Human vision with a lesion of the parvocellular pathway: an optic neuritis model for selective contrast sensitivity deficits with severe loss of midget ganglion cell function.

Achromatic visual function in primates is distributed between two pathways from retina to cortex, the parvocellular and the magnocellular. The relative contribution of these to human achromatic vision is controversial and largely unknown. Here, we use an optic neuritis (ON) model to investigate the effects of a severe loss of parvocellular function on human contrast sensitivity. In our first experiment, we use Gabor stimuli (0.5 cpd, 2 Hz) to show that, compared to normal control eyes, ON causes selective deficits in the two chromatic, cone opponent pathways, with L/M cone opponency affected more than S cone opponency, and a relative sparing of achromatic function. Since L/M cone opponency is carried exclusively by the midget ganglion cells of the parvocellular pathway, this demonstrates a selective deficit of parvocellular function. In a second experiment, we report on two subjects who have lost all L/M cone opponent response in both eyes, indicating a severe loss of parvocellular function. We measure the spatial and temporal contrast sensitivity functions of their remaining achromatic vision, compared with a normal control group, to determine the selectivity of the visual deficit caused by the differential parvocellular loss, and assess the relative contributions of the parvocellular and magnocellular pathways to achromatic contrast sensitivity. We find that parvocellular function contributes selectively at mid- to high spatial frequencies (at low temporal frequencies), whereas magnocellular function determines contrast sensitivity over a very broad temporal frequency range (at low spatial frequencies). Our data bear a striking resemblance to results obtained from primate parvocellular lesions.