VisualDude

Message deleted due to:

Please use the proper forum and thread. This would be medication>the link to "my keppra story" above

/Mod

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 ) …

My Phychiatrist I've had for yrs said she would back me up for disability due to extreme anxiety and bi/polar. What do I do next? I Never mentioned hppd so I guess I look for a lawyer who only works on cases they can gain a percentage out of. Then just throw paper work at them like lucid said. Usually you get denied atleast twice my doc said.....and by then they may not have disability???

Don't know anyways tomorrow looking for a lawyer I've worked my ass off for yrs w/ hppd, and I know so many ppl w/ disabilty because they're depressed. Give me a break fucking work out and stop eating so much this hppd is borderline suicide! I better win or fuck the world

You’ve passed the biggest hurdle – doctors who will stand behind you.

Assuming you are in the USA,

There are 2 disability ‘levels’ – SSD which is based on your recent (10 years) work history and SSI which is if your total income (including what you would get from SSD) is below poverty level ($791 ???)

The application is the same. Use a lawyer. In New York they are awarded 25% of your back payments (not future) and are only paid if they win. Also, suggest using a ‘greedy cut-throat’ lawyer – this isn’t the best place for a nice, personable, everybody’s-friend type guy (this is just a personal opinion). Perhaps your psychiatrist has suggestions here.

Social Security will probably send you to some of their doctors for additional ‘exams’. You will probably be denied initially, depending on medical evidence. It takes 2-5 years to win a case – so get the ball rolling now.

If you happen to get well by then, thank god and kiss the ground. But again, get it all started.

As a rule, they don’t care what you have got or why. They want proof that your ‘residual physical and mental capacities’ prevent you from working full-time or making $1000 / month.

Please note: One doctor recently told me that there has developed a ‘cottage industry’ of disability doctors. So was advised to video tape any examination – you have the legal right to do so. And take someone with you as well. The biggest problem is Workman’s Comp and the like.

Hope this helps…

Various things can alter body temperature: sauna, long hot bath, nasty hot weather, cold weather (hypothermia), fever, …

I ask because my visual symptoms are change this way. Most dramatic is when fighting a cold. Sometime temp is a degree lower and vision is more sluggish.

However, during a fever, vision speeds up – lock step with body temp. At 102°F or more, vision is normal – quick, smooth, depth perception good, natural, eyes feel relaxed. Of course the rest of me feels like crap and this isn’t a practical treatment modality.

It is well understood that body temperature affects nerve conduction. While velocity remains relatively constant, amplitude is reduce as temperature increase.

Appreciate your input...

distract yourself from your symptoms however you can. It isn't exactly a healthy way to deal with something but I have seen worse ways to deal with things. have a great day all.

Am new to this forum but have spent time at another doing as you said. It lifts my spirits (others have noticed it as well).

Partly i've been sulking - I felt the old board was a cumulative process of knowledge building so to have all that collaborative work deleted without warning or any effort to retain the knowledge therein, or even just giving us the opportunity to copy and paste some bits, felt like an insult. I spent a fair bit of thought, time and effort on some posts in the belief that it was adding to a permanent information base, which i obviously wasnt.

Perhaps the server for the old board had a major crash-n-burn, and there wasn’t any backup. (Surprised that there is NO backup – even a 1 or 2 year old copy would be useful)

So this is a new start. And hopefully efforts will be put in place (at least monthly backups?) to prevent catastrophic loss. Comments from Administrators would be welcome here.

I very much wish to hear people stories. What they have tried and how it affected them … how they cope … are the able to hold a job … where are they now with it … any progress made. Am also excited to share what has helped me.

A collection for permanent reference IS valuable. It is understandable to not wish to pour ones heart and soul into the project again. Also, a virtually empty forum doesn’t inspire energy. But perhaps just a summary, as each member feels so inclined, would help get things going again.

Although there is not established treatment protocol for HPPD, there are things that can help people. IMO, HPPD is symptomology of a mild brain injury. The treatments for such injuries are quite varied. Anti-seizure meds are common. Benzodiazepines (which many ARE anti-seizure meds) are common. ‘Physical’ therapies (rehabilitation) can be employed. In some cases, dopamine agonists are used successfully. In others, dopamine antagonists (anti-psychotics) have helped.

