Comitant misalignment is characteristically found in patients with congenital or early-onset strabismus. These patients 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. Suppression is often associated with amblyopia but may occur in patients with normal acuity in both eyes, especially in patients with an alternating exodeviation. Patients with a history of childhood strabismus may develop diplopia later in life, when the degree of ocular misalignment changes. Patients with a long-standing exophoria, for example, may develop horizontal diplopia in their fifth decade of life when accommodation and convergence capacities wane.
Conversely, a long-standing incomitant deviation may become comitant with the passage of time. This “spread of comitance” is related to a gradual resetting of the innervation to yoke muscles of each eye. This apparent violation of Hering’s law, which is probably mediated at a cerebellar level, produces an adjustment of the gain of the neural input signal to individual extraocular muscles. Spread of comitance may occur with either a restrictive or paretic incomitant deviation, especially with a fourth nerve palsy.
Comitant misalignment is characteristically found in patients with congenital or early-onset strabismus. These patients 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. Suppression is often associated with amblyopia but may occur in patients with normal acuity in both eyes, especially in patients with an alternating exodeviation. Patients with a history of childhood strabismus may develop diplopia later in life, when the degree of ocular misalignment changes. Patients with a long-standing exophoria, for example, may develop horizontal diplopia in their fifth decade of life when accommodation and convergence capacities wane.Conversely, a long-standing incomitant deviation may become comitant with the passage of time. This “spread of comitance” is related to a gradual resetting of the innervation to yoke muscles of each eye. This apparent violation of Hering’s law, which is probably mediated at a cerebellar level, produces an adjustment of the gain of the neural input signal to individual extraocular muscles. Spread of comitance may occur with either a restrictive or paretic incomitant deviation, especially with a fourth nerve palsy.
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