Fawkinchit

https://jnnp.bmj.com/content/early/2021/07/13/jnnp-2020-325881 Localised increase in regional cerebral perfusion in patients with visual snow syndrome: a pseudo-continuous arterial spin labelling study

They should help for sure, to assist in proper functioning of mitochondria, mitochondria are massively dense in synapses, and make all the work happen so they are crucial for a well function brain. Antioxidants may not make you live forever, but they do support and assist mitochondria massively, and niacin appears to be something special. So just eating healthy foods, fruits, veggies, nuts, and whole grains, will boost all these levels. Its a great place to start absolutely.

I can't really say that it has because mine got significantly better to the point where I'm not really in a position to try things out, my symptoms now are so vague it would be hard for me to tell improvement. Realistically as well any improvement would simply just mean slight improvement to 100% symptom free. The only symptoms I have anymore is if I drink too much coffee, I've also noticed an increase in heart rate after eating potatoes lol, but that could be completely unrelated, although it does seem to give me some mild anxiety. I think as well my brain doesn't regulate normal anxiolytic reactions from external sources as it should or used to. Other than that for my symptoms I can only say that sometimes I just feel like there is a certain joy missing that I used to have in life, but again that could be circumstantial and not symptomatic per say, it could also be an end result of suffering so severely for years from crushingly painful HPPD, this condition in a severe form I do believe does take a great deal of toll on the mental state of a human, as though being trapped in a tortuous prison.

Interesting! I saw a post by someone who claims to have gotten HPPD by an NMDA antagonist. See also: Olney's lesions Although NMDA antagonists were once thought to reliably cause neurotoxicity in humans in the form of Olney's lesions, recent research suggests otherwise. Olney's lesions involve mass vacuolization of neurons observed in rodents.[18][19] However, many suggest that this is not a valid model of human use, and studies conducted on primates have shown that use must be heavy and chronic to cause neurotoxicity.[20][21] A 2009 review found no evidence of ketamine-induced neuron death in humans.[22] However, temporary and permanent cognitive impairments have been shown to occur in long-term or heavy human users of the NMDA antagonists PCP and ketamine. A large-scale, longitudinal study found that current frequent ketamine users have modest cognitive deficits, while infrequent or former heavy users do not.[23] Many drugs have been found that lessen the risk of neurotoxicity from NMDA receptor antagonists. Centrally acting alpha 2 agonists such as clonidine and guanfacine are thought to most directly target the etiology of NMDA neurotoxicity. Other drugs acting on various neurotransmitter systems known to inhibit NMDA antagonist neurotoxicity include: anticholinergics, diazepam, barbiturates,[24] ethanol,[25] 5-HT2A serotonin receptor agonists,[26] anticonvulsants,[27] and muscimol.[28] "I was amazed to follow the discussion about vacuoles in the dorsal root ganglia neurons (Toxicol Pathol38, 554–59; 999; 39, 451–453). Vacuolation of neurons represents hydropic degeneration, which in the dorsal root ganglia may result in neuronal death and formation of nodules of Nageotte replacing the lost neurons. Obviously for some neuropathologists the only possible way neurons can die is through “apoptosis.” But this is not true. In our studies with toxicity of extremely high doses of pyridoxine (vitamin B6), we have demonstrated that cytoplasmic vacuoles can easily be produced experimentally and that they are harbingers of neuronal death (Krinke et al. 1981; Krinke et al. 1985; Krinke 1988). Neuronal vacuoles can appear spontaneously, especially in aging animals. They are unspecific, that is, not related to the chemical structure of the toxicant, and they can also be produced by trauma. In the context of “mad cow disease,” or bovine spongiform encephalopathy, the attention of European pathologists was focused on the occurrence of vacuolated neurons in the bovine brain. Examination of 378 bovine brains revealed that in 11.5% of the animals, there were large neuronal vacuoles in the brain stem, especially the red nucleus, that were nonspecific and spontaneous (Guarda and Fatzer 1995). More research into neuronal cytoplasmic vacuolation and its role as an alternative to apoptosis is needed." Georg J. Krinke Prof., MVDr, Dipl ECVP, Eggstrasse 26, CH-4402, Frenkendorf, Switzerland Abstract N-Methyl-D-aspartate (NMDA) antagonists cause neuronal vacuolation in the posterior cingulate and retrosplenial cortex of the rat. Because the nature of neuronal pathologic changes due to NMDA antagonists may affect the potential clinical use of this class of drugs, we undertook experiments to define the nature and time course of the vacuolation caused by high-dose (5 mg/kg) MK-801 (dizocilpine, 5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine). Ultrastructural examination revealed the vacuoles to be not a form of hydropic cellular degeneration, but rather a dilatation of several intracellular compartments, chiefly endoplasmic reticulum and mitochondria. Study of the time course of the alterations revealed no light or ultrastructural features of neuronal necrosis in over 1 thousand neurons examined in layers 3 and 4 of the cingulate and retrosplenial cortex, 153 of which were vacuolated. The vacuoles resolved over time by decreasing in magnitude. Oxalate-pyroantimonate methodology revealed no redistribution of cell calcium in either vacuolated or non-vacuolated neurons. At 6 h, when vacuoles were consistently prominent in glutaraldehyde-fixed plastic-embedded tissue, a separate series of experiments was undertaken to vary methods of tissue preparation, and determine conditions under which vacuolation occurs. Frozen sections revealed no vacuoles. Subsequent paraffin embedding of the previously frozen tissue revealed no vacuoles, but vacuoles were seen in paraffin after perfusion fixation. Immersion fixation with brain refrigeration for 12 h prior to fixation revealed no vacuoles. Alcohol fixation also led to no visible vacuoles.(ABSTRACT TRUNCATED AT 250 WORDS)

