Fawkinchit

So, I've been here, working on this, for 8 years now, and I think I have a conclusion. The main thing that I have noticed about HPPD, is that it is quite similar in presentation, though not so much in symptoms, to other mental health conditions, mainly epilepsy, and migraines. I have also found some convincing evidence that it is even somewhat similar in fashion to PTSD. Now, I believe its been quite discussed that as far as significant neuronal loss is concerned, it doesn't appear to be quite the case in HPPD, though I can't argue that some aren't lost, it doesn't appear to be the main driving factor involved. So, from there going on we have to look beyond the organ itself, the brain, and beyond the cell itself, the neuron, to the intricacies thereof involved within the structure, and within the metabolism. Given lack of studies this is a difficult thing, but if we take in to consideration the presentation of other similar conditions there is a common factor involved, this factor appears to be mitochondrial dysfunction. We can easily assert and know for certain that it is a definite and common finding within the investigations of epilepsy, and even in migraines as well, this is a proven fact. My idea is simple, that these are all the same conditions, effecting different areas of the brain, or possibly even different aspects of the mitochondrion. Now, this may all seem complicated, but there's no need to bewail over this matter, as I have found multiple ways of reversing mitochondrial dysfunction, some out of pure common sense, and others by proven scientific research. As for example the matter of migraines, it was shown in studies to be ameliorated by long term use of 400mg of riboflavin/vitamin b2, and reverse the condition of migraines all together. This is a great hope, and opportunity. Now, this isn't all, based on a lot of my reading, and findings, which I will not go in to depth about as to how I came to this conclusion, or that conclusion, there are other methods as well of achieving this outcome, which is very exciting, and may yield very positive and beneficial results. So, what I recommend also, is grape seed extract, because of the high content of proanthocyanins, which will also achieve the same goal of ameliorating mitochondrial dysfunction. Yet it would be better if you consume also a great deal of grapes with seeds in them, seedless however are rendered ineffectual, as the highest content of proanthocyanins are in the seeds. And if any are so inclined to try other things of the same magnitude, it would be wise to drink cinquefoil, and common sage as a tea, daily. All in my opinion are very fit for the amelioration of mitochondrial dysfunction, and the sage will help proliferations in the brain, and often gives a calming effect. So anyone can try this one or that one, or all together, its no matter to me. Just be safe and use increments in dosage to be sure there aren't any immediate worsening of symptoms, as some may react different than others. The time it should take for resolution is about 3-6 months. As for the dosage, grape seed extract should be minimum 8000mg, cinquefoil and sage just make a tea as anyone usually would. Good luck and if anyone is in want of a greater calming effect for their symptoms immediately, add cowslip to the tea.

Jay nailed it.

Completely agree with this, and at this point if I were you, cease all drug use for the rest of your life, there are a number of people that I have seen on here, that were where you are, and tried some weed or something mild even years down the road, and got full blown HPPD, dont risk it dude, its not worth it.

This is really fascinating.

Really, please, explain your symptoms and experience, its very interesting to hear stories like this. Thanks.

When my computer is back up and running I can take a look at it. Im just waiting for a new processor, should be a couple weeks though.

