dasitmane

Bit of an idea for possible CURE. Has some weight to it.

607 posts in this topic

-mg will a 5ht2a antagonist like lomerizine make me depressed? As agonizing 5ht2a receptors make you happy wouldn't reversing the process cause the opposite of happiness?

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I don't know for sure.  Ask Qaiphix(disitmane).  I would say that it is often thought that the ht2a receptor is responsible for delusions in psychotic patients.      

That's why we had initially started talking about ht2a inverse agonists which are in a weird way sort of like an antagonist.  

I don't know for sure.  

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Hey guys! Long time! I think I may have found something that can help!

 

I recently bought an herb that apparently was packing more punch than I thought. I was primarily getting it for memory increase, but starting doing some more reading about it.

 

This is what I found

 

"As people age, it’s common for age-related brain degradation to happen. The active compounds in Brahmi, known as bacosides, are beginning to be evaluated for their effects on the brain and human health. Some research has shown the compounds in Brahmi to positively influence brain cells that prompt the regeneration of brain tissue[1] In one animal study, long-term supplementation with bacosides showed therapeutic value against therapid degeneration associated with Alzheimer’s disease[2] Hopefully more will continue to explore its potential benefits for brain health." - http://www.globalhealingcenter.com/natural-health/9-facts-brahmi-bacopa-monnieri/#1

 

 

Then I looked up the case study its a bit confusing but down at the bottom it lists the herb, bacopa monnieri

 

Ayurveda is the oldest system of Medicine in the world, its antiquity going back to the Vedas. It adapts a unique holistic approach to the entire science of life, health and cure. The areas of special consideration in Ayurveda are geriatrics, rejuvenation, nutrition, immunology, genetics and higher consciousness. The Ayurvedic texts describe a set of rejuvenative measures to impart biological sustenance to the bodily tissues. These remedies are called Rasayana which are claimed to act as micronutrients. Some of these Rasayanas are organ and tissue specific. Those specific to brain tissue are called Medhya Rasayana. Such Rasayanas retard brain aging and help in regeneration of neural tissues besides producing antistress, adaptogenic and memory enhancing effect. In addition to the long tradition of textual and experience-based evidence for their efficacy, certain recent studies conducted on these traditional remedies on scientific parameters have shown promising results which have been reviewed in this paper for providing lead for further studies. The popular Medhya Rasayanas are Ashwagandha (Withania somnifera Dunal), Brahmi (Bacopa monnieri Linn), Mandukaparni (Centella asiatica Linn) and Sankhapuspi (Convolvulus pluricaulis Chois). - http://www.ncbi.nlm.nih.gov/pubmed/18931935

 

So apparently we have an herb that can potentially, and maybe, rejuvenate brain cells, and brain cell function.

 

Not sure how legit it is but its worth a try huh?

 

Who wants to try it first??

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I take 5HTP as a supplement. It helps me with my mood and sleep, but everyone is different. What works for me might be awful for you, I dunno.

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Annnd Im back with some new information. One thing that I always noticed about HPPD is that it has an impact on flight or fight type response, and I was thinking that if there were a way to inhibit that, it would probably significantly reduce the stress and anxiety induced on the body/mind. Today I was reading and found this little bit.

"Many sympathetic hormones and neurotransmitters are based on the phenethylamine skeleton, and function generally in "fight or flight" type responses, such as increasing heart rate, blood pressure, dilating the pupils, increased energy, drying of mucous membranes, increased sweating, and a significant number of additional effects."

Theres a possibility that HPPD may be a condition that stimulates the production of specific neurotransmitters in this area related to phenethylamine. One way to test this theory, would be something that reduces phenethalamine production, take it, and see if symptoms are lessened. IF this is the case and can be observed, we would have a potential trigger mechanism for the cause of HPPD. It also would give route for a potential method of treatment.

