N&PD Moderators: Skorpio
Hallucinogen(-Induced) Persistent Perception Disorder caused by cholinergics
TheTwighlight
Bluelighter
I agree, I just figured that maybe this might be sorta helpful information. There's no telling what really set this guy off, but he is a genius, he's a brilliant painter and musician, but he just can't facilitate the use of his intellect the way that he used to be able to.
pofacedhoe
Bluelight Crew
TheTwighlight
Bluelighter
^
I'm just saying, damn...
I could sure as hell imagins if i kept doing this crap the ghost like things may intensifie to creatures that follow me all day around.
Anticholinergics are fucking crap, just the histamine thats OTC had this feature... I've used antihistamines in high doses before without any problems.
ShaolinBomber
Ex-Bluelighter
HPPD is believed to be a neurobiological disorder, perhaps caused by changes in epigenetic coding of the cell, or long term potentiation aka reinforced excitatory pathways in the visual cortex.
It still amazes me how much people talk out of their ass about things they have no understanding of.
ShaolinBomber
Ex-Bluelighter
thank yoouuuuuuu. HPPD is not a "latent" mental disorder. People like to fall back on this absurd statement about drugs causing long term disorders when they dont know what the fuck they are talking about in the first place.
I've never had an actual psychiatric problem before my HPPD onset and mental disorders do not run in my family.
ShaolinBomber
Ex-Bluelighter
Oh that was one quick answer, thx!
Another question in this respect: Do you observe the same patterns when simply closing your eyes? I mean, it should theoretically be the same as when looking into the dark. Or not?
- Murphy
i have visual snow and real visual snow is seen eyes closed or open. This can be emphasized by simply closing your eyes and shining a flash light into it. I see a blueish/grey static in the eyes opened state in the dark, but i see a pure black static when i've done the activity stated above.
I am pretty sure tough that HPPD caused by anticholirenics is completely differend then when its caused by other psychedelics.
MurphyClox
Bluelighter
On what is this assumption based, if I may ask?
MurphyClox
Bluelighter
[1] Can you provide some reference for these theories?
[2] Well, that's why I asked, because I indeed have no real understanding about this.
- Murphy
Its completely unlike HPPD thats usually described.
Nothing like that, just ghost/wave like things that constantly flow if i look in the dark.
MurphyClox
Bluelighter
OK, I see. Thx for the pic though.
Interestingly, as a child I was willingly able to produce something that looked like those "floaters" ("mouches volantes"), just by defocussing the eyes.
Anyway, back on topic. I would be glad about some approaches to explain said phenomena, in particular those caused by anticholinergics.
- Murphy
ShaolinBomber
Ex-Bluelighter
i get the same kind of static and floaters as that picture has shown. My static is not as pronounced though.
There are currently no articles out right now about actually researching HPPD and cellular pathway activity so i cant directly back up that theory. I however do know that certain ligand activity can produce exctitation in MAPk/ERK pathways which produce cellular growth, or dendritic expansion in the brain, which COULD lead to enhanced synaptic connections between cells, making the brain offbalanced in the visual cortex, instead of equilibrium where the estimated 20% inhibitory cells can maintain the excitation caused by the estimated 80% of the excitatory cells.
There are large volume, strong EPSC(excitatory post synaptic current) producing spines on neurons, and there are weak, small volume EPSC producing spines on neurons. Synaptic efficacy COULD be increased via chemically induced long term potetiation (synaptic plasticity) amongst these neurons to the point where excitation cannot be inhibited enough by inhibitory afferents so the visual cortex remains on the excitated side of the spectrum, producing visual distortions in the sense that these neurons that get fired up when exposed to visual stimuli remian firing for longer periods of time and produce lingering visual information (afterimages, trails, floaters, starbursts.) This prolonged stated of firing is referred to as polysynaptic excitation or inhibition i believe.
http://www.sciencedirect.com/scienc...serid=10&md5=932b0f770a607f3bc6569f528f40e52f
"Inhibitory pathways in the neocortex display a variety of temporal and spatial patterns, maintaining a dynamic balance with excitatory synaptic activity. Recent studies have revealed prevalent polysynaptic subcircuits within the neocortical microcircuitry. These subcircuits involve excitatory and inhibitory connections that are activated by neurons both in supragranular and infragranular cortical layers and mediated by different mechanisms. Interestingly, in these subcircuits inhibition is induced by discharge of pyramidal cells, and excitation is caused by specific types of GABAergic interneurons. The different polysynaptic subcircuits are discussed with respect to their spatial and temporal properties and their possible functional role in cortical processing.
