Adderall and HPPD?

[jackie jones]

Pupil dilation is a side effect of adderall, and therefore enhances the visual cortex. If you experience HPPD, stimulants may trigger visual hallucinations.

 

[Bell Ringer]

i don't disagree

Pupil dilation is a side effect of adderall, and therefore enhances the visual cortex. If you experience HPPD, stimulants may trigger visuals.

I just think some people are getting carried away with visuals and negleting the gestalt. What effect would dopamine and norepinephrine have on one's pupil's?
More importently what effect would they, in combination with many other factors, have on the PNS and CNS. I think they would induce a mild fight/flight response which would override more complex but less esstaial systems in the nervous system, which may at least lessen one's perscecption of HPPD. Once the adderal is taken out of the picture or tolerance develops I predict a rebound. This is assuming the OP was correct.


Will fix spelling later must sleep

 

[seep]

Pupil dilation is a side effect of adderall, and therefore enhances the visual cortex. If you experience HPPD, stimulants may trigger visual hallucinations.

I think the focus is shifting not toward the primary sensory organ, but to the way the sensory input is processed. Most likely there's a deficiency in the way the brain filters out irrelevant data. There's a lack of feature extraction somewhere in the v. cortex.

I'm interested in the way the perceptual disturbances resemble what happens to a person who is extremely sleep deprived. This pins the tail on the mechanism of dreams, which I don't know enough about. Likely there's some kind of neuronal crossroads back there between the circuits for visual perception and the circuits of morpheus, so that a dysfunction in association takes place.

If that's the case, amps would nuke this fucker pretty effectively.

There's no reason that faulty editing and spontaneous dreaming (more at hypnagogia) can't both be at work here. The old theory about dreams being a form of memory assembly comes to mind.

Without empirical data about pathophysiology and how it relates to sensory processing/association, this is all just shamanistic wankery.

Bell Ringer, thanks.

Edit: To Mr. J: Apparently some level of signal processing (vs. simple transduction) happens at the eye level. The retina has, besides rods and cones, a third type of photoreceptor. They were recently discovered and analysis is still rudimentary, so much of this is tentative. They lie posterior to the rods and cones and utilize a different pathway to the thalamus. They are active even in people lacking rods and cones. They are sensitive to light intensity and respond primarily to blue light. Hence they play a role in regulating circadian rhythms and melatonin release. Also, they control pupil size. They are also claimed to be important in partitioning conscious and unconscious light perception. The PGRs are only present in mammals, process information more slowly and are not topically linked to anywhere in the cortex. Nevertheless, they respond to light more rapidly than rods and cones, and they exert some sort of control over what frequencies the R&Cs transduce. The previous two sentences makes me speculate they evolved prior to rods and cones. All of the above makes me think PGCs have a role in psychedelic experience. I don't have time to do the research right now.

 

[ShaolinBomber]

Shaolin, I'll be happy to put on a dunce cap and strum my lips while making semi-mammalian noises in a very public place and then post the video on you tube if we can break out of the circularity here.

Perhaps if I can see the Abraham paper, or any paper (whether it comes from Harvard or from the North Korean Ministry of Defense or from some guy named O-Dog) anything that explains or attempts to explain the pathophysiology of HPPD.

I'll go first, simply using Offerman's Encyclopedia of Molecular Pharmacology:

First the obvious:



So then, your (or Abraham's) claim is that hallucinogens damage this selfsame 5-HT2A pathway by permanently eliminating many of those receptors in specific areas of the visual cortex. This immediately prompts the question, "If the primary pathway is cut off, how can the hallucinogens' symptoms recur?"