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"This is for you out there, guys.....At least it doesn't block your NMDA receptor.....Now for my next song.....another 45 minutes of shitty music."

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Hey guys!

 

Came across something today and its something that we can try. Ill just brief it up as simple as I can. When I first started the thread the theory in my mind is that imbalance in the organs is essentially disease, however I was thinking more... physically rather that magnetically. Magnetically speaking though all organs in the body have their own resonances(you can think of it musically even if that helps, like a ringing, or instrument, and they all play together to make a symphony.), disease however, or dysfunction of a specific organ is simply just discordance in that organ on the magnetic level, which then drops down to the elemental level(bodies).

 

Its most likely that in the tragic case of HPPD, the brain is what is brought in to discordance, to relegate that discordance we must find something with a same sympathy, to restore concordance with in the organ. Which is easy to do, but I'll withdraw from explaining.

 

Thus, a plant that very well may restore concordance through sympathy should be spikenard, as according to Marsilio Ficino, "as the lodestone toward iron, rhubarb toward choler, saffron toward the heart, agrimony and spodium toward the liver, spikenard and musk toward the brain"

 

Agrimony as well has been proven very effective in jaundice and liver ailments, a true cure due to its sympathetic virtues to the liver. Our doctors have forgot its power and force though. Adhering to the almighty pharmacorps and FDA who monopolize our health for power, and monetary gain.

 

So spikenard may be our answer, not only that but it also has sedative type effects so could also help with anxiety along the way. It should be tried for I would say at least three months taken daily. Also it should be noted that spikenard may have been an old term for lavender as well, but im unsure as to that.

 

EDIT: After a little more reading I'm almost certain hes referring to lavender, being that according to Nicholas Culpeper the oil extracted was referred to as oil of spike. 

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Got some good news guys! Been reading all morning and im exhausted, but ill try and briefly sum up what I've found.

 

Basically when nerve tissue, like in the brain and spinal cord are damaged, even severe damage like stab wounds, the tissue doesn't actually form scar tissue, but rather glial scarring, which are just astrocytes replicating and migrating  to the area acting as a barrier. This is pretty good news, because if it were normal scarring(fibrin), the fibrous tissue would need to be removed. So realistically in this case, it seems that the nervous system just needs a push in the right direction for regeneration!! Which is remarkable!

 

Ill add to that there was a study done where they removed the astrocyte formation(glial scar) and the neurons/axons didn't fill in to that area, so it shows that its more than likely that the astrocytes may be a preliminary function towards neuronal regrowth, which is very exciting! 

 

Essentially is all we need to do is find something that will give the neurons that push that they need.

 

 

Also, if anyone is wondering if this condition is brought about by neuronal damage/death/apoptosis just read this.

 

Amphetamine abuse – Drugs like Adderall are not likely going to cause any major brain damage or loss of neurons if used properly. However, if you abuse amphetamines, it can have detrimental effects on cognitive functioning even years after use. Amphetamines release large amounts of dopamine to help stimulate brain activity. A point of exitotoxicity may be reached if amphetamines are abused and you could lose brain cells.

Source: http://news.bbc.co.uk/2/hi/health/692642.stm

 

Antipsychotics – The class of drugs known as antipsychotics is documented as being linked to brain shrinkage as well as killing brain cells. This is a double whammy for people that already have a disease like psychosis or schizophrenia. Their disease is causing significant distress and functional problems, and the medication that they are taking is actually slowly damaging the brain.

 

Source: http://www.nature.com/npp/journal/v32/n6/abs/1301233a.html

Bath Salts – There is not much scientific information regarding bath salts. However, this popular drug containes substituted cathinones. Most types contain mephedrone or methylenedioxypyrovalerone (MDPV). They cause major changes in brain activity and can certainly cause brain cell death. Elevated stress, paranoia, anger, stimulation, etc. are all side effects from this substance. By using bath salts you are likely going to get brain damage from the excessive stimulation and inability to wind down. Additionally, there may be chemicals in this drug that you are not aware of that may kill more brain cells.

