The Relation Between Migraine, Typical Migraine Aura and "Visual Snow"

[Syntheso]

The Relation Between Migraine, Typical Migraine Aura and "Visual Snow"

 

Abstract

OBJECTIVE:

To assess the relationship between the phenotype of the "visual snow" syndrome, comorbid migraine, and typical migraine aura on a clinical basis and using functional brain imaging.

BACKGROUND:

Patients with "visual snow" suffer from continuous TV-static-like tiny flickering dots in the entire visual field. Most patients describe a syndrome with additional visual symptoms of the following categories: palinopsia ("afterimages" and "trailing"), entopic phenomena arising from the optic apparatus itself (floaters, blue field entoptic phenomenon, photopsia, self-light of the eye), photophobia, nyctalopia (impaired night vision), as well as the non-visual symptom tinnitus. The high prevalence of migraine and typical migraine aura in this population has led to the assumption that "visual snow" is caused by persistent migraine aura. Due to the lack of objective measures, alternative diagnoses are malingering or a psychogenic disorder.

METHODS:

(1) The prevalence of additional visual symptoms, tinnitus, and comorbid migraine as well as typical migraine aura was assessed in a prospective semi-structured telephone interview of patients with "visual snow." Correlations were calculated using standard statistics with P < .05 being considered statistically significant. (2) Areas with increased brain metabolism in a group of "visual snow" patients in comparison to healthy controls were identified using [18 F]-2-fluoro-2-deoxy-D-glucose positron emission tomography and statistical parametric mapping (SPM8 with whole brain analysis; statistical significance was defined by P < .001 uncorrected for multiple comparisons).

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.

 

 

 

 

 

http://www.ncbi.nlm.nih.gov/pubmed/24816400

[Ghormeh Sabzi]

The hypermetabolic lingual gyrus confirms a brain dysfunction in patients with "visual snow."

 

 

 

Don't think that this is just another research articles guys. This is a very significant find. Take this article very seriously. 

 

Also be aware that they used a very specific set of patients for this study so it may be the case that the results are not replicated in other patients. I'd like to get scanned myself to see if the results are replicated in myself as I do not represent the type of patient they scanned.

[VisualDude]

Have you seen the results of the PET scans of VS patients?

 

[ From: http://hppdonline.com/index.php?/topic/3857-upcoming-eeg-test-with-neurologist-first-post ]

 

It kind of makes sense since the lingual gyrus is involved with dreaming - an abstract, imaginative process rather than 'cold' pixel processing.

 

As others have brought out before, the additional symptoms common with VS are common with HPPDers: palinopsia (afterimages and trailing), photophobia (sensitive to light), nyctalopia (night vision problems), tinnitus (ears ringing), entoptic phenomena (floaters, blue field, photopsia ('flashes'), blue field).

 

Some have attributed VS to the thalamus with as few as a hundred neurons involved.  But these other symptoms are way beyond that ... and imaged as hypermetablic activity.  Just as HPPD qEEGs show cerebral disinhibition (hyperactivity).

 

Many people with VS have had it all there life - so not linked to recreational drug use.  "None of the patients noted intake of illicit drugs prior the onset of visual snow" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620302/

 

So as with so many other brain studies, the same problem is being attacked from completely different fields.

 

Does anybody know of genetic studies being done for VS?

[Ghormeh Sabzi]

There are some flaws with their definition of VS and how (they think) it is unrelated to the intake of drugs. When they carried out a large survey (I was one of the people they interviewed) afterwards they said if you had not taken drugs one week prior to onset, then symptoms were unrelated to drugs. I, you and many others on this forum will probably disagree with that.

 

But they used a very specific set of patients for their study (introducing a bias towards migraine, people who had not taken drugs and other qualifications).

 

I understand they will be using the results of these scans to propose some possible treatments.

 

There are no genetic studies - we can be the first with that! If we can find some genetic markers for HPPD then we can transfer that over to the VS community and see if the markers relate.

 

I believe approx 3 years ago Dr. Abraham was planning to carry out research to find genetic markers for HPPD but he could not get the funding. He may have some ideas of which genes are involved but I'm not sure how willing he would be to help unless $$$ are provided to supplement his retirement fund (maybe I am cynical).

 

I have studied a small amount of genetics this academic year but next year there will be a lot more to study - so I am interested in the 23andme idea from both aspects. 

[VisualDude]

It's kind of annoying the limitations we need to work with.  23andMe and other companies predefine which SNPs they test.  This is generally based on which ones have any research regarding them - which makes sense.  At this time, getting entire 3 billion pair sequences is too costly ... although it should be below $1000 soon (that's too costly for nearly all of us still).  Also, at this time, entire sets wouldn't help much since nobody has been working with them.

