Onemorestep

Oh for sure. The article on hallucinogens and autoimmune is simply to further illustrate, after the pig study, that hallucinogens can have an effect on our immune functioning in a permanent way. And immune system dysfunction in the cns —> increased interleukins—>mitochondrial, astrocyte, microglial ros crazy time party. I am in no way am I suggesting that one should take them if you have hppd hahaha. I didn’t think I needed to point that out but for anyone who sees that article— please do not infer that a) hppd is an autoimmune condition—that, like everything else on this website, is theoretical or b) that taking more will alleviate your symptoms.

will it? Probably will improve for sure. You could also meditate, take cold showers, and reduce stress instead of meds.

Yes— imo this is inflammation. When I’ve had BAD hppd it’s felt like narcolepsy even. When the brain is under stress like this, endogenous cannabinoid activity also increases. Can add to that spacey sleepy feeling. low dose naltrexone, ibudilast, prednisone short term TAPER. Anything that reduces the following generally should help. Avoid herbs with complex mechanisms of action. You want very direct effects. interluekin-1b; il-b interleukin-6 , il-6 tnf-alpha; tnf-a ibudilast is your best bet IMO at getting a clear head real fast. Very safe profile. One other user and myself can attest but we’re the only ones to use it I think. first few days on it expect: super irritable, bored. That’s my experience at least. you can buy ibudilast online. I got mine from science.bio but tbh I didn’t get them at all. It seems to work haha.

You must reduce brain inflammation! Ibudilast is the safest thing i've found for this right now.

Hi Anna! im sorry to hear you are suffering so much I’m a bit short on time but to answer your post question: there is indeed a link between HPPD and seizure that is gaining credibility. Here is a post explaining why you can show this to your psychiatrist and it may help you get a prescription for this if you want. There are likely 100’s of different specific subtypes of hppd as it relates to treating it with chemicals, so while Keppra is always a good shot for those who are desperate, it doesn’t work for everyone. Other than that—live your best healthiest life. Nothing else matter but stress reduction and healthy lifestyle. Until more concrete science comes out about treatment we’re all just guessing. Listen to your body. Your life is not over. This too shall pass best, oms

I don’t know anything about nerve damage and psyche but I do know that psychs, by definition of how they work, leave your body extremely vulnerable for a period of time for latent virus’s living in the body to become active and spread very quickly. Psychedelics are “anti-inflammatory” which is also another way of saying “immune suppressing”. even if there is no link there, I would have yourself checked for Lymes and EBV. I have had all your symptoms during EBV flare ups.