 

Benzodiazepine abuse – Should you end up abusing a benzodiazepine drug like Xanax or Valium over the long term, you put yourself at risk to lose brain cells as well as develop dementia. Although not everyone taking this drug will experience the negative side effects, it can lead to cognition problems in the long term. There are a lot of conflicting results from benzodiazepine studies, but in most the long term effects do not seem favorable.

Cigarettes / tobacco products – A compound in tobacco products including cigarettes and chewing tobacco called NNK (procarcinogen) causes white blood cells in the body’s central nervous system (CNS) to attack healthy brain cells. Normally immune cells called “microglia” attack unhealthy and damaged cells in the brain to help promote healthy functioning. However the NNK causes the microglia to attack healthy cells.

Source: http://www.sciencedaily.com/releases/2009/06/090623090400.htm

 

Cocaine – Although using cocaine once or twice may not do much damage, there is significant evidence that cocaine use kills your brains pleasure cells. So the cells that allow you to get high off of cocaine are the very cells that become damaged and killed from the drug’s use. The cells that die from cocaine use are in your brain’s pleasure center, which help you feel good via the release of the neurotransmitter dopamine. Things that previously brought you pleasure may no longer bring you any pleasure due to all of the extinct pleasure neurons in the pleasure center.

Source: http://online.sfsu.edu/rone/Buddhism/FivePrecepts/cocainekillsbraincells.html

 

Ecstasy (MDMA) – One extreme myth regarding the popular rave drug ecstasy is that it will “put holes in your brain” – however, it does have the potential to kill brain cells – specifically ones that are of central importance to the serotonin system. Not only can it deplete natural stores of serotonin, it can damage axons and other nerve cells.  Some researchers believe that the brain is not able to restore its axons.  Read more about how ecstasy may cause brain damage if you are interested.

Source: http://www.sciencedirect.com/science/article/pii/0006899388913091

 

Inhalants – The poisons in inhalants can cause major problems in regards to brain functioning and can damage many brain cells. If you chronically sniff or huff things like paint and glue, you are risking your brain. Some people experience significant brain damage from years of huffing paint to get a high. Individuals that sniff paint are putting themselves at major risk for brain damage. Don’t huff paint or other inhalants as a way to get high – this is a surefire way to end up with brain problems.

 

Ketamine – Prolonged exposure to ketamine has been linked to the death of neurons and neuronal toxicity. The death was found to have happened in the frontal cortex of monkeys. Ironically enough ketamine is currently being investigated as an alternative treatment for depression. Short term exposure was not associated with any adverse effects; you really have to abuse ketamine to kill brain cells.

Source: http://www.ncbi.nlm.nih.gov/pubmed/19580862

 

Methamphetamines – If you want to severely damage your overall brain functioning, consider meth. Over time, this is a sure-fire way to roast your brain cells and cause long term damage to many areas of the brain. What’s interesting is that chronic use of meth can cause changes to the brain similar to those found in patients with Alzheimer’s disease and stroke victims. Scientists have found that the more you use meth, the more damage your brain cells will incur.

 

Nitrous Oxide – When used by a medical professional for anesthetic purposes, nitrous oxide is relatively safe – it will not damage the brain. However, when it is used recreationally in a repetitive manner to maintain a high, it can deplete oxygen levels may inhibit the uptake of vitamin B12. If you take “laughing gas” or “whippets” on the regular, you are putting your brain at risk for cell death – especially over the long term.

PCP – This drug was found to cause lesions on the brain in rats. This does not necessarily mean that it applies to humans. However abuse of Phencyclidine could still lead to brain cell death in humans as well. There is no way of knowing unless studies are actually conducted. Abuse of this dissociative over time has been linked to causing brain damage.