Mitochondria dysfunction in neurons could have a possible role. Obviously the article is geared more towards depression and suicide, but they mention PTSD as well, and I'm sure that the problems caused by mitochondrial dysfunctions could be expanded to HPPD as well. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4417658/ The Role of Nutrients in Protecting Mitochondrial Function and Neurotransmitter Signaling: Implications for the Treatment of Depression, PTSD, and Suicidal Behaviors Jing Du,1,3,*# Ming Zhu,1,* Hongkun Bao,1 Bai Li,1 Yilong Dong,1 Chunjie Xiao,1 Grace Y. Zhang,3 Ioline Henter,4 Matthew Rudorfer,2 and Benedetto Vitiello2 Author information Copyright and License information Disclaimer The publisher's final edited version of this article is available at Crit Rev Food Sci Nutr See other articles in PMC that cite the published article. Go to: Abstract Numerous studies have linked severe stress to the development of major depressive disorder (MDD), and suicidal behaviors. Furthermore, recent preclinical studies from our laboratory and others have demonstrated that in rodents, chronic stress and the stress hormone cortisol has caused oxidative damage to mitochondrial function and membrane lipids in the brain. Mitochondria play a key role in synaptic neurotransmitter signaling by providing adenosine triphosphate (ATP), mediating lipid and protein synthesis, buffering intracellular calcium, and regulating apoptotic and resilience pathways. Membrane lipids are similarly essential to central nervous system (CNS) function, because cholesterol, polyunsaturated fatty acids, and sphingolipids form a lipid raft region, a special lipid region on the membrane that mediates neurotransmitter signaling through G-protein coupled receptors and ion channels. Low serum cholesterol levels, low antioxidant capacity, and abnormal early morning cortisol levels are biomarkers consistently associated with both depression and suicidal behaviors. In this review, we summarize the manner in which nutrients can protect against oxidative damage to mitochondria and lipids in the neuronal circuits associated with cognitive and affective behaviors. These nutrients include ω3 fatty acids, antioxidants (vitamin C and zinc), members of the vitamin B family (Vitamin B12 and folic acid) and magnesium. Accumulating data have shown that these nutrients can enhance neurocognitive function, and may have therapeutic benefits for depression and suicidal behaviors. A growing body of studies suggests the intriguing possibility that regular consumption of these nutrients may help prevent the onset of mood disorders and suicidal behaviors in vulnerable individuals, or significantly augment the therapeutic effect of available antidepressants. These findings have important implications for the health of both military and civilian populations. Keywords: vitamin, oxidative stress, synaptic plasticity, lipid, suicide, zinc

When HPPD is really bad, paranoia and high anxiety is definitely a symptom. I initially had paranoia that I knew was most probable to be illegitimate thoughts, granted they were. The paranoia eventually resolved to some degree, the anxiety never did, it was crippling. Voices I never heard, that is more synonymous with schizophrenia, but HPPD sufferers typically reports a wide variety of symptoms, so its not impossible.

I left a comment, its just one doctor, and he clearly has a biased perspective, and possibly a biased "agenda" aka hes getting money to do work, this often sways researchers, especially if they are trying to get a foothold or build a name for themselves.

https://www.sciencedirect.com/science/article/pii/0041008X66901281 adding this for later

Completely agree, actually my HPPD no longer has symptoms revolving around the more recognized symptoms, it just seems to manifest in severe anxiety some times, like it literally feels like my entire nervous system is on fire. and it goes away after a couple hours. I rarely have issue anymore but sometimes it does flare up. I used to have a lot of the typical symptoms when I first got it and it was full blast. Anyways I want to post this write up by Dr. Royal Lee, from all the doctors I've seen I haven't seen many a greater, if any at all, and he does explain that brain dysfunction can stem from liver issues, and plainly states that narcotics can disrupt the urea(carbamide) production, which is specifically in the liver, so we may just have a liver issue. What I'm wondering is maybe there is a correlation, and in HPPD the narcotic induces long term change in the liver, or the livers function in metabolizing urea/carbamide.

