE 6B: Postoperative right medial rectus advance from 15 to 5 mm from limbus, right lateral recess 5 mm; right exotropia 5Δ in primary position, adduction OS improved (–1 ½). (Photos courtesy of author.) FIGURE 5B: Postoperative right superior recession 5 mm, left inferior recession 3 mm: improved head position, left hypotropia 4Δ, up-gaze 15Δ and downgaze 0Δ. (Photos courtesy of author.)
Restrictive strabismus can occur following strabismus surgery. This was seen in the “tight lateral rectus syndrome,” after insertion of superior oblique silicone spacers, after inferior oblique surgery (antielevation syndrome), and after multiple strabismus operations with contractures and adhesions. The patient in Figure 6A illustrates the features of the “tight lateral rectus syndrome.” There is an incomitant exotropia, a deficit of adduction of the left eye and an up-shoot and down-shoot. As part of the surgical plan, the left lateral rectus muscle should be recessed (Figure 6B). Silicone spacers inserted in the reflected tendons of the superior oblique muscles have a propensity to create scarring and adhesion in the superonasal
American Orthoptic Journal
quadrant and around the adjacent superior rectus muscle. This results in a limitation of down-gaze with significant functional problems. Some improvement in down-gaze can be seen after removal of the spacers, dividing adhesions, and recessing the superior recti. Antielevation syndrome is seen after inferior oblique surgery.13-15 Anterior transposition and postoperative adhesions at the surgical site inferiorly are factors in the pathogenesis of this condition (Figures 7A and 7B). Other surgical interventions have been implicated as causes of restrictive strabismus. These include blepharoplasty, sinus surgery, and scleral buckle retina surgery. The patient shown in Figure 8A experienced vertical double vision following blepharoplasty surgery16, 17 and was obliged to adopt an extreme chin-up head position to eliminate the diplopia. Adhesions around the inferior oblique / inferior rectus complex in the left eye resulted in a
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FIGURE 7A: Preoperative anti-elevation syndrome following left inferior oblique anterior transposition; left hypotropia 25Δ, elevation –2.5. (Photos courtesy of author.)
FIGURE 7B: Postoperative: 1) exploration left inferior oblique and excise adhesions and dysinsertionmyectomy; 2) right superior rectus recession 5 mm; left hypotropia 0, elevation –1. (Photos courtesy of author.)
severe up-gaze deficit that improved after two further operations (Figure 8B). Transcutaneous sinus surgery is performed in close proximity to the trochlea. Disruption in the movement of the reflected tendon of the superior oblique muscle can cause a restriction of motility that resembles both a Brown syndrome and a superior oblique palsy. When the surgical approach to the ethmoid sinus is endoscopic, the automated instrument can inadvertently penetrate into the medial orbit and injure the extraocular muscles. Scarring of the muscles and adhesions to the orbital walls can produce a complicated type of restrictive strabismus.18, 19 The surgical correction of post-scleral buckling strabismus is more rewarding.20, 21 The restricted eye movements and misalignment related to the placement of an encircling band around the globe can be corrected by removal of scar tissue, division of adhesions, and recession of tight muscles (Figures 9A and 9B). The clinical evaluation of restrictive
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FIGURE 8A: Preoperative patient with restrictive right hypotropia and marked chin-up head position, post-blepharoplasty; left hypotropia 20Δ, up-gaze 50Δ, down-gaze 0Δ, elevation OS –3. (Photos courtesy of author.)
FIGURE 8B: Left inferior recession 8.5 to 11.5 mm from limbus (excision of scar tissue), right superior recession 5.5 mm; improved head position, left hypotropia 6Δ, up-gaze 15Δ, down-gaze 0Δ. (Photos courtesy of author.)
FIGURE 9A: Preoperative patient following scleral buckling OS with esotropia 10Δ and left hypotropia 5Δ; esotropia increases to 20Δ in left gaze (associated with abduction OS –1 1 / 2), and hypotropia increases to 10Δ in up-gaze (associated with elevation OS –3). (Photos courtesy of author.)
FIGURE 9B: Postoperative left medial rectus recession and left inferior rectus recession; orthotropic in primary position, abduction and elevation OS normal. (Photos courtesy of author.)
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strabismus in association with thyroid orbitopathy sometimes requires monocular titration of ocular alignment (each eye separately) with head position.22-30 When there are restricted muscles in both eyes, the underlying principle of the prism and cover test is not applicable because the yoke muscle response during fixation is blocked by mechanical forces imposed by restricted muscles. Also, an eye with a mechanical restriction may be unable to take up fixation unless the head adapts a compensatory head posture. The secondary and tertiary functions of the vertical recti must be considered both in the preoperative assessment and also after surgical intervention. For example, “tight” inferior recti cause excyclotorsion and “tight” superior recti cause incyclotorsion. Recession of a “tight” inferior rectus creates exotropia in down-gaze and an “A” pattern. Recession of the inferior rectus frequently produces an early or late over-correction even if the deviation is initially under-corrected. Preexisting lower lid retraction is invariably exacerbated after inferior rectus recession. The patient in Figure 10A had a “tight” left inferior rectus associated with a large left hypotropia that increased in upgaze. She also had a “tight” right superior rectus with a significant right hypertropia in down-gaze. Recession of the two “tight” muscles resulted in a satisfactory postoperative alignment but an induced left lower lid retraction (Figure 10B). Longstanding paralysis of an extraocular muscle is often associated with a contracture of its antagonist muscle. In the case of a third nerve palsy with a paralysed medial rectus, the contracted lateral rectus muscle will mechanically restrict movement of the eye into adduction. A patient with a sixth nerve paralysis 31 will have limitation of abduction caused both by the paretic lateral rectus and the contracted medial rectus muscle. The patient in Figure 11A had a bilateral post-traumatic sixth nerve palsy. The left
American Orthoptic Journal
FIGURE 10A: Preoperative 58-year-old woman with Graves’ orbitopathy OS > OD and vertical diplopia; left hypotropia 45Δ in primary position, 50Δ in up-gaze and 30Δ in down-gaze; elevation OS –3, depression OD –2. (Photos courtesy of author.)
