I have spoken with Dr. Pelak and this study is open and actively recruiting participants. The study is taking place in Colorado. Eye On Vision has sent funding to ensure that this trial will continue.
All participants will undergo 2 weeks (5 times each week) of repetitive TMS.
Subject line for your email: NCT04925232, 20-0424, Transcranial Magnetic Stimulation For Visual Snow Syndrome
Contact: Visual Snow Study Coordinator 303-724-4644 VisualSnowColorado@cuanschutz.edu
Participants will be offered help if they cannot read the German questionnaire.
Location: Bergmannsheil-Klinikum, Bochum, NRW, Germany
Study takes place in #Germany
Researchers will be taking images of the thalamus hormone household with special research MRI and EEG devices.
It takes around 3-4 hours and they will pay you €150 for participating. This is not a treatment trial, but an important study to better understand the mechanism of Visual Snow #VS .
Please email the address below for more information if you are interested. Also please note that emails may takes a few weeks to be responded to based on patient experience.
Both male and female participants are being taken. Ideally the study would like more female participation as most of the patients who have competed the testing thus far have been male.
#EOVF is working with the non-profit, Visual Snow Syndrome Germany, to find the patients needed for this study.
#cureVSS #VSS #research
Visual snow syndrome, the spectrum of perceptual disorders, and migraine as a common risk factor: A narrative review
CONCLUSION: VSS, PPPD, fibromyalgia, and chronic tinnitus might lie on a spectrum of perceptual disorders with similar pathophysiological mechanisms and the common risk factor migraine. Understanding the underlying network disturbances might give insights into how to improve these currently very difficult to treat conditions.
VSS participants demonstrated delayed onset of IOR. Unlike controls, who exhibited IOR with 300 and 500 ms cue/target intervals, VSS participants only exhibited IOR with 500 ms cue/target intervals. These findings provide further evidence that attention is impacted in VSS, manifesting in a distinct saccadic behavioural profile, and delayed onset of IOR. Whether IOR is perceived as the build-up of an inhibitory bias against returning attention to an already inspected location or a consequence of a stronger attentional orienting response elicited by the cue, our results are consistent with the proposal that in VSS, a shift of attention elicits a stronger increase in saccade-related activity than healthy controls.
In conclusion, our results suggest that VSS is characterised by a complex disturbance in the interaction of multiple brain systems. This dysfunction particularly involves the pre-cortical and cortical visual pathway, the visual motion network, the attentional networks and finally the salience network; further, it does not depend on the activity state of the brain. What we observed suggests that there is a disruption in the filtering and integration of incoming sensory visual stimuli, versus the modulation of internally generated visual information. Future studies will help determine if this fingerprint of altered network dysfunction, indeed represents the main pathophysiological mechanism underlying the symptoms of this complex and disabling condition. In particular, it will be important to distinguish the impact of concomitant migraine, photophobia and aura on these findings, especially with regard to changes in connectivity affecting the visual system.
Given that no widely applicable treatment seems to fully suppress the symptoms of VSS, achieving an improved understanding of its underlying neurobiology is important, as it aids clinicians in explaining the condition to affected patients and also directs future research to more targeted approaches. In particular, the finding that diffuse brain networks are implicated in the genesis of VSS, could have the clinical implication of redirecting treatment from generic pharmacological interventions to a more focused modulation of brain function, possibly through techniques such as neuromodulation or neurofeedback.
Localised increase in regional cerebral perfusion in patients with visual snow syndrome: a pseudo-continuous arterial spin labelling study
ConclusionsIn conclusion, patients with VSS present increased activation in a wide network of intrinsic brain areas that are key in the processing of complex sensory and cognitive states. The fact that rCBF increases were independent of the presence of an external visual stimulus, suggests that these abnormalities could be a causal factor of the disorder.
This study expands on previous neuroimaging findings, confirms VSS to be a complex brain problem, and helps to improve our understanding of a condition for which treatment is still lacking.