 

Steroids – Taking steroids can lead to elevated levels of testosterone which in turn can kill brain cells. It was determined that at high concentrations, cell viability decreases. It is believed that the excess testosterone is what plays a role in damaging and knocking neurons out of commission. If you are getting your muscle by taking steroids, you may want to think twice before you have to deal with some brain damage.

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How is it posible that i am cured and the damage of anti psygotics and klonopin has left? I am sure my hppd had no differnts like the most with hppd and me to i losed lot of times i will noth recover. While on the meds for 2,5 years i didnt see improvements later when start to give a kick in the ass things became to change

I dont know any stuff how the brain works buth i believed in the theory of one doc he says the basic of a cure or repair of a organ depends on the booldflow to it how more bloodflow how faster it wil repair.

So this way i believed that sport do the job for increased bloodflow tho all part of the body

The understanding of the brain is a long story buth some logical knowledge can realy save lot people live this what i like to use in theory

The most horrible thing that while i used antipygotics "i became psygotic while i was noth it" i discoverd this later while i was off on it

You dont want to know what for thougt i was gething from it

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How is it posible that i am cured and the damage of anti psygotics and klonopin has left? I am sure my hppd had no differnts like the most with hppd and me to i losed lot of times i will noth recover. While on the meds for 2,5 years i didnt see improvements later when start to give a kick in the ass things became to change

I dont know any stuff how the brain works buth i believed in the theory of one doc he says the basic of a cure or repair of a organ depends on the booldflow to it how more bloodflow how faster it wil repair.

So this way i believed that sport do the job for increased bloodflow tho all part of the body

The understanding of the brain is a long story buth some logical knowledge can realy save lot people live this what i like to use in theory

The most horrible thing that while i used antipygotics "i became psygotic while i was noth it" i discoverd this later while i was off on it

You dont want to know what for thougt i was gething from it

Anhoter question : is this noth rare,that some where in your brain you start a point "so you?" "your soul?" to discover how your hole brain chemistry works

 

While you may have been completely relieved of your symptoms, there may still be damage, in most cases the symptoms do lessen quite significantly over time, but most people do not see a complete remission of their symptoms, especially in the more severe cases. You probably may even still have symptoms but due to perceptive adjustments you may not be noticing them. I'm fairly certain however that in this condition neurons are destroyed, quickly and abruptly for most usually. Then you see the the stages of the brain doing its best for repair, but for the most part it can do very little to no regeneration.

 

I dont understand your second question sorry.

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While you may have been completely relieved of your symptoms, there may still be damage, in most cases the symptoms do lessen quite significantly over time, but most people do not see a complete remission of their symptoms, especially in the more severe cases. You probably may even still have symptoms but due to perceptive adjustments you may not be noticing them. I'm fairly certain however that in this condition neurons are destroyed, quickly and abruptly for most usually. Then you see the the stages of the brain doing its best for repair, but for the most part it can do very little to no regeneration.

I dont understand your second question sorry.

Yes i have been completley relieved from my symptoms buth i know my hppd is still there somewhere in the background once i learnd to manage stress my health stay undercontrol

I can say its hard to cure if you have permanent hppd in this case i had it if you think when er is no improvment after 2 and half year

there is somehow posible that the brain repairs his self even the neurons has been desroyed maybe a adjusment or replacement from other cells thats why i believe in my case

Yea and my last question i deleted its shoud redicelous

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Just wanted to add more information that this condition is more than likely a neurotoxic effect.

 

Using lithium toxicity as an example of what can occur with the brain and hyperintensities. Lithium toxicity presents a permanent duration of neuronal damage especially in the cerebellum.

 

You can read this case study for an example of mistake by doctors prescribing to much lithium.

 

Since its first use in 1947, lithium is now commonly used as a least expensive mood stabilizer. However, because lithium has a low therapeutic index, lithium-induced drug toxicity is frequently seen in clinical practice.  Although most lithium-induced neurological side effects are reversible on discontinuation of the drug, there is evidence that lithium toxicity causes irreversible persistent neurologic disorders.  We report a case of syndrome of irreversible lithium-effectuated neurotoxicity (SILENT), who recovered partially after extensive treatment.