FIGURE 10B: Postoperative right superior rectus recession 4 mm and left inferior rectus recession 4.5 mm: left hypotropia 10Δ, normal depression OD and normal elevation OS; moderate, postoperative left lower lid retraction. (Photos courtesy of author.)
lateral rectus was marked paretic and the right one was moderately so. The patient was obliged to adopt a right head turn in order to physically line up his right eye with the object of regard. After a supramaximal right recess-resect procedure, abduction was moderately improved. After vertical transposition and an injection of BOTOX® into the left medial rectus, there was transient adduction paralysis of the left medial caused by the injection and an eventual recovery of medial rectus function, improved alignment, and a modest increase in abduction of the left eye (Figure 11B). Myopathies,32 such as chronic progressive external ophthalmoplegia and myotonic dystrophy, cause a progressive effect on extraocular motility. Gradual divergence of the eyes over time eventually results in a large exotropia with limitation of adduction. Presumably, this is related to progressive contracture of the lateral rectus muscles and is confirmed by the presence of a positive forced duction test. Large
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FIGURE 11A: 68-year-old man (motor vehicle accident with head trauma), horizontal diplopia; marked head turn to the right to facilitate fixation, abduction OD –3.5, OS –7, esotropia 70Δ in primary position. (Photos courtesy of author.)
FIGURE 12A: Preoperative patient with myotonic dystrophy, ptosis OD > OS, paralytic facies, orbicularis weakness OU, large right exotropia primary position, adduction OD –2, OS –3. (Photos courtesy of author.)
FIGURE 12B: Postoperative bilateral medial rectus resection 7 mm, bilateral lateral rectus recession 9 mm; exotropia 10Δ in primary position, abduction normal OU. (Photos courtesy of author.) FIGURE 11B: Upper row: preoperative alignment, Middle row: (1 week postoperative) right lateral rectus resection 9 mm, right medial rectus recession 8 mm, left superior rectus-inferior rectus temporal transposition and left medial rectus Botox® injection; large left exotropia in primary position; right gaze, improved abduction OD, poor adduction OS and left hypertropia (Botox®-induced); left gaze, improved abduction OS; Lower row: (3 months postoperative) orthotropic in primary position, restored adduction, improved abduction OD > OS. (Photos courtesy of author.)
recess-resect procedures can correct the large exotropia and improve the aesthetic appearance of these patients (Figures 12A and 12B). CONCLUSION The clinical spectrum of either purely or partially restrictive strabismus is very broad. The clinical evaluation of patients with this problem must include a careful and detailed history, which is crucial to establishing the diagnosis and must also explore the patient’s concerns. Analysis of fixation, head posture, and ocular align-
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ment require both traditional and special examination techniques. Patient and surgeon expectations must be synchronized preoperatively. A variety of surgical strategies can be applied to improve head posture, eliminate diplopia, and improve cosmesis. REFERENCES 1. Suh DW, Oystreck DT, et al.: Long-term results of an intraoperative adjustable superior oblique tendon suture spacer using nonabsorbable suture for Brown syndrome. Ophthalmology 2008; 115:1800-1804. 2. Santiago AP, Rosenbaum AL: Grave complications after superior oblique tenotomy or tenectomy for Brown syndrome. J AAPOS 1997; 1:8-15. 3. Yazdani A, Traboulsi EI: Classification and surgical management of patients with familial and sporatic forms of congenital fibrosis of the extraocular muscles. Ophthalmology 2004; 111:10351042. 4. Natan K, Traboulsi EI: Unilateral rectus muscle recession in the treatment of Duane syndrome. J AAPOS 2012; 16:145-149.
