Random1

Do you think it's possible that you have had double vision issues before the night you got hppd?

What is your visual snow like and how does the klonopin affect it?

My recovery was honestly about 100%. I have zero phsychological hppd symptoms and the only visuals i have are floaters (which my girlfriend sees in her vision too...shes never done any hallucinogen) and tracers (but i have to stare intently at the light at is moves past to even see it). Snow can be seen if i REALLY focus on seeing it, and even so the lighting has to be just right for me to even see the snow while intently focusing on seeing it. I mean, yah 100% may not be possible, but trust me, even a 75% symptom reduction is bliss and will have you functioning like your old self. Keep positive, its beatable...maybe not 100%, but cmon, 99% symptom reduction is having your hppd symptoms all but gone...which we all would give a limb for during the REALLY bad days with hppd.

Do your symptoms come back when you stop taking tramadol?

Yeah, the aniracetam sort of backfired on me and eventually made my visuals worse. Hopefully ill be back to baseline before too long. Shits pissing me off. My brain is so goddamn sensitive it seems like 99% of the things I try blow up in my face. Whatever. I guess ill just buckle down and ride it out until I feel moderately better or until my appt with dr abraham. Maybe then I can at least get some klonopin for occassional relief.

See which antidepressants he would suggest for use with HPPD.

Depressed people without HPPD act like you are all the time, you're just channeling your depression towards your HPPD rather than something else.

I apologise, I was hasty before. I'm quite interested in trying an anti-serotonergic approach, I see the potential for it to be palliative.

Any thoughts about what available antiserotonergic drugs would be best to try? As OP mentions 5-HT2a receptors make sense as the primary target.

5-HT_2A antagonists[edit source | editbeta]

• Clozapine blocks 5-HT_2A, 5-HT_2C and D₄ receptors. - don't like the idea of blocking dopamine receptors
• Cyproheptadine blocks 5-HT_2A, HI and is a mild anticholinergic. - seems like the best option. Would supp procholinergic. See studies on this too.
• Ketanserin blocks 5-HT_2A, 5-HT_2C and Alpha 1 (A1) adrenoreceptors. - sounds good.. 
• Methysergide is a 5-HT_2A antagonist and nonselective 5-HT₁ receptor blocker. It causes retroperitoneal fibrosis and mediastinal fibrosis - not digging the last bit...
• Quetiapine blocks 5-HT_2A, 5-HT_1A, dopamine receptors D₁ and D₂, histamine receptor H1, and A1 adrenoreceptors - again, don't like the idea of blocking the dopamine receptors

  Am working my way through list of other atypical antipsychotics that might fit the bill.

This is interesting;

 

Edit: Found some Cyproheptadine 15 x 4mg for £2.29, ordered. If anyone else wants to give it a whirl, let me know I'll send you the site (trusted vendor I have used a lot)

That's one of the ones I was going to suggest. The migraine dosage seems to be 4mg three times daily; I would try doing that, and experimenting with the amount of dosage at once (seeing if 8mg makes a difference over 4mg). This may require higher doses than normal, as we're trying to upregulate the receptors.

How long have you been drug-free with HPPD?

What type of doctor did you need to get a Keppra prescription (neurologist, etc.)?

I wish...

Why the disbelief? Just the lack of a precedent?

HPPD seems to be caused by substances of all types that cause excessive 5-HT2a agonism (such as psychedellics, serotonin drugs, and high-dose SSRI). This 5-HT2a agonism leads to severe down-regulation of the 5-HT2a receptors in the visual cortex (among other places), and this leads to severe overexcitation of the neurons and hence visual anomalies.

Research has shown that 5-HT2a agonists can provide temporary relief from visual symptoms (which would be expected, as the overload of 5-HT2a activation supercedes their downregulation), but can cause further 5-HT2a down-regulation and thus don't serve much benefit in the treatment of HPPD.

Now research has also shown that 5-HT2a antagonists cause exacerbations of HPPD visual symptoms, but this would be expected; as the already down-regulated 5-HT2a receptors are receiving even less activation than before. But, over time, the lack of activation of 5-HT2a receptors (due to the antagonists) would cause a significant upregulation in the 5-HT2a receptors; back to their normal level. This means that after a period use of the antagonists the 5-HT2a receptors will return to their natural level of activation, and the visual symptoms should subside; even though during treatment the visual symptoms would be exacerbated, it would eventually lead to complete remission.

