Visual Snow: Updates on Pathology

Abstract

Purpose of review: Until the last 5 years, there was very little in the literature about the phenomenon now known as visual snow syndrome. This review will examine the current thinking on the pathology of visual snow and how that thinking has evolved.

Recent findings: While migraine is a common comorbidity to visual snow syndrome, evidence points to these conditions being distinct clinical entities, with some overlapping pathophysiological processes. There is increasing structural and functional evidence that visual snow syndrome is due to a widespread cortical dysfunction. Cortical hyperexcitability coupled with changes in thalamocortical pathways and higher-level salience network controls have all shown differences in patients with visual snow syndrome compared to controls. Further work is needed to clarify the exact mechanisms of visual snow syndrome. Until that time, treatment options will remain limited. Clinicians having a clearer understanding of the basis for visual snow syndrome can appropriately discuss the diagnosis with their patients and steer them towards appropriate management options.

Keywords: Cortical hyperexcitability; Inhibitory mechanisms; Migraine; Palinopsia; Thalamocortical dysrhythmia; Visual snow.

Fig. 1

A proposed model for visual snow pathophysiology. Altered peripheral visual stimulation or a form of genetic predisposition could induce dysrhythmic connections between thalamic structures and cortical visual areas. The lateral geniculate nucleus (LGN) and pulvinar (Pv) in particular are directly connected to motion area V5 and the lingual gyrus (LG). Relevant to visual snow biology is the motion processing network, which is composed of areas within the primary visual cortex (V1/V2), area V3A within the cuneus (Cu), area V5 located ventrolaterally among the lateral occipital sulcus and inferior temporal sulcus, and Brodmann area 7 in the precuneus (Pc). Structures pertaining to the default mode network (PCC, posterior cingulate cortex; Pc; mPFC, middle prefrontal cortex) and/or the salience network (AI, anterior insula; ACC, anterior cingulate cortex) are involved in salience and interoception. Disruption of these networks, possibly through altered connectivity between cortical areas, could also play a role in visual snow pathophysiology. See main text for a more in-depth explanation. Available via open access – creative commons. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6923266/