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Medication Trial: Dr. Abraham


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I have been suffering some pretty heavy depression, frustration,anxiety and insomnia for the last several months, which the depression and frustration was very new to me

I would be interested to hear what meds (and their response) that you have tried.

Have you tried anything to increases dopamine levels?

The thing is, I haven't taken drugs at all. After the effexor debacle, I have been mortified for years to try anything besides a Klonopin here and a xanax there. Have you tried anything that has helped you in the dopamine arena? Anything for depression at all that has really helped and not caused an upheaval in symptoms? For over 14 years I suffered drug free with all the hope in the world. This depression crap is like stabbing a burn victim...

Jay,

no addictive qualities, nor upping doses, however, like I said, it is supposed to be a spot treatment drug anyway.

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The thing is, I haven't taken drugs at all. After the effexor debacle, I have been mortified for years to try anything besides a Klonopin here and a xanax there. Have you tried anything that has helped you in the dopamine arena? Anything for depression at all that has really helped and not caused an upheaval in symptoms? For over 14 years I suffered drug free with all the hope in the world. This depression crap is like stabbing a burn victim...

Jay,

no addictive qualities, nor upping doses, however, like I said, it is supposed to be a spot treatment drug anyway.

Have you tried anything that has helped you in the dopamine arena?

Requip, Selegiline, Sinemet, and Wellbutrin SR.

All of these have been beneficial for: visual symptoms, anxiety, insomnia, depression (anhedonia)

Anything for depression at all that has really helped and not caused an upheaval in symptoms?

If I take more than 75mg / day of Wellbutrin SR, then there is agitation and migraines, though it works wonders with visual symptoms. Presumably the problem is norepinephrine – too stimulating. So if you try this, start with small amounts. Don’t get Wellbutrin XL because you can’t break the pill smaller. Wellbutrin SR is usually a 150mg pill. Start with ¼ pill and only take in the morning. Increase after a week if you wish. If it becomes too strong, stop for a few days and then restart with a low amount.

Otherwise, no upheavals from these meds

A little history,

Based on researching symptomology, I knew a D2 agonist would be worth trying. Asked several doctors for a trial of Dostinex (cabergoline) or Parlodel (bromocriptine), but got the usual polite resistance – ‘no, you’re just nuts’. One doctor said, "it would take a quantum leap of faith the get a doctor to prescribe [dopamine meds] for you".

Since there are anecdotal reports from people with Parkinson’s disease about Wellbutrin being helpful, I reluctantly asked for this. (After all, many doctors dole out antidepressants like candy.) Got it but was pissed since I was convinced it was way too weak to do anything. It turned out to help a lot and in low doses.

Since there was very good response but higher (normal) doses caused problems, I got Requip. It was helpful but visual symptoms shifted a lot with the half life (how much was in the blood at any given moment).

So tried Requip XL (which is 2.2mg) – this was ‘smooth’ but the dose too high. It didn’t cause any distressing symptoms, but vision wasn’t as improved as with Wellbutrin.

Finally, the ‘quantum leap’ doc gave me Sinemet 25/100 to try. This was the best. Even though it has a very short half-life (45 min) and thus expected a ‘rough ride’, it works more like charging a battery. I take ½ pill 2-4 times a day.

Sinemet is levodopa, which is fuel (precursor) for the brain to make dopamine. It is FDA licensed for Parkinson’s Disease and Parkinsonism. Occasionally docs will use it for RLS, etc. If you wish to try and your doctor is resistant, emphasize that you have a HPPD diagnosis and it may (in your case) involve damage to dopamine pathways (Parkinsonism). Also, you just want to try it for a couple weeks.

 

Now, the whole focus was visual symptoms. So the other benefits ended up being a huge bonus.

If you wish, I can explain the mechanisms involved and why I concluded that dopamine was necessary to try. But otherwise, this is plenty to think about and don’t what the post to run on and on and on...

 

For over 14 years I suffered drug free with all the hope in the world. This depression crap is like stabbing a burn victim...

