Retinal abnormalities contribute to S-cone selective deficits in migraine

Past studies have shown that individuals with migraine have elevated thresholds to S-cone stimuli relative to the control population (Shepherd, 2005 Cephalalgia 25 412 ^ 423). However, it is unclear whether this deficit arises from dysfunction at cortical or precortical sites. To localise the source of this abnormality within the visual pathways, an experimental paradigm called transient tritanopia was employed (Mollon and Polden, 1977 Philosophical Transactions of the Royal Society of London, Series B 278 207 ^ 240). Defined as a reduction in sensitivity to short-wavelength stimuli in response to the extinction of a long-wavelength adapting display, there is strong evidence to suggest that this phenomenon is retinal in origin (Valeton and Van Norren, 1979 Nature 280 488 ^ 490). Thirty-two participants with migraine (meeting the International Headache Society diagnostic criteria), and thirty-two age-matched/sex-matched control participants were tested to determine S-cone detection thresholds in a 4AFC procedure, both before and after adaptation to (1) a long-wavelength, and (2) a chromatically neutral display. In both groups, long-wavelength adaptation increased subsequent detection thresholds to S-cone stimuli. However, this loss of sensitivity was significantly greater in the migraine group. In contrast, adaptation to Tenth Applied Vision Association Christmas Meeting, Abstracts 427 a chromatically neutral display (equal in luminance to the long-wavelength display) had no effect on S-cone sensitivity. In conclusion, retinal abnormalities may contribute to a loss of sensitivity in the detection of short-wavelength stimuli in migraine