Fawkinchit

Im starting to wonder if this could just be a depletion or depositing of elements or molecules in the CNS

Idk why tf you know that lmao, to my understanding all that is correct but i was under the impression that it was actually just inaccurately translated to sorcery in biblical scriptures, i could only assume roman catholics used it to dampen occult sciences that could possibly jeopardize their belief structure.

No neurotoxicity..... Behavioural and neurotoxic effects of ayahuasca infusion (Banisteriopsis caapi and Psychotria viridis) in female Wistar rat. Pic-Taylor A1, da Motta LG2, de Morais JA1, Junior WM1, Santos Ade F2, Campos LA3, Mortari MR3, von Zuben MV4, Caldas ED5. Author information Abstract Ayahuasca, a psychoactive beverage used by indigenous and religious groups, is generally prepared by the coction of Psychotria viridis and Banisteriopsis caapi plants containing N,N-dimethyltryptamine (DMT) and β-carboline alkaloids, respectively. To investigate the acute toxicity of ayahuasca, the infusion was administered by gavage to female Wistar rats at doses of 30X and 50X the dose taken during a religious ritual, and the animals observed for 14 days. Behavioural functions were investigated one hour after dosing at 15X and 30X using the open field, elevated plus maze, and forced swimming tests. Neuronal activation (c-fos marked neurons) and toxicity (Fluoro-Jade B and Nissl/Cresyl staining) were investigated in the dorsal raphe nuclei (DRN), amygdaloid nucleus, and hippocampal formation brain areas of rats treated with a 30X ayahuasca dose. The actual lethal oral dose in female Wistar rats could not be determined in this study, but was shown to be higher than the 50X (which corresponds to 15.1mg/kg bw DMT). The ayahuasca and fluoxetine treated groups showed a significant decrease in locomotion in the open field and elevated plus-maze tests compared to controls. In the forced swimming test, ayahuasca treated animals swam more than controls, a behaviour that was not significant in the fluoxetine group. Treated animals showed higher neuronal activation in all brain areas involved in serotoninergic neurotransmission. Although this led to some brain injury, no permanent damage was detected. These results suggest that ayahuasca has antidepressant properties in Wistar female at high doses, an effect that should be further investigated.

When i first got HPPD i didn't know what was wrong, it was so bad that i was always afraid to fall asleep because i thought that i may never wake up again not knowing what was wrong with me. It was a terrible time in my life, the worst really. I just had to continually convince myself i wasnt going to die if i fell asleep.