Sorry that you are suffering so. Also, understand what this is like, though my ‘journey’ has only be 4 years of hell. Benzos and Gabapentin have been useful too, but it wasn’t until trying the dopamine meds that things began to repair – even when I stop for a while, the improvement is largely permanent.

 

Hope this is helpful. Sorry it is so long winded – but it seemed necessary to convey as much info as possible

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He arrived at a diagnosis by a serious of questions, and probably observations. To my knowledge there is no other way to diagnose hppd. Wish there was-then we wouldn't have to spend years of our lives trying to convince the doctors we aren't making this up!

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wind, if that was towards me.. no not my liver..

lucky me i quit when this lil knowen, organ behind ur stomach called a pancreas, im a well study of anatomy... and i never even heard of it, untill a 6 day f/ing vist to a hospital hehe.. no food, no water.......... just 2mg of morphine and 1mg of lorazepam.. in the water-electrolyite iv im sry if i mispelled, i do that shiet alot.

they said, if i didnt have anything to eat for 10 days, they had to stick a tube down my throat...

lil did they know... it had alrdy been 22.

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Boy,there is a lot of different information here and I have some trouble processing a lot of information. As a matter of fact I try to process as little information as possible. My Dad was a doctor, probably of Dr. Abraham's generation and those guys didn't do a lot of drugs and mostly they don't understand addiction. It's sort of like if you were studying cures for liver disease you would be way to busy to council the patient's in your study about their alcoholism and depression You might suggest AA or psychotherapy,but that would be all you had time for. It seems to me that HPPD is one of the most seriously puzzling brain problems you can have.

I'm 58 yrs old and I have kind of a settled life. I can't imagine being young with HPPD and all the drugs that are around and having to go to work and school and all that. I don't even drive, because my vision is really bad. I write music in my little condo in Nashville. I'm a retired Nurse. I also took so much acid in the late 60s and 70s. That it came back on me after an operation 2 yrs ago where there were complications that put me in a ptsd state when I couldn't breath for an extended period of time. Hard to explain, but when I left ICU I was seeing hieroglyphics on walls and in certain light it looked like people's heads were shimmering. I had barely seen a little of that if I didn't get enough sleep or is I was hungover, but it was very brief.

Anyway as usual I got way off track. I'm a recovering alcoholic and drug addict and that's actually in my favor. If a Dr tries to give me klonopin I know from countless experiences that I will abuse it the minute I get home. I take Clondine, Neurontin,wellbutrin, cymbalta. Cymbalta is the only SNRI that's not as bad on my eyes and it really helps me. Depression is another defect of the brain. Great. Wellburin used to make me nervous, but the colodine offsets that. They give it to kids who take ritalin also for the same reason. I used to believe that it's better not to take any medicines, but it has to be on an indiviual basis. I tried not taking them for a goodwhile and ended up in the hospital for 2 weeks.

Good luck to all of us on here. This is a tough thing to have and I wish everyone well. I think HPPD screws with our emotions too

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If you wish, I can explain the mechanisms involved and why I concluded that dopamine was necessary to try. But otherwise, this is plenty to think about and don’t what the post to run on and on and on...

Great great great post; I do want you to explain those mechanisms, if not asking too much.

Thank you!

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Great great great post; I do want you to explain those mechanisms, if not asking too much.

Thank you!

Oh boy, Pandora’s box, god help the readers… There is so much to convey and not sure where to start. [Will skip lots of ‘proofs’ and references. Will try to be brief and summarize/categorize/illustrate. And, of course, this is primarily about dopaminergic neurons which are only part of the problem.]

Roles of Dopamine:

Attention

Cognition (making choices and learning)

Memory

Mood (anxiety, depression, optimism)

Motivation (incentive, wanting, "creative drive of idea generation") and Emotional learning (punishment and reward)

Movement control

Perception (pain, time, smell, vision…)

Sexual function and gratification

Sleep

Working memory (reasoning, comprehension and learning)

Dopamine is highest in the morning when waking up (motivation) and lowest in the evening (sleep – low motivation)

There is a seesaw relationship with Serotonin (calming), which is lowest in the morning and highest in the evening. And taking medications that increase serotonin will lower dopamine [Note: read the prescribing info on most SSRIs and you’ll see they can cause Parkinsonism – symptoms like Parkinson’s disease, low-dopamine]. One mechanism involved is that there are some synapses that can bind with both transmitters but once serotonin is attached, it cannot take in dopamine. Also, quite simply this is just part of our circadian rhythm.

