Memnoth

Theoretical treatments to visual snow

20 posts in this topic

As this is my first post, I feel by compulsiveness to express my hypothesizes on this matter. Compulsive by nature as I am autistic, and currently affected by ethanol and by a tryptamine hallucinogen called 4-HO-MET while writing this.

As the title of the topic suggests, I suffer from severe visual snow, and I feel obliged to inform others of my hypothetical treatments to this condition.

Number one: By empirical data at hand, I experienced less visual snow after watching television for at least 4 hours a day with bad SCART-cable connection. Which means I basically watched television with static distortions. This suggests 5HT-tolerance to visual perceptions, which would explain a decrease in visual snow. Maybe this has a therapeutic value to treat visual snow, by simply witnessing something of a resemblance to the symptom.

Number two: This is strictly by medicinal means, but I experienced less visual snow after tripping on 4-HO-MET while ingesting diazepam at the same time. If you have done your homework, by all humorous means, this means 5HT2C-tolerance is gained by engaging the surrounding areas, controversial to what 4-HO-MET or its analog Psilocin does, by simply applying a benzodiazepine with anti-epileptic properties at the same time.

I hope my experiences brings some perspective to you, and do please correct me if I'm wrong in some factual statements I have expressed.

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As for taking other hallucinogens to test if they improve your symptoms, that is an extremely risky idea. It has some merit, as we simply know so little about HPPD, every bit of information helps.

That being said. Don't take 4-HO-MET. It is very possible the 'decrease' in your symptoms is from the benzodiazapine alone.

As to 5ht-tolerance, that is currently over my head, but from what I do know now, it doesn't seem to make sense to me. I could be wrong, however. But 5HT is a serotonin receptor, so that receptor being somehow put into a more tolerant state (I don't know what you mean by tolerant. More receptive to serotonin? Less receptive?) would not seem to make sense to me.

I think you should keep coming up with hypotheses, but I absolutely have to encourage you to not do further hallucinogens. The affect of watching visual snow by watching static could be indeed a viable sort of technique. Or it could be completely placebo. Or it could be that you simply do not notice as much snow because you have beceom desensitized due to seeing so much of it on a TV.

So at the least we have a new idea on how to combat visual snow. It's a good idea. But do NOT take the hallucinogen anymore. It is too much of a risk. If you were in some kind of completely controlled, completely clinical lab setting, and there was data to suggest the hallucinogen might aid in reversing HPPD, it would still be a huge risk, and probably unethical. It would probably never be approved in a clinical trial if it is illegal.

So, that's it. Basically, my opinion is that further hallucinogen use should be avoided COMPLETELY by anyone with HPPD. There may be at some time a time and place to test different, potentially dangerous, chemicals on how they affect HPPD, but now is not the time. You take too huge a risk for too small a potential benefit. That's how I see it.

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I highly valuate your opinion, and thank you for expressing yourself. Though I have to say, I have had an autistic obsessive compulsion to study this, and this is basically my intellectual conclusions. I have had visual snow for six years now, and I have very much taken every drug genre that exists and it hasn't changed my visual snow at all, henceforth my expression of this very topic. I have taken 4-HO-MET at least 10 times during my condition, and it has not been getting worse. Personal experience only.

The 5HT-receptor or 5HT2C-receptor specifically is responsible for visual snow, inducing a perception disorder connected with a genetic predisposition of HPPD. Technically if you overstimulate the 5HT2C-receptor it becomes non-responsive, usually with presynaptic ion atoms, which reduces visual snow. Inducing a hallucinogen that overstimulates the 5HT-receptors will reduce visual snow only if you apply an anti-epileptic benzodiazepine at the same time, since it reprogrammes the neurosynaptic patterns in your brain to behave in a different pattern. If you have a hard time to understand the facts, I can simply put it as you will emotionally enforce the benzodiazepine effect to apply because the enforcement of the hallucinogenic drug stimulation will adapt to your experience, which will be less visual snow because of the benzodiazepine.

Again, please correct any factual statements that are wrong.

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Also, there have been some studies that I can remember reading, that concludes that supplements of melatonin of 5 milligrams or higher before sleep can reduce visual snow to some degree. I'm not really sure how, but as serotonin is a precursor to melatonin it may reduce visual snow by rebalancing the monoaminoacids somehow. Just something I'm thinking about.