After more research I wanted to post this, as I have been postulating that there could be adrenal dysfunction involved in HPPD. But there would likely have to be clear evidence that hallucinogens have impacts on the adrenals in the first place. So here I'm presenting this study. So it shows there could be some sort of adrenal dysfunction involved, which seems a bit misguided, but Dr. Royal Lee talks about caused hallucinations and their involvements with the adrenals, and I even found a case report of a man who was hallucinating badly, and it was eventually found that for some reason his adrenals weren't producing cortisol, on administration of synthetic cortisol there was a remission of the hallucinations. https://pubmed.ncbi.nlm.nih.gov/26849997/ Acute Effects of Lysergic Acid Diethylamide on Circulating Steroid Levels in Healthy Subjects P Strajhar 1, Y Schmid 2, E Liakoni 2, P C Dolder 2 3, K M Rentsch 3, D V Kratschmar 1, A Odermatt 1, M E Liechti 2 Affiliations expand PMID: 26849997 DOI: 10.1111/jne.12374 Abstract Lysergic acid diethylamide (LSD) is a serotonin 5-hydroxytryptamine-2A (5-HT2A ) receptor agonist that is used recreationally worldwide. Interest in LSD research in humans waned after the 1970s, although the use of LSD in psychiatric research and practice has recently gained increasing attention. LSD produces pronounced acute psychedelic effects, although its influence on plasma steroid levels over time has not yet been characterised in humans. The effects of LSD (200 μg) or placebo on plasma steroid levels were investigated in 16 healthy subjects using a randomised, double-blind, placebo-controlled, cross-over study design. Plasma concentration-time profiles were determined for 15 steroids using liquid-chromatography tandem mass-spectrometry. LSD increased plasma concentrations of the glucocorticoids cortisol, cortisone, corticosterone and 11-dehydrocorticosterone compared to placebo. The mean maximum concentration of LSD was reached at 1.7 h. Mean peak psychedelic effects were reached at 2.4 h, with significant alterations in mental state from 0.5 h to > 10 h. Mean maximal concentrations of cortisol and corticosterone were reached at 2.5 h and 1.9 h, and significant elevations were observed 1.5-6 h and 1-3 h after drug administration, respectively. LSD also significantly increased plasma concentrations of the androgen dehydroepiandrosterone but not other androgens, progestogens or mineralocorticoids compared to placebo. A close relationship was found between plasma LSD concentrations and changes in plasma cortisol and corticosterone and the psychotropic response to LSD, and no clockwise hysteresis was observed. In conclusion, LSD produces significant acute effects on circulating steroids, especially glucocorticoids. LSD-induced changes in circulating glucocorticoids were associated with plasma LSD concentrations over time and showed no acute pharmacological tolerance.

Whats up mgrade long time no see how have you been? Looks like you been doing some writing? Also to everyone: I just linked up with Oliver on Whatsapp, if anyone would like to join a group chat just send me your information for whatsapp and I will add you to the chat! Also for an update I am still doing a lot of work on trying to find something relevant for this disorder, after the long years of working on it though I'm extremely exhausted, and there have been so many other things in life that I have been trying to accomplish and keep together as well. I am still trying to make progress though and have been looking in to some interesting and relevant information involving other conditions that develop like symptoms and also hallucinations. Its become apparent that there are a lot of conditions of the body that are linked to healthy brain function, and when there are issues with these sections of the body, the brain does not function as it should, it isn't then per say, a requisite that the disorder lies solely in the brain, but could be elsewhere. I will try to share relevant information when I have time. I apologize to everyone that I haven't been as busy with this as usual. I do genuinely hope that we all end in a happy place and get a second chance, and I thank everyone that has posted here and talked with me and shared their information, it has been really encouraging and uplifting to continue trying. Thanks for everyone too that has been kind to me and reached out, I apologize also to anyone that I have not been able to help significantly, or have been rude to in the past, as I was under a lot of stress, and didn't have the best functioning brain for proper emotional handling. Also, Hope, the website looks good!

I can’t imagine any reason why Verapamil would make much difference. Its a calcium channel blocker, if I remember correctly its a minute dose of snake venom.

I’ve seen numerous posters here having a negative review, I never go there so I can’t speak for myself. I do believe that reddit can be very informative, but also over extensive in their liberal and modern views, while also using their broad knowledge base for an excuse to be close minded from anything different in their thought of concrete beliefs. I doubt that benzodiazepines have any drastic negative impact long term, but coming off them could have negative impacts on symptoms due to receptor adjustment, according to research it should only be temporary and symptoms within a month after discontinuation should technically return to baseline. However there are no studies I’m aware of that prove that, and in medicine thats really important.

Wow, this i the first case I have seen from nutmeg.

https://www.tapatalk.com/groups/thosewithvisualsnow/a-discussion-with-dr-weatherall-the-leading-visual-t7745.html found these people talking about their visual snow and found it interesting their non drug use sudden onsets...

Definitely expresses how I feel also.