Lmao.... its true.

Interesting that he eventually develops seizures. You see kids, doctors are fucking stupid, case in point. Now hes on topiramate, Im not sure about that one specifically but most anti seizure meds long term cause neuronal loss, and after about 20 years most patients so significant signs of reduced brain size. But as I have said I do believe that HPPD, migraines, and seizures are closely related.

Its your choice, I just don't understand exactly why you would though. I don't particularly understand a lot of peoples choices though.

Can you give at least a brief description of your symptoms, its not entirely common for HPPD to progress in symptoms after about a month of getting it.

I smoke a cigar every now and again, with little to no issues.

"Took me another year to get back to my semi normal state." Pretty much answered your own question. Edit: Im a little confused as to what was in the "blunt" though. if it was just tobacco thats a little strange.

Definitely! Its extremely safe, nothing more safe than vitamins, other than water and air lol. Just be sure to do a minimum of 500mg per day, max 1000mg should do the trick. And make sure to read up on niacin flush so it doesn't freak you out. Based on what I have read no flush is not as effective as normal niacin. But it would be great for even just a few people to try this, just to see if it works or not. If I remember correctly there was even a study on rat neurons that showed only 2 weeks of niacin therapy relegated all age related cellular conditions, so basically the cells in older rats became again as though they were young. If this condition is caused by neuronal dysfunction, as opposed to neuronal loss, then niacin will be the best treatment there is for HPPD, hands down.

Honestly if thats the only symptom you have consider yourself lucky as fuck. Dont do drugs ever again and enjoy your life.

Dude! Thank you so much for trying this, I talk about this in my thread, I think it may be one of the better if not possibly the best treatments for this, but I have found no one willing to try it as of yet. So thank you so much. Please keep updating, I would love to see how this turns out and I really hope the best. I have taken Niacin myself and I feel like it helped me feel better all around in general, but by the time I learned about it most of my symptoms have receded, so its great to see someone with more apparent symptoms trying it. If it doesn't help or work then so be it, but I feel it has enough potential that it should be tried. So thank you! This is my thread for anyone wondering.