Good post but it looks like most that report neurotoxicity are drugs like meth and mdma. This is what the section on hallucinogens says. The only “hallucinogens” they really list are ketamine and methoxetamine. Toxic Effects of Hallucinogen and Dissociative Drugs Preclinical studiesStudies in vitro have demonstrated that both acute and prolonged exposure to hallucinogen phenethylamines (2.4–100?μM) inhibit neuronal activity in rat primary cortical cultures (Zwartsen et al., 2018). Similarly, studies in users have demonstrated toxic effects of serotoninergic hallucinogens, including the newest ones, which have been frequently associated with acute serotonin syndrome, hyperthermia, seizures, hyponatremia and sympathomimetic toxicity (Hill and Thomas, 2011). Degree of symptoms can range from mild to severe; complications may include seizures and extensive muscle breakdown. Animal studies have described the behavioral components of the serotonin syndrome induced by hallucinogen drugs which include lateral head weaving, hind limb abduction, backward locomotion, and lower lip retraction (Halberstadt and Geyer, 2011; Gatch et al., 2017).Ketamine is a non-competitive antagonist of glutamate N-methyl-D-aspartate (NMDA) receptors that induces dissociative anesthesia and analgesia at clinical doses; however, at recreational doses of subanesthetic levels, ketamine may produce an intense psychedelic experience. Accordingly, although present on the drug market for long time, ketamine continues to be abused worldwide, and its consumption among adolescents is particularly worrying. A study in Cynomolgus monkeys has shown that repeated parenteral administrations of a recreational dose of ketamine (1 mg/kg) induce neurotoxic effects, involving the activation of apoptotic pathways in the prefrontal cortex, that lead to irreversible deficits in brain functions (Sun et al., 2014). In line with this, repeated parenteral administrations of sub-anesthetic doses of ketamine (5–50 mg/kg) increased cell death in hippocampal cornu ammonis area 3, caused irreversible changes in both brain structure and function in young adult mice (Majewski-Tiedeken et al., 2008) and induced apoptotic and necrotic neuronal cell death in the perinatal rhesus monkey (Slikker et al., 2007).Methoxetamine is an NPS structurally related to ketamine and phencyclidine, designed to mimic the psychotropic effects of its parent compounds (Zanda et al., 2016) and increasingly available on the Internet as ‘legal ketamine’ (EMCDDA, 2014). Methoxetamine acts as a NMDA receptor antagonist, but also potently inhibits neuronal activity and alters monoamine metabolism in in vitro models (Hondebrink et al., 2018). Moreover, acute repeated parenteral administration of methoxetamine (0.125–5 mg/kg) considerably stimulates the mesolimbic dopaminergic transmission in rats (Mutti et al., 2016), and affects brain functions and behavior in rodents (Zanda et al., 2017). A recent study in mice (Ossato et al., 2018) found that acute parenteral administration of methoxetamine (0.01–30?mg/kg) induced alterations in sensory function processing that resembled those reported by users (Kjellgren and Jonsson, 2013) and persisted for hours when methoxetamine was administered at high doses. Moreover, another recent study in rats found that repeated parenteral administrations of methoxetamine (0.1–0.5 mg/kg) induced persistent behavioral abnormalities in tests used to evaluate anxiety-like states and recognition memory (Costa et al., 2019). The same investigation also demonstrated that methoxetamine induced persistent damage of dopaminergic fibers and neurons in the nigrostriatal and mesocorticolimbic systems as well as of serotonergic fibers in the nucleus accumbens core (Costa et al., 2019). [Table 3] provides further details about the toxic effects of hallucinogen and dissociative drugs demonstrated by preclinical studies from the past 3 years. Table 3: Overview of the toxic effects of hallucinogen and dissociative drugs demonstrated in studies from the past 3 years Click here to view Human studiesIn 2007, tryptamine derivatives were listed as ‘narcotics’ or ‘designated substances’ and were quickly replaced on the online drug market by cathinones, phenethylamines, and piperazines. Yet, several novel tryptamines continue to appear on the online drug market as ‘legal highs’, which include AMT, 5-MeO-AMT, 4-HO-DALT and 5-MeO-DALT [Figure 2]. In addition to visual and auditory hallucinations, these drugs may induce agitation, tachyarrhythmia, hyperthermia and death (Wood and Dargan, 2013). Figure 2: Chemical structures of some hallucinogen/dissociative substances used as recreational drugs. AMT: α-Methyltryptamine; 5-MeO-DALT: N-allyl-N-[2-(5-methoxy-1H-indol-3-yl)ethyl]prop-2-en-1-amine; 25I-NBOMe: 4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine. Click here to view According to the EMCDDA (2015), some phenethylamines with hallucinogenic properties are very popular in the current drug market, including the so-called 2C series (e.g., 2C-B/‘Nexus’) and the NBOMe series drugs (e.g., 25I-NBOMe, [Figure 2]). Their use has been associated with serotonergic and sympathomimetic toxic effects, including vomiting/diarrhea, metabolic acidosis, mydriasis, convulsions, thrombocytopenia, renal failure, hyperthermia and coma (Schifano et al., 2017). Fatalities and hospitalizations have been reported following use of 25I-NBOMe and symptoms of acute toxicity included tachycardia, hypertension, agitation/aggression and seizures, while laboratory tests detected elevated level of creatinine kinase, leukocytosis and hyperglycaemia (Suzuki et al., 2015). Rhabdomyolysis is a relatively common complication of severe NBOMe toxicity, an effect that may be linked to NBOMe-induced seizures, hyperthermia, and vasoconstriction. Slightly different from 25I-NBOMe, 25C-NBOMe was found to induce aggression, unpredictable violent episodes, dissociation and anxiety (Lawn et al., 2014). Although studies on the pharmacology of hallucinogenic phenylethylamines from the 2C series are still scarce, it has been demonstrated that they may act either as agonists or antagonists of G-protein-coupled serotonin and α-adrenergic receptors (Villalobos et al., 2004; Fantegrossi et al., 2008) and some of them (i.e., 2C-C, 2C-D, 2C-E, and 2C-I) were found to act as full agonists at 5-HT2A/2C receptors (Eshleman et al., 2014).Use of methoxetamine by humans has been recently associated with acute neurological (Elian and Hackett, 2014; Fassette and Martinez, 2016) and cerebellar toxicity (Shields et al., 2012), including psychomotor agitation and altered motor coordination (Craig and Loeffler, 2014). Case reports described intoxicated patients with hypertension and tachycardia following use of methoxetamine (Thornton et al., 2017), ketamine (Kalsi et al., 2011), phencyclidine (Akmal et al., 1981) or methoxylated phencyclidine analogs (Bäckberg et al., 2015). Induction of gastrointestinal and urinary toxicity by ketamine have also been described (Wei et al. 2013). [Table 3] provides further details about the toxic effects of hallucinogen and dissociative drugs demonstrated by clinical studies from the past 3 years.Due to the numerous medical issues associated with the use of new hallucinogen and dissociative drugs, being aware of the toxicity of these compounds is of primary importance for health professionals. Since it is not always possible to know the exact compound(s) consumed, management of toxicity should be based on clinical symptoms that an individual presents with and training of medical staff should focus on the management of the pattern of toxicity, rather than on the specific drug(s) used. This view is supported by a recent study revealing that physicians and nurses have less confidence in managing acute toxicity related to the use of NPS compared with classical recreational drugs (Wood et al., 2016).

