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 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amblyopia or lazy eye is the most common cause of uniocular blindness in adults. It 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). Animal models based on extracellular recordings in anesthetized animals suggest that the earliest site of the anomaly in the primate visual pathway is the primary visual cortex (corresponding to the striate cortex, cytoarchitectonic area 17 and area V1), which is where inputs from the two eyes are first combined in an excitatory fashion, whereas more distal and monocular processing structures such as the retina and lateral geniculate nucleus (LGN) are normal. Using high-field functional magnetic resonance imaging in a group of human adults with amblyopia, we demonstrate that functional deficits are first observable at a thalamic level, that of the LGN. Our results suggest the need to re-evaluate the current models of amblyopia that are based on the assumption of a purely cortical dysfunction, as well as the role for the LGN in visual development.
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PMID:Deficient responses from the lateral geniculate nucleus in humans with amblyopia. 1929 Dec 31

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.
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PMID:The amblyopic deficit and its relationship to geniculo-cortical processing streams. 2046 93