Unless there is input, the forum will lose its purpose – to be a source of help other people.

Glad for you!

Was wondering what meds worked for you and which symptoms best resolved?

You earlier mentioned Keppra being very helpful (visual snow, trails, DP/DR, able to focus), so was this the main one? Are you still taking 1500mg or have you been able to taper down?

yea a little confusing. i dont close my eyes. i shut off all the lights waited for my eyes to adjust and just stared and i guess darker is the only way to explain it.

Have you had image persistance, trails, depth perception, and/or contrast problems?

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

For those who have seen Dr Abraham,

Was wondering, how did he arrive at the diagnosis of HPPD? Did he run tests? Or was it mainly discussing symptoms?

ive been doin it for a few days now and i notice a diff. might be for the good though. can't really tell lol. im smiling a lot more apparently according to my parents and i dont know if more energy is the way to say it but it feels foreign. as far as the memory goes i think its clearer but tbh it still feels a little weird. visuals are still there might not be as much though.

another question, has anyone turned off the lights and just stared? for some reason i did it last night and my whole field of vision got darker. spooked me a bit.

got off track there. yea it is weird how every person reacts differently though. again thanks for the responses.

my whole field of vision got darker

Please explain – after all it is supposed to be dark when you close your eyes

One of my first visual symptoms was it not being dark when closing eyes … the visual equivalent of tinnitus. Of the 3 meds that help this, Klonopin is one.

Glad to hear you are smiling more…

Just a report as to how the trial was...

I sat in front of Dr. A and for the first time in 14 years someone told me I have HPPD. That in itself was well worth the trip. I now don't have to convince doctors and psychologists that I have some strange disorder that none of them have ever heard of. Obviously I can't say the name of the drug that I was given but I can tell you this; the drug was never meant as a cure all. It was more of a spot treatment and its half life was less then a couple of hours and has the potential to be pretty harsh on the liver. This trial was obviously about defining mechanisms of HPPD and I was happy to be a part of it even though I was in the minority of people who the drug didn't help.

Dr. A is a brilliant man, but he is a man nonetheless. 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. After talking with him, I was a bit surprised at his suggestions. He first told me that he didn't have any firm evidence that SSRIs are contraindicated in HPPD, and if clinically needed, he would treat many folks with them without difficulty. Obviously we are all different, but I know from my experience that effexor made me think I was dying and I was a bit surprised that he was against, or unaware of, what I may have mistakingly thought was a staple of HPPD lore. He then made the suggestion that I get on a daily low dose of Klonopin and refuted any ideas of developing addiction or withdrawals from the drug, which knowing of a lot of users experiences here is pretty difficult pill to swallow (pun intended). I was very surprised but I do understand that when you put someone up on a pedestal as I had with him that finding out he isn't perfect is all the more disheartening.

Above all, it was a great experience and he was extremely knowledgeable and I suggest doing the trial if only to finally get a diagnosis and see the awesome Boston area. Me and my wife spent 6 days there and it was by far the best vacation I have had in awhile. I was able to get him to talk to my psychologist and finally say I have HPPD and that I need CBT over SSRI for my mild depression.

Please believe me when I say that I am not bashing Dr. A. I thought that the expense was so well worth it to talk to the man. I just wanted to share my experience and thoughts.

He then made the suggestion that I get on a daily low dose of Klonopin and refuted any ideas of developing addiction or withdrawals from the drug ... pretty difficult pill to swallow…

The key to preventing addiction and withdrawal problems IS low dose as he stated.

To illustrate: if you take hormones, the body compensates by reducing its own production … if you take a lot, the organs involved shut down … Take weight lifters who consume 50-100 times the normal production of androgen/testosterone, their testicles can literally atrophy if they keep it up.

This is true with neurotransmitter manipulation. The brain adjusts and discontinuance can make symptoms worse than before ever starting.

IMO, use medications like training-wheels on a bicycle. They are to help provide stability while you are learning. Eventually, they are just not needed. This is a problem with societal use of Prozac and other SSRIs. People take them but don’t follow through with CBT or whatever it takes to deal with their problems non-chemically.