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I have given this some more thought, and maybe trying to stimulate the 5HT2C receptor is the wrong way to go, do not do this, this will worsen your symptoms. Increasing dopamine in your brain slightly decreases the serotonin output in your brain synapses as a method to rebalance your blood pressure. This decreases 5HT2C-receptor stimulation thus experiencing a decrease in HPPD symptoms. This is why levadopa alleviates the symptoms while acting on the dopamine receptors. The only downside to this is that when dopamine returns to it normal quantity, after desensitizing its receptors, your symptoms will become worse. By personal postulate; this means you have to take levadopa for the rest of your life if you're going to use it.

Maybe a way to decrease visual snow would be to kill the 5HT-receptors causing this, which could mean taking MDMA or other empathogens, pure MDMA only though; that is, not Ecstasy (Ecstasy is a cocktail drug, usually containing amphetamines or other compounds as well), since too much serotonin and dopamine in your synapses at the same time makes the serotonergic enzymes that break down serotonin, accidentally break down dopamine as well, this produces hydrogenperoxide, and that is something you do not want in your brain, it is highly corrosive due to its oxidative effects. But do not try this, this is a mere hypothesis.

Please correct any factual statements as these are mere postulates.

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Visual-Any thoughts to this?

I just got a script for sinemet filled out and after reading this I"m shit scared of taking it!

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You shouldn't be scared. Even if you stop taking Sinemet after a while and the symptoms become worse, it will only be temporary as synaptic ion atoms will rebalance your receptor affinities again. Meaning your condition will become as it was before taking Sinemet. But do try the treatment, it could alleviate your symptoms and you could feel better as of it being a form of treatment. It is highly individual on how it works, but it will not permanently become worse either way.

Always read other peoples experiences on treatments though.

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hope1, I think the point he is getting at is that he does not think Sinemet is a cure - you're on it for life in the sense that you have to keep taking it in order to get the benefits from. If you stop taking it, then your symptoms will return. However, Visual reports some permanent improvement. However, his case appears a little more complex than a lot of ours.

Did you try it in the end?

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No, Sinemet is not a cure. Pharmacological tolerance is inevitable, no matter what psychoactive drug/precursor you ingest. By pure physics, tiny calcium ion atoms swim around inside our plasma membranes called axons. The receptors located on our axons have an electrical charge, and so does our cathecolamine- and monoamine-compounds, which are also called hormones. When a hormone reaches a receptor it shifts the electrical balance of the receptor itself, because it attracts ion atoms and switch electrons. This is how tolerance is gained.

The definition of Sinemet, nevertheless is that it's a treatment, a supplement to purposely alleviate the symptoms. But I'm back here now under the influence of Modafinil to tell you that my Visual Snow is almost gone completely. Temporary of course, but a huge relief nonetheless. According to my research, I see it as an Analeptic Nootropic agent actually, inducing Dopamine, Norepinephrine and even acting on the peptides of orexin, works a little on Serotonin as well though, which is regrettably. But also; it inhibits GABA-receptors and increases stimulation with Glutamic Acid in the brain. That's a cognitive stimulative nootropic by definition to me.

The half life time is quite long, longer than amphetamine. Eating is relatively easy to commit to, while on a low dosage (200 MG), I have now taken 2000 MG (Not all at once dear god), recreational purpose only, I've been programming on a game for 30 hours straight. My apologies for the off-topic. I realize that I can not start to shit chat while on a stimulant.

I hope my opinions are appreciated here. I am autistic so I can't really tell. But I will keep posting. I used to have social phobia, that's a bitch. Okay, I'm going to shut up now.

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Considering how many people here have HPPD from MDMA, why would you think that it's a possible cure?

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I wasn't speaking literally, I was trying to display how the damaged neurons could be eliminated without engaging myself in pharmacological terms, making myself more understandable to others.

But thank you for that information, I was not aware of that.

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And why do you assume that any neurons have been damaged? It seems to me that the brain is highly capable of adaptation as is evident by it's function of learning new things at rapid rates during childhood. Epigenetic responses from a very chaotic situation that arises quickly from drug use, like the mass release of neurotransmitters, a situation that someone's brain would never encounter otherwise, seems more plausible to me.

