Abstract

The paradigm that an underacting extraocular muscle (EOM) is always atrophic or hypoplastic, and an overacting EOM should always be enlarged, leads to inconsistencies with clinical observations. It is inconsistent with the findings of normal extraocular muscle diameters in patients with apparent superior oblique muscle palsy, “overacting” inferior oblique muscles, and the superior rectus muscle overaction/contracture syndrome, among other clinical entities. These inconsistencies can be reconciled if one accepts the possibility that EOM contractile activity may reflect a change in neural input to an anatomically normal muscle, and/or that muscle contractile activity may be altered by a shift in fiber type and distribution within a normal-sized muscle. This remodeling may occur as a result of vergence adaptation or any change in neural stimulus to the muscle. There is substantial evidence to suggest that both these theoretical possibilities may likely occur.

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