Another example: I know chronic pain suffers who take oxycodone and hydrocodone for over a decade. By carefully matching doses according to their current pain level, often cutting pills into ¼ and using titration (and never touching time-released versions), they are not addicted and the meds are very effective at even lower doses than they started with.

Back to Klonopin – while used for many things, this is an anti-seizure med. Brain injuries are often treated with anti-seizure meds. Again IMO, HPPD is a mild brain injury.

So, have to agree with the doctor here. (low dose meds to calm malfunctioning activity) What was the dose he suggested?

He first told me that he didn't have any firm evidence that SSRIs are contraindicated in HPPD, and if clinically needed, he would treat many folks with them without difficulty.

Again, technically he is correct – you just can’t say nobody with HPPD will benefit. Technicalities and probabilities differ. Like yourself (and general HPPD community comments), serotonin is NOT my friend. Low doses are tolerable (though my vision is worse) but stuff like Effexor – after just 8 days was told to stop and it took months to recover (a bad bad setback).

Doctors generally work with hard, established patterns. Something difficult with our kind of problems.

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?

Thank you very much for your post and glad, as an added bonus, you and your wife enjoyed the time there. [Did you stay at the Custom House overlooking Quincy market? It is great if you can do so.]

Interesting. A member on a DP forum has been taking 6 mg Klonopin for over 22 years with no change in dosage or in its effectiveness. Her memory is stellar and clearly she is intelligent. Amazing how this stuff goes.

For a while was taking 1800 mg Neurontin (not a benzo but has some similarities). When I started it gave me energy (unusual) and no memory problems. Now, as I have been getting better, 300 mg is plenty otherwise I can get dopey from it.

Well, bloodletting has been around for millennia. Curious this claimed affect on HPPD for some people. Of course spilling a pint of blood every 8 hours isn’t going to be a practical ‘cure’.

"This revelation led to the discovery that HPPD is not permanent brain damage and is not a mental disorder, but rather a complex problem related to pressure"

IMO this hypothesis is flawed. It is in the very nature of brain injuries to have problems with biochemical processes (metabolism). So the affected areas ARE sensitive to blood flow/pressure, sugar, oxygen, cortisol, …

Nevertheless, the report that "I discovered that these symptoms, as well as trails, tinitus and hallucinations can be completely relieved…8 hours" is interesting. Would be helpful to know more about these people. Perhaps it is just a fake…

Mutts,

Thank you for your post.

Perhaps I’ll try to see Dr Abraham too. Having additional diagnosis helps, even if there is no quick solution. Very much relate to frustration with 99% of doctors.

I am one of those few with HPPD symptomology who has never tried recreational drugs. Yea – there are actually some out there (kind of like the 40 year old virgin, lol). But my condition was directly caused from toxic poisoning and the experience should yield useful help for some.

Really appreciated Dr Abraham’s comment, "Developing HPPD without ever tripping on acid can also happen, but in my experience this is quite rare, and suggestive of another disorder in the nervous system that needs medical attention."

Lucid,

if he finds anything that would even help hppd at a 1% level

There are plenty of people that get better than 1% relief from all sorts of effort. The real clincher is to gain a lot more so life is easier.

People have to keep trying. And they have to change their lifestyle that caused the problem in the first place.

I’ve worked very hard for 4 years and have made perhaps 75% recovery. And I am 50 years old – an age when the body doesn’t heal quickly anymore. So many visiting this forum should hold on to hope. Even if the medical community isn’t up to par with this

In my opinion, HPPD and its ilk are forms of mild brain injury. It may not feel mild. But treating it medically as such can yield results. Not just medications, but the whole gambit of retraining the brain can help.

There are lots of possibilities…

How much klonopin have you been taking?

I've only used small amounts of benzos:

0.25 mg Xanax (PRN ~30 pills a year, 10 years)

10 mg Valium (couple weeks, 2 years ago)

1 mg Klonopin (couple years)

At these doses, have never noticed any memory issues.