The relation between migraine, typical migraine aura and "visual snow". Schankin CJ1, Maniyar FH, Sprenger T, Chou DE, Eller M, Goadsby PJ. Author information Erratum in Headache. 2015 Apr;55(4):592. Abstract OBJECTIVE: To assess the relationship between the phenotype of the "visual snow" syndrome, comorbid migraine, and typical migraine aura on a clinical basis and using functional brain imaging. BACKGROUND: Patients with "visual snow" suffer from continuous TV-static-like tiny flickering dots in the entire visual field. Most patients describe a syndrome with additional visual symptoms of the following categories: palinopsia ("afterimages" and "trailing"), entopic phenomena arising from the optic apparatus itself (floaters, blue field entoptic phenomenon, photopsia, self-light of the eye), photophobia, nyctalopia (impaired night vision), as well as the non-visual symptom tinnitus. The high prevalence of migraine and typical migraine aura in this population has led to the assumption that "visual snow" is caused by persistent migraine aura. Due to the lack of objective measures, alternative diagnoses are malingering or a psychogenic disorder. METHODS: (1) The prevalence of additional visual symptoms, tinnitus, and comorbid migraine as well as typical migraine aura was assessed in a prospective semi-structured telephone interview of patients with "visual snow." Correlations were calculated using standard statistics with P < .05 being considered statistically significant. (2) Areas with increased brain metabolism in a group of "visual snow" patients in comparison to healthy controls were identified using [(18) F]-2-fluoro-2-deoxy-D-glucose positron emission tomography and statistical parametric mapping (SPM8 with whole brain analysis; statistical significance was defined by P < .001 uncorrected for multiple comparisons). RESULTS: (1) Of 120 patients with "visual snow," 70 patients also had migraine and 37 had typical migraine aura. Having comorbid migraine was associated with an increased likelihood of having palinopsia (odds ratio [OR] 2.8; P = .04 for "afterimages" and OR 2.6; P = .01 for "trailing"), spontaneous photopsia (OR 2.9; P = .004), photophobia (OR 3.2; P = .005), nyctalopia (OR 2.7; P = .01), and tinnitus (OR 2.9; P = .006). Typical migraine aura was associated with an increased likelihood of spontaneous photopsia (OR 2.4; P = .04). (2) After adjusting for typical migraine aura, comparison of 17 "visual snow" patients with 17 age and gender matched controls showed brain hypermetabolism in the right lingual gyrus (Montreal Neurological Institute coordinates 16-78-5; kE  = 101; ZE  = 3.41; P < .001) and the left cerebellar anterior lobe adjacent to the left lingual gyrus (Montreal Neurological Institute coordinates -12-62-9; kE  = 152; ZE  = 3.28; P = .001). CONCLUSIONS: -Comorbid migraine aggravates the clinical phenotype of the "visual snow" syndrome by worsening some of the additional visual symptoms and tinnitus. This might bias studies on "visual snow" by migraineurs offering study participation more likely than non-migraineurs due to a more severe clinical presentation. The independence of entoptic phenomena from comorbid migraine indicates "visual snow" is the main determinant. The hypermetabolic lingual gyrus confirms a brain dysfunction in patients with "visual snow." The metabolic pattern differs from interictal migraine with some similarities to migrainous photophobia. The findings support the view that "visual snow," migraine, and typical migraine aura are distinct syndromes with shared pathophysiological mechanisms that need to be addressed in order to develop rational treatment strategies for this disabling condition.

Whenever my symptoms got any worse It was because of some external source. The degree of your symptom exacerbation is pretty strange though. This is an extremely strange condition.

Its normal, sometimes the symptoms get worse before they start to get better. For some strange reason my visual snow didn’t even appear till a month after I got HPPD. Didn’t know what the fuck was even happening to me because the doctors didn’t have an explanation.

Pretty interesting.

Anxiety, it was literally insane for me, it wasn’t from the other symptoms either, it was a thing of its own, it destroyed me every day, it was literally crippling. I never knew it was possible to suffer so much, back pain from herniation isn’t even close to comparable, maybe severe pain from a tooth infection, but i would even take that any day over HPPD, its not comparable to a physical pain.. The anxiety was so bad I wanted to just die, i remember the only time I got any relief was when I went to sleep.i spent so many years in so much pain that even today it effects me emotionally, like I’m scarred, sometimes I enjoy life so little because it was so bad that I think maybe I should still kill myself, like I said I never knew it was possible to suffer so much.

I agree, I bought a Jeep Cherokee once and whenever I would take long drives in it it would send my symptoms through the rough, eventually decided to sell it for that reason, next car didn’t have any problem with.

Im pretty sure use the shear stress from HPPD causes gastrointestinal issues sometime. Pretty sure it gave me an ulcer or something.