But I do agree with you on the Dopamine aspect to the HPPD question. I have a rather unfortunate opiate habbit and it seems that the opiate effect on the brain releases large amounts of dopamine and this counteracts my dissociation and visuals by quite a bit.

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And why do you assume that any neurons have been damaged? It seems to me that the brain is highly capable of adaptation as is evident by it's function of learning new things at rapid rates during childhood. Epigenetic responses from a very chaotic situation that arises quickly from drug use, like the mass release of neurotransmitters, a situation that someone's brain would never encounter otherwise, seems more plausible to me.

I made no such assumption. The statement itself establishes an absolute clarification asserting the implication to metaphorically provide information in a comprehensive convenient matter. Furthermore, Neural Darwinism along with Neuroplasticity renders any statements regarding neural damage and brain adaptability synonymous. Neurosynaptic patterns redefine their pathways when stimulated by electrical impulses for the purpose of optimizing the electrical time of travel between the stimulated areas. Consequently, we experience this as a result of tampering with our neurotransmitters.

Neuronal damage by MDMA consumption is proven both biochemically and neuropsychiatrically. When too much Serotonin and Dopamine are released in the same synapses, Dopamine gets accidentally broken down by 5HT enzymes. This produces hydrogenperoxide, which has highly oxidative effects and are thus corrosive. The long term effects of using MDMA frequently has been documented by neuropsychiatrists. Brain scans were taken on regular users and it showed visible gaps in their brain, largely affecting the areas that controls emotions, motivation, energy, joy and stress.

I need to come down now from Modafinil, I'm going to smoke some weed and take a handful of Valium. Been awake for 3 days studying evolution, biology, biochemistry, geochronology, geology, meteorology, tectonics, geochemistry and paleontology. Why? Because I'm programming an evolution-biology simulation game. Great fun, will upload when finished. I'm writing this off-topic now because I suffer from severe social anxiety when I'm not on a stimulant. I will be back though, maybe after 1 - 4 weeks. Autistic, eccentric and lonely.

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Visual-Any thoughts to this?

I just got a script for sinemet filled out and after reading this I"m shit scared of taking it!

Guess I don’t understand why this info is scary

As far as drugs go (recreational or prescription) problems are largely connected to amount taken. Seems that many people can occasional take some amount of recreational drugs for years with no obvious problems. Only a few are permanently altered with a few ‘hits’.

But lets pick on dopamine, plasticity and ‘damage’

How much Meth is safe? According to propaganda you see pictures like these - huge dopamine hits.

meth2.jpg

Have the brains of these people been altered?

Some definitions (from Google)

damage "Physical harm caused to something in such a way as to impair its value, usefulness, or normal function"

brain damage "Injury to the brain that impairs its functions, esp. permanently"

encephalopathy "A disease in which the functioning of the brain is affected by some agent or condition (such as viral infection or toxins in the blood)"

hppd "a disorder characterized by a continual presence of visual disturbances that are reminiscent of those generated by the ingestion of hallucinogenic substances."

Are brain functions altered while ‘high’ from drugs?

Once the drugs have cleared the system, are there any residual effects?

Could the desire to take drugs again be a residue effect? A learned experience (plasticity)?

Which drugs and what dosages are safe?

Few suffer HPPD for a little while. Fewer suffer HPPD for a long while.

Have there been any structural changes to the brain? Remember learning is a structural change.

Generally with the body, if there is too much of something it reacts by trying to reduce it. This is true with sugar, insulin, thyroid hormone, testosterone, cortisol, dopamine, serotonin, norepinephrine, etc… Likewise, with too little an effort will be made to increase it.

Eventually the body reaches homeostasis (balance) or the best it can do. If hormones are too high for too long, then the receptors change, such as ‘insulin resistance’ or ‘cortisol resistance’. This gets all the more complicated with changes in the body being only in some areas but not in others.

If neurotransmitter levels remain too high then structural changes happen. Plasticity occures by neurons deliberately increasing neurotransmitters at certain points to 'wire' in the change (cause structural changes). So systemic levels from drugs could cause this effect in unexpected areas. Sometimes structrual changes from 'overloads' are very negative – excitotoxicity being to worst (burnt synapses and/or neuronal death).

