Hermann Mühlendyck1. 1. Augenklinik der Universitätsmedizin Göttingen (UMG), Robert-Koch-Straße 40, 37075, Göttingen, Deutschland. hermann-muehlendyck@kabelmail.de.
Abstract
CLINICAL FEATURES: Acquired Jaensch-Brown syndrome is characterized by a mechanical limitation of elevation in adduction, with orthophoria in downward gaze. It was first described by Jaensch in 1928 after orbital trauma in his case and has the same motility pattern as congenital Brown's syndrome. For this reason, in 1973 Brown differentiated between the "true" and "simulated" cases. Further clinical findings of the different etiological factors must be considered in order to differentiate between the two groups. ORIGIN: The cause is an acquired restriction of the free passage of the superior oblique tendon through the trochlea. In most cases this is produced by a palpable swelling/nodule of the superior oblique tendon posterior to the trochlea. There are three possibilities to develop a swelling/nodule: 1. Shortly after birth due to an incomplete development at the time of birth of the sliding factors needed for a free passage. 2. An inflammation in combination with a systemic disease, such as rheumatism or idiopathic. 3. A blunt orbital trauma causing a hematoma of the superior oblique tendon. Additionally, the trochlear passage can be narrowed by a severe inflammation involving the trochlea, which is associated with a swelling and marked tenderness of the trochlear area and corresponds to stenosing tenosynovitis of the hand. TREATMENT: The therapeutic management of these four variations differs significantly depending on the cause of the swelling. CONCLUSION: The swelling of the superior oblique tendon posterior to the trochlea explains the motility disorder in acquired Jaensch-Brown syndrome. There are three different causes for the swelling, which require different therapeutic management.
CLINICAL FEATURES: Acquired Jaensch-Brown syndrome is characterized by a mechanical limitation of elevation in adduction, with orthophoria in downward gaze. It was first described by Jaensch in 1928 after orbital trauma in his case and has the same motility pattern as congenital Brown's syndrome. For this reason, in 1973 Brown differentiated between the "true" and "simulated" cases. Further clinical findings of the different etiological factors must be considered in order to differentiate between the two groups. ORIGIN: The cause is an acquired restriction of the free passage of the superior oblique tendon through the trochlea. In most cases this is produced by a palpable swelling/nodule of the superior oblique tendon posterior to the trochlea. There are three possibilities to develop a swelling/nodule: 1. Shortly after birth due to an incomplete development at the time of birth of the sliding factors needed for a free passage. 2. An inflammation in combination with a systemic disease, such as rheumatism or idiopathic. 3. A blunt orbital trauma causing a hematoma of the superior oblique tendon. Additionally, the trochlear passage can be narrowed by a severe inflammation involving the trochlea, which is associated with a swelling and marked tenderness of the trochlear area and corresponds to stenosing tenosynovitis of the hand. TREATMENT: The therapeutic management of these four variations differs significantly depending on the cause of the swelling. CONCLUSION: The swelling of the superior oblique tendon posterior to the trochlea explains the motility disorder in acquired Jaensch-Brown syndrome. There are three different causes for the swelling, which require different therapeutic management.