Had no idea you were 32 @Löken Honestly, IMO, why mess with it all. I will drink sometimes but thats it. Some HPPDers cant even do that.

Yah that sounds really difficult, especially after such a long interim. Its really hard to say what it could be, but large amounts of stress and emotion can definitely be hard on the neurons themselves, exhibiting like symptoms or causing reoccurrence thereof. That's one of the things about HPPD, is that normal life becomes much more difficult to deal with when things are hectic, its really a struggle for sure.

Damn 10 year later lmao

This may not be entirely accurate, I do believe there are rare cases that do not present much for visual disturbances. For myself in fact I didn't develop visual snow for a couple weeks, and eventually the visual snow went away, however other symptoms remained. It does however seem like something is going on, I agree it may not be HPPD, but it does seem like something neurological is going on, and given the series of events a form of HPPD is probable. To be honest though, what you're reporting Lucas is rather mild in comparison to what I have seen in other sufferers.

Edit

Those are valid points. However its unarguable that microdosing causes HPPD, there are numerous people to attest to the fact that thats how they got it. Just going to randomly throw this article in here lmao... wtf A woman took 550 times the usual dose of LSD, with surprisingly positive consequences https://www.cnn.com/2020/02/27/health/lsd-overdoses-case-studies-wellness/index.html

https://pubmed.ncbi.nlm.nih.gov/2780790/ This shows aggressive long term affects from microdosing. And there are plenty of people that have reported HPPD from microdosing. @NRFAdmin knows more examples of people than I do however. @Jay1 Also can probably attest to the fact that a good amount of people that post here got it from microdosing. Also a google or reddit search will probably help as well.

Microdosing can definitely cause HPPD, has, and may even have a higher potential than normal recreational use for causing it if the the microdosing is consistent. Studies have shown this.

