“…Rather than a single clinical malady with a specific organic cause, it can arise from any condition that prevents one or both eyes from focusing clearly or from having a normal binocular interaction during a critical period, which manifests in the stunted development of early visual cortex (Daw, 1998). The amblyopic eye has impaired contrast sensitivity relative to neurotypical observers (Baker, Simard, Saint-Amour, & Hess, 2015; Kiorpes, 2006; Levi, 2006; McKee, Levi, & Movshon, 2003), and even the fellow eye of amblyopes has degraded contrast sensitivity compared to the eyes of neurotypical observers (Chatzistefanou et al, 2005; Koskela, 1986; Leguire, Rogers, & Bremer, 1990). Amblyopia is often categorized into four subtypes, depending on etiology: (a) strabismic, or “lazy eye,” wherein the brain suppresses visual input from a deviated eye to prevent diplopia; (b) anisometropic, caused by a large interocular difference in refractive error; (c) deprivation, which emerges when there is a literal interruption of visual input, often due to congenital cataracts, ptosis, or corneal haziness; and (d) mixed, in which the amblyope suffers from a combination of one or more of these conditions (Levi, 2006; Levi & Carkeet, 1993; von Noorden, 1990; von Noorden & Crawford, 1978).…”