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D Somer, K Budak, S Demirci, S Duman; Corneal Topography in Establishing the Physiopathologic Mechanism of Cyclic Brown's Syndrome (Case report) . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1481.
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Purpose: To evaluate the responsible physiopathological mechanism in a patient with acquired Brown's syndrome presenting with cyclic characteristics. Methods: A 15 year old boy experiencing vertical diplopia upon waking in the morning was referred to our clinic. A spontaneous resolution occurred within 4-5 hours or the diplopia could then be overcome by attempted forced elevation in adduction while digitally pressing over the right trochlea. Limitation of elevation was first elicited at the age of 3.5 and the cyclic phase has since remained static and regular. Motility evaluation revealed a restriction of elevation in the right eye most remarkable in adduction which resolved completely after the episode. In addition to a full orthoptic assessment, magnetic resonance imaging (MRI) of the orbit and corneal topography were performed using the EyeSys Corneal Analysis SystemTM , during the diplopic period and during resolution in the afternoon. Computerized videokeratography data analysis included axial difference and refractive power maps and several numerical parameters obtained from the Holladay Diagnostic Summary. Results: Vision at the time was 20/200 OD and 20/20 OS. Cycloplegic refraction revealed - 7.50 × 75 OD and +.25S +.50C × 90 OS. The MRI scan demonstrated enlargement of the tendon-trochlea complex that was similar during the diplopic edisode and resolution. Afternoon topographic examination revealed steepening of the 55° meridian which suggested release of a former compression of trochlea onto the corresponding site. Corneal uniformity index and predicted visual acuity values were distorted in the topographic maps. The boy received an injection of depot betamethasone. Steepening of the 55° meridian on corneal topography persisted after steroid injection. The patient was symptom free for 7 months after steroid injection. Hard contact lens trial smoothened the corneal surface and the patient achieved 20/50 vision. Conclusion: An intermittent compression of trochlea onto cornea resolved by steroid injection suggests a vascular etiology for the condition of Brown's syndrome in this case. The highly vascular sheath of the intratrochlear portion of the superior oblique tendon may create the anatomic basis for vascular dilatation, edema or fluid accumulation in the bursa-like space between the vascular sheath and the trochlear saddle. The previously introduced concepts of remnants of embryological trabeculae or stenosing tenosynovitis as the etiology of Brown's syndrome seem unlikely to explain the intermittent trochlear compression observed in this case.
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