Good post but it looks like most that report neurotoxicity are drugs like meth and mdma. This is what the section on hallucinogens says. The only “hallucinogens” they really list are ketamine and methoxetamine. Toxic Effects of Hallucinogen and Dissociative Drugs Preclinical studiesStudies in vitro have demonstrated that both acute and prolonged exposure to hallucinogen phenethylamines (2.4–100?μM) inhibit neuronal activity in rat primary cortical cultures (Zwartsen et al., 2018). Similarly, studies in users have demonstrated toxic effects of serotoninergic hallucinogens, including the newest ones, which have been frequently associated with acute serotonin syndrome, hyperthermia, seizures, hyponatremia and sympathomimetic toxicity (Hill and Thomas, 2011). Degree of symptoms can range from mild to severe; complications may include seizures and extensive muscle breakdown. Animal studies have described the behavioral components of the serotonin syndrome induced by hallucinogen drugs which include lateral head weaving, hind limb abduction, backward locomotion, and lower lip retraction (Halberstadt and Geyer, 2011; Gatch et al., 2017).Ketamine is a non-competitive antagonist of glutamate N-methyl-D-aspartate (NMDA) receptors that induces dissociative anesthesia and analgesia at clinical doses; however, at recreational doses of subanesthetic levels, ketamine may produce an intense psychedelic experience. Accordingly, although present on the drug market for long time, ketamine continues to be abused worldwide, and its consumption among adolescents is particularly worrying. A study in Cynomolgus monkeys has shown that repeated parenteral administrations of a recreational dose of ketamine (1 mg/kg) induce neurotoxic effects, involving the activation of apoptotic pathways in the prefrontal cortex, that lead to irreversible deficits in brain functions (Sun et al., 2014). In line with this, repeated parenteral administrations of sub-anesthetic doses of ketamine (5–50 mg/kg) increased cell death in hippocampal cornu ammonis area 3, caused irreversible changes in both brain structure and function in young adult mice (Majewski-Tiedeken et al., 2008) and induced apoptotic and necrotic neuronal cell death in the perinatal rhesus monkey (Slikker et al., 2007).Methoxetamine is an NPS structurally related to ketamine and phencyclidine, designed to mimic the psychotropic effects of its parent compounds (Zanda et al., 2016) and increasingly available on the Internet as ‘legal ketamine’ (EMCDDA, 2014). Methoxetamine acts as a NMDA receptor antagonist, but also potently inhibits neuronal activity and alters monoamine metabolism in in vitro models (Hondebrink et al., 2018). Moreover, acute repeated parenteral administration of methoxetamine (0.125–5 mg/kg) considerably stimulates the mesolimbic dopaminergic transmission in rats (Mutti et al., 2016), and affects brain functions and behavior in rodents (Zanda et al., 2017). A recent study in mice (Ossato et al., 2018) found that acute parenteral administration of methoxetamine (0.01–30?mg/kg) induced alterations in sensory function processing that resembled those reported by users (Kjellgren and Jonsson, 2013) and persisted for hours when methoxetamine was administered at high doses. Moreover, another recent study in rats found that repeated parenteral administrations of methoxetamine (0.1–0.5 mg/kg) induced persistent behavioral abnormalities in tests used to evaluate anxiety-like states and recognition memory (Costa et al., 2019). The same investigation also demonstrated that methoxetamine induced persistent damage of dopaminergic fibers and neurons in the nigrostriatal and mesocorticolimbic systems as well as of serotonergic fibers in the nucleus accumbens core (Costa et al., 2019). [Table 3] provides further details about the toxic effects of hallucinogen and dissociative drugs demonstrated by preclinical studies from the past 3 years. Table 3: Overview of the toxic