Bilateral Brown Syndrome with Sequential Presentations with a 4-Years Interval

Brown syndrome is characterized by limitation of the elevation when the eye is in adduction. Both congenital and acquired cases, as well as constant or intermittent have been reported; it is bilateral in 10% of cases. Bilateral cases may occur simultaneously in most cases or sequentially in rare cases. Herein, we report a patient with a bilateral brown syndrome, who was diagnosed to be congenital in one eye and sequentially presented in the other eye.

A 4-year-old patient presented to Labbafinejad medical center with head tilt and strabismus since his childhood. In his examination, he had 30 PD hypotropia in the primary position and the same amount of esotropia accompanied by limitation of elevation in adduction in the left eye. The patient underwent two surgeries with a 3-year interval, including adhesion band release in superior oblique muscle and SO elongation and recession and resection of both horizontal recti. Nine months later, the patient presented with the complaint of strabismus in the fellow eye. In the ocular examination, the right eye had a limitation of elevation in the adduction. While the right eye was the fixator eye, hypertropia of the left eye in the primary position was evident at this stage. The patient was diagnosed to have acquired brown syndrome of the right eye. He underwent systemic work-ups, including rheumatologic consult and orbital and paranasal CT scan for sinusitis. All work-ups revealed negative results. After 5 months, the patient underwent two sequential surgeries on SO tendon for the correction of severe hypotropia including SO elongation and tenotomy, which resulted in acceptable residual hypertropia and esotropia in the left eye with no limitation in any direction.

In this s tudy, we reported a rare case of Brown syndrome with the congenital presentation in the first eye and idiopathic acquired type in the second eye after an 8-year delay. This bilateral sequential type has been reported rarely and we assume it may be the result of an anatomical anomaly in SO tendon and trochlea.