Hallucinogens, 5-ht, SSRI's, MDMA, all are active or increase activity at GABAergic interneurons which have 5-ht2 receptors on them. Over stimulation of these receptor areas of a neuron can produce cellular dendritic growth, perhaps causing increased efficacy at these spots on the synaptic connections, forming newer, stronger synaptic connections to the GABAergic interneurons responsible for the negative feedback loops between excitatory and inhibitory neurons.
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Mitchy=)
Bluelighter
EDIT:: Interesting information, have you guys heard about those piercing migraine's that make you hallucinate (not in a normal sense) that certain people get & alot of doctors recognise how close the two symptoms are? Well my mother used to get those, so interesting piece of information possibly suggesting it may somehow relate to gene's. Anyway, read on
I have HPPD, have had for almost 2 years now.
I got mine from abusing MDMA (pills that may of had other stuff in them)
I also used to abuse nangs(whip it's, w.e you call em) while abusing mdma.
If i had to guess, i would say i was eating between 3-10 pills every weekend for about 6months, most of which had 100+mg of MDMA in them. I also smoked weed on occasion (which seemed to make me notice it alot more) I believe i started to 1st notice it after a night heavy on the pills (both high dose mdma and ketamine), lack of water, and alot of hallucinating.
I have never taken LSD, but i believe some of the pills i had in this period of 6months had a substantial dose of MDA in them.
DR Rick Strassman's theory on this was you brain resetting itself. Explanation: His theory was that we started out seeing like this when we where born, then our vision adjusted/changed, as we grew older, then by abusing(maybe not even abuse, but something happened that changed the chemicals in the brain) drugs we changed it back to how it was when we where young.
Thats not a quote, i reworded that to how i think he tried to put it across, and i believe that it sounds reasonable, as there are success stories of people getting rid of HPPD after 5+/- years and regaining normal vision.
I don't want to rant much more, i could talk about it for ages and i have alot of views on what has happened, if you would like to hear more or want me to elaborate on anything just let me know and i will be happy to
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TheTwighlight
Bluelighter
^
The headaches you're talking about that make you hallucinate are migraines with aura. I happen to suffer from both migraines with and without aura, and the ones with are weird. I could be totally sober and just all of a sudden feel like I'm on a low dose of LSD, or the come-up or something. But it never progresses anywhere, except that 18 hours later I have a horrible migraine.
My first Datura stramonium trip (roots, then stems, then leaves, then fuck it half a CUP of seeds sent me into a 4 day stay in the ICU. MY vision didnt return to normal for a week? 2 weeks? after that, Any writing Eg a newspaper would blur the moment i focused on it, and there were rainbows and halos on anything bathed in light. also i could focus on things and they would warp and change quite a bit. Used Brugmunsia 100's of times to even up pinpoint pupils from opiate use so my girl would notice, same thing might happen sometimes, but NOTHING persistent. nothing without there being some drug in my system causing it, except maybe the first time[
QUOTE=MurphyClox;7226790]Yep, it was one purpose of this thread to collect personal experience from Bluelighters.
In this context I remind all readers of ADD to check THIS THREAD! The so-called 'spring cleaning' is supposed to clear out all threads (meaningful ones, useless ones...ALL!) if they hadn't been marked before. Personally, I prefer a "delete nothing"-approach for ADD in particular and I would be pleased to see others join my opinion. Please check the thread and post!
- Murphy[/QUOTE]
Mitchy=)
Bluelighter
Cheers for clearing that up about the migraine aura TheTwighlight, that's what i was talking about.
ShaolinBomber
Ex-Bluelighter
There are studies showing sufficient gene expression changes in synaptic plasticity genens with use of psychedelics and MDMA. Most people i think can ward off any kind of attempts of their brains to reinforce excitatory pathways, or have no need to because they can manage the excitation.
