Comitant and Incomitant Deviations
As previously mentioned, comitant misalignment is characteristically found in patients with congenital or early-onset strabismus. Patients with this condition typically do not report diplopia because of suppression, an adaptation that reduces the responsiveness of the visual neurons in the occipital cortex to the input from 1 eye (see BCSC Section 6, Pediatric Ophthalmology and Strabismus, Chapter 5, Fig 5-5). Patients with a history of childhood strabismus may experience diplopia later in life if their ocular misalignment changes. For example, in patients with a long-standing exophoria, horizontal diplopia may develop in the fifth decade of life, when accommodation and convergence capacities wane.
Conversely, an incomitant deviation may become comitant with the passage of time. This spread of comitance may occur with either a restrictive or paretic incomitant deviation and is especially likely with a CN IV palsy.
Incomitant strabismus is most frequently acquired and usually causes diplopia. If the deviation is very small, fusion may align the eyes and eliminate diplopia. Relatively small misalignments may produce blurred vision rather than an obvious perception of 2 images. Patients with subnormal vision may not recognize diplopia or may have difficulty articulating how their visual perception changes in various positions of gaze. Congenital incomitant deviations, such as those caused by overaction of the inferior oblique muscles, typically do not produce diplopia, even when the strabismus is quite obvious. Generally, gross observation alone is not sufficient for the clinician to distinguish with confidence whether subnormal ductions are secondary to a paretic or restrictive process.
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.