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5. Barbe ME, Scott WE, et al.: A simplified approach to the treatment of Duane syndrome. BJO 2004; 88:131-138. 6. Rosenbaum AL: Costenbader Lecture. The efficacy of rectus muscle transposition surgery in esotropic Duane syndrome and VIth nerve palsy. J AAPOS 2004; 8:409-419. 7. Kubota N, Takahashi H, et al.: Outcome of surgery in 124 cases of Duane’s Retraction Syndrome (DRS) treated by intraoperatively graduated recession of the medial rectus for esotropic DRS, and of the lateral rectus for exotropic DRS. Binocul Vis Strabismus Q 2001; 16:15-22. 8. Prieto-Diez J, Gamio MS: The surgical innervational effect: utilizing it to treat monocular elevation deficiency strabismus. Binocul Vis Strabismus Q 2007; 22:169-178. 9. Dal Canto AJ, Linberg JV: Comparison of orbital fracture repair performed within 14 days versus 15 to 29 days after trauma. Ophthal Plast Reconstr Surg 2008; 24:437-443. 10. Jordan DR, Allen LH, et al.: Intervention within days for some orbital floor fractures: The white-eyed blowout. Ophthal Plast Reconstr Surg 1998; 14:379-390. 11. Mauriello Jr JA, Antonacci R, et al.: Combined paresis and restriction of the extraocular muscles after orbital fracture: A study of 16 patients. Ophthal Plast Reconstr Surg 1996; 12:206-210. 12. Biesman BS, Hornblass A, et al.: Diplopia after surgical repair of orbital floor fractures. Ophthal Plast Reconstr Surg 1996; 12:9-16. 13. Goldchmit M, Felberg S, et al.: Unilateral anterior transposition of the inferior oblique muscle for correction of hypertropia in primary position. J AAPOS 2003; 7:241-243. 14. Stager DR: Costenbader lecture. Anatomy and surgery of the inferior oblique muscle: recent findings. J AAPOS 2001; 5:203-208. 15. Mims III JL, Wood RC: Anti-elevation syndrome after bilateral anterior transposition of the inferior oblique muscles: Incidence and prevention. J AAPOS 1999; 3:333-336. 16. Syniuta LA, Goldberg RA, et al.: Acquired strabismus following cosmetic blepharoplasty. Plast Reconstr Surg 2003; 111:2053-2059. 17. Ghabrial R, Lisman RD, et al.: Diplopia following transconjunctival blepharoplasty. Plast Reconstr Surg 1998; 102:1219-1225. 18. Flanders M, Hwang SY, et al.: Endoscopically assisted strabismus surgery. Am J Rhinology 2007; 21:297-301. 19. Thacker NM, Velez FG, et al.: Extraocular muscle damage associated with endoscopic sinus surgery: An ophthalmology perspective. Am J Rhinology 2005; 19:400-405.
American Orthoptic Journal
20. Chang JH, Hutchinson A, et al.: Effect of scleral buckle removal on strabismus surgery outcomes after retinal detachment repair. J AAPOS 2012; 16:e12. 21. Farr AK, Guyton DL: Strabismus after retinal detachment surgery. Curr Opin Ophthalmol 2000; 11:207-210. 22. Kerr NC: The role of thyroid eye disease and other factors in the overcorrection of hypotropia following unilateral adjustable suture recession of the inferior rectus (an American Ophthalmological Society thesis). Trans Am Ophthalmol Soc 2011; 109:168-200. 23. Wright KW: Late overcorrection after inferior rectus recession. Ophthalmology 1996; 103:15031507. 24. Meyer DR, Simon JW, et al.: Primary infratarsal lower eyelid retractor lysis to prevent eyelid retraction after inferior rectus muscle recession. Am J Ophthalmol 1996; 122:331-339. 25. Maino AP, Dawson EL, et al.: The management of patients with thyroid eye disease after bilateral orbital three-wall decompression. Strabismus 2011; 19:35-37. 26. Nicholson BP, De Alba M, et al.: Efficacy of the intraoperative relaxed muscle positioning technique in thyroid eye disease and analysis of cases requiring reoperation. J AAPOS 2011; 15:321325. 27. Rajendram R, Bunce C, et al.: Smoking and strabismus surgery in patients with thyroid eye disease. Ophthalmology 2011; 118:2493-2497. 28. Thomas SM, Cruz OA: Comparison of two different surgical techniques for the treatment of strabismus in dysthyroid ophthalmopathy. J AAPOS 2007; 11:258-261. 29. Dal Canto AJ, Crowe S, et al.: Intraoperative relaxed muscle positioning technique for strabismus repair in thyroid eye disease. Ophthalmology 2006; 113:2324-2330. 30. Nguyen VT, Park DJJ, et al.: Correction of restricted extraocular muscle motility in surgical management of strabismus in Graves’ ophthalmopathy. Ophthalmology 2002; 109:384-388. 31. Bagheri A, Babsharif B, Abrishami M, Salour H, Aletaha M: Outcomes of surgical and nonsurgical treatment for sixth nerve palsy. J Ophthalmic Vis Res 2010; 5:32-37. 32. Durmus H, et al.: Oculopharyngeal dystrophy is a distinct entity. Neurology 2011; 76:227-235.
Key words: restrictive strabismus, strabismus surgery
63
Restrictive Strabismus: Diagnosis and Management Michael Flanders, M.D., F.R.C.S.C.
ABSTRACT Introduction: Restrictive strabismus is a type of ocular misalignment with limitation of motility caused by intrinsic or extrinsic mechanical forces. The clinical spectrum of either purely or partially restrictive strabismus is very broad. Most cases are of congenital, traumatic, endocrine, post-paralytic or myopathic origin. The surgical treatment strategies are designed to correct abnormal head posture, to eliminate diplopia in primary and functional positions of gaze and to enhance aesthetic and psychosocial aspects of a patient’s life. Purpose: The objective of this paper is to present a clinical approach to the diagnosis and evaluation of patients with restrictive strabismus and to propose a logical surgical approach to the correction of this type of ocular misalignment. Patients and Methods: As representative of the broad spectrum of restrictive strabismus problems, twelve cases are presented and the preoperative and postoperative clinical finding are illustrated with photographs. Conclusion: The clinical spectrum of either purely or partially restrictive strabismus is very broad. The clinical evaluation of patients with this problem must include a careful and detailed history, which is crucial to establishing the diagnosis and must also explore the patient’s concerns. Analysis of fixation, head posture, and ocular alignment require both traditional and special examination techniques. Patient and surgeon expectations must be synchronized preoperatively. A variety of surgical strategies can be applied to improve head posture, eliminate diplopia, and improve cosmesis.