 

  Case Report   arrow_top.gif

A 45-year-old Mr. S presented with a history of altered sensorium for the past 2 days. The patient had a history of five episodes of mania and two episodes of depression in the last 15 years. Six weeks ago he had an episode of mania, for which he was treated at a tertiary care center as inpatient and given a tablet each of olanzapine 20 mg, lithium 900 mg, and chlorpromazine 300 mg daily. A week after he was discharged from the center, while still on regular medication, he developed coarse tremors affecting the whole body and was unable to walk. When he was brought to the Accident and Emergency Department of our hospital, he was afebrile and was not responding to painful commands. His pulse rate was 105/min with exaggerated deep tendon reflexes. His investigations showed a raised serum lithium level of 3.9 mEq/L, creatinine of 1.8 mg/dl, and raised white blood cells of 24,800/μl. His liver function tests and sugar level were within the normal range. All his previous medications, including lithium were stopped, and he was treated with intravenous (IV) normal saline, IV ceftriaxone 2 g, and vancomycin 500 mg twice a day for 2 weeks. In order to rule out any infection, his blood was sent for culture, and a cerebrospinal fluid (CSF) analysis was done to rule out any neuro-infection. However, both blood culture and CSF results were found to be normal. A magnetic resonance imaging (MRI) of the brain showed T2 and flair hyperintensities in the bilateral parietal lobe and periventricular white matter changes, both suggestive of lithium toxicity [Figure 1]a. In view of his low Glasgow coma scale (8/15), the patient was intubated. Also, because of the severe lithium toxicity, hemodialysis was started. After two cycles of hemodialysis, the patient started responding to painful commands. His serum lithium level fell to 1.8 mEq/L. He was extubated on day 5 of admission. From day 6 onward, he started responding to oral commands, even though his speech was slurred. However, he had coarse tremors, truncal ataxia, and difficulty in deglutition. Subsequently, the patient was shifted to the psychiatry ward of our hospital for further management and for observation of manic symptoms. Physiotherapy was started, and within 2 weeks of intensive physiotherapy the patient started walking with support. His speech too improved. After 3 weeks, when his blood serum lithium level fell to 0.2 mEq/L, he started showing symptoms of mania. He was then treated with oral quetiapine, which was gradually increased to 300 mg/day. Thirty-six days after the first MRI, a second MRI was done. The second MRI showed up to 40% reduction in periventricular white matter hyperintensities in the bilateral parietal lobes [Figure 1]b. Even after about 6 months of follow-up the patient continues to have coarse tremors, dysarthria, and significant limb ataxia.

 

Brain MRI showing hyperintensities. 

JMentalHealthHumBehav_2015_20_2_80_17460

 

 

 

So even after 6 months he was showing symptoms, which clearly demonstrates damage to the neural tissue. There are multiple examples of this that can be found. I would assume that this is similar to HPPD, but rather effecting different areas of the brain.

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More information on the neurotoxicity involving drugs.

 

"Recently, two other penethylamine hallucinogens 3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA) have been demonstrated to produce apparently irreversible neurotoxicity to serotonin neurons."

 

Clearly the reason why not all get HPPD is dose dependant and others may be more sensitive to the drugs, and more perceptive to the sensory changes after use.

 

Entire case study can be found here.

 

https://www.ncbi.nlm.nih.gov/pubmed/10899362

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Here is one more case study proving the fact that these types of drugs are causing neuronal death and apoptosis like I had expected.

 

The neurotoxicity of hallucinogenic amphetamines in primary cultures of hippocampal neurons.

