Alison M. Harris
Department of Psychological Science, Claremont McKenna College, Claremont, CA, United States
Visual snow syndrome, characterized by persistent flickering dots throughout the visual field, has been hypothesized to arise from abnormal neuronal responsiveness in visual processing regions. Previous research has reported a lack of typical VEP habituation to repeated stimulus presentation in patients with visual snow. Yet these studies generally used pattern-reversal paradigms, which are suboptimal for measuring cortical responses to the onset of foveal stimulation. Instead, these responses are better indexed by the C2, a pattern-onset VEP peaking 100–120 ms after stimulus onset. In this case study, we analyzed the C2 and its adaptation profile in data previously collected from a single patient with visual snow using a “double-pulse” presentation paradigm. In controls, shorter intervals between stimulus pairs were associated with greater attenuation of the C2 VEP, with recovery from adaptation at longer stimulus onset asynchronies (SOAs). However, the visual snow patient showed the opposite pattern, with reduced C2 amplitude at longer SOAs despite distinct C2 peaks at the shortest SOAs. These results stand in contrast not only to the pattern of C2 VEP attenuation in controls, but also to a lack of adaptation previously reported for the pattern-onset P1 VEP in this patient. Exploratory source localization using equivalent current dipole fitting further suggested that P1 and C2 VEPs in the visual snow patient arose from distinct sources in extrastriate visual cortex. While preliminary, these results support differential patterns of VEP attenuation and potentiation within the same individual, potentially pointing toward multiple mechanisms of abnormal neuronal responsiveness in visual snow syndrome.
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