Jump to content

Medication Trial: Dr. Abraham


Recommended Posts

I psyched myself into believing that Sinemet actually was doing anything positive for me. After I read what the other drug was in this thread it got me very curious with wondering if it's the key to allowing other meds to do their job in the brain. I got absolutely nothing from Sinemet by itself and nothing from Keppra by itself.

My next bet was to try Flunarizine but now I really want to see if this COMT inhibitor would do anything for me.

Link to comment
Share on other sites

Visual> Just wanna add that it was during WD, just like Rollinggreat, that i didn't benefit from sinemet. If i would only take Sinemet without Clonazepam post any other WD symptoms things might have turned out different.

Thanks -- Just wanted to clarify ... it is most helpful to everyone for each to put all their cards on the table.

Tasmar isn't something you can use for a long period of time without damage to the liver. It's not worth it. The study was never meant to reveal a long-term medication for HPPD.

Tasmar can clearly be used safely. http://www.ncbi.nlm....pubmed/17909307

"Tolcapone ... generally well tolerated, with the most common adverse events being dopaminergic related. However, clinical trials demonstrated dose-related increases in liver enzymes, and postmarketing surveillance noted 4 cases of acute hepatotoxicity with 3 fatalities that were attributed to tolcapone. For this reason, the drug was withdrawn from the market in some countries, and its use was severely restricted in the United States. An analysis of safety data indicates that, since the labeling restrictions in 1998, there have been more than 40,000 patient-years of tolcapone treatment worldwide, with only 3 reports of severe, but reversible, liver injury and no reports of hepatic fatality. It can be concluded that severe liver injury due to tolcapone is a rare event. Based on these data, the drug has been reintroduced to the market in several European countries, and the Food and Drug Administration in the United States has modified monitoring requirements. The new labeling recommends monitoring of liver function every 2 to 4 weeks for 6 months and at the physician's discretion thereafter. In addition, patients must be taken off the drug if blood tests show enzyme elevation of greater than twice the upper limit of normal."

Another thing to keep in mind is that most people with advanced Parkinson's are elderly - those with weakest organ/biological functions (bluntly: being old is pre-death). These are the ones using Tasmar.

Lastly, a few years ago I had elevated liver enzymes from a product (cough syrup) with acetaminaphen (Tylenol) - something VERY common. This OTC pain relief is massively consumed in the USA with about 100-200 yearly deaths from liver failure. Aspirin and ibuprofen are easy alternatives without the hepatotoxity of acetaminaphen. So without knowing it, most of us are facing 'liver dangers' all the time.

7597W.jpg

The most likely problem with Tasmar is affording it. Most insurance companies don't cover it. At about $3 per pill most people won't OD it, lol. Generics may become available starting as soon as this December.

There are a couple important reasons for a person to try Tasmar. First, if you do not respond to Sinemet (or respond weakly), then a trial will give you more info: How much of your HPPD involves dopamine? Does it significantly help you?

The second is: "Tocapone ... may determine a significant improvement in cognitive resources of patients" http://www.ncbi.nlm..../pubmed/9451720 . For some of us, visuals are minor compared to other cognitive functions - visuals stink but the other is crippling. Addressing the later is important for these people.

Tasmar targets (passively) the prefrontal cortex and may address what is most frustrating. Dopamine is eliminated by DAT (reuptake mechanism) and COMT (breakdown). There is very little DAT in the prefrontal cortex - the area accredited with most our symptoms. It is already known that COMT polymophisms are connected with problems such as developing schizophrenia later in life. So this is a significant area ... one that Dr A chose to target for HPPD treatment.

Frankly, this info does bother me ... It is exciting to find a possible key ... And it is frightening to need a med that must be closely monitered and can't afford. I seriously consider a few weeks trial even though low dose Sinemet does a lot. Since some symptoms have permanently improved (such as frame-rate) with Sinemet, will others improve on a lasting basis with temporary dosing of Tasmar?

This raises other questions: Am I the only one with lasting improvement? Or have others not reported this since almost no one has tried taking Sinemet for a while? Just as with the hepatotoxicity issue, this is all individualistic.

