Strabismic amblyopia results from competitive or inhibitory interaction between neurons carrying nonfusible input from the 2 eyes. Constant, nonalternating heterotropias are the most likely deviations to cause amblyopia. The visual cortex becomes dominated by input from the fixating eye, with reduced responsiveness to input from the nonfixating eye. In young children with strabismus, suppression develops rapidly. This visual adaptation serves to avoid diplopia and visual confusion (see Chapter 5), but in a child who does not alternate fixation, constant suppression of input from the same eye can lead to amblyopia.
Several features distinguish strabismic amblyopia from other types of amblyopia. Grating acuity (see Chapter 1), the ability to resolve uniformly spaced stripes, is often reduced less than recognition acuity. Measurements obtained with Teller Acuity Cards II (Stereo Optical, Inc, Chicago, IL) and the LEA Grating Acuity Test (Good-Lite Company, Elgin, IL) may overestimate recognition visual acuity. Visual acuity measured through a neutral density filter declines less sharply for patients with strabismic amblyopia than for those with ocular disease (neutral density filter effect).
Eccentric fixation is the consistent use of a nonfoveal region of the retina during monocular viewing. Minor degrees of eccentric fixation, detectable only with special tests such as visuoscopy, are present in many patients with strabismic amblyopia. Clinically evident eccentric fixation results in a decentered position of the corneal light reflex when the amblyopic eye is fixating monocularly and implies visual acuity of 20/200 or worse, as well as a poorer prognosis. It should not be confused with an abnormal angle kappa (see Chapter 7).
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.