INTRODUCTION: Although Brown syndrome classically is considered to be limited to the SO tendon sheath and trochlea, it does not always respond to SO surgery. We investigated mechanisms of Brown syndrome by magnetic resonance imaging (MRI). METHODS: Three patients with congenital and 8 with acquired Brown syndrome were compared with matched normal subjects under a prospective protocol of high-resolution, multipositional orbital MRI using surface coils. Muscle size and contractility were determined using digital image analysis. RESULTS: Five of 8 patients with acquired Brown syndrome had a history of trauma or surgery and demonstrated extensive scarring, avulsion, or fracture of the trochlea. One of the 8 had a cyst in the SO tendon. One congenital and one acquired case demonstrated inferior displacement of the lateral rectus (LR) pulley in adduction, with a normal SO tendon-trochlear complex. Such cases of Brown syndrome responded to surgical stabilization of the LR pulley. Two congenital cases had clinical findings of ipsilateral SO palsy confirmed on MRI by atrophy or absence of the SO belly. In congenital absence of the SO belly, the anterior tendon was present but terminated directly on the trochlea. CONCLUSION: High-resolution MRI demonstrates a variety of abnormalities in patients presenting with Brown syndrome, including atrophy or absence of the SO belly. Management in Brown syndrome should be tailored to the pathophysiology of the individual patient.
INTRODUCTION: Although Brown syndrome classically is considered to be limited to the SO tendon sheath and trochlea, it does not always respond to SO surgery. We investigated mechanisms of Brown syndrome by magnetic resonance imaging (MRI). METHODS: Three patients with congenital and 8 with acquired Brown syndrome were compared with matched normal subjects under a prospective protocol of high-resolution, multipositional orbital MRI using surface coils. Muscle size and contractility were determined using digital image analysis. RESULTS: Five of 8 patients with acquired Brown syndrome had a history of trauma or surgery and demonstrated extensive scarring, avulsion, or fracture of the trochlea. One of the 8 had a cyst in the SO tendon. One congenital and one acquired case demonstrated inferior displacement of the lateral rectus (LR) pulley in adduction, with a normal SO tendon-trochlear complex. Such cases of Brown syndrome responded to surgical stabilization of the LR pulley. Two congenital cases had clinical findings of ipsilateral SO palsy confirmed on MRI by atrophy or absence of the SO belly. In congenital absence of the SO belly, the anterior tendon was present but terminated directly on the trochlea. CONCLUSION: High-resolution MRI demonstrates a variety of abnormalities in patients presenting with Brown syndrome, including atrophy or absence of the SO belly. Management in Brown syndrome should be tailored to the pathophysiology of the individual patient.