Abstract

3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") and 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) are hallucinogenic amphetamines with addictive properties. The hippocampus is involved in learning and memory and seems particularly vulnerable to amphetamine's neurotoxicity. We evaluated the neurotoxicity of DOI and MDMA in primary neuronal cultures of hippocampus obtained from Wistar rat embryos (E-17 to E-19). Mature neurons after 10 days in culture were exposed for 24 or 48 h either to MDMA (100-800 μM) or DOI (10-100 μM). Both the lactate dehydrogenase (LDH) release and the tetrazolium-based (MTT) assays revealed a concentration- and time-dependent neuronal death and mitochondrial dysfunction after exposure to both drugs. Both drugs promoted a significant increase in caspase-8 and caspase-3 activities. At concentrations that produced similar levels of neuronal death, DOI promoted a higher increase in the activity of both caspases than MDMA. In the mitochondrial fraction of neurons exposed 24h to DOI or MDMA, we found a significant increase in the 67 kDa band of apoptosis inducing factor (AIF) by Western blot. Moreover, 24h exposure to DOI promoted an increase in cytochrome c in the cytoplasmatic fraction of neurons. Pre-treatment with an antibody raised against the 5-HT(2A)-receptor (an irreversible antagonist) greatly attenuated neuronal death promoted by 48 h exposure to DOI or MDMA. In conclusion, hallucinogenic amphetamines promoted programmed neuronal death involving both the mitochondria machinery and the extrinsic cell death key regulators. Death was dependent, at least in part, on the stimulation of the 5-HT(2A)-receptors.

 

https://www.ncbi.nlm.nih.gov/pubmed/22983118

 

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This CLEARLY shows to a significant degree that HPPD is caused by neuronal tissue damage and apoptosis. Meaning that it will not be cured by means of chemical alteration, and requires neurogenesis. 

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This report here seems to imply that there is the possibility that MDMA acting on serotonin receptors may cause acute brain infarction in the forebrain and brain stem/mid brain.

 

Keep in mind most hallucinogens act on the serotonin receptors, so could have similar effects to that of MDMA.

 

HUMAN STUDIES

Evidence of neurotoxicity

Evidence from human studies has accumulated more slowly, but it is becoming apparent that the toxic effect of MDMA on central serotonergic systems found previously in animal studies has a clear parallel in human users of the drug.There is now direct evidence of a lasting decrease in 5-HT uptake sites (a marker for the integrity of 5-HT nerve terminals) in human volunteers with a past history of MDMAabuse.13 Moreover, this decrease correlates positively with the extent of their self-reported previous exposure to the drug, and is in keeping with decreases in more general biochemical markers for central serotonergic activity reported elsewhere.14Positron emission tomographic (PET) imaging has revealed that the consequences of MDMA toxicity may be even more widespread than predicted from animal experiments. In addition to the hippocampal formation, both the amygdala andareas of neocortex may be affected byMDMA.15

Cognitive changes in ecstasy users

The manifestations of this neurotoxicity, in terms of altered cerebral function and behavioral change, range from neuroendocrine impairments16 to deficits in verbal memory and reasoning,17short-term memory and semantic recognition,14 and visual memory.18More general indices of intelligence are also adversely affected,19 but reports of serious long-term psychiatric disorders are still rare, with the possibility that previous exposure to MDMA merely accentuates preexisting negative personality features.20 One particularly worrying feature that has emerged is that chronic psychosis, when manifest in MDMA users, reportedly responds poorly to therapy.21

The effects of MDMA on cognitive performance arising directly from drug—induced neurotoxicity may be compounded by indirect effects on the cerebral circulation. As well as providing extensive innervation of forebrainneuronal systems, there is also evidence that cerebral blood vessels are innervated by the same serotonergic neurons arising from themesencephalon.22 It should not be surprising then that both acute and chronic treatments with MDMAproduce cerebrovascular effects. In rats, the acute effect of MDMA is to produce pronounced focal cerebrovascularhyperemia,23 which, in anatomic distribution, is directly parallel to the occurrence ofMDMA-associated hemorrhagic stroke in humans.24 In contrast, the chronic cerebrovascular effects of MDMA are more subtle under normal physiologic conditions and require the superimposition of physiologic stress before becoming fully apparent.25 It is now evident that MDMA abuse is an important risk factor for cerebrovascular accidents in young people. If these vascular accidents are neurologically silent, however, they may only become apparent at a later date. This effect may parallel the type of cognitive decline seen in patients with multi-infarctdementia.

