eMedicine Specialties > Ophthalmology > Extraocular Muscles

Brown Syndrome: Treatment & Medication

Author: Kenneth W Wright, MD, Director, Wright Foundation for Pediatric Ophthalmology and Strabismus; Director, Pediatric Ophthalmology Research and Education, Cedars-Sinai Medical Center; Clinical Professor of Ophthalmology, University of Southern California Keck School of Medicine
Coauthor(s): Maria Gabriela Salvador, MD, Consulting Staff, Department of Ophthalmology, Division of Pediatric Ophthalmology and Strabismus, Colonia Polanco Chapultepec Morales
Contributor Information and Disclosures

Updated: Dec 3, 2007

Treatment

Medical Care

Spontaneous resolution of Brown syndrome rarely occurs; if it does, it is more likely in nontraumatic acquired cases. Because of the possibility for late spontaneous recovery, a conservative approach to management is justified, especially for patients with nontraumatic acquired cases.

• Patients with acquired Brown syndrome should be evaluated medically for coexisting systemic disease.
  • If a disorder, such as rheumatoid arthritis or sinusitis, is identified, treat accordingly.
  • Once systemic disease is excluded, patients who have acquired Brown syndrome with signs of inflammation can be treated with anti-inflammatory medication. Oral ibuprofen is a good first-line choice. Local steroid injections in the area of the trochlea and oral corticosteroids can be used for inflammation.
  • Once the inflammatory disease process is controlled, patients with inflammatory Brown syndrome may show spontaneous resolution.
• Congenital Brown syndrome is unlikely to improve spontaneously; therefore, surgery is important to consider as an option.

Surgical Care

The most important indications for surgery are the presence of chin elevation and severe limitation of elevation in adduction, which significantly interferes with the quality of life. Acquired nontraumatic cases should be observed conservatively, because spontaneous resolution may occur. Consider surgery for long-standing cases.

Treatment of Brown syndrome should release the restriction without causing a superior oblique palsy. The first phase is to identify the restriction's cause, inelastic superior oblique tendon or no superior oblique tendon (eg, fat adhesion). The most important signs of inelastic tendon etiology include positive forced duction that is worse with retropulsion, intorsion in upgaze, and negative forced duction after transecting the superior oblique tendon.

• Wright silicone tendon expander technique (preferred method)
  • This technique consists of elongating the superior oblique tendon by performing a tenotomy and then of inserting a segment of medical-grade silicone 240 retinal band between the cut ends of the tendon.
  • Silicone must be placed within the tendon capsule without disrupting the floor of the tendon capsule; otherwise, complications, such as postoperative adherence of the silicone to the sclera or spontaneous extrusion of the implant, may occur.
  • This technique has been effective.
  • The silicone tendon expander procedure is not easy to perform because tenotomy or tenectomy requires special surgical techniques.
• Superior oblique split tendon lengthening technique
  • This technique splits the tendon on the nasal side of the superior rectus muscle. The halves of the tendon are removed and then joined to lengthen the tendon.
  • The function of the superior oblique tendon remains intact and the cut tendon ends are separated in a controlled manner.
  • The author has used this procedure on one patient with excellent results.
• Tenotomy
  • This treatment has been relatively successful for primary superior oblique overaction in nonfusing patients. However, patients with bifoveal fusion do not tolerate induced postoperative cyclovertical deviations.
  • A major problem with this technique is the uncontrolled separation of tendon ends.
  • The incidence of postoperative superior oblique paresis is reported to be 50-85%.
  • Parks and Eutis added a simultaneous ipsilateral inferior oblique recession with a superior oblique tenotomy to reduce the incidence of a secondary superior oblique palsy.⁵
  • Use of a 5-6 mm suture bridge can keep the cut tendon ends from separating too much. Unfortunately, this suture bridge can act as scaffolding for fibrosis to reunite the cut tendon ends, resulting in undercorrections.
• Superior oblique recession
  • This procedure produces a graded slackening of the tendon.
  • The results are mixed, because undercorrections are common.
  • The problem with recessing the superior oblique tendon is that it dramatically changes the characteristics of the superior oblique tendon insertions and alters its functional mechanics. This results in postoperative complication of limited depression.
• Superior oblique and trochlear luxation consists of removing the tendon from the trochlea by luxating the trochlea. This procedure has been abandoned.
• Sheathectomy has been abandoned.

Consultations

Consult a rheumatologist in acquired nontraumatic cases.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ibuprofen (Motrin, Ibuprin, Advil)

Inhibits inflammatory reaction and pain by decreasing the activity of the enzyme cyclooxygenase, which results in prostaglandin synthesis.

• Search for CME/CE on This Topic »