Jump to content
Hallucinogen Persisting Perception Disorder (HPPD) Support Forum

dasitmane

Members
  • Content Count

    420
  • Joined

  • Last visited

  • Days Won

    46

Everything posted by dasitmane

  1. Like I make mention of in the second post anyone can try sage if they want, I do believe for various reasons this is a suitable treatment for this condition. How long the treatment takes on average I have no idea. Sufferers can also try cinquefoil as well as this may have long term beneficial effects on the condition as well. Also someone could simply try a mineral supplement with ALL minerals, not just the basic minerals. Its possible that there was simply a depletion of one of the said minerals in the brain that takes a long time to build up and once depleted is in a state of deficiency causing said symptoms. There is still a lot that science doesn't know. The one that I recommend trying is colloidal minerals by NOW. If anyone does try this please report your findings. When deficiencies occur for various reason though they are rare they can be hard to bring the organ back up to the requisite levels, for example the case of zinc deficiency and the liver. So this is worth a shot or try as well.
  2. Thanks for posting too, your case is very interesting.
  3. What drugs did you do? There have been occurrences of peoples hppd getting worse from certain medications. Im sure the phenergen triggered it. A lot of people on this forum have had symptoms as bad as you. Sorry this is happening. I had symptoms as bad as yours, i had to lean on tables at work because i was so unstable, my derealization was so bad it was like i wasnt even in my body. And my anxiety was so bad my hair was falling out, lots of it in the shower etc. hang in there eventually it gets better.
  4. It does say it has a “weak affinity” to 5ht2a receptors, theyre the same that hallucinogens interact with.
  5. Im honestly not sure that is kind of strange.
  6. How many did you consume?
  7. Awesome, thanks for the response. You never called me back....
  8. Ah the Unicorn's butthole.... interesting. Please stop doing drugs of any kind so you do not further your condition.
  9. Super weird that it is out of the brain in 20 minutes.... The drug moves quickly to the brain and throughout the body and acts on both the central and autonomic nervous systems. All traces of the drug disappear from the brain rapidly in about 20 min, although the effects may last many more hours.
  10. This is nuts because I always noticed my anxiety would slightly increase as the sun was going down and everything was getting darker, probably effects alpha waves to some degree likened to that of closing of the eyes, and found in high frequencies in our brains. Alpha waves are neural oscillations in the frequency range of 8–12 Hz[1] arising from the synchronous and coherent (in phase or constructive) electrical activity of thalamic pacemaker cells in humans. They are also called Berger's waves after the founder of EEG. Alpha waves are one type of brain waves detected either by electroencephalography (EEG) or magnetoencephalography (MEG), and can be quantified using quantitative electroencephalography (qEEG). They predominantly originate from the occipital lobe during wakeful relaxation with closed eyes. Alpha waves are reduced with open eyes, drowsiness and sleep. Historically, they were thought to represent the activity of the visual cortex in an idle state. More recent papers have argued that they inhibit areas of the cortex not in use, or alternatively that they play an active role in network coordination and communication.[2] Occipital alpha waves during periods of eyes closed are the strongest EEG brain signals. These faster alpha waves could be the whole cause of HPPD, and could explain the disinhibition of the cortex/cerebrum. Visually everything routes through the thalamus too, to be communicated to the visual cortex. Interesting indeed.
  11. What da fawk Nicotine[edit] One reason people report they like smoking cigarettes is nicotine's ability to aid their selective attention.[3] In order to alleviate the stress of not being able to gate sensory input, nicotine can correct sensory gating deficits for individuals with schizophrenia, but the effects only last about 30 minutes after nicotine intake.[9] The same self-medication is present among those with attention-deficit/hyperactivity disorder and even those on the autism spectrum as well.