INTRODUCTION Restrictive strabismus is a type of ocular misalignment with limitation of motility From the Department of Ophthalmology, McGill University, Montreal, Quebec, Canada. Requests for reprints should be addressed to: Michael Flanders, M.D., F.R.C.S.C., Department of Ophthalmology, McGill University, 4095 Tupper Street, Westmount, Quebec H3Z 3E5, Canada; e-mail: [email protected] Presented at The Canadian Orthoptic Society annual meeting in Montreal, Quebec, Canada, June 17th, 2013.
caused by intrinsic or extrinsic mechanical forces. The clinical spectrum of either purely or partially restrictive strabismus is very broad. Most cases are of congenital, traumatic, endocrine, post-paralytic, or myopathic origin. The objective of this paper is to present a clinical approach to the diagnosis and evaluation of these patients and to use this approach to explore this exciting subject of restrictive strabismus. The surgical treatment strategies are designed to correct abnormal head posture, to eliminate diplopia in primary
© 2014 Board of Regents of the University of Wisconsin System, American Orthoptic Journal, Volume 64, 2014, ISSN 0065-955X, E-ISSN 1553-4448
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and functional positions of gaze, and to enhance aesthetic and psychosocial aspects of a patient’s life. CLINICAL ASSESSMENT History The history is an essential part of the evaluation because it establishes the etiology, dates the onset, clarifies the degree of functional and / or psychosocial difficulty, and explores the expectations of the patient. The onset of diplopia or ocular misalignment may be congenital or acquired and can be further clarified by examining the family album or reviewing the family history. A previous history of ocular or orbitofacial trauma, thyroid orbitopathy, or previous neurological or neurosurgical problems provides useful information. Characterizing the diplopia (horizontal, vertical, oblique, or torsional), and relating it to a compensatory head posture allows for a focused approach to the orthoptic examination. Examination Concepts and Techniques Certain concepts are helpful in understanding and examining the patient with restrictive strabismus. “Fixation duress” occurs when the fixating eye generates extra motor input against a restrictive or paralytic force in order to maintain the eye in its desired position of gaze. This extra input is transferred to the yoke muscle of the fellow eye in accordance with Hering’s law of equal innervation of yoked muscles. It also explains the concept of primary and secondary deviation which is seen in patients with paralytic strabismus. Patients with restrictive strabismus adopt abnormal head positions not only to eliminate diplopia or to achieve single binocular vision. They are sometimes obliged to position their head in order to align a re-
American Orthoptic Journal
stricted eye with its object of regard. If both eyes are restricted in their movements and cannot physically move into primary position, it may be necessary to measure the misalignment of each eye relative to head position by introducing enough prism in front of each eye separately to allow the head to rotate into primary position. When performing the prism-and-cover test, the corrective prism should always be placed before the restricted eye so that it will be able to remain in its deviated position behind the prism and will not be subject to “fixation duress.” Prism and cover test measurements at distance and near, in up-gaze and down-gaze and in the cardinal positions of gaze should be performed. Incomitance is a consistent feature of restrictive strabismus and will become evident during the course of the examination. Alignment and Motility Examination of ocular motility involves several techniques. Versions (binocular eye movements) demonstrate the presence of an incomitant deviation and quantify the function of individual muscles in their functional fields of gaze. Ductions (monocular eye movements) can help differentiate between paretic or restrictive limitation of movement. A paretic muscle will produce a better duction than a restricted muscle. Rapid saccades indicate normal agonist muscle function whereas slow saccades indicate paresis. Muscle-Force-Generation-Test measures the function of the agonist muscle by feeling the pull of the muscle against a forceps that is grasping the eye and preventing its displacement in the direction of the agonist contraction. This test should correlate with the results of the saccadic velocity test. The Forced-Duction-Test signals the presence of a restrictive force. The eye is grasped with a forceps, the patients looks in a direction away from the restrictive element, and the eye is forcibly rotated in that direction. The degree of resistance to rotation defines
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the amount of restrictive element present. Finally, a prism adaptation test can be done in the office to provide a surgical simulation of what is performed in the operating room. Patterns of Restriction Patterns of restriction can be organized into different categories based on the direction of restriction as follows: An abduction deficit could be seen in patients with infantile esotropia, Duane type I, sixth nerve palsy, and thyroid orbitopathy; adduction deficit in third nerve palsy and “tight” lateral rectus syndrome; elevation deficit in orbital floor fracture, thyroid orbitopathy, monocular elevation deficit, congenital inferior rectus fibrosis, and Brown syndrome; depression deficit in thyroid orbitopathy and inferior rectus palsy; combined horizontal and vertical deficit in thyroid orbitopathy. Associated Findings Associated findings will provide clues to the etiology and pathogenesis of the problem. Lid malposition such as ptosis and retraction should be documented. The presence of palpebral fissure narrowing as well as exophthalmos or enophthalmos should be noted. The pupils should be examined. Conjunctival scarring should be observed. Informed Consent Informed consent involves much discussion to achieve the goal of synchronizing patient and surgeon expectations. Topics to be discussed include perceived postoperative changes and improvements in head position, double vision, ocular alignment, lid changes, and aesthetics. Possible need for secondary surgery or for postoperative glasses and / or prisms should be included in the discussion.