There are 5 know dopamine receptor types grouped in 2 families. D1 and D5 (D1 family) act directly (stimulate). D2, D3 and D4 (D2 family) act inversely (attenuate).

While there are many feedback loops involving all the neurotransmitters, dopaminergic neurons control glutamate and GABA levels/activities. Glutamate comprises ~40% of neurotransmitter activity. Glutamate is the bullet; dopamine is the rifleman. GABA suppresses neuronal activities [just take a benzo and you will understand]

There are also close ties with opioid receptors as well.

Unlike other neurotransmitters, virtually all dopamine in the brain is manufactured in one spot, the VTA (ventral tegmental area). [As an ‘artsy’ way of viewing this, since dopamine is about emotion and emotions are the core of being alive, think of the VTA as a ‘fountain’ of life flowing into the rest of the brain, and dopamine as ‘water’. (After all, life without emotion isn’t living)] Side point: as an example of feedback looping, ~70% of synaptic innervation of the VTA is by glutamatergic axons.

So what happens if dopaminergic neurons are not up to par. Dysregulation – overactivity (and over response) is some places, underactity (and under response) in others, and sluggish or stuck responces.

Disease/Disorder examples involving dopamine:

Addiction

ADHD (low)

Anhedonia (low)

Autism

Bipolar Disorder

Tourette’s syndrome

Parkinson’s disease (low)

RLS

Schizophrenia (high – ‘positive’ symptoms: delusions; low – ‘negative’ symptoms: anhedonia)

Social anxiety (low)

IMO, Dopamine’s major purpose is to regulate/adjust to situations. Dopamine "does not act like like a fast ionotropic neurotransmitter like acetylcholine, AMPA, NMDA or GABA but rather seems to modulate other receptor channels: activation of DA receptors alone does not induce large postsynaptic currents but modifies the cell’s excitability or the synaptic transmission of other neurotransmitters"

Analogy:

Plumbing: flow adjust valve

Electronics: volume control on radio (mechanical adjustable), transistor (electrically adjustable)

Examples:

There are D2 receptors on the back of each photoreceptor in the retina. This allows for ‘spot’ adjusting contrast (compare: take a picture indoors without a flash – some things will be well ‘exposed’, others will be too bright or too dark. Yet the healthy eye doesn’t have this problem)

Dopamine receptors on penis. This allows sexual sensations to be turned on or off. Furthermore (during ‘on’ cycles), D1 receptors facilitate erections (via parasympathetic system) and D2 receptor activities increase during the shift to seminal emission (via sympathetic system).

Dopamine controls learning via its control of glutamate. Normally glutamate activity is at a certain level, but to form new association (plasticity), it becomes ‘supercharged’ (~10 fold increase). This is cleverly regulated with dopamine. Dopamine is known to "enhance signal-to-noise ratio" – analogous to ‘choosing’. Increasing dopamine suppresses some activities (D2) and increases other activities (D1). [this is an exhaustive topic but note: Learning is highly dependant on emotional response (dopamine again), not rational choice.] Once more, dopamine is the rifleman.

Dopamine regulates testosterone: D2 > Prolactin (Pituitary) > testosterone production.

Dopamine regulates movement – note Parkinson’s in which dopaminergic neurons are badly damage (basil ganglia). Part of the movement control system uses acetylcholine and remains in tack, but the other part using dopamine is crippled – causing tremors, cog-wheeling, jerky movement. People with this disease not only shake but ‘get stuck’. In this case, dopaminergic neurons are involved in unconscious decision making (how to move).

Its use in visual processing is massive and thus a subject for other posts.

These are just a few to wet the appetite and build appreciation for dopamine’s functions.

