Objective: To characterise the psychiatric symptoms of visual snow syndrome (VSS), and determine their relationship to quality of life and severity of visual symptoms.Methods: One hundred twenty-five patients with VSS completed a battery of questionnaires assessing depression/anxiety, dissociative experiences (depersonalisation), sleep quality, fatigue, and quality of life, as well as a structured clinical interview about their visual and sensory symptoms.Results: VSS patients showed high rates of anxiety and depression, depersonalisation, fatigue, and poor sleep, which significantly impacted quality of life. Further, psychiatric symptoms, particularly depersonalisation, were related to increased severity of visual symptoms. The severity/frequency of psychiatric symptoms did not differ significantly due to the presence of migraine, patient sex, or timing of VSS onset (lifelong vs. later onset).Conclusion: Psychiatric symptoms are highly prevalent in patients with VSS and are associated with increased visual symptom severity and reduced quality of life. Importantly, patients with lifelong VSS reported lower levels of distress and milder self-ratings of visual symptoms compared to patients with a later onset, while being equally likely to experience psychiatric symptoms. This suggests that the psychiatric symptoms of VSS are not solely due to distress caused by visual symptoms. While no consistently effective treatments are available for the visual symptomology of VSS, psychiatric symptoms offer an avenue of treatment that is likely to significantly improve patient quality of life and ability to cope with visual symptoms.

Objective:To determine whether changes to cortical processing of visual information can be objectively evaluated using three simple ocular motor tasks to measure performance in patients with visual snow syndrome (VSS).Methods:Sixty four patients with VSS (32 with migraine and 32 with no migraine), and 23 controls participated. Three ocular motor tasks were included: prosaccade (PS), antisaccade (AS), and interleaved antisaccade-prosaccade (AS-PS) tasks. All these tasks have been used extensively in both neurologically healthy and diseased states.Results:We demonstrated that, compared to controls, the VSS group generated significantly shortened PS latencies (p = .029) and an increased rate of AS errors (p = .001), irrespective of the demands placed on visual processing (i.e., task context). Switch costs, a feature of the AS-PS task, were comparable across groups, and a significant correlation was found between shortened PS latencies and increased AS error rates for VSS patients (r = .404).Conclusion:We identified objective and quantifiable measures of visual processing changes in patients with VSS. The absence of any additional switch cost on the AS-PS task in VSS suggests that the PS latency and AS error differences are attributable to a speeded PS response rather than to impaired executive processes more commonly implicated in poorer AS performance. We propose that this combination of latency and error deficits, in conjunction with intact switching performance will provide a VS behavioural signature that contributes to our understanding of VSS and may assist in determining the efficacy of therapeutic interventions.

Visual snow syndrome (VSS) is a poorly understood neurological disorder that features a range of disabling sensory changes. Visual processing changes revealed previously in VSS appear consistent with poor attentional control, specifically, with difficulty controlling environmentally driven shifts of attention. This study sought to confirm this proposal by determining whether these changes were similarly evident where attention is internally driven. Sixty seven VSS patients and 37 controls completed two saccade tasks: the endogenously cued saccade task and saccadic Simon task. The endogenously cued saccade task correctly (valid trial) or incorrectly (invalid trial) pre-cues a target location using a centrally presented arrow. VSS patients generated significantly shorter saccade latencies for valid trials (p = 0.03), resulting in a greater magnitude cue effect (p = 0.02), i.e. the difference in latency between valid and invalid trials. The saccadic Simon task presents a peripheral cue which may be spatially congruent or incongruent with the subsequent target location. Latencies on this task were comparable for VSS patients and controls, with a normal Simon effect, i.e. shorter latencies for saccades to targets spatially congruent with the preceding cue. On both tasks, VSS patients generated more erroneous saccades than controls towards non-target locations (Endogenously cued saccade task: p = 0.02, saccadic Simon task: p = 0.04). These results demonstrate that cued shifts of attention differentially affect saccade generation in VSS patients. We propose that these changes are not due to impairment of frontally-mediated inhibitory control, but to heightened saccade-related activity in visual regions. These results contribute to a VSS ocular motor signature that may provide clinical utility as well as an objective measure of dysfunction to facilitate future research.