  12. Super fucking interesting In electroencephalography, the P50 is an event related potential occurring approximately 50 ms after the presentation of a stimulus, usually an auditory click.[1] The P50 response is used to measure sensory gating, or the reduced neurophysiological response to redundant stimuli. Research has found an abnormal P50 suppression in people with schizophrenia, making it an example of a biological marker for the disorder.[2][3] Besides schizophrenia, abnormal P50 suppression has been found in patients with traumatic brain injury, recreational drug use, and post-traumatic stress disorder.[4]
  13. More shit, I'm going to try and find any correlations with qEEG and other disorders, that could give some more leads as to the cause of this. Here's a study where they already did this with 44 HPPD patients. I dont know anything about qEEGs or what everything means, all I made out was "disease severity was highly significant". All I can make out is faster alpha frequency(brainwave), and visual evoked response, which has something to do with LSD induced cortical(outer areas of the brain) disinhibition. Abstract Hallucinogen persisting perceptual disorder (HPPD) may follow the ingestion of LSD or other hallucinogens in a subset of users. It is characterized by chronic, intermittent or constant visual hallucinations of many sorts persisting beyond the period of acute drug effects. We studied 44 LSD-induced HPPD subjects and 88 matched controls to search for spectral and evoked potential differences using quantitative EEG (qEEG). HPPD subjects demonstrated faster alpha frequency and shorter VER (visual evoked response) latency, consistent with prior animal and human data on response to acute LSD administration which suggest LSD-induced cortical disinhibition. AER (auditory evoked response) latency was prolonged consistent with a differential LSD effect upon visual and auditory systems. The exploratory T-statistic significance probability mapping (T-SPM) technique demonstrated HPPD-control differences mostly involving temporal and left parietal scalp regions, confirmed by a split-half analysis. Significant variables were all derived from the long latency flash VER and click AER. None were derived from spectral analyzed EEG data. Canonical correlation between SPM-derived measures and variables reflecting disease severity was highly significant. A between-group stepwise discriminant analysis based upon a full set of qEEG measures demonstrated 87% prospective classification success by jackknifing and 88% success in a separate split-half analysis. https://www.ncbi.nlm.nih.gov/pubmed/8912957 Heres another. "in HPPD, there is widespread cortical inhibition in the eyes-opened state, but localized and isolated occipital disinhibition upon eye closure, a state known to facilitate hallucinatory experiences." Abstract LSD use in certain individuals may result in chronic visual hallucinations, a DSM-IV syndrome known as hallucinogen persisting perception disorder (HPPD). We studied 38 HPPD subjects with a mean of 9.7 years of persistent visual hallucinations and 33 control subjects. Measures of local and medium distance EEG spectral coherence were calculated from all subjects. Coherence, a measure of spectral similarity over time, may estimate cortical coupling. In the eyes-open state in HPPD subjects, widespread reduction of coherence was noted. However, upon eye closure, the occipital region demonstrated augmented regional coherence over many frequencies but with reduced coherence of the occipital region to more distant regions. This occipital coherence increase correlated with previously reported shortened occipital visual evoked potential latency for HPPD subjects. We speculate from coherence and known clinical and psychophysical data that, in HPPD, there is widespread cortical inhibition in the eyes-opened state, but localized and isolated occipital disinhibition upon eye closure, a state known to facilitate hallucinatory experiences. An analogy is drawn to findings in the interictal and ictal epileptic focus. In HPPD, we speculate that occipital EEG hypersynchrony resulting from increased regional coherence, when coupled with relative isolation of visual cortex, especially upon eye closure, facilitates hallucinations and illusions. https://www.ncbi.nlm.nih.gov/pubmed/11566431 Basically the cerebrum(outer parts of the brain/front back and side) is disinhibitied or overreacting for some reason. Very interesting. Heres a study that probably rules out the GABA interneurons theory. It doesn't definitively, but leans away from the idea more so. https://www.jneurosci.org/content/jneuro/20/16/6232.full.pdf
