Antagonistic Relationship Between VEP Potentiation and Gamma Power in Visual Snow Syndrome

Abstract

Objective.-Using a "double-pulse" adaptation paradigm, in which two stimuli are presented in quick succession, this study examines the neural mechanisms underlying potentiation of the visual evoked potential (VEP) in visual snow syndrome.Background.-Visual snow is a persistent visual disturbance characterized by rapid flickering dots throughout the visual field. Like the related condition of migraine with aura, visual snow has been hypothesized to arise from abnormal neuronal responsiveness, as demonstrated by a lack of typical VEP habituation to repeated visual stimulation. Yet the exact neural mechanisms underlying this effect remain unclear. Previous "double-pulse" experiments suggest that typical VEP habituation reflects disruptive gamma-band (50-70 Hz) neural oscillations, possibly driven by inhibitory interneurons. Given that migraine has been associated with reduced cortical inhibition, we propose here that visual snow may likewise reflect diminished inhibitory activity, resulting in decreased gamma power following initial visual stimulation and concomitant potentiation of the subsequent VEP response.Methods.-We compared VEP responses to double-pulse adaptation in a 22-year-old man with a 2-year history of visual snow versus a group of age-and gender-matched controls (N 5 5). The patient does not have a comorbid diagnosis of episodic migraine or migraine with aura, and controls had no personal or family history of migraine.Results.-In contrast to the pattern of habituation observed in controls, visual snow was associated with persistent potentiation of the VEP response. Consistent with our predictions, time-frequency analysis revealed reduced gamma-band power following the initial stimulus in visual snow relative to controls.Conclusions.-These results support an antagonistic interplay between gamma power and rapid neural adaptation, shedding new light on the neural mechanisms of VEP potentiation in visual snow.

The Clinical Characteristics and Neurophysiological Assessments of the Occipital Cortex in Visual Snow Syndrome With or Without Migraine

“…Later, another case report of a patient with visual snow syndrome was also reported to have loss of VEP habituation and reduced gamma power. 21 Here, in this study, we were able to show that although the habituation response was prominent in the healthy controls, both the VS m and VS wom groups showed loss of habituation. In pairwise comparisons of the 10th/1st block N1-P1 amplitude ratios measured from the right eye stimulations, there were statistically significant differences between the VS m vs the healthy control group and also between the VS wom vs the healthy control group.…”

“…Our preliminary study promoted us to further characterize the clinical and neurophysiological characteristics of VS patients with or without migraine. Later, another case report of a patient with visual snow syndrome was also reported to have loss of VEP habituation and reduced gamma power . Here, in this study, we were able to show that although the habituation response was prominent in the healthy controls, both the VS m and VS wom groups showed loss of habituation.…”

Prevalence of visual snow syndrome in the UK

“…3. Minor physiological alterations in visual association pathways appear compatible with this notion [6,7]. Although speculative, this may perhaps also explain the poor response to various attempts at medical treatment [5].…”

“…The biological mechanisms of the syndrome are poorly understood [6][7][8]. Empirical data are based on isolated case reports and smaller case series [6] or on surveys of self-help groups with people who have taken the initiative to register their symptoms with a web-based platform dedicated to visual snow syndrome [9].…”

Insular and occipital changes in visual snow syndrome: a BOLD fMRI and MRS study

“…Hallucinogenic persisting perceptual disorder 3,4 can sometimes mimic VS, although the two are certainly separate conditions. 5 VS pathophysiology is currently unknown; hypotheses include thalamo-cortical dysrhythmia of the visual pathways, 6 hyperexcitation of primary and secondary visual cortices, [7][8][9] increased saliency of normally ignored subcortical activity or perhaps a combination of all these mechanisms. 10 In particular, evidence for dysfunctional visual processing within the association cortices has emerged in VS, through the use of visual-evoked potentials.…”