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To Better Understand the Various Etiologies of Brown's

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To Better Understand the Various Etiologies of Brown's BROWN'S SYNDROME: DIAGNOSIS AND MANAGEMENT BY Kenneth W Wright, MD' ABSTRACT Purpose: To better understand the various etiologies of Brown's syn- drome, define specific clinical characteristics of Brown's syndrome, describe the natural history of Brown's syndrome, and evaluate the long- term outcome of a novel surgical procedure: the silicone tendon expander. Also, to utilize a computer model to simulate the pattern of strabismus seen clinically with Brown's syndrome and manipulate the model to show potential surgical outcomes of the silicone tendon expander. Methods: Charts were reviewed on patients with the diagnosis of Brown's syndrome seen at a children's hospital ophthalmology clinic from 1982 to 1997, or seen in the author's private practice. Objective fundus torsion was assessed in up gaze, down gaze, and primary position in 7 Brown's syn- drome patients and in 4 patients with primary superior oblique overaction. A fax survey was taken of members of the American Association of Ophthalmology and Strabismus (AAPOS) listed in the 1997-1998 directo- ry regarding their results using the silicone tendon expander procedure for the treatment of Brown's syndrome. A computer model of Brown's syn- drome was created using the Orbit 1.8 program by simulating a shortened superior oblique tendon or by changing stretch sensitivity to create an inelastic muscle. Results: A total of 96 patients were studied: 85 with Brown's syndrome (38 with congenital and 47 with acquired disease), 6 with masquerade syn- dromes, 1 with Brown's syndrome operated on elsewhere, and 4 with pri- mary superior oblique overaction in the torsion study. Three original clin- ical observations were made: 1. Significant limitation of elevation in abduction occurs in 70% of *From the Department of Ophthalmology, University of California, Irvine College of Medicine and Cedars-Sinai Medical Center, Los Angeles, CA. TR. AM. OPHTH. SOC. VOL. XCVII, 1999 1024 WVright Brown's syndromie cases surgically verified as caused by a tight superi- or oblique tendon. Contralateral pseudo-inferior oblique overaction is associated with limited elevation in abtductioin. 2. Traumiatic Brown's syndrome cases have larger hypotropias than non- traumatic cases (P<.001). There was no significant hypotropia in pri- mary position in 56 (76%)of 74 congenital and nontrauimatic acquired cases despite severe limitation of elevation. 3. Of 7 patients with Brown's syndrome, 6 had Ino significant fundus tor- sion in primary position, but had significant (+2 to +3) intorsion in up gaze. Spontaneous resolution occurred in approximately 16% of acquired nontraumatic Brown's syndrome patients. The silicone tenldoil expander was used on 15 patients, 13 (87%) were corrected with 1 surgery and 14 (93%) witlh 2 surgeries. The only failure was a Brown's syndrome not caused by superior obliquie pathology. Five of the silicone tendon expander patients had at least 5 years follow-tip (range, 5 to 11 years). Four (80%) of the 5 patients had an excellent outcome with 1 surgery, final results graded between 9 and 10 (on a scale of 1-10, 10 is best). The fifth patient had a consecutive superior oblique paresis and a good out- come after a recession of the ipsilateral inferior oblique muscle. The AAPOS survey had a mean outcome score of 7.3, with 65% between 8 and 10. There were 9 (6%) complications reported: 4 related to scarring and 5 extrusions of the implant. Three of the 5 extruisions were reported from the same surgeon. The computer model of an inelastic superior oblique muscle-tendon complex best simulated the motility pattern of Brown's syndrome with severe limitation of elevation in adduiction, mild limitation of elevation in abduction, minimal hypotropia in primary position, no superior oblique overactioni, and intorsion in up gaze. Concltusion.s: The presence of mild to moderate limitatioin of elevation in abduction is common, and its presence does not eliminate the diagnosis of Brown's syndrome. The majority of Brown's syndrome patients have a pat- tern of strabismus consistent with an inelastic superior oblique muscle- tendon complex that does not extend, but can contract normally; not the presence of a short tendon. The presence of inelastic or tethered superi- or oblique muscle-tendon can be diagnosedc without forced duction testing by observing the pattern of strabismus including torsion. Because of the chance for spontaneous resolution, conservative management, not surgery, should be the first line of treatment for acquired Brown's syndromne. If surgery is indicated, a novel procedure, the .silicone tenclon expatndler, is an effective option with excellent long-term outcomes. Brown's Syndrome: Diagnosis and Managenent 1025 INTRODUCTION A small subset of patients presents with an interesting pattern of strabis- mus, the most prominent feature being restriction of ocular rotations upward and nasally. This distinctive pattern of strabismus has come to be known as Brown's syndrome.'