  14. Here's a study where they already did this with 44 HPPD patients. I dont know anything about qEEGs or what everything means, all I made out was "disease severity was highly significant". All I can make out is faster alpha frequency(brainwave), and visual evoked response, which has something to do with LSD induced cortical(outer areas of the brain) disinhibition. Abstract Hallucinogen persisting perceptual disorder (HPPD) may follow the ingestion of LSD or other hallucinogens in a subset of users. It is characterized by chronic, intermittent or constant visual hallucinations of many sorts persisting beyond the period of acute drug effects. We studied 44 LSD-induced HPPD subjects and 88 matched controls to search for spectral and evoked potential differences using quantitative EEG (qEEG). HPPD subjects demonstrated faster alpha frequency and shorter VER (visual evoked response) latency, consistent with prior animal and human data on response to acute LSD administration which suggest LSD-induced cortical disinhibition. AER (auditory evoked response) latency was prolonged consistent with a differential LSD effect upon visual and auditory systems. The exploratory T-statistic significance probability mapping (T-SPM) technique demonstrated HPPD-control differences mostly involving temporal and left parietal scalp regions, confirmed by a split-half analysis. Significant variables were all derived from the long latency flash VER and click AER. None were derived from spectral analyzed EEG data. Canonical correlation between SPM-derived measures and variables reflecting disease severity was highly significant. A between-group stepwise discriminant analysis based upon a full set of qEEG measures demonstrated 87% prospective classification success by jackknifing and 88% success in a separate split-half analysis. https://www.ncbi.nlm.nih.gov/pubmed/8912957 Heres another. "in HPPD, there is widespread cortical inhibition in the eyes-opened state, but localized and isolated occipital disinhibition upon eye closure, a state known to facilitate hallucinatory experiences." Abstract LSD use in certain individuals may result in chronic visual hallucinations, a DSM-IV syndrome known as hallucinogen persisting perception disorder (HPPD). We studied 38 HPPD subjects with a mean of 9.7 years of persistent visual hallucinations and 33 control subjects. Measures of local and medium distance EEG spectral coherence were calculated from all subjects. Coherence, a measure of spectral similarity over time, may estimate cortical coupling. In the eyes-open state in HPPD subjects, widespread reduction of coherence was noted. However, upon eye closure, the occipital region demonstrated augmented regional coherence over many frequencies but with reduced coherence of the occipital region to more distant regions. This occipital coherence increase correlated with previously reported shortened occipital visual evoked potential latency for HPPD subjects. We speculate from coherence and known clinical and psychophysical data that, in HPPD, there is widespread cortical inhibition in the eyes-opened state, but localized and isolated occipital disinhibition upon eye closure, a state known to facilitate hallucinatory experiences. An analogy is drawn to findings in the interictal and ictal epileptic focus. In HPPD, we speculate that occipital EEG hypersynchrony resulting from increased regional coherence, when coupled with relative isolation of visual cortex, especially upon eye closure, facilitates hallucinations and illusions. https://www.ncbi.nlm.nih.gov/pubmed/11566431 Basically the cerebrum(outer parts of the brain/front back and side) is disinhibitied or overreacting for some reason. Very interesting. Heres a study that probably rules out the GABA interneurons theory. It doesn't definitively, but leans away from the idea more so. https://www.jneurosci.org/content/jneuro/20/16/6232.full.pdf
  15. To some degree, I agree with this post. I do however have some innate desire to recommend against suicide, granted in severe doomable cases of intolerable suffering with no possible positive outcome I can't see why it can't be an option. HPPD is definitely tough though, insane rather, but to say that we are completely doomed, I can't throw in the towel yet. Glad to see you're back posting though.
  16. Its highly unlikely that its chemical imbalance. I think people tend to jump to it because chemicals in the brain are the most talked about thing, and its an idea that offers hope. There are a lot of possibilities that it could be... I line a lot of them out in my thread on the front of the forum. "Idea for a possible cure...etc", you can read about all the possibilities there, they're the areas that require research. If its not neuronal loss its probably highly correctable. It could be neuronal loss though... HPPD sufferers may have some metabolic disorder or something that does present naturally and maybe cant break down the metabolites of the hallucinogens or something to that matter, which would explain why some get it and most dont. There are a lot of possibilities though, just check out my thread. I think a lot of people do recover to some degree though, I did, but it was still extremely difficult of the first year or two.
