Amblyopia (“lazy eye”) is a visual impairment secondary to abnormal visual experience during early childhood. About 3% of the population suffers from this disorder. The causes can be strabismus (crossed eye), anisometropia (unequal refractive error in the two eyes), or form deprivation (congenital cataract or ptosis). For more than half a century, the neural basis of amblyopia in humans has been studied with animal models. Much of this work has indicated that the amblyopic deficits due to strabismus and/or anisometropia are largely cortical, mainly located in early cortical areas V1 and V2 (Bi et al.,
2011; Chino, Bi, & Zhang,
2004; Kiorpes, Kiper, O'Keefe, Cavanaugh, & Movshon,
1998; Kiorpes & Movshon,
2003; Movshon et al.,
1987; Schmidt & Lowel,
2008; Shooner et al.,
2015; Tychsen, Wong, & Burkhalter,
2004). These deficits include fewer fine-scale (high spatial frequency) neurons driven by the amblyopic eye, physiological and anatomical disruption of binocular organization, and interocular suppression. Importantly, these studies have reported that the cortical abnormalities in V1 and V2 do not entirely explain the behavioral deficits associated with the amblyopic eye, suggesting that additional losses must arise beyond V1 and V2 (Kiorpes,
2006; Shooner et al.,
2015). Indeed, in a large body of tasks that activate the extrastriate cortex, amblyopic individuals showed abnormal performance as assessed by behavioral measures (Chandna, Pennefather, Kovacs, & Norcia,
2001; Hess, McIlhagga, & Field,
1997; Ho & Giaschi,
2006; Ho et al.,
2006; Kovacs, Polat, Pennefather, Chandna, & Norcia,
2000; Popple & Levi,
2000; Simmers, Ledgeway, & Hess,
2005; Simmers, Ledgeway, Hess, & McGraw,
2003; Simmers, Ledgeway, Mansouri, Hutchinson, & Hess,
2006; Tripathy & Levi,
2008), functional imaging (Ho & Giaschi,
2009; Lerner et al.,
2003,
2006; Muckli et al.,
2006; Secen, Culham, Ho, & Giaschi,
2011; Thompson, Villeneuve, Casanova, & Hess,
2012; Wang et al.,
2012), and electrophysiological measures (Hou, Pettet, & Norcia,
2008,
2014). These extrastriate deficits appear more severe in strabismic amblyopes than in anisometropic amblyopes (Ho & Giaschi,
2009; Wang et al.,
2012). The normal-acuity fellow eye also showed abnormal performance for motion tasks (Aaen-Stockdale, Ledgeway, & Hess,
2007; Davis et al.,
2008; Giaschi, Regan, Kraft, & Hong,
1992; Ho & Giaschi,
2007,
2009; Ho et al.,
2005; Hou et al.,
2008; Secen et al.,
2011; Simmers et al.,
2003) and for stimuli defined by illusory contours (Hou et al.,
2014). The fellow eye deficits were seen more often in strabismic amblyopes than in anisometropic amblyopes (Hou et al.,
2014).