individual case studies and by using the examination techniques illustrated above. A small “x” has been placed on many of the photographs to indicated the location of a restrictive element or a restricted muscle. Postoperative results will be presented and the rationale for the surgical strategies will be explained. Restrictive strabismus can become evident in infancy and is presumed to be of congenital origin. Brown syndrome, congenital fibrosis of the extraocular muscles, Duane syndrome, and monocular elevation deficit are examples. The first case shows a patient with Brown syndrome as well as intermittent exotropia.1, 2 He had a marked chin-up position and a moderate head turn to the right (Figure 1A). There was a marked limitation of elevation in adduction of the left eye. The forced duction test was positive. A left superior oblique tenotomy and bilateral lateral rectus recessions were performed. Postoperatively, primary position ocular alignment has been restored, elevation in adduction of the left eye is significantly improved, and the head posture is normal (Figure 1B). Congenital fibrosis of the extraocular
FIGURE 1A: Preoperative Brown Syndrome and intermittent exotropia. (Photos courtesy of author.)
ILLUSTRATIVE CASES The clinical spectrum of restrictive strabismus will now be illustrated by using
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FIGURE 1B: Postoperative left superior oblique tenotomy with chicken suture and bilateral lateral rectus recession. (Photos courtesy of author.)
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FIGURE 2B: Postoperative bilateral inferior rectus recession 8 mm and bilateral facia lata sling. Improved ptosis and head position and reduced hypotropia. Poor elevation and decreased depression. (Photos courtesy of author.) FIGURE 2A: Twenty-two month old baby girl with congenital fibrosis of the extraocular muscles: Preoperative marked chin-up position, severe ptosis, brow elevation, marked bilateral hypotropia, and variable esotropia. Bilateral elevation deficit greater than depression deficit. (Photo courtesy of author.)
muscles is a rare, inherited, restrictive, nonprogressive ophthalmoplegia.3 Historically, it was thought to be a primary fibrosis of the extraocular muscles. It is now considered to be a congenital cranial disinnervation defect associated with aberrant development of motor nuclei in the midbrain and pons. An example of this condition is shown in Figure 2A. The baby girl had a marked chin-up position, severe ptosis with brow elevation, marked hypotropia, and a variable esotropia. There was a marked bilateral elevation and depression defect. Large inferior rectus recessions to release the restriction in these muscles and bilateral fascia lata slings to elevate the ptotic lids reduced the hypotropia and improved head posture (Figure 2B). Duane syndrome is another congenital eye- movement disorder involving failure of the sixth cranial nerve to develop normally.4-7 There are varying degrees of abduction and adduction deficit, narrowing of the palpebral fissure with retraction of the globe on adduction, and characteris-
American Orthoptic Journal
tic up-shoots and down-shoots. Duane type I is the designated category when there is a predominance of abduction deficit, an esotropia in forced primary position, and a head turn toward the affected eye (Figure 3A). Large recessions of the medial recti, more so in the affected eye, can produce straight eyes in the primary position, normal head posture and a modest improvement in abduction, related to relieving a contracture in the medial rectus (Figure 3B). In the case of the Duane type II patient, there was a significant adduction defect, an exotropia in forced primary position, and a head turn away from the affected eye. In addition to fissure narrowing and globe retraction on adduction, there was an up-shoot and down-shoot on adduction and an associated “X” pattern. A large left lateral rectus recession produced good alignment in primary position, improved adduction (relieves a contraction in the lateral rectus muscle), restored normal head posture, diminished the globe retraction, dampened the up-shoot and down-shoot, and corrected the associated “X” pattern. Monocular elevation defect (MED) is also a type of congenital cranial disinnervation disorder.8 The elevation deficit is evident both in abduction and adduction and increases in up-gaze. A chin-up compensatory head position will be present in fusing
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FIGURE 3A: Patient with Duane type I: Preoperative moderate left head turn, left esotropia 20Δ in primary position and abduction deficit OS –4. (Photos courtesy of author.)
FIGURE 4A: Three-month-old baby with congenital elevation deficit (–6) and large left hypotropia of 45Δ. Forced duction test strongly positive. (Photos courtesy of author.)
FIGURE 3B: Postoperative left medial recession 8 mm and right medial recession 5 mm. Head straight, orthotropic in primary position, adduction OD –2, abduction OS –3. (Photos courtesy of author.)
patients. Ptosis and / or Marcus-Gunn jawwinking are variably present. The elevation deficit may be caused by an inferior rectus restriction and / or a superior rectus paresis. The patient in Figure 4A had decreased elevation and a large hypotropia of the left eye since birth. Forced duction testing demonstrated a significant contracture of the left inferior rectus. A large inferior rectus recession followed by a vertical (upward) transposition of the horizontal recti (Knapp procedure) improved the primary position alignment (Figure 4B). Periocular and orbital trauma, either accidental or iatrogenic, are frequent causes of restrictive strabismus. In the case of a blow-out fracture,9-12 a restriction to elevation is caused by entrapment of the inferior rectus muscle in a fracture site in the floor of the orbit. A restriction to depression may be related to swelling, hemorrhage, or direct injury to the inferior rectus muscle and / or secondary contracture in the ipsilateral superior rectus. The patient in Figure 5A had an elevation deficit and a chinup position associated with an entrapped
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FIGURE 4B: Postoperative: 1) left inferior recession 6 mm 2) left Knapp procedure: left hypotropia reduced to 10Δ and elevation OS improved to –3. (Photo courtesy of author.)
inferior rectus. The left hypotropia was corrected by combining a modest left inferior rectus recession (to avoid creating a down-gaze deficit), with a moderate right superior rectus recession (to enhance upgaze in the left eye by means of increasing yoke muscle activity in the left superior rectus muscle) (Figure 5B).