One thing for sure: Do NOT take Tasmar without getting liver enzymes monitered repeatedly. This will likely mean no internet purchasing unless you are going to regularly get blood tests some how.

Link to comment
Share on other sites

Visual>>

Great info right there! Just one thing i didn't get about the schizo thing, i read it as we could be more vulnurable to schizoprenia due to the COMT-thing? Or is it that people with COMT-issues pre-HPPD are in the risk zone? If there is something i fear more the HPPD its schizoprenia.

Link to comment
Share on other sites

Many people with DP, DR and HPPD fear schizophrenia. Afterall, we have altered/distorted visual perceptions. I was a little concerned about trying dopamine agonists ... would it flare symptoms since schizophrenia is treated by reducing dopamine? So have taken comfort that Sinemet didn't make me 'mad', lol.

Dr A wrote: "Studies of HPPD patients with qEEG mapping show that the disorder is represented by disinhibition in the cerebral cortex. Inhibition of catechol-Omethyl transferase (COMT) increases inhibition of sensory input in humans carrying the G/G polymorphism"

I do not know what the G/G polymorphism is ... is it the same as val/met or val/val? These two functional polymorphism substitute 1 or 2 valine (val) aminos for methionine (met) in gene expression. The val substitution is 4 times more effective in breaking down dopamine, thus 'rarification' of dopamine occures. There is a correlation between these polymorphisms and developing schizophrenia later in life. Confusing to me is, this ploymorphism reduces dopamine, so why would schizophrenia be treated by further reducing dopamine???

Dr A also wrote: "and a determination of COMT polymorphism in responders and non-responders". Genetic testing would be beneficial for HPPD research. Do all of us on this forum have this altered gene expression? Or just the ones who respond to Sinemet (and the like)? Or any of us?

Now remember, Parkinson's disease, Tourette's, and Schizophrenia are major disorders of dopamine 'processing' - but there is nothing similar between these 3 disorders. So too with HPPD. Distortions are not the same as Delusions. And there are a few members around who have had HPPD for 10, 20, or 30 years - they don't report needing dopamine antagonists (which schizophrenics must have).

Link to comment
Share on other sites

i have a few questions because i havent the time to research alot these days.

do you think these findings suggest that HPPD is a gene problem?

is there a problem with our COMT-gene? i read on a german site, that there are assumptions shizophrenia "triggered" by cannabis is caused by a problem with the COMT-gene.

and if so, is there a possibility to affect these gene without "hardcore" drugs like these COMT-inhibitors?

Link to comment
Share on other sites

Until a bunch of HPPDers get gene testing done, we don't know about the connection with genes. What we do know is most people who use drugs do NOT get HPPD.

It is curious that cannibus use before age 20 has been linked with schizophrenia. Some types (Skunk) have been singled out as being more troublesome. Seems to be lots of Google hits for cannabis schizophrenia COMT such as http://www.sciencedaily.com/releases/2012/05/120508112748.htm.

Is there a possibility to affect these gene without "hardcore" drugs like these COMT-inhibitors?

Tasmar doesn't change genes, it (somehow) reduces the activity of (or how much there is of) "catechol-O-methyltransferase" - the stuff the COMT genes make which breaksdown dopamine. Basically anything that increases dopamine will affect dopaminergic synapsis. Tasmar MAY better target the part of brain they THINK is mainly responsable for our symptoms - plenty of IFs and MIGHT-BEs. Too bad we can't just drink a lot of prune juice to purge our toubles away...

Link to comment
Share on other sites

Until a bunch of HPPDers get gene testing done, we don't know about the connection with genes. What we do know is most people who use drugs do NOT get HPPD.

yeah thats true, but i think its impossible to get all genes checked so there must be a selection of genes which could be involved and i could imagine this finding could encircle maybe a few possible genes.

like there are a few other meds which seem to have an effect on some people like flunarizine maybe this is also helpful to isolate possible involved genes.

Link to comment
Share on other sites

Thanks for the info Visual, it is great to have you on this site.

