Distinct Patterns of P1 and C2 VEP Potentiation and Attenuation in Visual Snow: A Case Report.

Alison M Harris

doi:10.3389/fneur.2021.723677

Abstract

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.

Highlights

Visual snow syndrome is a debilitating neurological condition characterized by the persistent and continuous experience of tiny flickering dots in the visual field (1)
The polarity of the C2 varies depending on which hemifield is visually stimulated, it has typically been reported as a negative deflection emerging from 100 to 130 ms after stimulus onset (11), perhaps due to superposition with the N1 component in the same time window (13)
In line with previous findings, the controls showed a pattern of decreasing adaptation at longer stimulus onset asynchronies (SOAs) (16), with the C2S2 responses at shorter SOAs of 50 and 67 ms appearing partially integrated with the initial C2S1 response

Summary

Introduction

Visual snow syndrome is a debilitating neurological condition characterized by the persistent and continuous experience of tiny flickering dots in the visual field (1). Similar to migraine aura (2), the visual disturbances in visual snow syndrome have been hypothesized to arise from changes in neuronal responsiveness to sensory stimulation (3). Habituation, the phenomenon of reduced responsiveness over repeated stimulus presentation, is commonly observed in measurements of visual evoked potentials (VEPs) for healthy individuals (4). Loss of VEP habituation has been reported both in migraine with aura (5) and visual snow syndrome (6, 7). Prior measurements of VEP habituation in visual snow have largely utilized pattern-reversal paradigms, in which a patterned stimulus switches polarity repeatedly over time. While pattern-reversal stimulation produces a reliable and consistent VEP across participants, the Distinct VEP Patterns in Visual Snow pattern-reversal P1001, this protocol is limited in terms of the cortical activity it represents. The pattern-reversal P100 appears to largely reflect neural responses to the offset, rather than the onset, of the stimulus (8, 9), with contributions from both magnocellular and parvocellular pathways (10)

Methods

Results

Conclusion