The Amblyopic Deficit and Its Relationship to Geniculo-Cortical Processing Streams

Abstract

Amblyopia or lazy eye is the most common cause of uniocular blindness in adults and is caused by a disruption to normal visual development as a consequence of unmatched inputs from the two eyes in early life, arising from a turned eye (strabismus), unequal refractive error (anisometropia), or form deprivation (e.g., cataract). Using high-field functional magnetic resonance imaging in a group of human adults with amblyopia, we previously demonstrated that reduced responses are observable at a thalamic level, that of the lateral geniculate nucleus (LGN). Here we investigate the selectivity of this deficit by using chromatic and achromatic stimuli that are designed to bias stimulation to one or other of the three ascending pathways (the parvocellular, magnocellular, and koniocellular). We find the greatest LGN deficit is for stimuli modulated along the chromatic, L/M cone opponent axis of color space, suggesting a selective loss of parvocellular function in the LGN. We also demonstrate a cortical deficit that involves all the visual areas studied (V1, V2, V3, VP, V3A, V4), and we find this is greatest for the two chromatic responses (S cone opponent and L/M cone opponent) versus the achromatic response, as might be expected from a loss of segregation of chromatic pathways in the cortex.