In the article entitled “Multiple Mechanisms of Extraocular Muscle ‘Overaction,’” Dr Kushner provided lucid and well-illustrated descriptions of loss of elasticity (contracture, true shortening) and gain in elasticity (expansure, true lengthening) of extraocular muscles.1 Dr Kushner, however, failed to mention alternate explanations2 for 2 examples of the inferior oblique (IO) muscle “overaction” (IOOA) that he analyzed. Overaction of the IO muscle secondary to superior oblique muscle palsy may be almost exclusively contracture with no hypertrophy seen on magnetic resonance imaging3 for the majority of patients for whom the hypertropia in contralateral upgaze is no larger than the hypertropia in straight contralateral gaze,4 with the positive Bielschowsky result mainly due to the superior oblique muscle paresis, which is Bielschowsky's original explanation. In contrast, the primarily overacting IO muscle associated with infantile esotropia usually appears greatly hypertrophied at surgery,5 a hypertrophy that explains why the contralateral upgaze hypertropia is larger than the hypertropia in straight contralateral gaze in primary IOOA; the lack of change on head tilt in primary IOOA (negative Bielschowsky result) may be due to an as-yet-unknown central nervous system disconnect.
Mims JL. Alternate Explanations for Inferior Oblique Muscle “Overaction”. Arch Ophthalmol. 2006;124(12):1797–1798. doi:10.1001/archopht.124.12.1797-b
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