Each eye is rotated by four recti muscles pulling on the globe against the elastic restraint of the orbital connective tissue. At equilibrium the net muscle torque balances the elastic restoring torque:
τ_muscle = r · (F_agonist − F_antagonist)
τ_elastic = −k · θ
equilibrium: θ_eq = (r/k) · (F_agonist − F_antagonist)
Here the sliders directly set the medial-vs-lateral and superior-vs-inferior force imbalance on the affected eye; the model converts it to a deviation angle θ (esotropia/exotropia horizontally, hyper/hypotropia vertically) while the other eye keeps fixating the target normally — exactly the asymmetry seen in a unilateral extraocular muscle palsy.
Because the two visual axes no longer intersect at the fixation target, each eye's fovea receives a different retinal image of the same object. The brain cannot fuse them into one, so a second, offset image is perceived — diplopia — separated by an angle equal to θ. Clinically this is measured in prism diopters: Δ = 100·tan(θ). A corrective prism placed base-out bends the incoming light so the misaligned eye's image lands back on the fovea without correcting the muscles themselves, which is why the eyes here still visibly point in different directions even at full prism correction.
If the misalignment persists uncorrected, the visual cortex progressively suppresses the deviated eye's competing image to avoid constant diplopia — the readout accumulates a suppression signal that, past ~60%, can mature into amblyopia (a "lazy eye" the brain has learned to ignore even though the eye itself sees normally). Occlusion therapy — patching the stronger, fixating eye — forces the visual system to use the weaker eye again, which is modelled here as a slow reversal of the suppression signal.