Before we get into the significance of this connection, we must first learn a little bit about what Levetiracetam and SV2A are. click (LINK) for links. Keppra In 1999, Levetiracetam (LEV—commercial name: Keppra©) was approved by the Food and Drug administration as a novel anti-epileptic drug. It is particularly useful in patients suffering from partial seizures, patients less responsive to conventional drugs or showing risks of drug interactions (Hovinga, 2001). Even if the exact mechanism by which LEV acts on seizures is still undefined (we don’t even known if LEV is an agonist or antagonist of SV2A), we know that it binds to SV2A and that this binding is required for its anti-epileptic action (Lynch et al., 2004). Implicated residues in this binding are depicted in Figure 4 (Shi et al., 2011; Lee et al., 2015). It is worth noting that LEV is able to normalize under- and over-expression of SV2A in autaptic hippocampal neurons by controlling the concentration of SV2A in the synapse (Nowack et al., 2011). More recently, other compounds were added to the racetam family—Brivaracetam, Selectracetam—and show promises for epilepsy therapeutic control. (LINK) The major mechanism of action of LEV is considered to involve binding to synaptic vesicle glycoprotein 2A (Lynch et al., 2004), although other pharmacological actions have also been demonstrated, such as inhibition of N‐type voltage‐sensitive Ca2+ and K+ channels, AMPA receptors and Ca2+ release from intracellular Ca2+ stores mediated by inositol 1,4,5‐trisphosphate (IP3) receptors (Carunchio et al., 2007; De Smedt et al., 2007b; Fukuyama et al., 2012). In particular, activation of the AMPA receptor plays important roles in the initiation of epileptic seizures and propagation of epileptic discharge (Rogawski, 2002), whereas hyper‐activation of the IP3 receptor contributes to the neuronal damage induced by epileptic seizure, seizure maintenance and dysfunction of GABA exocytosis during epileptic discharge (Pal et al., 2001; Fukuyama et al., 2012). (link) Sv2A SV2A belongs to the Synaptic vesicle (SV) protein 2 family, which also includes SV2B and SV2C. These three paralogs can be found in vesicles of neuronal or endocrine cells. SV2A is the only member of the SV2 family ubiquitously expressed in the adult brain, and is also found in neuroendocrine cells and at neuromuscular junctions (Buckley and Kelly, 1985; Bajjalieh et al., 1994; Dong et al., 2006). SV2A is found in all areas of the brain, including the trigeminal nuclei (Edvinsson et al., 2015) and the sphenopalatine ganglion (Steinberg et al., 2016) where it was recently found. (LINK) One of the first trials on the role of SV2A was the extreme phenotype displayed by SV2A KO mice. Mice that survive birth seem to be normal during their first days of life. However, after 1–2 weeks, they experience seizures, quickly followed by weight loss and death around P20 (Crowder et al., 1999; Janz et al., 1999). (LINK) A more recent electrophysiological study performed on hippocampal slices showed that in the absence of SV2A, EPSC amplitudes remain unchanged while the associated frequencies increase (Venkatesan et al., 2012). The author emphasized that the opposite effect of SV2A on excitatory and inhibitory currents observed in hippocampal slices of SV2A KO likely underlines an effect of SV2A on GABAergic network subsequently impacting the Glutamatergic synapses rather than a direct effect of SV2A on both networks. Interestingly, overexpression of SV2A in autaptic hippocampal neurons produced the typical neurotransmission defect observed in SV2A KO mice (Nowack et al., 2011). (x) Mice models where higher levels of SV2A are found, experience “evoked” seizures in response to convulsing chemicals or mild electrical stimulations rather than real spontaneous seizures (Sharma et al., 2007). (LINK) Now-- On to the show A Single Dose of Psilocybin Increases Synaptic Density and Decreases 5-HT2A Receptor Density in the Pig Brain A single dose of psilocybin, a psychedelic and serotonin 2A receptor (5-HT2AR) agonist, may be associated with antidepressant effects. The mechanism behind its antidepressive action is unknown but could be linked to increased synaptogenesis and down-regulation of cerebral 5-HT2AR. Here, we investigate if a single psychedelic dose of psilocybin changes synaptic vesicle protein 2A (SV2A) and 5-HT2AR density in the pig brain. Twenty-four awake pigs received either 0.08 mg/kg psilocybin or saline intravenously. Twelve pigs (n=6/intervention) were euthanized one day post-injection, while the remaining twelve pigs were euthanized seven days post-injection (n=6/intervention). We performed autoradiography on hippocampus and prefrontal cortex (PFC) sections with [3H]UCB-J (SV2A), [3H]MDL100907 (5-HT2AR antagonist) and [3H]Cimbi-36 (5-HT2AR agonist). One day post psilocybin injection, we observed 4.4% higher hippocampal SV2A density and lowered hippocampal and PFC 5-HT2AR density (-15.21% to -50.19%). These differences were statistically significant in the hippocampus for all radioligands and in PFC for [3H]Cimbi-36 only. Seven days post-intervention, there was still significantly higher SV2A density in hippocampus (+9.24%) and PFC (+6.1%) whereas there were no longer any differences in 5-HT2AR density. Our findings suggest that psilocybin’s antidepressive actions are linked to increased persistent synaptogenesis and possibly also to an acute decrease in 5-HT2AR density. Levetiracetam Reverses Synaptic Deficits Produced by Overexpression of SV2A Levetiracetam is an FDA-approved drug used to treat epilepsy and other disorders of the nervous system. Although it is known that levetiracetam binds the synaptic vesicle protein SV2A, how drug binding affects synaptic functioning remains unknown. Here we report that levetiracetam reverses the effects of excess SV2A in autaptic hippocampal neurons. Expression of an SV2A-EGFP fusion protein produced a ∼1.5-fold increase in synaptic levels of SV2, and resulted in reduced synaptic release probability. The overexpression phenotype parallels that seen in neurons from SV2 knockout mice, which experience severe seizures. Overexpression of SV2A also increased synaptic levels of the calcium-sensor protein synaptotagmin, an SV2-binding protein whose stability and trafficking are regulated by SV2. Treatment with levetiracetam rescued normal neurotransmission and restored normal levels of SV2 and synaptotagmin at the synapse. These results indicate that changes in SV2 expression in either direction impact neurotransmission, and suggest that levetiracetam may modulate SV2 protein interactions. TLDR: Mushrooms increase SV2A. Levetiracetam "normalizes" SV2A. Although we cannot assume causation, this correlation may have something to do with the etiology and treatment of HPPD. More to come Full Links: https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1111/bph.14491 https://core.ac.uk/download/pdf/322961503.pdf https://www.frontiersin.org/articles/10.3389/fnmol.2017.00148/full https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0029560 https://www.preprints.org/manuscript/202011.0742/v1

