Visual Snow Syndrome (VSS) is a condition where people constantly see tiny flickering dots, like TV static, across their entire field of vision. Many also experience other symptoms such as afterimages, light sensitivity, poor night vision, tinnitus, and migraines. Although it strongly affects daily life, doctors currently diagnose VSS mainly based on what patients describe, because there are no clear objective tests.
Research suggests that VSS may be caused by overactivity in the visual parts of the brain and disruptions in larger brain networks involved in perception and attention. However, most existing brain imaging methods can only show associations, not direct cause-and-effect relationships.
In this recently published preprint study (awaiting peer review), researchers combined two techniques to better understand VSS:
- Transcranial magnetic stimulation (TMS) was used to stimulate the visual cortex and produce brief visual sensations called phosphenes (flashes or shapes of light that appear without actual visual input).
- Eye-tracking measured how participants’ eyes moved before and after stimulation.
Compared to healthy individuals, people with VSS showed more spread-out phosphene perceptions, faster initial eye movements toward targets, and slower eye movement speed after brain stimulation.
Methods
The study included 12 participants: four individuals with Visual Snow Syndrome (VSS) and eight healthy controls. The goal was to compare how their visual systems respond to direct brain stimulation and how this affects eye movements.
To investigate this, researchers used MRI-guided transcranial magnetic stimulation (TMS) to precisely stimulate the occipital cortex — the visual processing area at the back of the brain.
First, they measured each participant’s phosphene threshold, meaning the lowest level of stimulation that reliably produced a phosphene (a brief flash or visual sensation without actual light entering the eye).
Once this threshold was established, single TMS pulses were delivered to different visual cortex locations. After each pulse, participants used a tablet to draw what they saw and where they saw it on a digital grid.
At the same time, eye movements were recorded with a high-resolution eye-tracker. All systems were synchronized so researchers could analyze eye movements occurring within 500 milliseconds after each stimulation.
In a separate session, participants completed a prosaccade task. They fixated on a central cross, and then a target appeared either 10 degrees to the left or right of it. Participants were instructed to look at the target as quickly and accurately as possible.
Researchers measured:
- Latency — how quickly the eye movement began after the target appeared
- Peak velocity — the maximum speed of the eye movement
All data including TMS timing, stimulation location, eye movements, and tablet drawings were merged using shared timestamps for precise alignment.
Phosphene drawings were digitized and converted into visual field coordinates. Individual and group maps were created to show where phosphenes were perceived. Phosphene thresholds, gaze velocity after TMS, and prosaccade performance were statistically compared between VSS participants and healthy controls.
What the Findings Suggest About Visual Snow Syndrome
Please note: This study is an early research report and has not yet been peer-reviewed, so the findings are considered preliminary and may be refined as more research is completed.
The results show clear differences in how the visual brain functions in people with VSS.
First, VSS participants had lower phosphene thresholds, meaning weaker stimulation was enough to produce visual sensations. This suggests their visual cortex is more excitable than in healthy individuals, consistent with previous research indicating increased visual brain activity in VSS.
Second, phosphene maps in VSS were more spread out and less precise compared to the compact and stable maps seen in controls. This may reflect reduced inhibitory control in the visual cortex, leading to less precise visual processing. Such reduced filtering could help explain the persistent “visual noise” experienced in VSS.
Third, after TMS stimulation, VSS participants showed slower eye movement responses, suggesting altered communication between the visual cortex and motor systems. This points to broader changes in visual and sensorimotor network function.
Together, these findings suggest that Visual Snow Syndrome involves both increased cortical excitability and network-level dysregulation, possibly related to impaired sensory filtering or thalamocortical disturbances.
Importantly, the combination of TMS, phosphene mapping, and eye-tracking may offer a promising objective approach to measuring visual and oculomotor abnormalities in VSS — pointing to potential future biomarkers and deeper insight into the disorder.
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