  17. I agree with this statement 100%. Also have you read my thread on here? Neuroplascicity is a thing but if the issue is neuronal loss it wont do much, if its not neuronal loss, then neuroplacicity wont do anything lol. If you dont want to live like this for the rest of your life you can always help with research.
  18. Lemon balm helps Edit: It will improve btw, give it some time.
  19. As far as I know its pretty useful for epileptics. Granted if these alternative theories are wrong, then its discordance/desyncronization in the feedback loops involved due to white matter neuronal loss, which would be for the most part unrepairable even with neurogenesis. It is a very curious thing though that Risperidone is working in some of these patients...
  20. In some cases it does appear risperidone makes symptoms worse. Maybe an antagonist would be better. EDIT: Antagonists like trazodone seem to do nothing, but I was thinking that maybe its nessasary to have a highly specific 5HT2A inverse agonist.
  21. Here is another case where the patient is prescribed 1mg of risperidone, and within two months reports that they are cured. Ill post more if I find any. Looks like one month in though they discontinued Risperidone and added the lamotrigine. This is the lamotrigine person I mentioned in the previous post. Also if anyone has had any EEGs done please do post the results. Would like to add too that its possible that the Risperidone could exasperate symptoms initially, but then resolve them, sometimes in medicine when there is a cure, the symptoms get worse before better. Not always, but there are cases. Heres a post from another member, stating that it worsened his symptoms, he doesn't give the dose that he was prescribed though unfortunately. Posted December 29, 2012 Firstly they gave me risperidone, this amplified my symptoms and i stopped taking them. They then gave me amisulpride, that didnt go well either. Then seroquel, it was the better of the three.Once i got used to the side effects it doesnt seem so bad, although im really not sure how much good its doing me. Thats pretty much all I could find on the forum, if theres anything else anyone can find please share. Thanks! If all this is true and accurate, these desyncronization or discordances in the brain could be the cause of a lot of mental disorders.
  22. HUGE post today. Last night I was reading an LSD study and the effects on the brain, going on about areas that are upreg/downreg or something. Anyways the down regulated areas he mentioned are desyncronized. I had to look up what that meant because I had no idea, but it started going on about brain frequencies etc. Basically the neurons in areas pulse with a feed back loop from other areas through resonance, the neurons fire in waves, as groups, its exactly what I was talking about really early on in my first thread. So I started conjecturing that maybe in a few minor users of hallucinogens their brain becomes permanently desynced so to speak, or the harmony between the two areas become discordant, exactly like I used to conjecture, only now there is physical evidence to the idea being possible. So, it comes back to the very first and original posts I made here when I joined 7-8 years ago, about using an antagonist, or maybe even an inverse agonist to "resync" the brain areas. It appears that the issues are predominately in the temporal lobes for people who have anxiety, and the occipital lobes for visual effects. I found a study involving Dr. Abraham where they did EEG studies on post drug users with and without anxiety, most of the users with anxiety showed irregularities in these areas, these are also areas in with patients with seizures can be effected. Dr. Abraham and the other doctor also mentioned how before seizures, patients will report high fear/anxiety. The condition of HPPD could very well be brother/sister relationship with epilepsy interestingly enough. Then I searched the HPPD forum for any posts involving 5HTP2A receptor antagonists or agonists. What found is shocking. Heres the posts from "Victor" Posted March 31 In my case the disorder healed in two months with risperidone and paroxetine. Paroxetine acting upon anxiety and risperidone over visual distortions. Well you know the risk of self-medicating, do not do that, I had facial spasms with only 3 days of use of quetiapine (prescribed by shrink). Doctors actually know about the disorder, but since it is something very recent and vague hardly anyone is diagnosed with it, even because