Articles (use Google for more):

5-HT2a antagonist causing HPPD symptoms in someone without HPPD:

http://www.erowid.org/archive/rhodium/pharmacology/risperidone.palinopsia.html

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

"While MAOIs, TCAs and SSRIs increase serotonin levels, others prevent serotonin from binding to 5-HT_2A receptors, suggesting it is too simplistic to say serotonin is a happy hormone. In fact, when the former antidepressants build up in the bloodstream and the serotonin level is increased, it is common for the patient to feel worse for the first weeks of treatment. One explanation of this is that 5-HT_2A receptors evolved as a saturation signal (people who use 5-HT_2A antagonists often gain weight), telling the animal to stop searching for food, a mate, etc., and to start looking for predators. In a threatening situation it is beneficial for the animal not to feel hungry even if it needs to eat. Stimulation of 5-HT_2A receptors will achieve that. But if the threat is long lasting the animal needs to start eating and mating again - the fact that it survived shows that the threat was not so dangerous as the animal felt. So the number of 5-HT_2A receptors decreases through a process known as downregulation and the animal goes back to its normal behavior. This suggests that there are two ways to relieve anxiety in humans with serotonergic drugs: by blocking stimulation of 5-HT_2A receptors or by overstimulating them until they decrease via tolerance."

Notice the bolded text. This effect of 5-HT2a receptors is analagous to the effect it has on the visual system. With HPPD-downregulated 5-HT2a receptors, our visual system continues to search for visual information (is disinhibited), and very rarely receives the "saturation signal" from the 5-HT2a receptors. This causes the visual anomalies. Using 5-HT2a antagonists would understimulate them and cause them to upregulate themselves to normal levels, causing a normal amount of "saturation signals" in the visual cortex and eliminating any visual anomalies.

Further evidence:

Many people with HPPD verify remission of the most debilitating visual symptoms over time, leaving them with only a light case of visual snow. This would be expected, as their 5-HT2a receptors begin to upregulate themselves to approach their normal range, the severe visual symptoms disappear; however, they may only upregulate themselves to the bottom of their normal activation range which would leave a light speckling of visual snow and not a complete natural remission, as most anecdotal evidence shows; and an extremely light level of visual snow is considered a normal occurrence, even people not affected by HPPD can see it if they concentrate very hard and look for it. This 5-HT2a antagonist treatment would allow the 5-HT2a receptors to upregulate even beyond the bottom level of the normal range, to a level where the visual snow becomes virtually invisible.

Anecdotal reports, even on these very forums, show exacerbation of visual symptoms while on 5-HT2a antagonists, followed by a strong reduction in visuals after their discontinuance. Had these cases been treated in an intelligent manner with supporting actions, it is very likely they would have received a complete remission of all symptoms.

Any input from knowledgeable others?

It is quite possible that visual snow is the product of some type of brain-proxy that filters stimulus as it passes between the hemispheres of your brain. I'd imagine that most of the symptoms of HPPD can easily be emulated with this type of technology. I'd highly recommend contacting your local intelligence agency to see if they are involved in anyway.

 

I'd imagine that the simulation of visual snow could easily disorient someone and could also prevent the formulation of visual memories. I'm pretty sure there are people electrocuting my brain and when I contacted the CIA, they refused to communicate with me.

 

 

Also, my father is turning into a hyper-vigilant asshole that threatens me passively when ever I think about telling people to contact the CIA for me. (I believe he may have been given ear pieces by 'Skull and bones' members while on the Dr. Phil show). For example, right as I was deciding to write this post he started violently twisting a water bottle in a very intimidating and threating way.

 

He also dragged me to the hospital and got me diagnosed as a schizophrenic after beating me up for complaining about him masturbating in the living room with a back massager (because the neighbors down stairs might have heard me complaining)

 

I'm pretty sure there are federal agents lying on my profile, so if any CIA official could come in and evaluate my situation, i'd really appreciate it. I don't want to end up being one of those sorry assholes that end up getting dragged into the entertainment industry to become a robot actor because I was unable to get in touch with the Central Intelligence Agency.

Thanks for the thread bump, see a psychiatrist about your schizophrenia.

Still looking for people to partake in this experiment, it has profound implications for discovering the causes of visual snow.

Where did you find the release date?

I am looking more into the nature of this visual snow, its causes, and its implications for the visual cortex.

Please go to the following link: http://dragon.uml.edu/psych/mach.html

Read the description, and take a look at the Mach Bands image.

Please supply the following information in your reply:

- Do you see the Mach Band effect as described, or do you see 7 uniformly colored bands without any effect?
- How did you get your visual snow?
- Any other accompanying symptoms?

If you do not see the Mach Band effect, try to confirm with someone who doesn't have visual snow that they see the Mach Band effect and post the result with your reply. Determine whether they experience greater or lesser Mach Band effect (greater would mean larger discolored bands near the edges), if possible.

The information gathered from this experiment will be helpful in pinpointing the neurological nature of visual snow and help all sufferers.

Thanks, I await your replies.