A motor theory for monocular eccentric fixation of amblyopic eyes.
A motor theory is proposed to explain monocular eccentric fixation of amblyopic eyes. Clinical observations that suggest the involvement of a motor anomaly related to strabismus are cited. The model proposes that potentiation (after discharge) of the agonist muscle in strabismus results in a nonregistered error of monocular fixation of the amblyopic eye. The position error goes undetected as a result of reduced sensitivity of the amblyopic eye. Evidence is cited for normal muscle potentiation in nonamblyopic eyes. A suggestion is made that amblyopia be considered both a sensory and a motor disorder. The sensory disorder is the reduced acuity at the fovea of the amblyopic eye. The motor disorder is muscle potentiation that causes the amblyopic eye to fixate with an eccentric retinal region that has lower acuity than the fovea. A distinction is made between motor anomalies that have a sensory basis, such as unsteady fixation in anisometropic amblyopia, and motor anomalies that have a motor basis, such as eccentric fixation in strabismic amblyopia.
D000550:Amblyopia / Q000503:physiopathology*; D005133:Eye Movements; D005403:Fixation, Ocular; D005584:Fovea Centralis / Q000503:physiopathology; D006801:Humans; D008954:Models, Biological; D009801:Oculomotor Muscles / Q000503:physiopathology; D013285:Strabismus / Q000503:physiopathology; D014792:Visual Acuity; D014795:Visual Pathways / Q000503:physiopathology