It appears I may have overstated the dangers of Tasmar, I must admit I have only researched it a little. Some of my info comes from Dr. Abarham ... one member said Dr. Abarham said there 'would be blood on his hands if the medication was revealed', hence the secerecy. Dr. Abraham also told me it was not a long term solution to HPPD because of side effects such as damage to the liver, or if not liver then other side effects. I cannot remember fully. But what he did say was that it's use, if any, was to allow someone to occasionally take a break from HPPD, when driving at night for example. So it would be taken on an as needed basis. But perhaps he has overstated the dangers of Tasmar as well.

But nevertheless, I would still be concerened with taking Tasmar for a long period of time. It can clearly, in rare cases, do damage to the liver, and so over a long period of time it could do damage to the liver in the same way that alcohol might, for example. But as with alcohol, it may not show up on any tests until significant enough damage is done. I don't know the long term effects, and so this is just speculation on my part.

Additionally, Tasmar has to be taken with Sinemet, and will therefore increase blood levedopa levels, and so potentially increase the chance of side effects associated with dopamine boosting medication. This is a great cause for concern.

Tasmar has been studied thoroughly in clinical trials. In these studies, the side effects that occurred in a group of people taking Tasmar (along with carbidopa-levodopa) were documented and compared to side effects that occurred in another group of people taking just carbidopa-levodopa (without Tasmar). As a result, it was possible to see what side effects occurred, how often they appeared, and how they compared to the group taking just carbidopa-levodopa.

In these studies, the most common side effects of Tasmar plus carbidopa-levodopa included:

  • Involuntary body movements (dyskinesia) -- in up to 51 percent of people
  • Nausea -- up to 35 percent
  • Sleeping problems -- up to 25 percent
  • Loss of appetite -- up to 23 percent
  • Uncontrollable, sustained muscle contractions (dystonia) -- up to 22 percent
  • Excessive dreaming -- up to 21 percent.

Other common side effects (occurring in 1 to 20 percent of people) included:

  • Muscle cramps
  • Drowsiness or fatigue
  • Diarrhea, constipation, abdominal pain (stomach pain), or vomiting
  • Headaches
  • The flu or upper respiratory tract infections, such as the common cold
  • Increased sweating
  • Dry mouth
  • Urine discoloration
  • Loss of balance
  • Gas
  • Increased muscle movements (hyperkinesia) or decreased muscle movements (hypokinesia)
  • Chest pain
  • Unusual sensations, such as burning, pricking, or tingling
  • Arthritis, stiffness, or neck pain
  • Bladder problems
  • Sinus congestion
  • Hyperactivity
  • Hair loss
  • Blood in the urine.

Many of these side effects are caused by carbidopa-levodopa, not by Tasmar. However, this is of little importance because Tasmar is always used in combination with carbidopa-levodopa (it is not effective at treating Parkinson's disease when used by itself). Also, because the drug increases the level of levodopa in the blood, Tasmar may increase the risk for or worsen the side effects of carbidopa-levodopa.

http://parkinsons-di...de-effects.html

Cases of severe hepatocellular injury, including fulminant liver failure resulting in death, have been reported in postmarketing use. As of May 2005, 3 cases of fatal fulminant hepatic failure have been reported from more than 40,000 patient years of worldwide use. This incidence may be 10- to 100-fold higher than the background incidence in the general population. Underreporting of cases may lead to significant underestimation of the increased risk associated with the use of TASMAR (tolcapone) . All 3 cases were reported within the first six months of initiation of treatment with TASMAR (tolcapone) . Analysis of the laboratory monitoring data in over 3,400 TASMAR (tolcapone) ­treated patients participating in clinical trials indicated that increases in SGPT/ALT or SGOT/AST, when present, generally occurred within the first 6 months of treatment with TASMAR (tolcapone)

---

Although a program of periodic laboratory monitoring for evidence of hepatocellular injury is recommended, it is not clear that periodic monitoring of liver enzymes will prevent the occurrence of fulminant liver failure. However, it is generally believed that early detection of drug-induced hepatic injury along with immediate withdrawal of the suspect drug enhances the likelihood for recovery. Accordingly, the following liver monitoring program is recommended.

http://www.rxlist.com/tasmar-drug.htm

To anyone thinking of taking Tasmar (called different things in in different counties, but the actual name is tolcapone) - please make sure you do your research of side effects (of levdopa/cardidopa as well as Tasmar), and regularly get you liver tested. Having posted the study, I'd hate to be partly responsible for something bad happening to someone.