I wonder if there’s a way to quickly get more vitamins in. (Sulbutiamine, magnesium threonate.?)

I stand corrected--- Valerian is a bit more than just a natural benzo.... "Valeriana officinalis (Valerianaceae) has been of great interest for its therapeutic uses for treating mild nervous tension and temporary sleeping problems. In traditional European medicine it has been also reported as an antiinflammatory remedy. This study reports that the EtOAc extract of the underground parts of V. officinalis showed inhibitory activity against NF-kappaB at 100 microg/mL in the IL-6/Luc assay on HeLa cells and provided protection against excitotoxicity in primary brain cell cultures at micromolar concentrations. Bioassay-guided fractionation of the EtOAc extract led to the isolation of three known sesquiterpenes: acetylvalerenolic acid (1), valerenal (2) and valerenic acid (3), 1 and 3 were active as inhibitors of NF-kappaB at a concentration of 100 microg/mL. Acetylvalerenolic acid (1) reduced NF-kappaB activity to 4%, whereas valerenic acid (3) reduced NF-kappaB activity to 25%."

Psychedelics as a novel approach to treating autoimmune conditions Definitely worth a read. Glad science is finally getting off it’s ass.... lots of interesting stuff in here that can tie to your thoughts Fawk

https://www.pnas.org/content/115/36/9002 IL-18 deficiency—>increased neuronal activity—>reversed by levetiracetam. hallucinogens/ssri’s/cannabis/antibiotics —> alterations in neural immune system—> increased neuronal activity??

I have used it once at a very low dose and didn’t notice anything. But I was also smoking a bunch of weed at the time hehe... hmm never feeling awake? I would do a little research first but it would be very interesting to see if you react well to a dose of prednisone. I’ve been wondering if acute stage hppd could be neuro inflammatory/neuro immune. But it’s really just a theory. Been wondering about the connection between cannabinoids and encephalopathy which does exist. I would try what your doctor gave you first, of course I’m sure it feels kinda scary to try something but I very much doubt you would have a bad reaction to lamictal that wouldn’t wear off in time. It doesn’t appear to interact with hppd in a bad way and if there is glutamate issues this will prevent them from getting worse, at the very least, and allow your brain to get a foothold again.