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FIGURE 5A: Preoperative patient with left blow-out fracture, chin-up head position and left hypotropia 20Δ, increasing to 35Δ in up-gaze and decreasing to 2Δ in down-gaze. (Photos courtesy of author.)
FIGURE 6A: Preoperative patient with “tight” lateral rectus syndrome: right exotropia 30Δ, right gaze 20Δ, left gaze 50Δ, adduction OD –3, up-shoot OD in upgaze to the left and down-shoot OD in down-gaze to the left. (Photos courtesy of author.)
FIGURE 6B: Postoperative right medial rectus advance from 15 to 5 mm from limbus, right lateral recess 5 mm; right exotropia 5Δ in primary position, adduction OS improved (–1 ½). (Photos courtesy of author.) FIGURE 5B: Postoperative right superior recession 5 mm, left inferior recession 3 mm: improved head position, left hypotropia 4Δ, up-gaze 15Δ and downgaze 0Δ. (Photos courtesy of author.)
Restrictive strabismus can occur following strabismus surgery. This was seen in the “tight lateral rectus syndrome,” after insertion of superior oblique silicone spacers, after inferior oblique surgery (antielevation syndrome), and after multiple strabismus operations with contractures and adhesions. The patient in Figure 6A illustrates the features of the “tight lateral rectus syndrome.” There is an incomitant exotropia, a deficit of adduction of the left eye and an up-shoot and down-shoot. As part of the surgical plan, the left lateral rectus muscle should be recessed (Figure 6B). Silicone spacers inserted in the reflected tendons of the superior oblique muscles have a propensity to create scarring and adhesion in the superonasal
American Orthoptic Journal
quadrant and around the adjacent superior rectus muscle. This results in a limitation of down-gaze with significant functional problems. Some improvement in down-gaze can be seen after removal of the spacers, dividing adhesions, and recessing the superior recti. Antielevation syndrome is seen after inferior oblique surgery.13-15 Anterior transposition and postoperative adhesions at the surgical site inferiorly are factors in the pathogenesis of this condition (Figures 7A and 7B). Other surgical interventions have been implicated as causes of restrictive strabismus. These include blepharoplasty, sinus surgery, and scleral buckle retina surgery. The patient shown in Figure 8A experienced vertical double vision following blepharoplasty surgery16, 17 and was obliged to adopt an extreme chin-up head position to eliminate the diplopia. Adhesions around the inferior oblique / inferior rectus complex in the left eye resulted in a
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FIGURE 7A: Preoperative anti-elevation syndrome following left inferior oblique anterior transposition; left hypotropia 25Δ, elevation –2.5. (Photos courtesy of author.)
FIGURE 7B: Postoperative: 1) exploration left inferior oblique and excise adhesions and dysinsertionmyectomy; 2) right superior rectus recession 5 mm; left hypotropia 0, elevation –1. (Photos courtesy of author.)
severe up-gaze deficit that improved after two further operations (Figure 8B). Transcutaneous sinus surgery is performed in close proximity to the trochlea. Disruption in the movement of the reflected tendon of the superior oblique muscle can cause a restriction of motility that resembles both a Brown syndrome and a superior oblique palsy. When the surgical approach to the ethmoid sinus is endoscopic, the automated instrument can inadvertently penetrate into the medial orbit and injure the extraocular muscles. Scarring of the muscles and adhesions to the orbital walls can produce a complicated type of restrictive strabismus.18, 19 The surgical correction of post-scleral buckling strabismus is more rewarding.20, 21 The restricted eye movements and misalignment related to the placement of an encircling band around the globe can be corrected by removal of scar tissue, division of adhesions, and recession of tight muscles (Figures 9A and 9B). The clinical evaluation of restrictive
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FIGURE 8A: Preoperative patient with restrictive right hypotropia and marked chin-up head position, post-blepharoplasty; left hypotropia 20Δ, up-gaze 50Δ, down-gaze 0Δ, elevation OS –3. (Photos courtesy of author.)
FIGURE 8B: Left inferior recession 8.5 to 11.5 mm from limbus (excision of scar tissue), right superior recession 5.5 mm; improved head position, left hypotropia 6Δ, up-gaze 15Δ, down-gaze 0Δ. (Photos courtesy of author.)
FIGURE 9A: Preoperative patient following scleral buckling OS with esotropia 10Δ and left hypotropia 5Δ; esotropia increases to 20Δ in left gaze (associated with abduction OS –1 1 / 2), and hypotropia increases to 10Δ in up-gaze (associated with elevation OS –3). (Photos courtesy of author.)
FIGURE 9B: Postoperative left medial rectus recession and left inferior rectus recession; orthotropic in primary position, abduction and elevation OS normal. (Photos courtesy of author.)
