Primary oblique muscle overaction: the brain throws a wild pitch.

Abstract

Sensorimotor and orbital anatomical mechanisms have been invoked to explain primary oblique muscle overaction. Review of primitive visuo-vestibular reflexes and neuroanatomical pathways corresponding to vestibulo-ocular reflexes, and correlation with known clinical abnormalities in patients with primary oblique muscle overaction. Bilateral superior oblique muscle overaction, which corresponds to a backward pitch in lateral-eyed animals, can occur when structural lesions involving the brainstem or cerebellum increase central otolithic input to the extraocular muscle subnuclei that modulate downward extraocular muscle tonus. Bilateral inferior oblique overaction, which corresponds to a forward pitch in lateral-eyed animals, may result from visual disinhibition of central vestibular pathways to the extraocular muscle subnuclei that modulate upward extraocular muscle tonus. Primary oblique muscle overaction recapitulates the torsional eye movements that occur in lateral-eyed animals during body movements or directional luminance shifts in the pitch plane. These primitive ocular motor reflexes become manifest in humans when early-onset strabismus or structural lesions within the posterior fossa alter central vestibular tone in the pitch plane.