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This study shows not only the areas of the brain most likely effected in this condition, but also, that during hallucinogen use, these areas of the brain are stimulated(and possibly overstimulated?(such as in the lithium study))

 

Brain imaging studies

Until recently, many neural circuit models were based on animal studies, and implications for the effects of hallucinogenic drugs or disease models in humans were based on inferences from these studies. However, functional neuroimaging studies enable one to examine these neural circuit models directly and test specific hypotheses about the role of specific neural systems in the expression of ASC.

PET with the radiotracer 18F-fluorodcoxyglucose (18FDG) was used to assess drug-induced changes in the regional cerebral metabolic rate of glucose (CMRglu), as an index of cerebral activity. We found that a hallucinogenic dose of racemic ketamine increased neuronal activity in the prefrontal cortex (hyperfrontality) and associated limbic regions, as well as in striatal and thalamic structures in healthy volunteers, giving the first evidence that functional alterations in CSTC loops may underlie the symptomatology of drug-induced ASC.50 This hyperfrontality finding was corroborated and extended in subsequent studies in healthy volunteers in which the effects of hallucinogens and NMDA antagonists including psilocybin, racemic ketamine, and S-ketamine were compared.

In particular, we found that, despite different primary mechanisms of action, the two classes of drugs produced strikingly similar brain activation patterns as indexed by normalized CMRglu. Both psilocybin and ketamine markedly increased brain activity bilaterally in the frontomedial and frontolateral cortex, including the anterior cingulate. Lesser increases were found in the temporomedial, superior, and inferior parietal cortices, striatum, and thalamus. Decreases were found in the left caudate nucleus, bilaterally in the ventral striatum, occipital lobe, and visual pathway.9-11 A correlational analysis revealed that the metabolic hyperfrontality in ketamine and psilocybin subjects was associated with a depersonalization/derealization syndrome, thought disturbances, and mania-like symptoms.9-11 The hyperfrontality finding in ASC was further supported by evidence from brain imaging studies with ketamine and psilocybin in healthy volunteers27,51 and was also found in subjects treated with the classic pheny le thyl amine hallucinogen mescaline.52

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181663/

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Hi everyone, 

After several years of putting together an HPPD non profit, it looks like it's going to happen. Took me several years but I finally found an attorny who will be filing the necessary forms to help us attain 501c3 status with the intent on finding a cure for HPPD and quite possibly Visual Snow as the two seem very interrelated. I should have some more news in the first quarter of 2017 barring any hangups. If anyone would like to get involved, we can certainly use your help. This is afterall a patient powered organization. I can be reached at info@neurogroup.org 
Best

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Well guys, its a sad day, because here is pretty much the nail in the coffin that hallucinogenic use does in fact like I theorized produce an excitotoxic effect, resulting in loss of neurons. Finding this article was difficult for even me to read because it really sinks in the reality of the situation of HPPD. The good news is, believe it or not, that this still is a curable disease. More so than others, or has a better potential outcome. The reason being for this is that central nervous system tissue damage, like this, or in the case of a stroke or paralysis, does not form any scar tissue, so healing remains only to just stimulating neuronal growth. The only detriment I see to this is by possibility that the purkinje cells in the heart are also reduced, in which case I would assume fills with scar tissue rendering that area much more difficult to remedy, and possibly... impossible, which could have great consequences in the case that they send any signals to the brain that modern science is unaware of. Anyways, here it is.