Lets just say I am depressed. Not from being unable to perceive a straight line without a skew, mostly because I am lonely for much of the time and The people I associate with are callus and dramatic. Social/personal issues have be-fronted me for the past few years to the point that my visual stress has been on the back burner for a good while now. being distracted from my sensory milieu has been "peaceful" but the distraction is damaging as a medication. I tried to kill myself with a bottle of meth/molly/vodka a couple weekends ago and lets just say that supportive friends are really a good thing to have. Pursuing Biotechnology and botany and shmoozing with the local minds about such ideas and projects has helped but a lack of personal companionship leaves me an empty craftsman putting all of his love into artifacts to time. So thats what keeps me from going to this site and complaining about my symptoms. What keeps you from stressing over knowing that you wont ever see things the same again?

What keeps you from stressing over knowing that you wont ever see things the same again?

First off, I see a lot better than in the past – so don’t know if I will or won’t. I’ve worked damn hard to get this far. Get so tired of it all, so take breaks. Find other topics…

Perhaps trying to help other people has helped – but this is the opposite of what you asked as the topic of this thread: "Things that affect your life more than HPPD".

Can’t really think of anything worse for me. The fatigue from it is the worst part – can’t work which is humiliating.

But the rest of crap in life (which is plenty) is so much more manageable – you CAN do something about most of it.

In certain lighting conditions, hppd has given me x-ray vision. None of you guys knew this?....

I better make sure I wear clean underwear around you ...

Don't know if you are serious with x-ray stuff but here is something that, when first experiencing it, thought I had totally lost my mind:

Would look at an instructor and as they were moving back and forth, sometimes their head and/or arms would disappear and I would see the wall behind them.

Eventually figured out that it only happened if I had just recently seen what was behind a person. It never, for example, happened with a picture. Perhaps it is like looking at the blades of a ceiling fan that are moving too fast to see.

A doctor told me that vision is extremely memory intensive, so this experience isn't as strange as it seemed. Just merging information from earlier frames.

As far as advantages, think of the money you save not buying HDTV and BlueRay videos. And if it keeps some of us out of Walmart – that’s gotta be a good thing.

Some with HPPD report getting floaters or an increase of floaters upon the onset of the disorder.

Floaters are defined as: "Deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent."

At first glance it seems a little unusual for this to be part of HPPD symptomology.

Is the increase of floaters,

A - More and/or larger floaters? [ actual changes in the vitreous humour ]

B - More noticeable because of visual hyper-sensitivity due as response to malfunctioning vision?

C - More visible due to breakdown of visual filtering which formerly ‘removed’ the sight of them?

Any thoughts?

1- What are afterimages and why and how they happen?

http://en.wikipedia.org/wiki/Afterimage

http://en.wikipedia.org/wiki/Palinopsia

2- What exactly is HPPD? Death of neurons? Damage on receptors? Changes on synaptic strength? Wrongly rewired synapses? What?

Probably any combination of the above, depending on the individual (genes, age, health, diet), cause, duration of cause, how many times the neurons have been ‘assaulted’, and sum total of ‘stressors’ being experienced before, during and after injury(s).

neurons … hold built-in structures that should not be changed during your lifetime … but I can't imagine how our vision could work if those neurons didn't hold a very reliable anti-replication mechanism.

Love your logic and thinking! And you are very right about something here.

Nearly all cells in the body grow old and replace themselves. The brain is different (with very minor exceptions) – it does NOT replace its neurons, but must keep them alive and healthy. This is because of all the complex synaptic connections that would be lost if a neuron replaces its predecessor (think what would happen to memory when a neuron actually dies).

So brain growth (learning) is not through cell growth/replacement but through the growth of new synaptic connections and changes in existing synaptic connections.

What do you mean with seeing in frames? You could only see 1 image per second? Seriously?

Yes, 1 image per second. Like a slow web ‘network’ meeting.

For me, there would be a frame (whole picture), then (when someone was moving) a perceptible blur (comet trail?) then another whole frame, …

A couple medical words for this sort a thing are Akinetopsia and Dyskinetopsia

There are even some people who suffer multiple frames (old one hang around). So a guy is watching a dog running and it becomes a bunch of dogs running. See: http://www.ajo.com/article/S0002-9394(99)00177-4/abstract and http://www.nature.com/eye/journal/v17/n9/full/6700551a.html

Why?

