dasitmane

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dasitmane last won the day on May 6 2016

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  1. I also wanted to add that its very unlikely that the purkinje fibers in the heart would be affected in this condition. As for the nodes and such of the heart I hardly doubt as well, Im not ruling that out completely yet though. But I hope to God that the neurons in the heart are not affected in this case, as it would be quite detrimental if they by any chance send anxiety/fight/flight responses to the brain triggering it, then the anxiety would most likely be incurable, where as if all the damage is located specifically to the central nervous system it should be fine and curable up to I would guess anywhere from 80% to 99% improvement, which realistically is remarkable, and would make life bearable for this horrific disease. So anyways to wrap all this up its extremely clear at this point as to the cause of this disease, and how it develops, etc.
  2. 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 WRITTEN BY: The Editors of Encyclopædia Britannica LAST UPDATED: 5-15-2015 See Article History RELATED TOPICS Jan Evangelista Purkinje cell organ cerebellum mirror neuron brain neuron hindbrain nervous system neuroplasticity Purkinje cell, large 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 … 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.
  3. It doesn't sound like it to much, if it is it sounds very mild. Stay away from synthetics btw.
  4. Have you taken a look at my thread? Theres been a lot of progress made.
  5. 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. https://www.researchgate.net/publication/14821234_Degeneration_of_Purkinje_cells_in_parasagittal_zones_of_the_cerebellar_vermin_after_treatment_with_Ibogaine_or_harmaline
  6. Lol what would be the gain of making up some disease?? People are ridiculous.
  7. Hey Jay! Would you be willing to post results of your MRI? Maybe you could screen shot it if they find anything. I've been making a lot of advancement in reading. It turns out that brain tissue doesn't "scar" like most people think but its a glial scar, and really not even a scar at all, in essense it just liquefies the dead tissue/neurons and removes them, leaving a vacant area. Which really is good news because actual fibrin scar tissue would impede any kind of healing. Which means realistically is all we have to do is find something that stimulates neuron replication. I'm pretty certain as well that the issue in cases of HPPD there is a minor, widespread neuronal loss in the areas affected. Primarily the the limbic system, and prefrontal lobes. just check out my thread I posted quite a bit of new stuff.
  8. 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 studiesUntil 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/
  9. 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 neurotoxicityEvidence 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 usersThe 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.
  10. If you're not getting the symptoms of it, it could be gone, that is if you mean specifically DP/DR, if you mean HPPD its rarely never completely resolved and in the few cases that it is claimed, its probably just lack of perception from the party claiming it to be gone. Basically whenever its seemed to have been resolved just drink enough coffee and you'll realize its still there. The DP/DR can definitely go away though. Generally DP/DR is seen in the earlier stages of HPPD, and typically can resolve, but it seems to just depend on person to person, and is probably dependent on which type of drug they used and what part of the brain was more affected.
  11. 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.
  12. 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. Capela JP1, da Costa Araújo S, Costa VM, Ruscher K, Fernandes E, Bastos Mde L, Dirnagl U, Meisel A, Carvalho F. Author information 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
  13. 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
  14. 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 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. 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.