 

So its like technology.  The longer you wait to jump in, the better the initial purchase will be.  With early hobby computers (shortly before the 'PC'), memory was sold in 1K cards for a lot of money.  Now you get 1G chips for a fraction of the cost.  However, there is over 30 years between the two.  Most of us don't want to wait 30 years before getting more help.

 

But with over 600,000 SNP pairs, we have a lot to work with.  And many SNPs are picked because they have ended up being the most disease/disorder part of a whole sequence.

 

Do you know any more about Dr A's marker search?

[Ghormeh Sabzi]

Here is something from the visual snow forum:

 

 

 

Just got off the phone with Dr. Abraham  ......He is super smart, he is currently conducting a trial study and his studies have
shown that in 50% of his patients in the study have found that all symptoms went away within an HOUR of treatm...ent, but
that was for only 50% -- He also had very hopeful news, he said that in all of his studies and treating patients with our condition,
also watching them over time etc, that half of them found resolution and eventually visual phenomena went away. But, this was
for the HPPD cases. I am not an HPPD sufferer since I have never used illicit drugs but my symptoms are very similar. He also
said that their research studies are showing that it may not be the drugs at all for the HPPD sufferers, they are finding that
there is a defected gene. It may be that we were born with a defected gene!!! Actually he said there was evidence. Also, he
mentioned that for the trial study the meds work to help the defected gene. And lastly, he talked about how our symptoms are
not a disease, but rather a syndrome. Meaning for example, people who have for example a fever, the fever is not the disease, it is a sign/symptom. Same with visual snow, it is not a disease in itself, it is a symptom. So, as of right now his theories are that we are born with a defected gene that makes us suseptible to visual pathway disturbances, and if certain things are thrown into the mix we can alter the brain. For example, I was born with a defected clotting gene called Factor V Leiden. This just means that I am more likely to have a blood clot then someone without the defected gene. It also means that because I have this I am highly recommended not to smoke or take birth control because those things naturally increase your risk for clots. So, if we have a say defected visual pathway gene (he told me the name of it but I forget) and if throw things into the mix it can cause a problem. Example, if I do in fact have this visual pathway defected gene and I took Paxil for 6 years it puts me at a risk for palinopsia etc. Then, for those that are VS lifers, it may be that they have BOTH defected genes and naturally just born with it. There are 2 genes associated with this and it could be some of us have 1 and others have both. Using the Factor V example, I am heterozygous for the mutation, so that means I only have 1 defected gene, some people are homozygous and can easily have clots without even taking birth control pill or smoking etc....Hope this helps.
pm:
Guys I also want to clarify, he specifically works with HPPD patients, he did mention that there were people that went to him and had further testing to show that there were other causes to their VS - such as brain tumor however he did mention that if you had a full workup, ex brain mri cat scan etc and are able to rule out the big, nasty things then you could be considered PPD (without the H) and there is still lots of research between people who have never used illegal drugs vs the HPPD sufferers - Pls know that all of this is still under investigation, LONG road ahead to confirm the defected gene but he specifically told me that there is evidence of a defected gene in the HPPD patients. Apparently he needs grants and so on in order to even move forward with this complex study to confirm the theories he cannot go in front of the medical board without granst and such, I hope that he receives funding, I know Im willing to pitch in!! I will give him Dr Schankin's number.

 

When I spoke to Dr. Abraham he confirmed that he was trying to get funding for research into the genetic marker.

 

There was a post I read a couple of years ago which said which named a gene he thought was involved but I remember when looking it up it did not seem likely as the gene was associated with a disease which we would know about. I can no longer find that post.

 

Maybe email him but he doesn't come across as too helpful unless you give him money.

[VisualDude]

Sound like the conversation was about the rs4680 G:G polymorphism, which involves over rapid removal of dopamine via COMT action.  I tested as A:A so should not respond to COMT inhibitors ... which I don't.  However I respond to Sinemet.  He hasn't done a Sinemet drug trial ... and would not likely do so without understanding a reason to do so.  He is focused on COMT and is (was) pursuing that ... probably doesn't even know that some respond to Sinemet by itself.

 

As for money, it makes the world turn.  Don't know the man so can't really comment on that aspect of his morality.  But most 'giving' doctors get used up fast ... and often taken for granted in the end.  An ugly reality.

 

But on the positive, we will do what we can.  And it is encouraging to find another group (the VSers) that are actually working on the same thing - PPD.  Ironic for this thread, visual snow is not one of my symptoms (just mild and specific stuff) ... and I don't know if those who have responded to Sinemet have had their snow improve (and if they had snow either).