effects of hallucinogen and dissociative drugs demonstrated in studies from the past 3 years Click here to view Human studiesIn 2007, tryptamine derivatives were listed as ‘narcotics’ or ‘designated substances’ and were quickly replaced on the online drug market by cathinones, phenethylamines, and piperazines. Yet, several novel tryptamines continue to appear on the online drug market as ‘legal highs’, which include AMT, 5-MeO-AMT, 4-HO-DALT and 5-MeO-DALT [Figure 2]. In addition to visual and auditory hallucinations, these drugs may induce agitation, tachyarrhythmia, hyperthermia and death (Wood and Dargan, 2013). Figure 2: Chemical structures of some hallucinogen/dissociative substances used as recreational drugs. AMT: α-Methyltryptamine; 5-MeO-DALT: N-allyl-N-[2-(5-methoxy-1H-indol-3-yl)ethyl]prop-2-en-1-amine; 25I-NBOMe: 4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine. Click here to view According to the EMCDDA (2015), some phenethylamines with hallucinogenic properties are very popular in the current drug market, including the so-called 2C series (e.g., 2C-B/‘Nexus’) and the NBOMe series drugs (e.g., 25I-NBOMe, [Figure 2]). Their use has been associated with serotonergic and sympathomimetic toxic effects, including vomiting/diarrhea, metabolic acidosis, mydriasis, convulsions, thrombocytopenia, renal failure, hyperthermia and coma (Schifano et al., 2017). Fatalities and hospitalizations have been reported following use of 25I-NBOMe and symptoms of acute toxicity included tachycardia, hypertension, agitation/aggression and seizures, while laboratory tests detected elevated level of creatinine kinase, leukocytosis and hyperglycaemia (Suzuki et al., 2015). Rhabdomyolysis is a relatively common complication of severe NBOMe toxicity, an effect that may be linked to NBOMe-induced seizures, hyperthermia, and vasoconstriction. Slightly different from 25I-NBOMe, 25C-NBOMe was found to induce aggression, unpredictable violent episodes, dissociation and anxiety (Lawn et al., 2014). Although studies on the pharmacology of hallucinogenic phenylethylamines from the 2C series are still scarce, it has been demonstrated that they may act either as agonists or antagonists of G-protein-coupled serotonin and α-adrenergic receptors (Villalobos et al., 2004; Fantegrossi et al., 2008) and some of them (i.e., 2C-C, 2C-D, 2C-E, and 2C-I) were found to act as full agonists at 5-HT2A/2C receptors (Eshleman et al., 2014).Use of methoxetamine by humans has been recently associated with acute neurological (Elian and Hackett, 2014; Fassette and Martinez, 2016) and cerebellar toxicity (Shields et al., 2012), including psychomotor agitation and altered motor coordination (Craig and Loeffler, 2014). Case reports described intoxicated patients with hypertension and tachycardia following use of methoxetamine (Thornton et al., 2017), ketamine (Kalsi et al., 2011), phencyclidine (Akmal et al., 1981) or methoxylated phencyclidine analogs (Bäckberg et al., 2015). Induction of gastrointestinal and urinary toxicity by ketamine have also been described (Wei et al. 2013). [Table 3] provides further details about the toxic effects of hallucinogen and dissociative drugs demonstrated by clinical studies from the past 3 years.Due to the numerous medical issues associated with the use of new hallucinogen and dissociative drugs, being aware of the toxicity of these compounds is of primary importance for health professionals. Since it is not always possible to know the exact compound(s) consumed, management of toxicity should be based on clinical symptoms that an individual presents with and training of medical staff should focus on the management of the pattern of toxicity, rather than on the specific drug(s) used. This view is supported by a recent study revealing that physicians and nurses have less confidence in managing acute toxicity related to the use of NPS compared with classical recreational drugs (Wood et al., 2016).

