Transactions 29th European Strabismological Association Meeting – de Faber (ed) © 2005 European Strabismological Association, ISBN 04 1537 211 9

Long term outcome of silicone expander for Brown’s syndrome

H. Kadircan Keskinbora* & Nuray Karakus¸çu Pulur

Bakirköy Dr. Sadi Konuk Education and Research Hospital, Clinic of Ophthalmology*, Istanbul, Turkey

ABSTRACT: To evaluate the long term outcome of silicone tendon expander for Brown’s syndrome. Records of 22 eyes of 16 patients with diagnosis of Brown’s syndrome reviewed. The mean followup period was 54,7 months. The expander, which varies 5 to 7 mm.in length was placed in all patients in the tenotomized superior oblique muscle tendon 5 mm. nasal border of the superior rek-

tus muscle using 6–0 nonabsorbable suture.

Elevation in adduction obtained in all operated eyes. Two eyes had undercorrection and 3 eyes had overcorrection postoperatively. Four eyes has a severe postoperative inflammatory reaction. Two eyes developed granuloma and 6 eyes had foreign body sensation. One eye reoperated for extrusion. The silicone bands extirped from 3 eyes. Two eyes developed consecutive SO palsy.

The silicone expander surgery is successful in treating overacting superior oblique muscle. No cyclotorsion symptom occurred after this surgery. This procedure is reversible and can repeat.

1INTRODUCTION

Brown syndrome is characterized by limited elevation in adduction. It is described as superior oblique (SO) muscle tendon sheath first by Dr. H. Whaley (Brown 1950). Later, Brown stated this theory does not explain the etiology sufficiently (Brown 1973). In 1977, Parks expressed SO muscle tendon does not have a sheath; so it is clarified that the syndrome defined by Brown is not a sheath syndrome (Parks 1977). The syndrome may present in a congenital, acquired, constant or intermittent form.

The silicone tendon expander technique as a weakening procedure can be succesfully used in the surgical treatment of SOOA on Brown syndrome in addition to various other surgical procedures (Wright 1991, Wright et al. 1992).

We investigate the results of SO silicone tendon-expander procedure in a series of patients with SOOA for surgical treatment of Brown’s syndrome.

2MATERIALS AND METHODS

Records of 22 eyes of 16 patients with diagnosis of Brown’s syndrome have been reviewed between January 1995 and January 2002. Nine of the patients were female and 7 were male. Criteria for exclusion included previous SO muscle surgery, previous or concurrent other rectus muscle surgery. We aimed to observe only the results of the patients on whose SO muscles expander was applied. As a summary, silicon expander was applied to only single or both of the SO muscles tendons according to unilateral or bilateral presence of the disease.

Preoperative patient measurements included detailed ocular examination, versions and ductions in the diagnostic positions of gaze, primary position deviation at distance and at near and with head tilt.

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The operation criteria were as follows:

1.Evident hypotropia on affected eye in primary position.

2.The presence of compensatory head tilt.

3.The presence of limited elevation which cannot be accepted aesthetically in adduction.

The aims of the surgery were to provide binocularity of vision and prevention of the available physical abnormalities after a long lasting head position.

Forced duction test was performed to SO muscle before the operation under general anesthezia, thus the diagnosis of Brown’s syndrome was confirmed. The conjunctiva and Tenon’s capsule were incised nasally on the superior quadrant. SO tendon was brought out with a hook from nasal side of insertion of SR muscle. SO tendon was pulled out gently with a hook. It is essential to be careful to avoid traumatisation of SO tendon sheath and intermuscular septum in this step. After dissection of SO tendon sheath, the tendon was clearly seen. The part of the sheath which touches the sclera was not dissected. Two non-absorbable sutures were applied to tendon separetely with a distance of 1–1,5 mm. from each other. The expander was prepared with proper length with silicone band No. 240. The silicone band was sutured with mentioned two sutures to the tendon. After that, the SO tendon was cut between the sutures, silicone band was brought close to the tendon and the sutures were tied. The elongated tendon was pushed into its sheath. Tenon capsule and conjunctiva were closed separetely. The forced duction test was repeated at the end of the operation to assure whether the tendon was cut completely.

3RESULTS

The Brown’s syndrome was congenital in 11 patients and acquired in 5 patients. Bilateral SO tendon-expander procedure was performed on six patients out of the mentioned sixteen.

The mean age of patients at surgery was 9.7 years (range: 3.4 years to 49.1 years). The silicone expander was applied for 5 mm in 8 eyes, for 6 mm in 10 eyes, and for 7 mm in 4 eyes.

The average figure of SOOA was 3.0 preoperatively while 0.3 postoperatively. The preoperative average for “A-pattern” was 23.15 prism diopter while it became 3.56 prism diopter postoperatively.

The postoperative temporary complications included: inflammation in 4 eyes (18.1%), granuloma in 2 eyes (9.0%) and irritation in 6 eyes (27.2%). The inflammation was succesfully treated with local corticosteroids and oral NSAI drugs.

The complications which required surgical intervention were extrusion in 1 eye (4.5%) and SO palsy in 2 eyes (9.0%). In addition, the implanted silicone band had to be removed in 2 cases (9.1%). However, a complete improvement occurred 2 and 4 months after removal of silicone band. An overcorrection appeared in 3 cases. Paretic hypercorrection developed in 2 cases in postoperative period although a diplopia or restriction in down gaze was not present. While an anterior transposition was performed on inferior oblique muscle in one of these patients, silicone band was removed on the other one. A complete recovery was observed in 3 cases 2 to 4 months after explantation of silicone band. No cyclotortion symptom occurred after surgery.