I do believe this could be due to genetic factors, and its a situation of being in the wrong place (bad environment in your body to take a potent 5-ht2 agonistic drug) at the wrong time (taking the drug.)
I wish i could talk more about the work "they" are doing at the moment for HPPD and the acceleration they are working at for answering questions. I mean the team working and contributing to this HPPD research is like OVER 9,000 in powerlevel if you're into DBZ you'll get that one I truely believe in the enxt 5 years at the most they will have the answers to why this happens and why it happens to only a few individuals.
Here's an article I found
"J Clin Psychopharmacol. 1989 Oct;9(5):347-51.
Dopaminergic activity of the antimuscarinic antiparkinsonian agents.
Modell JG, Tandon R, Beresford TP.
Department of Psychiatry, University of Michigan, Ann Arbor.
The antimuscarinic antiparkinsonian agents are widely used in psychiatric practice to reduce the extrapyramidal motor symptoms caused by the neuroleptic antipsychotic medications. Although the antimuscarinic antiparkinsonian agents are effective in reducing extrapyramidal symptoms, their use in conjunction with neuroleptic treatment of psychosis has been reported to antagonize the therapeutic effects of the neuroleptic; there are also several reports of the antimuscarinic antiparkinsonian agents variously causing psychotic syndromes, mood elevating and stimulant effects, stereotypy, dyskinesia, behavioral agitation, and drug dependence in both psychiatric and normal populations. These drug-related phenomena are generally attributed to the antimuscarinic properties of these agents. A large body of data, however, has shown that the antimuscarinic antiparkinsonian agents also function as potent, indirect dopamine-agonists. Benztropine, the most widely prescribed of these medications, is one of the most potent known inhibitors of presynaptic dopamine reuptake. These antiparkinsonian agents also have potent agonist activity at the noradrenergic synapse, as well as minor activity at the serotonergic synapse. This paper reviews neuropharmacologic evidence suggesting that significant neurophysiologic effects can result from the dopaminergic--and possibly noradrenergic--activity of the antimuscarinic antiparkinsonian agents, similar in some cases to those observed with amphetamine. Greater attention to these properties may aid in interpretation of clinical and research observations involving these so-called "antimuscarinic" agents."
From what I gather from this, the antimuscarinics (anticholinergic) drugs blocks the reuptake of dopamine from the synapse, and slightly blocks reuptake of serotonin and norepinephrine. It would almost induce a "amphetamine-like" state. So I assume in large quantities, this effect in the CNS would be shown. Dopamine is the key neurotransmitter in psychosis, which is why D2 is targeted in schizophrenia.
Also, one would see anticholinergic side effects from diphenhydramine, such as blurry vision, urinary retention, tachycardia, dry mouth, etc. but whether diphen actually binds the specific M5 receptor in the CNS that causes the psychosis effects, I have no idea. I've never gotten a high of Benadryl, but then again, the max I've ever taken is 50 mg...
This is another abstract I found that makes a little more sense and is clearer:
Clin Drug Investig. 2006;26(10):603-6.
Psychotic disorder induced by oxybutynin: Presentation of two cases.
Gulsun M, Pinar M, Sabanci U.
Tatvan Military Hospital, Psychiatry Service, Tatvan, Bitlis, Turkey. [email protected]
Anticholinergic agents are muscarinic receptor antagonists that suppress the activity of the acetylcholine system in the brain. Some of these agents also increase the concentration of dopamine in the synaptic cleft, which may result in psychotic symptoms. Oxybutynin is an antimuscarinic drug that may have adverse effects on the CNS, including memory impairment, confusion, delirium and hallucinations in elderly patients. To date, several case reports have been published about the association between oxybutynin and psychotic symptoms in elderly subjects, but we were unable to find any case reports describing oxybutynin-induced psychotic disorders in young people. Here we report on two patients, a 7-year-old boy and a 21-year-old man, who developed a brief psychotic disorder that may have been caused by oxybutynin. The first patient was kept under observation with vital functions supported but no medication. All his psychotic symptoms regressed and his general condition improved. The second patient was treated with olanzapine 10 mg/day. His psychotic symptoms resolved within 3 weeks. Our two case reports provide evidence that oxybutynin may induce psychotic disorders, and in younger patients.
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")
