Abstract

ABSTRACT Importance Phoria adaptation is a central tonus mechanism that provides plasticity to binocular alignment. However, its slow dissipation inevitably adulterates our clinical strabismus measurements. Purpose To examine the role of phoria adaptation in normal binocular control, understand its neural substrate, and explore how it can alter our clinical measurements in common forms of strabismus. Methods Investigation into the role of phoria adaptation in maintaining binocular alignment and its role in altering clinical strabismus measurement. Results Phoria adaptation permeates all aspects of binocular alignment. It accounts for the stability of orthophoria, “latent” phorias, tenacious proximal fusion in intermittent exotropia, large fusional vertical amplitudes in congenital superior oblique muscle palsy, the “eating up” of prisms in accommodative esotropia, the smaller measured distance deviation in patients with high AC/A ratio or convergence excess, absence of physiologic skew deviation during head tilt, fusional divergence amplitudes, and spread of comitance. This binocular control system probably arises from a cerebellar learning mechanism that involves input via climbing fibers to the inferior olive, which provide a powerful timing and error signal to the cerebellar Purkinje cells to produce activity-dependent modification analogous to long-term potentiation. Conclusions Phoria adaptation is generated by a central neural integrator that provides inertia, plasticity, and positional stability to human binocular vision.

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