Microstructure in patients with visual snow syndrome: an ultra-high field morphological and quantitative MRI study
Myrte Strik, Meaghan Clough, Emma J Solly, Rebecca Glarin, Owen B White, Scott C Kolbe, Joanne Fielding
Brain Communications, Volume 4, Issue 4, 2022, fcac164, https://doi.org/10.1093/braincomms/fcac164
It is clear that visual snow syndrome is a disorder of the central nervous system. However, the underlying pathophysiological mechanisms remains elusive. Here, we reveal no evidence of gross morphometry changes in the visual snow syndrome brain, but widespread changes in the microstructure of the GM, the most notable of these occurring in caudal regions including the occipital cortex. None of these changes are directly associated with the co-occurrence of migraine. While we were unable to determine the specific brain tissue that underlies microstructural changes, they do focus further investigations, contributing significantly to our understanding of visual snow syndrome.
* GM refers to gray matter
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The Psychiatric Symptomatology of Visual Snow Syndrome
Emma J. Solly
Owen B. White
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.
Full article: https://www.frontiersin.org/articles/10.3389/fneur.2021.703006/full
I am absolutely thrilled to announce that with a global effort funds have been raised for VSS research to move forward at Monash University! More details will be coming, but I wanted to let all of our supporters and donors know that we did it! Big changes are ahead in the lives of Visual Snow sufferers!
Patient advocate/consumer Patricia and Associate Professor Joanne Fielding talk about respectively the experience of living with Visual Snow Syndrome, and the challenges of research.
Hello. We have enrolled 9 participants. We have so many terrific volunteers and have over 75 active on the waitlist. We plan to recruit 3 more for the study and have identified those three with preliminary screening. Stay tuned as we evaluate the data – likely in the summer of 2023.
The recruitment is clearly terrific as you can see. Thank you to Eye On Vision for allowing us to keep going with the study that originally started in 2019, even though COVID-19 had hit us hard and made it difficult to keep the study up and running.
Published: August 21, 2019
Updated: September 23, 2021
Migraine aura without headache, sometimes referred to as “silent migraine,” does not feature any head pain.
By Dr. Jennifer Robblee
Headache can be a common migraine symptom. But not all forms of migraine come with headache. “Migraine aura without headache”—previously known as “acephalgic migraine” and sometimes called “silent migraine”—is when someone has a migraine aura without any head pain.
Despite a lack of head pain, migraine aura without headache is still disabling for those who live with it. It also has its own set of considerations for diagnosis and treatment. The following is a breakdown of the basics of this form of migraine.
To read full article, please click here
Alison M. Harris
Department of Psychological Science, Claremont McKenna College, Claremont, CA, United States
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.
To read the full article please click here or download PDF below.