sequels of psychedelic drugs are not the only reason for the cause of false visual perceptions or other senses without loss of lucidity. So go to the psychiatrist anyway, because only then will you get these medications and then heal. Other than this, physical activities are great for diverting your focus from the problem, but the visual symptoms will only disappear with treatment using remedies. I also suggest meditation and some artistic activity such as writing, drawing, playing an instrument, etc. And also temporary abolition of coffee, alcohol and cigarette consumption. Posted March 25 Hello ! Your story is very similar to everyone here, including mine. When I had HPPD, I also got the symptoms very fast and only noticed them after smoking marijuana days after my trip with LSD. What matters is that as quickly as the symptoms came, they left. This is because I did psychiatric treatment, initially using paroxetine for anxiety, risperidone for visual distortions and clonazepam for anxious seizures. Risperidone is an antipsychotic and a major antagonist of LSD as well as quetiapine and chlorpromazine (I have taken all of these, but risperidone was the most effective). In a matter of two months the false hallucinogenic perceptions were gone. With you it would not be different, but for this you need to look for a psychiatrist and explain what happens to you, as he will know the right medication to apply. Please do not self-medicate, as these medicines can have horrible adverse reactions. I for example had facial spasms when I took quetiapine (this I only took for 3 days). I recommend that you do not look for it on the internet, because it is still very vague, unfortunately it is difficult to find information about it and almost all are scary, as it comes from a sensational and anti-drug media. Rest assured, what happens to you is nothing serious and has a cure. Avoid using drugs at this time, including marijuana, alcohol, cigarettes, and coffee. Stay in peace ! If you read most of his posts he is very adamant that Risperidone cured his HPPD. I found another poster too... Posted October 26, 2013 I have HPPD consisting of marihuana-like derealization, LSD-like movements of surfaces, and optical noise. The LSD-like movements had gotten much better over the course of 7 years until they were barely noticeable, until I took Ritalin. Within two weeks, the LSD effects were almost as bad as in the beginning. The rest of my visual effects were not affected. I discontinued Ritalin. The LSD effects remained unchanged (other than going through their usual cyclical fluctuation over 5 days (IIRC) for the next few weeks. Then I started taking low-dose Risperidone (2mg, I think). For the first two days, nothing happened. On day 3, the LSD effects were basically turned off, back to barely noticeable. It was like flipping a switch. In the morning they were there, in the afternoon they were almost gone. I continued taking Risperidone for a few weeks, even increased the dosage, but nothing else happened. There was no effect on my other visuals. After discontinuing Risperidone, the LSD effects did not return, even when I started taking Ritalin again (strange, huh?). I've been taking Ritalin for a few years now. The HPPD symptoms are stable. Caffeine never affected my symptoms. I also found another poster saying he was cured by 200mg of Lamotrigine, which is an antiseizure medication, but it would be clear that this would only treat the symptoms since they are probably similar to epilepsy like disruptions in the brains resonations. Also, there are arguements that Risperidone, an inverse agonist of 5HTP2A exasperates symptoms of HPPD, which is also probably very true, as per the drug in itself without history of HPPD can cause palinopsia. I'm guessing the difference is just in the dose, as the one guy listed his dose which was very smart of him, and as far as I'm concerned is a pretty low dose, not the lowest, but pretty low, as the high does is 200mg. So the answer may very well be in inverse agonists, and maybe even antagonists as well. whichever being the case I'm not entirely sure. Interestingly enough this is probably the "reversal" that hope's research team may have in mind, whether they read my initial ideas/post in my first thread I have no idea, and if that is what they have in mind I'm not entirely sure. But this may very well be it. The cure for HPPD.
  23. Yah, I'm aware of the virus situation, if its a virus I dont know what to do. I'll read those thread you posted later today to see what they all say. Healthier life definitely helps, but placebo effect should be considered as well.
×
×
  • Create New...

Important Information

By using this site, you agree to our Terms of Use.