https://pubmed.ncbi.nlm.nih.gov/10998193/ https://scholar.google.com/scholar?q=experimental+autoimmune+encephalitis&hl=en&as_sdt=0&as_vis=1&oi=scholart#d=gs_qabs&u=%23p%3DZk7M4-de-goJ

You know interestingly enough there is mounting evidence that epilepsy, schizophrenia, migraines are all immune system related. It really does make sense that hppd could be as well. in fact, I think neural immune system issues can account for everything you mentioned in terms of mitochondria, astrocytes, etc. You may find this interesting: https://www.google.com/amp/s/www.psypost.org/2021/01/psilocybin-produces-an-immunology-related-genetic-response-in-the-prefrontal-cortex-of-pig-brains-59115/amp might be worth looking into. you also might find this interesting, as it lines up with your thinking. Baclofen helps amelioriate a large chunk of my cognitive dysfunctions. It did not return my long term memory to exactly what it was, but I could retain information again about facts well. When I began it, I had an INSATIABLE URGE TO EAT EGGS. In fact all I ate for three weeks was eggs. Folates and choline I guess hehe... anyway, I ran across this recently. Baclofen eventually had a deleterious effect on my ability to feel pleasure (complete anhedonia lasting 3 years after reaching 100mg per day after 9 months of use... god it made me high too hehe) but I suspect this was a side effect and possibly just from overuse. https://www.frontiersin.org/articles/10.3389/fpsyt.2018.00506/full

Metformin inhibits mitochondrial ROS. Wanted to throw that in here before I forgot.

Yea I wouldn’t risk it for a very long time if ever. I do think you can have brain specific areas of hppd. Most of the people on this website have emotional anxiety symptoms. Many of the people on Reddit are just enjoying constant visuals and a dreamy headspace (lucky bastards). at the end of the day, we don’t know what causes this but we do know it’s volatile as all fuck and a single dose of a drug can have hppd onset upwards of 6 MONTHS later. Wild right? Just read a case of doctor prescribed ketamine induced hppd for a teenager that got it that long after. but who am I to say this. I give good advice and rarely take it lol.

Hi Ruskin! people absolutely do heal. Abstaining from any psychoactive drug will certainly help your chances. So sorry to hear you are going through this. just remember—this isn’t your fault. Many people smoke a little pot. There’s no way you could have expected this. Go easy on yourself :). its very easy to get sucked into your condition when it’s new. Give it time and do whatever you need to help you pass the time.

https://www.frontiersin.org/articles/10.3389/fneur.2014.00017/full

https://www.google.com/amp/s/www.psypost.org/2021/01/psilocybin-produces-an-immunology-related-genetic-response-in-the-prefrontal-cortex-of-pig-brains-59115/amp

Hi Hall! if part of the etiology of hppd does indeed lie in the loss of gaba inter neurons, resulting in a loss of the “break pedal” and then subsequent glutamate storm—then taking lamictal would help creat an artificial break pedal. It’s a Bandaid... but bandaids are good! They help you heal. And they help prevent you from opening up the wound. hppd has cascade effects for some, it seems. Usually there is initial onset, and then a series of events that take place later (for some). Some people report a see-sawing effect. Some report a worsening after the first, second, or third month. If you are going to take drugs, a good focus is on drugs that offer neuro-protection from glutamate excitotoxic events. Lamictal is one of those. gabapentin also can help, but it comes with its own dependency issues. Benzos are like this too, but the relief, and dependency, seems to be greater. I wouldn’t touch benzos unless you absolutely have to. I think they can be used sparingly, but the temptation if they provide relief is almost too overwhelming to resist for most. something that would very much interest me, is if you have had or currently have Epstein Barr Virus. Although that’s a whole other thing hehe. anyways, I don’t think it will permanently worsen your symptoms or hamper recovery. Most likely it will help your recovery. Will it make u feel better? Not sure. Your personal etiology will decide that. I am currently finding some relief in lithium orotate. Very few people on here seem to have experience with it. One member wrote a long post on why it’s bad but it seemed to be all conjecture so I gave it a shot and it’s been helpful. Magnesium has helped me too in the past.

