As new research becomes available I will try to keep up to date. Here are a couple updates that you may have missed or been unaware of.
James Fulton On Visual Snow
James Fulton was one of the speakers at the recent “Visual Snow Conference”. The full video footage from that event is at the time of writing not yet available but his presentation slides have actually been viewable online via his website for a while now. I would recommend looking over the slides, but perhaps even more so reading this additional material that I imagine many like myself may previously have been unaware of.
Fulton refers to himself an independent investigator in neuroscience, and he has done a lot of independent research into vision, hearing, and the neural system. Based on his knowledge, some of his research theories and findings from a set of surveys, he has focused on helping to pinpoint where the “errors” leading to visual snow may occur within the neural system. He wrote about the “perception and cause” of visual snow a few years ago, but has now been able to add to that groundwork with more information now being available.
Here is a brief summary of some of those points (as I understood them, and simplified):
Visual Snow Type And Location
The visual system can be split up into various stages. In these stages information travels from the eyes through to different parts of the brain to form and complete the images which our brains can comprehend. Because of this and with how visual snow seems to be uniform across the field of vision, Fulton says the noise cannot originate from one hemisphere or quadrant of the brain – this would add noise to a section of our vision but not all of it. So instead the likely source of visual is beyond a certain stage where consequent noise would be uniform across the visual field. Fulton says this could be the thalamus or parietal lobe.
Visual snow he says is likely to be the result of a neuron or small group of neurons that fire inappropriately to add noise into an otherwise normally operating visual system. At what stage exactly this noise is located, and what role the misfiring neuron(s) plays, may determine the type of noise and therefore static. According to Fulton’s surveys there are three types of static possibly seen in visual snow syndrome – Popcorn noise (“pulse type visual snow”), White noise and Pink noise (“broadband type visual snow”). These have different frequencies and originate at different stages, therefore they also have distinct visible characteristics. As he describes them: popcorn noise presents scattered dots, white noise a TV like blotchy field of vision, and pink noise a fuzziness across vision.
According to the surveys pink noise is the most common, and tinnitus commonly also has pink noise. A possibility that Fulton raises is that there could be a “reference voltage supply” serving both auditory and visual circuits, which when it fails to function properly could introduce noise as both tinnitus and visual snow.
Fulton comments that cortical hyperexcitability is too general a term for all of this and says that the thalamus may be an area of interest, but not in the sense of an arrhythmia or dysrhythmia. He criticises previous work which described visual snow as a potential thalamocortical dysrhythmia.
Cause Of Visual Snow
Fulton underlines that visual snow does not involve a hallucination. It is not a psychotic failure to interpret an image but likely an actual circuit failure within the visual system as described above – so an “organic” disease. Imaging techniques to locate the source of this failure (because it is just a few neurons) have not yet been available, although this is something which I think is currently being looked into by the Visual Snow Initiative.
In terms of what could cause this inappropriate firing to happen in the first place, Fulton suggests either chemical or vascular failure leading to a change in the porosity of tissue in the thalamus or parietal lobe of the brain. This in turn he writes could either change the availability of glutamic acid (glutamate) or make it harder for GABA or CO2 to be removed from a certain area – either way causing a problematic change in the “electrical operating condition” of a few neurons.
In addition, he discusses how Marijuana could be a cause of visual snow, where it would have a slightly different potential mechanism relating to dopamine.
Other Symptoms And Observations
Fulton makes a point of differentiating visual snow (static) from other symptoms, saying that most other symptoms are effectively unrelated or a psychotic reaction to visual snow.This is probably the case for depersonalisation and anxiety but I feel this is an unsatisfactory conclusion for some symptoms. Their organic appearance in connection with visual snow otherwise still remains unexplained, and yet potentially important.
That Fulton says visual snow is a function of attention and that it appears to diminish in sufficiently complicated scenes is true in my experience, but of course this is compounded by other symptoms which are just as bothersome.
Here are a few quick considerations for the thalamus:
Interesting for me was the mentioned opinion of a “well respected and experienced medical researcher” who as Fulton writes believes the cause of visual snow could be down to either a viral infection or altered output from microglia. These are both things I have been considering recently and to me seem very reasonable suggestions, particularly in the idiopathic/family member scenario.
Practical Steps And My Conclusions
Vascular failures? I mentioned recently that my circulation has been poor for a while now, and since starting a ketogenic diet this appears to have changed (and my vision also seems to have improved). Potentially a connection in my case, although other instances such as erythromelalgia may be more what Fulton is referring to.
New Lamotrigine Case Report
There was also this recent new case report. Unfortunately it doesn’t really add much for those with visual snow – mainly owing to a lack of detail, but also several other problems.
The case report says a patient received lamotrigine and had a “complete resolution of symptoms”. There is no clarification as to what this phrase means or much information given about the patient. The author has also received compensation from pharmaceutical companies in the past. For these reasons the case report isn’t that suitable to be acted upon by those with visual snow, though we are not the target audience here anyway.
In terms of the merit of lamotrigine in general, there is only an indication that it may help in some cases, in others not so much. As is mentioned in the case report, previous studies have generally found a lack of response to lamotrigine. Online, you can also find anecdotal reports of worsening from lamotrigine. We know that people seem to have visual snow caused by different triggers, with differing symptoms and different responses to attempted treatment. Consider the complexity that Mr Fulton’s research evokes and compare it to this case study – trying to treat a condition for which there is so little information with a non-specific drug with a range of potential side effects is very contentious and overly simplistic at this stage, in my opinion.
As I understand a sodium channel blocker such as lamotrigine may stop or reduce the firing of action potentials but it will affect not just the small group of neurons, and won’t get to the root of the problem. So an important point to stress here is that “treated” ≠ cured, and I believe you would have to keep taking lamotrigine, without knowing what the long-term effects will be. This is a big issue, even if the treatment seems to be helping. My personal stance, especially given the improvement that I have seen naturally is to advise caution here, and as a general point please always think critically when looking at new research and articles.
I will be updating the site’s visual snow research overview in the next few weeks to add some more detail and make some potential corrections in the way the information there is presented.