Strabismus is prevalent in the US. It is usually treated surgically with imperfect results. This results from an imperfect understanding of orbital anatomy and the biomechanics of binocular alignment. Recent evidence in humans and monkeys shows that orbital connective tissue containing elastin and smooth muscle cells form pulleys to guide muscle paths. Pulleys play a crucial role in binocular alignment, and abnormalities can cause pattern strabismus, as in genetic connective tissue diseases. Consequences of pulley abnormalities are best understood with a computational biomechanical model. Parallel, multidisciplinary studies in monkeys and humans are proposed. Functional anatomy of pulleys: 1) Technical refinement of MRI resolution. 2) More accurate determination of muscle, pulley, and connective tissue positions as a function of gaze in normal and strabismic humans (and static positions in cadaveric monkeys). 3) A new mathematical formulation of the biomechanical model. 4) Application of the improved model to validate description of common strabismus syndromes and surgeries. Composition of pulleys: 5) Characterization of changes in composition of EOM connective tissue and smooth muscle with gender, age, and race by correlating dynamic MRI in living subjects (functional anatomy) with cadaver CT, MRI, and immuno and histochemistry (microscopic anatomy). Pathophysiology of pulleys: 6) Prospective testing of the new biomechanical model in patients with pulley and connective tissue abnormalities undergoing strabismus surgery. 7) Correlation in genetic connective tissue disorders of abnormalities of binocular alignment with orbital connective tissue histology. 8)Seeking molecular genetic evidence for local connective tissue diseases associated with pulley abnormalities. 9) Use of alert, behaving monkeys with implanted measuring devices to explore and model effects of orbital smooth muscle stimulation and inactivation.
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