Results(1) Of 120 patients with “visual snow,” 70 patients also had migraine and 37 had typical migraine aura. Having comorbid migraine was associated with an increased likelihood of having palinopsia (odds ratio [OR] 2.8; P = .04 for “afterimages” and OR 2.6; P = .01 for “trailing”), spontaneous photopsia (OR 2.9; P = .004), photophobia (OR 3.2; P = .005), nyctalopia (OR 2.7; P = .01), and tinnitus (OR 2.9; P = .006). Typical migraine aura was associated with an increased likelihood of spontaneous photopsia (OR 2.4; P = .04). (2) After adjusting for typical migraine aura, comparison of 17 “visual snow” patients with 17 age and gender matched controls showed brain hypermetabolism in the right lingual gyrus (Montreal Neurological Institute coordinates 16-78-5; kE = 101; ZE = 3.41; P < .001) and the left cerebellar anterior lobe adjacent to the left lingual gyrus (Montreal Neurological Institute coordinates -12-62-9; kE = 152; ZE = 3.28; P = .001).
Conclusions—Comorbid migraine aggravates the clinical phenotype of the “visual snow” syndrome by worsening some of the additional visual symptoms and tinnitus. This might bias studies on “visual snow” by migraineurs offering study participation more likely than non-migraineurs due to a more severe clinical presentation. The independence of entoptic phenomena from comorbid migraine indicates “visual snow” is the main determinant. The hypermetabolic lingual gyrus confirms a brain dysfunction in patients with “visual snow.” The metabolic pattern differs from interictal migraine with some similarities to migrainous photophobia. The findings support the view that “visual snow,” migraine, and typical migraine aura are distinct syndromes with shared pathophysiological mechanisms that need to be addressed in order to develop rational treatment strategies for this disabling condition.
ResultsWe found reduced BOLD responses to the visual stimulus with respect to baseline in VS patients compared to controls, in the left (k = 291; P = 0.025; peak MNI coordinate [-34 12 -6]) and right (k = 100; P = 0.003; peak MNI coordinate [44 14 -2]) anterior insula. Our spectroscopy analysis revealed a significant increase in lactate concentrations in patients with respect to controls (0.66 ± 0.9 mmol/L vs. 0.07 ± 0.2 mmol/L; P < 0.001) in the right lingual gyrus. In this area, there was a significant negative correlation between lactate concentrations and BOLD responses to visual stimulation (P = 0.004; r = −0.42), which was dependent on belonging to the patient group.
The prevalence of visual snow syndrome in the UK is
1.4%–3.3%. Visual snow syndrome is associated with
tinnitus and, possibly, to a lesser degree with mood
impairment and headache. It is of note that unprimed
laypeople with visual snow syndrome in the general
population are on average older than those seeking
medical attention and, perhaps, less concerned.
Although prospective follow-up data are needed,
visual snow syndrome is very unlikely to be a progres-
sive disorder. We suggest that reassuring information
can be given to those seeking medical attention for
visual snow syndrome.
From the data presented here, almost all patients with ‘visual snow’ have a variety of additional visual symptoms (palinopsia, enhanced entoptic phenomena, photophobia, and nyctalopia), which do not sound like typical migraine aura at all. Visual snow therefore represents a unique clinical syndrome. Our data acknowledge an overlap of migraine and visual snow but do not support the hypothesis that migraine attacks or individual episodes of migraine aura ‘cause’ visual snow. Our data do not support a view the visual snow syndrome is caused by anxiety, depression or the intake of illicit drugs, such as LSD. Remarkably, most patients with visual snow have normal best corrected visual acuity, perimetry and fundoscopy. Any association with visual loss or acute onset of visual symptoms similar to visual snow, especially floaters and photopsia, would therefore require appropriate assessment by a specialist before calling it ‘visual snow’.
We would define the ‘visual snow’ syndrome by the presence of visual snow as the main criterion, with some additional visual criteria, and exclusion of migraine aura, and overlapping diseases, such as ophthalmological pathology or intake of psychotropic drugs (Table 4).