Vision is a time-consuming task, so the brain pre-processes the next frame (what you are viewing) while still working on the older one(s).

The brain makes this all smooth so people don’t normally see in frames. Something to consider:

Old silent movies 18 frames / sec

Modern films 24 frames / sec

TV (in USA) 30 frames / sec

TV (in UK) 25 frames / sec

Yet (with possible exception of old silent movies) you do not notice flicker or ‘jumping’ movement

Vision is a massive process and there are actually multiple systems involved.

The nerve fibers from the peripheral retina go to a fast section called Ambient Visual Processing. This is foundational for much cognition since it literally feed-forwards its info to 99% of the Cortex.

This section is responsible for orienting a person in space and time. It is how you ‘feel’. It allows you to jump and respond to a ‘fast ball’ (feeds into the Amygdala for sudden ‘flight/fight’ response).

The nerve fibers from the central retina go to the Focal Visual Processing centers. This is where you ‘think’.

When the ambient system is struggling, then the focal system tries to compensate and you get all sorts of problems. Frames, stationary objects ‘move’ or wiggle, reading is difficult, walls seem bowed, fatigue, anxiety, …

Also, since you see with two eyeballs, both sets of information need to be processed and coordinated. Problems here (binocular convergence) can further delay and confuse vision.

So … lots of weird, complicated stuff going on … it is amazing that it works so well and that we can 'see' at all

Do u feel physically weak

Yes, suffer fatigue.

This is part of the nature of brain injuries. The various systems in the brain are not in balance/harmony, so more effort is expended than when healthy – even for simple tasks

HPPD is a neurological dysfunction. Throwing molecules at your neurons won't fix them. It's like trying to fix a damaged computer punching it until it rewires by itself

At the heart of rehabilitative exercises/therapy/whatever is to rebuilt/relearn activities and thinking patterns. Drugs CAN be used therapeutically.

A personal experience: Used to see in frames for over a year. The frames were about 1 sec apart. Within 4 hours of 75mg Wellbutrin CR (dopamine and norepinephrine agonist) frames noticeably improved. In 3 days frames were about 1/2 sec apart. On 6^th day increased dose to 150mg. By day 7 frames about 1/8 sec. On 10^th day discontinued altogether (dose too high causing other problems). Frame problem slowly degraded (at rate of drug half-life) but never got worse than about 1/4 sec.

How did this work? Did it ‘un-stuck’ ‘jammed’ neural circuits? Did it stimulate growth and repair? Did it ‘knock-out’ some sort of toxin? I don’t know but would put my money on #1 and 2 because this is characteristic of nerve cells.

Today (18 months later) frame-rate is tight enough that I would never have ever guessed it is frames. More like drunkish

Another personal experience: Pulse dosing B12 with GPC and MSM. This improved visual acuity (but didn’t affect frames). This also repaired nerve damage to left fingers – despite being told by a neurologist that too much time had gone by for it to ever repair.

Moral of story – you just have to try things (but not fry things). Drugs can help fix things.

Why do you think molecules could be capable of intelligently rewiring synapses, resynthetizing dead neurons and messing with receptors to give your brain to the exact structure it had before HPPD?

Drugs can NOT intelligently rewire synapses. But your brain design (DNA) will try to do its best. If you feed and stimulate it, it will do even better.

Rule of Thumb: Nerve repair is NEVER the same as the original. But if damage isn’t too extensive, you won’t even notice the difference.

Thanks guys.

Visual, I would like to know more about your treatment and the effects on you.

1998, thanks for that very helpful information. Some disturbing thing just happened the other day. I had a book that had red squares on a green cover. Moving the book, the red squares came off the book, you know th affect. I hope you are correct in my case.

I started the valium and it was worse. Then my doc called and said she spoke to a specialist and said that there really is not a substitute and that I should not change the med. I should ween off from that.

Larry

Larry,

So you have tinnitus as well. Am curious about other non-visual symptoms. Do you have (or had),

change in pain perception?

reduction in sense of smell?

muscle cramping?

numbness anywhere?