So I've been doing some more reading, as per usual. Whenever I have any new ideas that I haven't checked I always google. Anyways I was reading about DMT and its effects on the brain and if there are any signs of neurotoxicity, I didn't exactly look to far in to the details but according to everything I read not only does it show limited neurotoxicity, but it doesn't even appear to be neurotoxic even when injected in large quantities, which is extremely interesting. Also, believe it or not it even showed neuroprotective abilities, very interesting. DMT is originally what triggered my HPPD, and it was bad. I also used Syrian Rue in conjunction of the DMT source, as is typical in Ayahuasca concoctions, so I also had to read up on the possibility of Harmala and related alkaloids having any neurotoxicity, which interesting enough not only do they not show any significant signs of being neurotoxic, but they have neuroprotective effects by inhibiting glutamate caused apoptosis. So absolutely remarkable, and fascinating information. To be completely honest this is a great deal of information that I almost feel that neuronal loss in the case of HPPD as a cause, very well may at this point be removed as a possibility. At this point its a VERY confusing subject of what causes this disease.

Its probably just the novacaine, it has a slight effect similiar to cocaine, they also put a small percentage of epinephrine in there, so there is some stimulant effect. This could possibly explain the symptoms getting worse. I believe they are vasodilators though, do you know the actual numbing agent they gave you? Also did they specifically say it was vasoconstrictive?

That is interesting, thanks for sharing.

Lmao yah I would like to see this study as well. Looks like he edited that comment out?

Mgrade did you read all the info on my new thread, the continuation of this one?

Visual snow, or visual static is the common term. If you’re meaning the lamp diagram that is. The other colorful stuff i believe is referred to halos and auras.

Thats a report for lithium overdose and I’m just using it as an example for evidence of the possibility for neuronal loss. We still don’t have definitive evidence that it is in fact neuronal loss. Also in the case of neuronal loss neurogenesis is not a complete impossibility. It may be impossible currently in modern medical science, but it doesn't mean it cant be done.

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.

Ill hit you up.

Awesome, thanks for the response. You never called me back....

Ah the Unicorn's butthole.... interesting. Please stop doing drugs of any kind so you do not further your condition.

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.

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.

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.

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]

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

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

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.

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.