No discussion would be complete without mentioning the Amygdala. This is a dopamine rich structure that some consider an extension of the basil ganglia. This is our ‘fight or flight’ processor – FEAR and ANXIETY. Most of us suffer a persistent anxiety that is hard to get under control. Over-activity here is involved - be sure to read up about this one.

Ok, what is the relevance to people with HPPD?

Many HPPD symptoms involve vision. Visual processing involves dopamine. http://www.visuospatial-cognition.org/publications/P11.pdf Google "dopamine vision", "dopamine visual processing", and various permutations.

Nearly all recreational drugs mess with dopamine circuitry either directly or indirectly. When these systems get overloaded, either there is injury (oxidative stress, excitotoxicity) or changes in synaptic connection/strength (plasticity).

So the goal is to repair and/or re-teach our pathways. By opening the door of considering HPPD to be a mild brain injury, doctors should start with the brain injury basics: control inflammation (excessively active areas) [benzos, antiseizures], stimulate suppressed areas, and begin brain rehabilitation.

Note: brain inflammation takes 10 months to resolve after the cause of inflammation is removed – TBI or chemical. If your ‘injury’ is from drugs and you continue to take them, the problem is aggravated and inflammation continues. Also, remaining in high states of emotion turmoil contributes to brain inflammation (by elevated cortisol and other mechanism). So it is important to get persistent anxiety under control. [An excellent book to read about what chronic stress does to the body is Why Zebras Don’t Get Ulcers]

Increasing dopamine MAY be useful here. Perhaps not as a first step, but somewhere along the line. Also, only low doses should be used – you don’t ‘rev’ a damage engine. [Disclaimer: Resolving ‘dopamine issues’ is not always so simple as taking agonists or antagonists. Take schizophrenia as an example – treated with anti-psychotics (anti-dopamine) to reduce delusional states, but this aggravates anhedonia.]

Unfortunately, many doctors just view our symptoms as anxiety and/or psychosis, thus only trying SSRIs, SNRIs, and anti-psychotics. This only helps a minority. (As a hypothesis, dopamine pathways overstimulated by drugs are going to be altered in a underactive state. These pathways need to be gently encourage – putting a derailed train back on tract).

Fortunately we have DNA (blueprint) and the bodies self-repair mechanism on our side.

Well, hope this helps (as a start laugh.gif ) …

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I don't think the treatment was meant to be a cure but to prove the theory on the drugs potential efficacy and direct researchers on where to go from here.

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No I am not taking the drug on an ongoing basis. The risk/reward is too great. Like I said it is a means of proving what the problem is and to move forward with tedesrch

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I took the trial about a year ago.. The visuals did decrease quite a bit, for a while, even for a few days i felt my vision was pretty similar to what it was pre-HPPD

but the risks are too great with the medication that is prescribed.. Perhaps when better parkinsons drugs come out, and there is a lot of research on that area.. maybe there will be a cure for HPPD..

But ths drug can seriously fuck up your liver it seems.. If taken improperly or even properly to the wrong person.. Anyways, it was great meeting DR, abraham.. He is a smart and kind man.

He told one good thing that has stuck on my mind though, that some of his patients include, Doctors, lawyers and investment banker.. Saying that HPPD isnt an obstacle of pursuing a normal life and career..

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I took the trial about a year ago.. The visuals did decrease quite a bit, for a while, even for a few days i felt my vision was pretty similar to what it was pre-HPPD

but the risks are too great with the medication that is prescribed.. Perhaps when better parkinsons drugs come out, and there is a lot of research on that area.. maybe there will be a cure for HPPD..

But ths drug can seriously fuck up your liver it seems.. If taken improperly or even properly to the wrong person.. Anyways, it was great meeting DR, abraham.. He is a smart and kind man.

He told one good thing that has stuck on my mind though, that some of his patients include, Doctors, lawyers and investment banker.. Saying that HPPD isnt an obstacle of pursuing a normal life and career..

For those who want to try if it works, there is supplemental L-dopa.. maybe it might help a small bit with HPPD.. although that is just a guess.