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strabismus in association with thyroid orbitopathy sometimes requires monocular titration of ocular alignment (each eye separately) with head position.22-30 When there are restricted muscles in both eyes, the underlying principle of the prism and cover test is not applicable because the yoke muscle response during fixation is blocked by mechanical forces imposed by restricted muscles. Also, an eye with a mechanical restriction may be unable to take up fixation unless the head adapts a compensatory head posture. The secondary and tertiary functions of the vertical recti must be considered both in the preoperative assessment and also after surgical intervention. For example, “tight” inferior recti cause excyclotorsion and “tight” superior recti cause incyclotorsion. Recession of a “tight” inferior rectus creates exotropia in down-gaze and an “A” pattern. Recession of the inferior rectus frequently produces an early or late over-correction even if the deviation is initially under-corrected. Preexisting lower lid retraction is invariably exacerbated after inferior rectus recession. The patient in Figure 10A had a “tight” left inferior rectus associated with a large left hypotropia that increased in upgaze. She also had a “tight” right superior rectus with a significant right hypertropia in down-gaze. Recession of the two “tight” muscles resulted in a satisfactory postoperative alignment but an induced left lower lid retraction (Figure 10B). Longstanding paralysis of an extraocular muscle is often associated with a contracture of its antagonist muscle. In the case of a third nerve palsy with a paralysed medial rectus, the contracted lateral rectus muscle will mechanically restrict movement of the eye into adduction. A patient with a sixth nerve paralysis 31 will have limitation of abduction caused both by the paretic lateral rectus and the contracted medial rectus muscle. The patient in Figure 11A had a bilateral post-traumatic sixth nerve palsy. The left
American Orthoptic Journal
FIGURE 10A: Preoperative 58-year-old woman with Graves’ orbitopathy OS > OD and vertical diplopia; left hypotropia 45Δ in primary position, 50Δ in up-gaze and 30Δ in down-gaze; elevation OS –3, depression OD –2. (Photos courtesy of author.)
FIGURE 10B: Postoperative right superior rectus recession 4 mm and left inferior rectus recession 4.5 mm: left hypotropia 10Δ, normal depression OD and normal elevation OS; moderate, postoperative left lower lid retraction. (Photos courtesy of author.)
lateral rectus was marked paretic and the right one was moderately so. The patient was obliged to adopt a right head turn in order to physically line up his right eye with the object of regard. After a supramaximal right recess-resect procedure, abduction was moderately improved. After vertical transposition and an injection of BOTOX® into the left medial rectus, there was transient adduction paralysis of the left medial caused by the injection and an eventual recovery of medial rectus function, improved alignment, and a modest increase in abduction of the left eye (Figure 11B). Myopathies,32 such as chronic progressive external ophthalmoplegia and myotonic dystrophy, cause a progressive effect on extraocular motility. Gradual divergence of the eyes over time eventually results in a large exotropia with limitation of adduction. Presumably, this is related to progressive contracture of the lateral rectus muscles and is confirmed by the presence of a positive forced duction test. Large
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FIGURE 11A: 68-year-old man (motor vehicle accident with head trauma), horizontal diplopia; marked head turn to the right to facilitate fixation, abduction OD –3.5, OS –7, esotropia 70Δ in primary position. (Photos courtesy of author.)
FIGURE 12A: Preoperative patient with myotonic dystrophy, ptosis OD > OS, paralytic facies, orbicularis weakness OU, large right exotropia primary position, adduction OD –2, OS –3. (Photos courtesy of author.)
FIGURE 12B: Postoperative bilateral medial rectus resection 7 mm, bilateral lateral rectus recession 9 mm; exotropia 10Δ in primary position, abduction normal OU. (Photos courtesy of author.) FIGURE 11B: Upper row: preoperative alignment, Middle row: (1 week postoperative) right lateral rectus resection 9 mm, right medial rectus recession 8 mm, left superior rectus-inferior rectus temporal transposition and left medial rectus Botox® injection; large left exotropia in primary position; right gaze, improved abduction OD, poor adduction OS and left hypertropia (Botox®-induced); left gaze, improved abduction OS; Lower row: (3 months postoperative) orthotropic in primary position, restored adduction, improved abduction OD > OS. (Photos courtesy of author.)
recess-resect procedures can correct the large exotropia and improve the aesthetic appearance of these patients (Figures 12A and 12B). CONCLUSION The clinical spectrum of either purely or partially restrictive strabismus is very broad. The clinical evaluation of patients with this problem must include a careful and detailed history, which is crucial to establishing the diagnosis and must also explore the patient’s concerns. Analysis of fixation, head posture, and ocular align-
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ment require both traditional and special examination techniques. Patient and surgeon expectations must be synchronized preoperatively. A variety of surgical strategies can be applied to improve head posture, eliminate diplopia, and improve cosmesis. REFERENCES 1. Suh DW, Oystreck DT, et al.: Long-term results of an intraoperative adjustable superior oblique tendon suture spacer using nonabsorbable suture for Brown syndrome. Ophthalmology 2008; 115:1800-1804. 2. Santiago AP, Rosenbaum AL: Grave complications after superior oblique tenotomy or tenectomy for Brown syndrome. J AAPOS 1997; 1:8-15. 3. Yazdani A, Traboulsi EI: Classification and surgical management of patients with familial and sporatic forms of congenital fibrosis of the extraocular muscles. Ophthalmology 2004; 111:10351042. 4. Natan K, Traboulsi EI: Unilateral rectus muscle recession in the treatment of Duane syndrome. J AAPOS 2012; 16:145-149.