Keppra inhibits cd8 T cells I have shit tons of immune system issues. They just keep accumulating too.

The first time I got it I didn’t realize I had it, tbh. Symptoms subsided within 6 months if I remember correctly. yymv but I was using harder drugs than you and I imagine that is in your favor. Some symptoms may take longer to go away than others. Don’t assume one is linked to the other. Different brain regions, different rates of recovery time, different symptoms etc. Most of my visuals have subsided in intensity over the years. Some aspects of them gone. I did a LOT OF DRUG man so don’t sweat it. If mine got better you’re will absolutely get better. You’re on the right track. Man I wish I had stumbled across this website before I took traditional psychedelics and really poked the beast... my life would probably be very different. Can’t look back now though. You, on the other hand, have a very bright future ahead of you. This will probably be a year where you periodically feel stronger anxiety than you are used to, but be assured it will pass. And it will not return unless you use drugs. a lot of hppd can resolve on its own or get better with mild therapies. What you don’t wanna do is get yourself in a place where you need to try and do surgery with the sword that cut you. It’s rough (and maybe dumb who knows) trying to find chemicals to dig oneself out of a whole chemicals put themselves in.

After having Epstein Barr enter my brain recently and cause a lot of crazy symptoms I associate with hppd, I’m seriously wondering about possible viral components to this disorder. 95% of people have this virus in them. It can resurface, albeit its “rare” (I’ve had it twice last 4 years... last time I thought I was losing my mind but the doctor didn’t inform me. I simply found out via blood tests.) Psychedelics influence the immune system/would make it easier for latent https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500993/ EBV can cause hallucinations that are eerily similar to the ones I had after getting mushroom hppd. https://www.prweb.com/releases/2013/12/prweb11448461.htm Theres a huge list of symptoms for EBV reactivation. One not need have every one. Last time I had no sore thoat. both times I had EXTREME PANIC waking up one day. Like ungodly panic. This time I wished only for death for 9 straight days. It was the most humbling experience of my life. Is hppd Epstein Barr? Maybe it’s a part of it. Or maybe hppd is a different virus going wild. Perhaps the body gets confused—immune system dysfunction ensues. this might also explain how some people get HPPD NOT from psychedelics as well. Epstein Barr can cause post concussive symptoms not detectable by MRI. its all really interesting stuff. No way I know of to test it haha. Just interesting to find a virus that almost everyone has and can sometimes resurface with emotional or biological triggers, can cause visual hallucinations, alters monoamine status, causes grave emotional changes, and can stick around for a long time (often 8 month-2 years but sometimes forever). or it does nothing and I get a sore throat for a month haha.

I believe in time you will heal on your own a few people on here (myself included) reaaaallly pushed the envelope. It’s a slippery slope and no one here really knows what happened unfortunately. ssris gave me a lot of weird physical anxiety in my abdominal area. It was highly distracting and a huge relief when I came off them and it disappeared. But I would say if you feel better on them, it’s not going to change much. first time I got hppd I was on ssris and it was better on them than off. When I got hppd BAD that’s when I couldn’t tolerate them anymore. Kinda forgot about this. Give this some time and then return to us if it’s still a problem in a year if you really can’t handle the anxiety, or your cognition seems to worsen overnight, try some gabapentin. baclofen returned my cognition to me. Probably because of this: https://pubmed.ncbi.nlm.nih.gov/24838625/ ... but who knows. It also gave me anhedonia after 8 months of high dosing. Not exactly a case study haha.

Did you end up taking it? Doesn’t seem like many people here have. I imagine it’s safe just by it’s moa and in fact there’s some cool stuff about occipital lobe gaba increase with it. it might make you feel dumb af; be prepared.