So where does an individual with HPPD stand?

Do they have altered brain function?

Is there synaptic damage?

Is there plasticity that has simply changed the way the brain in now wired?

The DNA blue print ‘wants’ things to be ‘normal’. Provided that genes have not be ‘silenced’, it will work to fix changes ‘sensed’ on the molecular biology level. There are already studies indicating that LSD silences some genes.

It seems impossible to know for sure. So what can a person do?

Living ‘healthy’ gives the body the greatest possibility to repair.

It is very important to address chronic anxiety since this IS damaging to the brain and body. See Why Zebras Don’t Get Ulcers by Robert M. Sapolsky

One can do ‘visual rehabilitation’ to try to teach the brain the way you want it to work.

One can try prescription drugs to attempt to restore normal functions.

It seems that Klonopin helps lots of people but I haven’t heard of reports of permanent changes. And discontinuing is often unpleasant.

My experience with dopamine agonists seem unique in that some areas have been permanently improved (permanent being defined as persistent improvement even without the meds for weeks). But there aren’t many here who have tried it. And those who have a positive response have so far expressed concern about discontinuing and perhaps loosing the benefit altogether.

Did dopamine ‘unjam’ stuck neuronal circuits? Did it fuel the brain to reroute certain functions? It took only a few hours to notice improvement. Merkan said that in 15 minutes of ½ pill of Sinemet 25/100 he felt its effect. In 30 minutes began to cry since for the first time in over 4 years he could feel again and his vision sharpened from a blur. It helps his DR (but doesn’t for me). He is also taking Klonopin and Keppra.

There is nothing simplistic about all of this. Vision is complex. Perception is complex. The whole brain is complex. HPPD is complex. Life is complex – so there is little to fear.

Each person must decide how to manage their condition. It is understandable that there is reluctance to try drugs to get better "once bitten twice shy". And doctors often respond with SSRIs and/or anti-psychotics – meds that do not have a good tract record for HPPDers.

Learning about how the brain functions should not be frightening. But if it is too squeamish, then perhaps it is best to occupy oneself with another topic. Really, other than personal interest (hobby or profession), the only reason to try to learn is because very few doctors have time to adequately help a person – you often have to do all the footwork.

The most important thing is to try to live ones life the way they wish, and not get swallowed in the negatives of the current situation.

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I've been taking Prozac the last few weeks, could that be making my VS worse?

I just finished taking a bunch of speed, too, and I have a bad headache and my VS is incredibly bad. Could amphetamines make it worse, too?

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How much Meth is safe? According to propaganda you see pictures like these - huge dopamine hits.

Have the brains of these people been altered?

Yes, neurosynaptic patterns by neuroplasticity follows the flow of electric activity in the brain, throwing a neurotransmitter out of balance by ingesting a psychoactive drug slowly causes priority changes in the brain. Damage may then be defined by how much cognitive decline the reconstruction results in, as this defines the very value of our brain. Safe drug usage of this sort can only be achieved by balancing the intake in response to neuroplastic reconstruction, staying off the drug long enough to enforce normal functionality between every high.

Are brain functions altered while ‘high’ from drugs?

Brain functions simply react differently when a neurotransmitter is unbalanced, it becomes altered in the long run from abusive usage.

Once the drugs have cleared the system, are there any residual effects?

Yes, neuroplasticity defines functions as altered when tampered with by the influence of a drug, though reshaped into normal function, if possible, during normal state of mind using the power of time. Studies have confirmed residual alteration in neurosynaptic patterns on experiments with giving amphetamine to mice. The alteration persisted for 8 months after a single dose of amphetamine.

Could the desire to take drugs again be a residue effect? A learned experience (plasticity)?

Only if the psychoactive substance has a euphoric property, then it's compared to any positive feeling, like the simple desire to indulge in an emotional state of joy. Speaking from an objective perspective, reconstruction of neurosynaptic patterns involving pleasure areas of the brain can be driven to the point of it overriding any conflicting electric activity. This can be converted to being defined as addiction, as the desire is overriding thoughts of repercussions. There are instances of amphetamine users growing so fond of the instantaneous rush by injecting intravenously, they feel that using the syringe has become such a joyous activity they would inject water in lack of amphetamine.