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5. Barbe ME, Scott WE, et al.: A simplified approach to the treatment of Duane syndrome. BJO 2004; 88:131-138. 6. Rosenbaum AL: Costenbader Lecture. The efficacy of rectus muscle transposition surgery in esotropic Duane syndrome and VIth nerve palsy. J AAPOS 2004; 8:409-419. 7. Kubota N, Takahashi H, et al.: Outcome of surgery in 124 cases of Duane’s Retraction Syndrome (DRS) treated by intraoperatively graduated recession of the medial rectus for esotropic DRS, and of the lateral rectus for exotropic DRS. Binocul Vis Strabismus Q 2001; 16:15-22. 8. Prieto-Diez J, Gamio MS: The surgical innervational effect: utilizing it to treat monocular elevation deficiency strabismus. Binocul Vis Strabismus Q 2007; 22:169-178. 9. Dal Canto AJ, Linberg JV: Comparison of orbital fracture repair performed within 14 days versus 15 to 29 days after trauma. Ophthal Plast Reconstr Surg 2008; 24:437-443. 10. Jordan DR, Allen LH, et al.: Intervention within days for some orbital floor fractures: The white-eyed blowout. Ophthal Plast Reconstr Surg 1998; 14:379-390. 11. Mauriello Jr JA, Antonacci R, et al.: Combined paresis and restriction of the extraocular muscles after orbital fracture: A study of 16 patients. Ophthal Plast Reconstr Surg 1996; 12:206-210. 12. Biesman BS, Hornblass A, et al.: Diplopia after surgical repair of orbital floor fractures. Ophthal Plast Reconstr Surg 1996; 12:9-16. 13. Goldchmit M, Felberg S, et al.: Unilateral anterior transposition of the inferior oblique muscle for correction of hypertropia in primary position. J AAPOS 2003; 7:241-243. 14. Stager DR: Costenbader lecture. Anatomy and surgery of the inferior oblique muscle: recent findings. J AAPOS 2001; 5:203-208. 15. Mims III JL, Wood RC: Anti-elevation syndrome after bilateral anterior transposition of the inferior oblique muscles: Incidence and prevention. J AAPOS 1999; 3:333-336. 16. Syniuta LA, Goldberg RA, et al.: Acquired strabismus following cosmetic blepharoplasty. Plast Reconstr Surg 2003; 111:2053-2059. 17. Ghabrial R, Lisman RD, et al.: Diplopia following transconjunctival blepharoplasty. Plast Reconstr Surg 1998; 102:1219-1225. 18. Flanders M, Hwang SY, et al.: Endoscopically assisted strabismus surgery. Am J Rhinology 2007; 21:297-301. 19. Thacker NM, Velez FG, et al.: Extraocular muscle damage associated with endoscopic sinus surgery: An ophthalmology perspective. Am J Rhinology 2005; 19:400-405.
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20. Chang JH, Hutchinson A, et al.: Effect of scleral buckle removal on strabismus surgery outcomes after retinal detachment repair. J AAPOS 2012; 16:e12. 21. Farr AK, Guyton DL: Strabismus after retinal detachment surgery. Curr Opin Ophthalmol 2000; 11:207-210. 22. Kerr NC: The role of thyroid eye disease and other factors in the overcorrection of hypotropia following unilateral adjustable suture recession of the inferior rectus (an American Ophthalmological Society thesis). Trans Am Ophthalmol Soc 2011; 109:168-200. 23. Wright KW: Late overcorrection after inferior rectus recession. Ophthalmology 1996; 103:15031507. 24. Meyer DR, Simon JW, et al.: Primary infratarsal lower eyelid retractor lysis to prevent eyelid retraction after inferior rectus muscle recession. Am J Ophthalmol 1996; 122:331-339. 25. Maino AP, Dawson EL, et al.: The management of patients with thyroid eye disease after bilateral orbital three-wall decompression. Strabismus 2011; 19:35-37. 26. Nicholson BP, De Alba M, et al.: Efficacy of the intraoperative relaxed muscle positioning technique in thyroid eye disease and analysis of cases requiring reoperation. J AAPOS 2011; 15:321325. 27. Rajendram R, Bunce C, et al.: Smoking and strabismus surgery in patients with thyroid eye disease. Ophthalmology 2011; 118:2493-2497. 28. Thomas SM, Cruz OA: Comparison of two different surgical techniques for the treatment of strabismus in dysthyroid ophthalmopathy. J AAPOS 2007; 11:258-261. 29. Dal Canto AJ, Crowe S, et al.: Intraoperative relaxed muscle positioning technique for strabismus repair in thyroid eye disease. Ophthalmology 2006; 113:2324-2330. 30. Nguyen VT, Park DJJ, et al.: Correction of restricted extraocular muscle motility in surgical management of strabismus in Graves’ ophthalmopathy. Ophthalmology 2002; 109:384-388. 31. Bagheri A, Babsharif B, Abrishami M, Salour H, Aletaha M: Outcomes of surgical and nonsurgical treatment for sixth nerve palsy. J Ophthalmic Vis Res 2010; 5:32-37. 32. Durmus H, et al.: Oculopharyngeal dystrophy is a distinct entity. Neurology 2011; 76:227-235.
Key words: restrictive strabismus, strabismus surgery
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![[New strategies of strabismus diagnosis and surgery].](/assets/img/hold.png)