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Obviously, it has been a conscious decision for me to stay out of this discussion (for the most part). This is not because I am formally associated with any aspect of Dr. Abraham's work, but because I have experience working in the research and clinical landscapes and do not want to damage or potentially affect any ongoing research project because it does not benefit the community as a whole or HPPD members. I want to first say that I am very impressed with a few parts of this discussion:

1) Many individuals who participated in trial medication(s) have remained silent on the issue despite their discussion with me regarding their personal outcome. I know this is difficult.

2) Individuals who chose (as is your right) to discuss any treatment or treatments in your experience have pointed out a few key themes that should be repeated. First, all medications have risks and I am happy to see that these are discussed. My personal fear is that someone will decide on their own to try a new medication without supervision and harm themselves. The worst outcome is any person harming themselves whether it be taking a new substance being prescribed for HPPD, for example: individuals becoming addicted to a drug like clonazepam because they were using it from illicit sources and taking the drug in dose ranges (or with alcohol) resulting in addiction/etc or someone taking a trial medication or medication simply based on the recommendation of another member. We all have a unique brain chemistry, variations of a theme (HPPD has different flavors), and as a whole because we have HPPD we have shown we have a unique reaction to substances and should be careful with what we take. Not to be a hypocrite, I will admit that in the past I have not followed this advice and learned the hard way that I have only further compounded my problem in other ways. I am glad the reports are honest, do not exaggerate claims, and in many cases focus on some of the ways HPPD can be managed simply by knowing a few things:

A) HPPD does not have to control your life. I have spoken with perhaps a 1,000 individuals with HPPD including jobs requiring a high level of functioning, focus, and overall positive emotional outlook on their health including: high-rankingm ilitary officers, medical doctors, students graduating with highest honors, multimillionaires, mothers, and the list goes on.

B) The thread is discussing hope, even for those individuals reporting no effect with any trial medication.

C) The Dopamine Hypothesis. I started this topic off a few months ago in another section with hesitation, but decided to let it pass because the information is present in the scientific literature if you piece it together. I recommend any person wanting to get a "feel" for the complexity of the mechanism(s) of action with hallucinogens read an excellent paper by Dr. David Nichols, which is available along with many interesting literature articles at Erowid.org.

The link is: <a href="http://www.erowid.org/references/texts/show/6318docid5883">http://www.erowid.org/references/texts/show/6318docid5883</a>

Brief excerpt of timed writing exam asking about current psychological and pharmacological treatments and HPPD for degree

"The current standard treatment for the symptoms of visual disturbances and associated anxiety with HPPD is clonazepam. Clonazepam is effective at reducing symptoms and in many cases prescribed for long periods. In some HPPD cases, individuals are unable to drive at night or distinguish stars from visual static without the use of clonazepam. However, the potential for dependence and abuse is a concern if the patient has a history of substance abuse, but HPPD alone does not necessitate a diagnosis of substance abuse. Individuals with HPPD can be strongly adverse to new psychotheraputics and resist medication treatment. The discovery of a therapy providing the same type of amplification of the inhibitory transmitter GABA, as exists with clonazepam, but without dependence could be a breakthrough for this population. Areas including increasing dopamine in the ventral tegmentum, which projects to the limbic system, is one area to consider increasing inhibition in the system. The limbic system is strongly associated with lasting effects from trauma and the processing of visual information."

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I don't think the treatment was meant to be a cure but to prove the theory on the drugs potential efficacy and direct researchers on where to go from here.

I spoke (had a phone consultation) with Dr. Abraham. He mentioned that it is not a cure. And that the effect, if working, lasts for 2 hours. He is working on a hypothesis of another mechanism through another med that works through a different biochemical channel than klonopin. He said that if it works for a person then the benefit is that they get a couple of hours to do productive things, use a computor without the visual distortion for example. If it works on enough people then the mechanism is valid and more work would need be done to find a drug that would work for a longer time.

Currently in the trials, he said that it has affected positively 30 to 50% of the trial participants.

I was going to have a trial with my neurologist with the assistance of Dr. Abraham but I moved out of the area so that shot that possibility.

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