Abstract
The indole alkaloids ibogaine and harmaline are beta-carboline derivatives that cause both hallucinations and tremor. Reports that ibogaine may have potent anti-addictive properties have led to initiatives that it be tested for the treatment of opiate and cocaine addiction. In this study, ibogaine-treated rats were analysed for evidence of neurotoxic effects because human clinical trials of ibogaine have been proposed. We recently found that ibogaine induces a marked glial reaction in the cerebellum with activated astrocytes and microglia aligned in parasagittal stripes within the vermis. Based on those findings, the present study was conducted to investigate whether ibogaine may cause neuronal injury or degeneration. The results demonstrate that, after treatment with ibogaine or harmaline, a subset of Purkinje cells in the vermis degenerates. We observed a loss of the neuronal proteins microtubule-associated protein 2 and calbindin co-extensive with loss of Nissl-stained Purkinje cell bodies. Argyrophilic staining of Purkinje cell bodies, dendrites and axons was obtained with the Gallyas reduced silver method for degenerating neurons. Degenerating neurons were confined to narrow parasagittal stripes within the vermis. We conclude that both ibogaine and harmaline have selective neurotoxic effects which lead to degeneration of Purkinje cells in the cerebellar vermis. The longitudinal stripes of neuronal damage may be related to the parasagittal organization of the olivocerebellar climbing fiber projection. Since these drugs produce sustained activation of inferior olivary neurons, we hypothesize that release of an excitatory amino acid from climbing fiber synaptic terminals may lead to excitotoxic degeneration of Purkinje cells.
Edited by dasitmane
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Here is some more detailed information of the probable occurrence in HPPD at hand, and linear with the theories that i had before, that we have lost some neurons that are involve in inhibitory responses. Just read the article, typically purkinje cells are involved with just fine motor control but it does show that they release GABA and have an inhibitory effect on the brain. It could be the case that these cells exist else where or are communicating with other areas of the brain and have been lost, hence the over stimuli effect such as visuals and anxiety etc. Its very clear that certain areas of the brain are not being properly regulated/inhibited.

Purkinje cell

ANATOMY
LAST UPDATED:
 5-15-2015 See Article History

Purkinje celllarge neuron with many branching extensions that is found in the cortex of the cerebellum of the brain and that plays a fundamental role in controlling motor movement. These cells were first discovered in 1837 by Czech physiologist Jan Evangelista Purkinje. They are characterized by cell bodies that are flasklike in shape, by numerous branching dendrites, and by a single long axon. Most Purkinje cells release a neurotransmitter called GABA (gamma-aminobutyric acid), which exerts inhibitory actions on certain neurons and thereby reduces the transmission of nerve impulses. These inhibitory functions enable Purkinje cells to regulate and coordinate motor movements.

  • A Purkinje cell that has been isolated from a mouse brain, injected with fluorescent dye, and imaged using confocal microscopy.
    A Purkinje cell that has been isolated from a mouse brain, injected with fluorescent dye, and …
    Maryann Martone—CCDB/NCMIR/UC San Diego
 

The cerebellar cortex is made up of three layers, consisting of an outer synaptic layer (also called the molecular layer), an intermediate discharge layer (the Purkinje layer), and an inner receptive layer (the granular layer). Sensory input from all sorts of receptors is conveyed to specific regions of the receptive layer, which consists of enormous numbers of small neurons (hence the name granular) that project axons into the synaptic layer. There the axons excite the dendrites of the Purkinje cells, which in turn project axons to portions of the four intrinsic nuclei that make up the vestibular nucleus within the fourth ventricle of the brainstem. Because most Purkinje cells are GABAergic and therefore exert strong inhibitory influences upon the cells that receive their terminals, all sensory input into the cerebellum results in inhibitory impulses’ being exerted upon the deep cerebellar nuclei and parts of the vestibular nucleus.

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