----

On a side note, there is also some more interesting research in the UK which I will post about at a later date once I have an appointment at the research clinic (just waiting for the NHS to agree to fund me). I don't know much yet, but I was told by the doctor over the phone that those with visual snow etc perform differently on tests to those who do not have it. On some tests, they do better, and on others, they do worse.

Link to comment
Share on other sites

Also, following on from the discussion above, Dr. Abraham told me a while back that he was trying to obtain funding for research into a genetic marker. Someone on the visual snow forum even said they had identified a gene. I asked for an update in relation to that in my last email to him. He replied, but not to that specific question. If anyone speaks with him, then that's something you might want to bring up.

Link to comment
Share on other sites

yeah thats true, but i think its impossible to get all genes checked so there must be a selection of genes which could be involved and i could imagine this finding could encircle maybe a few possible genes.

like there are a few other meds which seem to have an effect on some people like flunarizine maybe this is also helpful to isolate possible involved genes.

Yes, we don't know what genes to check. However, Dr A has opened the door on testing COMT polymorphisms. Probably only useful for research - how would it really affect treatment?

So Visual you're saying that Tasmar can be taken safely for longer periods of time while being monitored by a doctor and having regular testing/check-ups done?

That is what the article said. It remains to be seen what long term consequence for having elevated liver enzymes - doesn't make me feel comfortable. But is rather stands in contrast to Tasmar being some sort to "death drug".

Many meds raise liver enzymes. I have seem people die from liver failure ... it is terrible. But it isn't the norm. Taking a drug like Tasmar without monitoring is playing russian roulette. And a poorly functioning liver can contribute to brain damage.

Flat out, what is the truth about all medications. In this country people are all excited about taking statins. Yet these drugs raise liver enzymes. They also can cause muscle weakness and wasting. A friend of mine has an atrophied heart from Lipitor. Know of a doctor whos wife died within a week of starting Lipitor ... from Lipitor.

People take Fosamax to reduce osteoperosis. Yet it is known to eat a whole in your stomach, cause your teeth to fall out and your jaw bones to literally rot.

The list goes on and people are influenced by ads. The reason meds are available by prescription is that they are dangerous for some, if not all.

How about this parital list of Klonopin side-effects: serious dysphoria, Thrombocytopenia, serious psychological and psychiatric side-effects, induction of seizures, personality changes, behavioural disturbances, confusion, ataxia, psychosis, incontinence, liver damage, depression, disinhibition, sexual dysfunction.

Additionally, Tasmar has to be taken with Sinemet, and will therefore increase blood levedopa levels, and so potentially increase the chance of side effects associated with dopamine boosting medication. This is a great cause for concern.

If a person doesn't need increased dopamine, doing so can cause problems. Even if a person does need increased dopamine, they can suffer side effects. Most 'psychiatric' drugs are needed only in part of the brain. Treating the whole brain causes problems - but you can't treat just parts of the brain.

Some of my info comes from Dr. Abarham ... one member said Dr. Abarham said there 'would be blood on his hands if the medication was revealed', hence the secerecy. Dr. Abraham also told me it was not a long term solution to HPPD because of side effects such as damage to the liver, or if not liver then other side effects. I cannot remember fully. But what he did say was that it's use, if any, was to allow someone to occasionally take a break from HPPD, when driving at night for example. So it would be taken on an as needed basis. But perhaps he has overstated the dangers of Tasmar as well.

Taking a break from HPPD is interesting idea. Jay reports doing this with Klonopin on occasion.