A slight esotropia in one case and an exotropia in 3 cases developed in postoperative period. The exotropia recovered in one of them later whereas in 2 patients it continued. Diplopia, phoria or even no aesthetic problem has been observed neither in exotropic nor esotropic cases. All other patients were ortophoric in primary position. The head tilt improved in all cases. Downgaze restriction was not seen in any cases.

4DISCUSSION

The etiology of Brown’s syndrome is multifactorial: 1) Anomalies of tendon or trochlea, 2) Tendon tightness, 3) The reasons which lead to dyskinesia of SO tendon on trochlea, 4) Dysgenesis of SO

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muscle, 5) Secondary defects on trochlea and SO tendon because of infection or trauma, 6) SO anomalies, developed secondary as a result of anomalies of inferior oblique (IO) itself or its neighbourhood, 7) After surgery of SO tendon, 8) Paradoxical innervation, 9) Secondary development of Brown’s syndrome because of IO muscle palsy (Von Nooerden 1996).Considering the theories describing Brown syndrome, many operation techniques have been proposed to treat the disease.

SO tendon silicon expander technique is a recently described technique for the treatment of Brown syndrome, which provides a quantitative expansion in the SO tendon (Wright 1992). This techique is superior to the other techniques because it causes a quantitative relaxation in the functions of the SO tendon without impairing its functions. This is due to the broad insertion of the muscle that enables it to run three functions which are: The tendon fibrils in front of the equator are responsible for the incyclotorsion and the posterior fibrils are responsible for the depression and adduction.

Stager et al. reported that placement of a 5 to 8 mm. silicone expander in the tenotomized SO muscle tendon is an effective means of correcting Brown syndrome with a low rate of reoperation. Initial undercorrection should not discourage the surgeon because improvement may continue for up to 3 years. This technique reduces the need for either simultaneous or subsequent inferior oblique muscle weakening and represents an advance in the treatment of Brown syndrome (Stager et al. 1999). In our study, the SOOA reduced to 0.3 after surgery while it was 3.0 on the average preoperatively. The average amount of “A-pattern” reduced to 3.56 from 23.12 as prism diopter. The average improvement of “A-pattern” was 19.56 prism diopter. It was observed that 5 years’ post operative results have improved compared to the 6 months’ post operative results. Our study supports the improvement in the long term.

Awad et al. performed a SO tendon lengthening procedure, using a 10 to 12 mm. long silicone band on each patient. All patients had a hypotropia equal or higher than 20 prism diopter in primary position. All patients experienced an improvement in their severe Brown syndrome. Hypotropia in postoperative primary-position was less than 8 prism diopter in all patients. No patient required further surgery, and no extrusions of the implants were noted (Awad et al. 2003). In our study, even if the “A-pattern” was very severe, we did not implant expanders as long as the expanders used by Awad et al. In spite of this fact, may be not in short term but in long term, satisfactory results have been achieved. Regarding further surgery and extrusion, we were not as lucky as Awad et al. One patient had extrusion. On the other hand, band extraction had to be applied for 3 patients.

The silicon band, by keeping the tendon ends apart, prevents postoperative scar contractures that may develop following suture expansions. This technique is superior to SO retraction operations because the localization of the tendon insertion and the functional characteristics are left unchanged. In addition, the length of the expander silicon band may vary according to the clinical situation. Besides, retraction of ipsilateral inferior oblique muscle retraction which is performed frequently after SO tenotomy operations is not necessary in this technique.

REFERENCES

Awad AH, Digout LG, Al-Turkmani S, Khan AO, Fallata A. 2003. Large-segment superior oblique tendon expanders in the management of severe congenital Brown syndrome. J AAPOS Aug;7(4):274–278.

Brown HW. 1950. Congenital stuructural muscle anomalies. In Allen JH., editor: Strabismus ophthalmic symposium. St.Louis Mosby Co, s.205–206.

Brown HW. 1973. True and simulated superior oblique tendon sheath syndromes. Doc Ophthalmol. 34:123–136.

Parks MM. 1977. The superior oblique tendon. 33rd Doyne Memorial Lecture. Trans Ophthalmol Soc UK. 97:288–304.

Stager DR Jr, Parks MM, Stager DR Sr, Pesheva M. 1999. Long term results of silicone expander for moderate and severe Brown syndrome (Brown syndrome “plus”). J AAPOS Dec;3(6):328–332.

Von Noorden GK. 1996. Binocular vision and ocular motility, theory and management of strabismus. St. Louis. CV Mosby Co s:437–442.

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Wright KW. 1991. Superior oblique silicone expander for Brown syndrome and superior oblique overaction.

J Pediatr Ophthalmol Strabismus. 28:101–107.

Wright KW. 1992. Surgical management of superior oblik overaction and Brown’s syndrome. Ophthalmology Clinics of North America. 5:67–78.

Wright KW, Min B, Park C. 1992. Comparison of superior oblique tendon expander to superior oblique tenotomy for the management of superior oblique overaction and Brown syndrome. J Pediatr Ophthalmol Strabismus. 29:92–97.

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