Which drugs and what dosages are safe?

All drugs not affecting your visual perception to the extent of stimulating the same receptors causing HPPD are safe to use in that aspect. Though even if they affect those receptors, a brief high, relatively speaking, does not need to cause more neurosynaptic reconstruction that increases symptoms. Moderation is the keyword. Electric conflictions in the basic need of gaining nutrition, fluids and sleep are statistically the largest factor of body decline.

Have there been any structural changes to the brain? Remember learning is a structural change.

Yes, according to neuropsychiatric studies, ecstasy abusers for example, have been reported having a decline in mass among brain cells covering the areas of emotions like motivation, decision and safety. Long term bensodiazepine use can cause cognitive dysfunction because of neuroplasticity selectively killing off cells as a response to lowered electric activity in the brain.

Generally with the body, if there is too much of something it reacts by trying to reduce it. This is true with sugar, insulin, thyroid hormone, testosterone, cortisol, dopamine, serotonin, norepinephrine, etc… Likewise, with too little an effort will be made to increase it.

Sounds like an archetypical axiomatic statement of neuroevolutionary adaption.

So where does an individual with HPPD stand?

Do they have altered brain function?

Is there synaptic damage?

Is there plasticity that has simply changed the way the brain in now wired?

It seems impossible to know for sure. So what can a person do?

Living ‘healthy’ gives the body the greatest possibility to repair.

It is very important to address chronic anxiety since this IS damaging to the brain and body. See Why Zebras Don’t Get Ulcers by Robert M. Sapolsky

One can do ‘visual rehabilitation’ to try to teach the brain the way you want it to work.

One can try prescription drugs to attempt to restore normal functions.

It seems that Klonopin helps lots of people but I haven’t heard of reports of permanent changes. And discontinuing is often unpleasant.

Did dopamine ‘unjam’ stuck neuronal circuits? Did it fuel the brain to reroute certain functions?

There is nothing simplistic about all of this. Vision is complex. Perception is complex. The whole brain is complex. HPPD is complex. Life is complex – so there is little to fear.

Concepts are only complex when fundamental understanding is conflicted or inadequate. Neuronal circuit priorities are defined by our genetic predisposition to maintain brain functions in a specific manner. The visual disturbances can therefore be linked to a rudimentary group of neurons, assigned genetically to their lost functionality. Not reshaping into normal function because of an adjacent group of purpose-fulfilling neurons sharing stimulation, promoting the area to exist and cause output. One factor as an example could be the constant stream of visual inputs stimulating the rudimentary group of neurons. Psychoactive substances would then be the cause of this shift in functionality by reacting with the neuroplasticity that defines the binding around the dysfunctional group of neurons.

With this data at hand, it suggests that dopamine alters the behavior of function but fails to alter the neurosynaptic patterns enough to delete the output of symptoms. Klonopin or other anti-epileptic bensodiazepines works by suppressing enough electrical activity in the brain to leave the rudimentary function in the shadow of active neurons. It behaves as a benign tumor, fueled by its surrounding biomatter, giving the impression that counteractions or cures have to be invasive surgical removal, intense selective psychoactive stimulation or, if you possess the genes where the rudimentary neurons are distant enough to lose stimulation while in a normal state of mind, simply avoid drugs until full recovery.

Contemplating on the concept of curing this condition with the psychoactive substances of today, probability calculates ineffective use. Theoretical treatments established as treating symptoms only (semantic tautology observed). Seems as though you either have the genes enabling neurochemical activation of HPPD neuronal activity and the ability to decline it with time, or activation with the aftereffect of growing a strong connection in the dysfunctional neurosynaptic patterns. The latter being seemingly permanent.

Did I cover everything?

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I've been taking Prozac the last few weeks, could that be making my VS worse? I just finished taking a bunch of speed, too, and I have a bad headache and my VS is incredibly bad. Could amphetamines make it worse, too?

Speaking with personal experience on both questions, fluoxetine (brand name Prozac) worsens visual snow permanently, after 5 days of treatment it increased my symptoms by 300%. Taking amphetamine while having visual snow appears to only worsen the symptoms during comedown, 5 years of sporadic amphetamine use have not worsened my symptoms permanently as far as I can tell.

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