What is hard to define is "as needed". Most people drive some a night every day in the winter. Others report not being able to read from HPPD ... would you not need to read to stay employed? All this depends on how bad a person suffers or is disabled. There is nothing ideal about facing the decision of using a harsh medication. I will not deside for some time - even though I took one dose.

I find myself looking for meds to try briefly in some sort of rehab way. But this may be a holy grail.

Having posted the study, I'd hate to be partly responsible for something bad happening to someone.

You cannot be responsible for what others do. You are just another anonymous person on the internet. Perhaps Dr A would be more concerned about what he says because he has a huge positive reputation behind him that some might take as an endorsement (which it is not) when all he is doing is testing a theory. Tasmar as been rumored for some time. And until publicly published, it is still a rumor.

But nevertheless, I would still be concerened with taking Tasmar for a long period of time. It can clearly, in rare cases, do damage to the liver, and so over a long period of time it could do damage to the liver in the same way that alcohol might, for example. But as with alcohol, it may not show up on any tests until significant enough damage is done. I don't know the long term effects, and so this is just speculation on my part.

Yes, that is a problem. What do you do if your liver enzymes remain elevated even if you quit a med?

This also highlights a paradox: a number of members feel it is safe to binge drink. Others feel that weed is safe - even though it is mentioned in research in context of COMT polymophism problems.

There is no easy answer. However if 50% of people eventually recover from HPPD, then waiting it out would be the first thing to do.

Link to comment
Share on other sites

Yes, we don't know what genes to check. However, Dr A has opened the door on testing COMT polymorphisms. Probably only useful for research - how would it really affect treatment?

Even if this has been a one dose only, it might be that some need to take it for a longer period. It would be a real mindbender if those who respond to the treatment has a different setting of polymorphism then other HPPD:ers. Or that everyone with HPPD symptoms have a common setting against a control group.

Anyway, does anyone know yet where this was published? My doc would probably need a reference to check out for herself.

Link to comment
Share on other sites

Yes, we don't know what genes to check. However, Dr A has opened the door on testing COMT polymorphisms. Probably only useful for research - how would it really affect treatment?

in my opinion there are maybe a few diffrent genes involved. there are a lot of diseasses which are caused by diffrent gene defects, but with the same symptoms.

also maybe in future gene therapy is able to help if the gene is detected. and the most important point i am able to teach my children(hope i will have a lot of children^^) that they could get into big trouble by taking drugs. not in a form "anti drug parents" do and their kids do it because of their propaganda, but in a way of: "maybe you are predisposed to a fucking disorder which can mess up your life completly"

Link to comment
Share on other sites

As I said there is talk that Dr. Abraham has already identified one of the genes involved.

If anyone wants the PDF of the study, send me a PM with your email address and I'll send it to you. I don't think it has been published in any journal yet, although it was presented to a large group of professionals.

Link to comment
Share on other sites

  • 2 weeks later...

It's really hard for me to post this privacy is very important to me as I'm sure it is to all of you. I felt after reading this I needed to share it with you. I've already told dr.a about this as well. My child at a very early age around 6 told me in away only a child could express that at night in the dark he sees ants marching all over (visual snow) later years he expressed a concern that he sees colors flashing on his wall (I dont even have this) and images in the dark. He's young never tried drugs or even tasted alcohol and no anti depressants or add meds. This is passed down and I feel I need to share this with you because you need to know that it can be passed down.

I have posted before about myself but would have never about my child exept to let you know that your child never has to tuch a drug to get hppd. The hardest part for me is I have no answers for him. Dr.a said I better make sure he never tries a drug. Could you imagine. My husband is very well known in certain areas and has mastered life educationally but I do wonder because he is OCD if together we passed this down. I don't know may never know but there it is anyway. I really hope this helps in some way.

Link to comment
Share on other sites

I know I never thought I would pass this on to my child. It's one thing to know you did the drugs and this is the punishment but a complete other for someone who's done nothing. What will his life hold. It's really hard when I can't offer help and I know that it can make life very hellish.

Link to comment
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now
×
×
  • Create New...

Important Information

By using this site, you agree to our Terms of Use.