` Much remains to be learned regarding the cause, treatment, and clinical course of this intriguing syndrome. Prior to the present report, there have been no large comprehensive studies on Brown's syndrome since Brown's series published in 1973.5 The goals of this thesis are to better understand the etiology of Brown's syndrome, define specific clinical characteristics of Brown's syndrome, describe the natural history of Brown's syndrome, and evaluate the long-term outcome of a novel surgical procedure, the silicone tendotn expander. This will be accomplished by a literature review, a clinical study on a large number of patients with Brown's syndrome, and postoperative evaluation of patients who underwent the silicone tendon expander procedure for Brown's syn- drome. Computer modeling of Brown's syndrome will be used to help elu- cidate the mechanisms and predict the effect of elongating the superior oblique tendon. BACKGROUND AND HISTORY In 1950, Harold Whaley Brown' first reported on an unusual motility dis- order characterized by limited elevation when the eye is in adduction. This was a preliminary report on the clinical features and surgical out- comes of 8 patients. The clinical features were similar to an inferior oblique palsy, but there was little or no associated superior oblique mus- cle overaction (Fig 1). At surgery, Brown found "their most striking fea- ture a short tendon sheath of the superior oblique tendon that restricts passive movements of elevation in the nasal field." The clinical features of these patients as summarized by Brown are listed in Table I. Brown reported the surgical results on 4 of 8 patients studied." All 4 patients underwent excision of the superior oblique tendon sheath, and 1 patient also had a partial superior oblique tenotomy. He noted that excis- ing the superior oblique sheath improved forced ductions at the time of surgery, but did not significanitly improve postoperative ductions in all 4 cases. Despite these results, Brown attributed the limited elevation to a short or tight ainterior superior oblique tendon sheath and termed this newly discovered syndrome the .superior oblique tendon sheath syndrome. The tight anterior superior oblique tendon sheath theory explained a pas- sive restriction to elevation in adduction found at the time of surgery. Brown demonstrated that the distance from the trochlea to the insertion of the superior oblique tendon normally increases on elevation in adduc- 1026 Wright FIGURE 1 Composite gaze photograph from Harold Brown's original 1950 article first describing what became known as Brown's syndrome.6 Patient shows a classic right Brown's syndrome with limited elevation in adduction without significant superior oblique overaction. Pafient was noted to have orthotropia in primary position. TABLE I: CLINICAL FEATURES DESCRIBED BY BROWN 1. The most striking feature is limited elevation in adduction. 2. In straight up gaze there is usually divergence (V-pattern). 3. The degree of limitation is the same on versions, ductions, and forced duction. 4. Usually, there is widening of the palpebral fissure on adduction. 5. Normal or near normal elevation in abduction. 6. Restricted forced ductions to elevation in adduction. 7. Head tilt backwards (compensatory chin elevation for binocular fusion). tion; thus, a short tendon sheath would restrict this movement. He further hypothesized that the short sheath was due to a complete congenital pare- sis ofthe ipsilateral inferior oblique muscle and secondary sheath contrac- ture because of "a lack of force during its development."6'7 Brown's preliminary report stimulated investigation into this newly identified syndrome.8'14 The syndrome could be acquired, intermittent, and in some cases show spontaneous resolution.l.13 Electrophysiological studies showed that inferior oblique muscle activity was normal and that the muscle was innervated.5'15 Clinical observations also indicated that the pattern of the strabismus of the sheath syndrome was not consistent with an inferior oblique paresis.'6'2' The sheath syndrome is associated with a V-pattern and minimal to no superior oblique overaction, in contrast to inferior oblique paresis that is associated with an A-pattern and marked superior oblique overaction. These findings brought into doubt Brown's original hypothesis that a complete inferior oblique palsy contributed to the elevation deficit and secondary contracture of the superior oblique Brown's Syndrome: Diagnosis and Management 1027 tendon sheath. In 1971, Brown redefined the sheath syndrome and dropped the idea that a congenital inferior oblique paresis was part of the syndrome (later published in 1973).5 He reported on 126 patients and divided them into true sheath and simulated sheath syndromes. True sheath syndrome was defined as "only those cases which have a congenital short anterior sheath of the superior oblique tendon." Simulated sheath syndrome was defined as "all cases with the clinical features of a sheath syndrome caused by an anomaly other than a congenital short anterior sheath of the superior oblique tendon." True sheath syndrome was subdivided into typical and atypical forms based on ipsilateral superior rectus muscle function.
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