Ghormeh Sabzi

Very much so. Various parts of my body shake when put in certain positions. I have tremors in my hands and the palm of my left hand has had a 24/7 fasciculation for 2 and a half years. Curious.

Can you talk us through your symptoms and which ones improved?

I take a flupirtine (indirect NMDA antagonist) and Keppra combination which helps my symptom of pain somewhat. I associate the pain with HPPD. It does nothing for the visuals.

I got some from DocSimon.com approx 2 years ago which arrived here in the UK without problems. I never tried it in the end, though. Still tucked away in the drawer!

The site has various bugs. Some have been fixed thankfully.

Annoyingly I only just the other day received a notification of a PM which I received in March. 

I think people have offered to help out David in the past, but as far as I am aware no offers have been taken up.

http://www.telegraph.co.uk/news/uknews/10878625/Fasting-for-three-days-can-regenerate-entire-immune-system-study-finds.html

I'd love to hear details of the qEEG.

 

I am still experimenting with T-DCS and knowing which parts of the brain are over/under stimulated would be very helpful.

Check out the recent study with regards to visual snow and hypermetabolism in the lingual gyrus. 

I don't see this as any less likely to help than visiting a spiritual healer in Brazil, Jess.

A chemical brain injury - what do you even mean by that? It's so vague that it is an essentially pointless term. Everything is chemical. 

If you mean a lack of or misappropriation of neurotransmitters (is that what HPPD is?!) - well neurofeedback has been shown to improve the symptoms of Parkinson's.

Oh, and have you seen this thread? http://hppdonline.com/index.php?/topic/3665-temporary-visual-snow-treatment/ - how can watching a video for a couple of minutes temporarily correct a chemical brain injury? 

It may also cause kidney and bladder failure.

Uridine has anecdotally been associated with tinnitus. Taking uridine (for a few weeks) coincided with much increased tinnitus for myself which took ages to go away again after stopping uridine (although my tinnitus is now very minor again, I'm not sure it every returned to baseline). Other than that I noticed nothing from it.

Rhodiola rosea increases serotonin. This was the first supplement I ever took and coincided with 'pre HPPD' turning into standard HPPD. I took it before fully informed about HPPD because I was feeling fatigued and struggling to study. I think my brain was in the process of going completely haywire when I took it.

Of course these can be coincidences, but need be mentioned nonetheless. I personally think uridine was more likely to have a negative effect on myself than rhodiola rosea.

Just a heads up - there's an additional charge of $79.95 for international shipping if you're not located in the US.

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.

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. 

Can you list your physical symptoms?  This might narrow down the class of med you would respond well to.

 

EEGs are usually 'normal' for HPPDers.  But it is good to have this test done.  qEEGs are EEGs with more mathamatical analysis applied.  These show differences associated with HPPD.  Not sure if they can take the EEG data and send it to be 'crunched' or if you have to do it as its own proceedure ... but it is worth asking.

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

http://hppdonline.com/index.php?/topic/3849-the-relation-between-migraine-typical-migraine-aura-and-visual-snow

I was going to reply why genetic testing can be controversial but Visual has done all the hard work for me .... cheers!

I'll be sure to get myself tested in June. Well done for getting this started.

No, no, no, no, no, no, no, no, nope.

No. No. No.

No.

Look into bupropion.

It was posted on the VS Facebook group.

Here's a longer version that some people are trying and are saying the longer they look the longer their symptoms stay away for:

It's quite annoying though. I'm sure there's better videos out there.

I'd be interested to see if it would work with a VS simulator - I haven't had a chance to try it out yet.

no but i wouldn't dare! i know that anxiety is half my problem, and just the thought of taking a hallucinogenic makes my heart feel like its trying to jump out of me haha 

MDMA has hallucinogen properties. 

You're back here after some of your symptoms returned. You really think use of drugs has nothing to do with that?

Just stay away from all drugs. It's the ONLY sensible choice.

Watch this video on YouTube in full screen:

Now look around the room. Does your visual snow improve?

For me all the dots stop moving for 30 seconds - a (very) temporary, yet very interesting, treatment for visual snow.

I would like to think the published articles I have read will have ensured active ingredient concentrations are reliably within certain parameters, yet they detail significant differences in effectiveness of (multiple?) brand v generic Keppra. I would suggest that inactive ingredients aren't always technically inactive, because tablets can contain substances to allow for better absorption of active ingredients, for example. 

I even upped my dosage and my symptoms did not get better, yet very quickly after switching back to generic Keppra my symptoms subsided again, suggesting significant differences, regardless of the reasons for those differences.

Yet I confess comments are based on very limited research I carried out when switching between the products, but it is certainly an interesting discussion and something I'd like to research in more detail when time allows, which would also allow me to speak with more authority. As you suggest I'm sure things aren't always as rosy as we think. Here in the UK we like to think things go through strict processes before products can reach the market, but things surely do slip through the net from time to time, as last year's horse meat scandal demonstrates. 

I have temporarily abandoned talkppd.com because it didn't turn out as I hoped and I haven't had the time to push forward with it. But I will revisit in the summer when I have the time and will try and make it successful with some new ideas so that it becomes active. I haven't logged in or commented for a while because I am working a lot and I am also trying to focus on my studies, but I do visit these forums occasionally to see what's going on. 

Under EU laws active ingredients have to be within certain percentages but there will be slight differences. But effectiveness of medications can depend on other things such as how the tablets are pressed, how the active ingredient is released, what else is in the tablet, etc.

I also read some articles that suggest that brand Keppra is more effective than generic for epilepsy.

I have a private prescription, but normally you would only pay a small prescription charge in England, with the NHS covering the rest of the cost. The NHS provides the much more expensive brand Keppra rather than the generic version, which says a lot, I think.

I've been using Keppra in combination with flupirtine to control symptoms of pain which I'm convinced is intertwined with my HPPD. I switched to the generic version briefly because it is a lot cheaper but my symptoms returned and so I had to switch back to the brand Keppra, at which point my symptoms subsided again. 

I thought it useful to post this information to demonstrate differences between different versions of levetiracetam.

First I've heard of it and, like Visual, do not understand the reasoning behind such thoughts.

I am still on a combo of flupirtine (NMDA antagonist properties) and Keppra which has reduced my worst symptom (pain, which increasingly seems connected to my HPPD) by 70-80%, which has allowed me to continue with my studies. There is no change in any of my other symptoms (except possibly tinnitus, which I rarely notice these days). However, I don't want it to be a long-term solution for a few reasons and so I will explore other options in the summer when my exams are over and I have a break.