Pathophysiology

In early postnatal development, there are critical periods of cortical development during which neural circuits display a heightened sensitivity to environmental stimuli and are dependent on natural sensory experience for proper formation (see also Chapter 5). During these periods, the developing visual system is vulnerable to abnormal input due to visual deprivation, strabismus, or significant blur resulting from anisometropia or isoametropia. Conversely, the visual system’s plasticity early in development allows the greatest opportunity for amblyopia reversal. The window of opportunity for treatment depends on the type of amblyopia (see the next section, Classification). For example, the critical period for reversal of visual deprivation amblyopia (eg, due to infantile cataracts) is shorter than that for reversal of infantile strabismic or anisometropic amblyopia.

Amblyopic visual deficits result primarily from visual cortical changes. With abnormal visual experience early in life, cells of the primary visual cortex can lose their ability to respond to stimulation of 1 or both eyes, and the cells that remain responsive show significant functional deficiencies, including abnormally large receptive fields. Visual cortex deficiencies may account for the crowding phenomenon, in which optotypes are easier to recognize when isolated than when surrounded by similar forms (see Chapter 1). Abnormalities are also found in neurons within the lateral geniculate body, but the retina in amblyopia is essentially normal. Amblyopia is primarily a defect of central vision; the peripheral visual field is usually normal.

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.