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Medication Trial: Dr. Abraham


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The results were published a couple of weeks ago. I spoke with him on the phone yesterday. He is going to scan the published results summary and email it to me. From this hopefully we can find which journal to locate the full results in. I imagine he will email me at the start of next week. I will post the results on the forum.

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The results were published a couple of weeks ago. I spoke with him on the phone yesterday. He is going to scan the published results summary and email it to me. From this hopefully we can find which journal to locate the full results in. I imagine he will email me at the start of next week. I will post the results on the forum.

Yes, Yes, Yes !!! (and thank you)

I've been salivating for this so long I fell asleep

slobber.jpg

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I am so excited!

I hope he will comment on why not everyone respond to the treatment and if he has any idea of the mechanism of action as well as the best treatment option (like if a inhibitor is important to the success and dosing etc.) However this is a great thing to be able to show the docs as well a step further to understanding HPPD

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No email yet. If he doesn't send it by the weekend I'll chase him up.

Since the results have now been published, I don't suppose there's much harm in revealing the drugs involved. From what I understand through this forum, they are levedopa and Tasmar. One dose only.

Dr. Abraham has in the past told me that about a third of patients responded to the medication with about a 75% improvement in symptoms.

Tasmar is very hard on the liver, and so is not a viable long-term solution to those with HPPD. Levedopa also has long-term side effects. But this trial shows that dopamine clearly has a role to play in this complex disorder, for some people at least.

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I hope this isn't getting those people with no response down. I am glad that i am one of those who has that 75% inprovement. Keppra and Clonazepam takes care of the rest. Seems legit. I wonder though what the bext step with this knowledge is. Does it mean that there are subtypes of HPPD or that we can atleast distinguish two areas where the fundamental "injury" is located and if there is something in the symptom description of those who got relief vs. those who didn't that can give the researchers a clue what that would be.

I find it crucial to find out why only 1/3 statisticly get relief.

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945. Catechol-O-Methyl Tranferase lnhibition Reduces Symptoms of Hallucinogen Persisting Perception Disorder

Henry D. Abraham

Psychiatry, Tufts University, Boston, MA

Background: Hallucinogen persisting perception disorder (HPPD) is a poorly understood disorder arising from the use of hallucinogens. It is characterized by continuous visual disturbances which can be lifelong. There is no known treatment. 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. Accordingly, I hypothesized that inhibition of COMT would reduce symptoms in HPPD.

Methods: A single-dose, open label trial of a tolcapone, carbidopa, and L-dopa was conducted in 17 consecutive HPPD subjects. Visual symptoms in

each subject were coded on a 0 to 7 Likert scale before, and two hours after, drug administration. A paired Student t-test was used to determine statistical significance.

Results: The mean pre-drug visual symptom score for the entire sample was 4.7 +l- 2.6, compared to the post-drug score af 3.7 +l- 2.8 (P= .001). A post hoc median split of the percent response of each subject was 51% symptom reduction in the upper half of responders compared to 1% in the lower half, suggesting a bimodal sample.

Conclusions: Inhibition of COMT is a novel approach in the treatment of HPPD. The bimodal treatment response is consistent with the action of a functional polymorphism in the COMT gene. Future directions include a double blind, placebo controlled trial of this treament and a determination of COMT polymorphism in responders and non-responders.

Keyword(s): HPPD, COMT, tolcapone, carbidopa, DOPA

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thx mate. but i read this stuff is really dangerous. it was forbidden in europe for 6 years. since 2004 its possible to getit pescribed for parkinson again but no doc wants to pescribe it because of its sideeffects.

so lets take it as a step forward into finding the cause but that will never be a possible treatment.

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Yes, its side effects outweigh any benefits. There was talk that Dr. Abraham wouldn't let anyone do the trial unless they had a liver test. Its side effects were also the reasoning behind the secrecy of the drugs used in the trial. But it provides useful information in relation to the disorder, and provides information for the possibility of other drugs that may work. I think the trial was to find out information about the disorder, rather that to propose a treatment option.

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Just to give you my perspective on the drug(s): Dr. A said they were intended for use in an acute situation, sort of like how people might use Xanax. He gave me the example of when someone had a lot of reading to do and needed their vision improved for a couple of hours or for driving.

Personally I felt barely anything from it, but perhaps the fact that I've been suffering from a messed up klonopin cut (part of the reason I went to see him -- to validate to my doc that I had HPPD so she would stop trying to get me off) had something to do with it.

I don't think the drug is intended as a longterm "solution" like klonopin, rather as something to temporarily alleviate symptoms. The only thing that would be promising immediately would be possible mechanisms for targeting different systems (Dopamine in this case) as opposed to blanket GABA bombing.

The subtype issue is an interesting one. I'm certain we suffer from different degrees and categories of not only visual but also somatoform (physical) symptoms.

Ghormeh, did you just call him up to ask him about the study? I'm still waiting on his reply to my email. I'm assuming that's not gonna happen.

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I wonder if entakapon, the other COMT-inhibitor could be just as useful. It wont stress your liver. I know that Tasmar (tolkapon) is harsh on the liver, although its a last resort in PD, i would take it if my neuro would accept it. Hands down. A healthy liver tolerates Tasmar, atleast for some years with monitoring but the real hazard is if there is just a slight issue with the liver. Potentially lethal.

But if entakapon, which is a part of the med "Stalevo", would work it would be great. Then you have a pill that consist of a COMT-inhibitor, carbidopa and l-dopa all in one. However, there must be a reason why Doc. A choosed Tasmar in the trial.

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Personally I felt barely anything from it, but perhaps the fact that I've been suffering from a messed up klonopin cut (part of the reason I went to see him --

Well, i had little effect of levodopa alone when i cut my Clonazepam. As soon as i stabilized it had and still have a tremendous effect on my symptoms. Cannot imagine a day without it.

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