Just posting this for further reading Ion channels have key functions in the nervous system, including the generation, repression and propagation of action potentials. The opening of Na+ channels depolarizes neurons, while the opening of K+ channels will lead to hyperpolarization. The situation is more complex with Cl− channels, because the cytoplasmic chloride concentration depends upon the cell type, and changes during development. Thus, an opening of Cl− channels may lead to a hyperpolarization (as in most neurons of the adult CNS) or to a depolarization (as in early development). Given the very large transmembrane gradient of Ca2+, Ca2+ currents will always be depolarizing. However, the role of Ca2+ as a second messenger is more important under most circumstances. Taking these considerations into account, loss-of-function mutations in neuronal K+ or Cl− channels, or gain-of-function mutations in neuronal Na+ channels, should give rise to hyperexcitability and perhaps epilepsy. While this indeed turns out to be true in some cases, it should be borne in mind that the systemic effect depends on the particular neuronal circuitry that is affected. For instance, ion channel mutations leading to a selective hyperexcitability of inhibitory interneurons are expected to rather decrease CNS excitability. Although K+ channel defects were long suspected to underlie some forms of epilepsy, this was proven only in 1998, when it was shown that mutations in KCNQ2 and KCNQ3 underlie benign familial neonatal convulsions, a generalized epilepsy of the newborn (21,22,51). KCNQ2 and KCNQ3 are neuron-specific K+ channels that are broadly expressed in the CNS, where they assemble to heteromeric channels (11,52). KCNQ2/KCNQ3 heteromers are a molecular correlate of the M current (53). This current was first described in sympathetic neurons as a non-inactivating K+ current that could be inhibited by muscarinic stimulation (hence its name ‘M current’) (54). M currents are involved in regulating the subthreshold excitability of neurons and their responsiveness to synaptic inputs. This physiological, extremely sensitive regulation of neuronal excitability probably explains why a small loss of M currents suffices to cause epilepsy (55). From in vitro studies, it was concluded that mutations found in BFNC reduce current amplitudes by merely 25% (11). Interestingly, the homozygous knockout of KCNQ2 in mice is lethal, and heterozygous animals have a reduced seizure threshold (56). Recently, a particular mutation in the voltage sensor of KCNQ2 was shown to lead to neonatal epilepsy with myokymia (involuntarily contractions of skeletal muscles), pointing to a role of M currents in motor neuron control (57). A dominant form of episodic ataxia that is accompanied by myokymia was previously shown to be caused by mutations in the Kv1.1 K+ channel (encoded by KCNA1) (58). This K+ channel is strongly expressed in myelinated peripheral nerves and cerebellar interneurons, where it contributes to the repolarization of action potentials. Mutations in pore-forming α and accessory β subunits of voltage-gated Na+ channels of the CNS were found to underlie other forms of epilepsy (59–61). Mutations in the SCN1A α subunit (59) and in the SCN1B β subunit (60) cause generalized epilepsy with febrile seizures (GEFS+), while mutations in another α-subunit isoform (SCN2A) (61) yield a somewhat different clinical picture (generalized epilepsy with febrile and afebrile seizures). Similar to previous findings with skeletal muscle Na+ channel mutations, for example in periodic paralysis (12), the mutant channels do not inactivate properly (15). Mutations in the Ca2+ channel gene CACNA1A (encoding Cav2.1) can cause ataxia and migraine (62,63), and this gene may also be associated with epilepsy (64). Mutations in another channel type whose opening leads to depolarization, namely two different subunits of the nicotinic acetylcholine receptor, have also been shown to be associated with epilepsy (65,66). Although the mutants have been studied in heterologous expression systems, the mechanism by which they lead to autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is incompletely understood (67). Rather surprisingly, no unambiguous association with human genetic disease has been established so far for the major class of CNS excitatory neurotransmitter receptors, the glutamate receptors. The main inhibitory neurotransmitters, GABA and glycine, exert their fast inhibitory effect through ligand-gated Cl− channels: the GABAA and glycine receptors. Because intracellular Cl− is usually below its electrochemical equilibrium in adult neurons, opening of these receptors leads to a hyperpolarizing Cl− influx. The sedative and anxiolytic effects of benzodiazepines depend on a modulatory upregulation of GABAA receptor activity. Only recently, two GABAA receptor subunit genes were found to be affected in epilepsy. Mutations in the γ2 subunit of the GABAA receptor (GABRG2) were identified in childhood absence epilepsy and febrile seizures (68), as well as in generalized epilepsy with febrile seizures (GEFS+) (69). A mutation of GABRA1, which encodes the α1 subunit of the GABAA receptor, was recently associated with an autosomal dominant form of juvenile myoclonus epilepsy (70). Mutations of the α1 glycine receptor cause autosomal dominant hyperekplexia (startle disease) (71), which is characterized by marked muscular hypertonia in infancy and a grossly exaggerated response to unexpected stimuli. As the electrophysiological effect of GABA and glycine depends on the intracellular Cl− concentration, one may speculate that mutations in transporters involved in intracellular Cl− concentration regulation may also affect neuronal excitability. In fact, a locus for rolandic and idiopathic generalized epilepsy maps close to KCC3, a K–Cl co-transporter that is expressed in the CNS. Like other KCCs, it is expected to contribute to postsynaptic inhibition by lowering [Cl−]i. However, no mutations were found in SLC12A6, the gene encoding KCC3, in the linked families (72). In contrast, the disruption in mice of the neuronal-specific isoform KCC2 caused severe motor deficits due to defective GABA- and glycine-mediated synaptic inhibition, and led to early postnatal death (73). Mice with an incomplete gene disruption survived for a couple of weeks and displayed severe seizures (74).

No not at all, not for HPPD, sounds more like a peripheral neurology issue(if it is anything), if it gets worse or doesn't go away typically its cause by various vitamin deficiencies.

Sounds pretty mild to be honest. Just give it time and definitely never touch hallucinogens again or you'll end up back here. Typically when you have HPPD you KNOW you have HPPD. Cause its a nightmare. The symptoms are synonymous with HPPD though, but again, sound very mild.

That awesome bro! Edit: Just realized this is a thread bump lol