Or course we are all just getting older, but changes such as these should not be quick.

As for things that have helped, to start with I’ve always approached this as treating a mild brain injury (oxidative stress and/or undesirable plasticity changes).

‘Alternative’ stuff. Big topic. Couple pointers:

1) Glutathione – major converter of intermediate metabolites. Glutathione is mainly made from Vitamin C, E and Selenium with cystine as the major catalyst (which are cheaper to buy).

2) Encourage nerve repair/growth with nutrition

~5000 mcg of sublingual B12 – 1 week on, 2 weeks off

~1000 mg GPC – 1 week on, 2 weeks off

~3000 mg MSM – 1 week on, do what you want the rest of the time

Medication:

Increase Dopamine (agonists) – there are only a few available. You want to use small doses (think of it like super nutrition instead of medication that is often dosed like a sledgehammer)

Sinemet 25/100 (carbidopa/levodopa) has been the overall best. Dose ½ pill 1-4 times a day. But some doctors don’t like to prescribe it if you don’t have Parkinson’s disease. Note: Parkinsonism is brain injury involving dopamine pathways – thus a no-brainer for this application.

The second best has been Wellbutrin CR 150mg. Many doctors readily dole out anti-depressants. This is the first DA I tried. It is harder to take because in increases Norepinephrine (and thus pro-convulsive at high doses). Dose 50-75mg in morning only. I found 150 mg improved vision more but caused problems. Note: noticed significant improvement of visuals (and non-visuals) within a few hours of first dose of 75mg.

You can try Requip and others, but they are more selective (D3) and do affect visuals – but not good enough for me.

[ In harmony with above, SSRIs and anti-psychotics can make visuals worse ]

DA is used by some doctors for brain injuries. Perhaps not used much with HPPD as the gut reaction is ‘psychosis’ and in the medical community, you just don’t give dopamine to a psychotic individual.

Recently a doctor just recently told me that seeing trails and/or tracers is definitely a dopamine problem.

Increase GABA – this is common with both brain injuries (to slow excessive activity) and anxiety. Benzos are anti-seizure. You mention having problems with Klonopin – I would like to understand your story more.

I’ve used Gabapentin (Neurontin) with success. It is considered a mild anti-seizure. Only a little help with visuals, but reversed deterioration. Started 1800mg a day but now 600mg and reducing.

Well, hopefully this is helpful to you and other members here. For me there has been immediate improvement of frames, contrast issues and depth perception.

Hi Larry (and everyone else),

It is joyful for me to meet people also suffering this vision crap - though it is sad that you are suffering such.

New to this forum but have visual anomalies do to toxic poisoning (am the fellow Ludwig mentioned in #10)

Am happy to share my experience - details are long so will be brief to start now...lol

Cutting to the chase,

Vision is a massive, multiple system that some feel is like the operating system (the foundation) in a computer.

It takes time to cognitively see. And so to make this smooth, instead of actually seeing in frames normally, the Ambient visual process system is a high speed, feed-forward system and pre-process information for the rest of the brain (actually feeds 99% of all cortical functions). It provides orientation and 'feeling' for ones environment. It feed right into the midbrain for motor control and balance. A lot of its processes use dopamine (anyone familiar with Parkinson's might know about dopamine and the midbrain areas).

So, for whatever reason, these pathways have been compromised (oxidative stress? placidity changes?) When this system isn’t up to snuff, then most cognitive functions suffer from this to some degree.

While everyone is different, so it isn't as straight forward as swallowing dopamine, this neurotransmitter is intimately involved. Note: virtually all recreational drugs affect the dopamine system directly or indirectly. Overloading any neuronal circuit causes changes.

I've had wondrous help with dopamine agonists - but you must use only small amounts. And sometime you need to compensate other areas with calming meds such as Gabapentin or benzodiazepine. Have just begun working with a vision rehabilitater who is familiar with many of these symptoms – time will tell on this but at least it is refreshing to find a doctor who understands.

If anyone wishes more information, then I’ll describe it. (otherwise this post will go on and on and on…)

Question: Has anyone here actually used carbidopa/levodopa (Sinemet 25/100)?

Best wishes for everyone here …