So then, the claim is that the hallucinations et al of HPPD are not caused by the 5HT2a pathway, but rather by a critical lack of GABA molecules in the relevant synapses and the consequent hyper-exitation. It is also claimed that benzodiazepine drugs (especially clonazepam) ameliorate the symptoms of HPPD. This sets up a contradiction:


Also, it's claimed that the reason there's a decreased GABA concentration in the synapse is that since the 5HT2A's are decimated, pre-synaptic GABA release is insufficiently stimulated. This assumes that one of the principal catalysts of presynaptic GABA release is serotonin activity, principally at the 5-HT2A receptor. I don't know enough about triggers for GABA release, but I assume the triggering has something to do with all exitatory transmitters; if so, the hypervigilance and anxiety which accompany flashbacks (to call a steer a steer) are necessarily the products exitatory transmitters and depolarization. So then, given all that's been said about GABA release, there seems to no dearth of triggers. This is speculation on my part. Offerman only gives me this:


One or two of us is oversimplifying or overlooking key aspects of the process. Either that or the 5HT2A-receptor-attenuation theory is incomplete. I'd really like to see that Abraham paper.

I'm keeping this up because I honestly want to know, not because I think you're wrong.

point #1: Not every HPPD patient has reduction in visuals from benzo administration. I have slight reduction in SOME, but most visuals still persist through klonopin treatment. The papers and studies you're referring to are talking about the anxiety symptoms that come along with the HPPD and the visuals. Basically clonazepam reduces anxiety so that the HPPD'er isnt constantly freaked out by what they're seeing. Benzos dont effect the GABAergic cells through the same way that the serotonergic/GABAergic pathway would. There are GABAa receptors on both pre and post synaptic cells. Benzos just make the GABA thats around more efficient by opening the ion channels. But if there isn't enough GABA being produced through this negative feedback loop in the VISUAL CORTEX, then benzos aren't gonna do shit for reduction of visual disturbances. They'll have anxiolytic effects and reduce anxiety in other GABAergic cells around the cleft, but the visuals are gonna be left untouched.

Point #2: The receptors that are talked about in the current theory are primarily located upon POST-SYNAPTIC GABAERGIC INHIBITORY CELLS. When serotonin binds to these 5-ht2a receptors located upon the post-synaptic neuron, it causes an inhibitory response(this is called the negative feedback loop between the pre-synaptic serotonergic cells, and the post-synaptic GABAergic cells. Basically its a system that keeps the visual cortex in check), therefore releasing GABA to SLOW OR TOTALLY STOP THE EPSC(excitatory post synaptic current) caused by the pre-synaptic serotonergic cell. Now you ask why do the current researchers and i think this? Because if theres no receptor to stimulate this inhibitory response, then you have excitation running wild in the visual cortex, much like what you would see in a normal persons brain on a psychedelic drug.


Now onto Adderall.

1. the point about pupil dilation. well pupil dilation is controlled by a neurotransmitter called acetylcholine, or Ach for short. Look it up if you want. I'm not sure how amphetamines would effect this system but if you're interested give it some reading.

 

[seep]

Fair enough. Sounds somewhat like Huntington's, with the breakdown of inhibition leading to hyperbolic visual perception instead of motor conniptions (totally different regions of the brain, but yeah). This is interesting shit. How is it not degenerative?

I wasn't aware you had it. I've had 30-50 hits of acid and several dozen rolls and never had a single flashback. I wonder if there's a genetic precipitant, and why the positive symptoms are so much like those of SCPT. Actually, the latter is why I've been so keen on this thread. I've gotten so picqued by dealing with people who hallucinate (schizos in my case) that watching and studying their breakdown in perception is more appealling to me now than actually experiencing it firsthand again.

Maybe when the 5th DSM finally makes it to press, they won't append the word Flashbacks to the heading for HPPD. They're authoring it without peer review, so anything can happen.

Re the Ach and mydriasis: I thought so too, but I stumbled accross the photosensitive ganglion cell today and there looks like there's something to that. Haven't read up on it tho.

Thanks for putting up with my badgering.

 

[permastoned]

1. the point about pupil dilation. well pupil dilation is controlled by a neurotransmitter called acetylcholine, or Ach for short. Look it up if you want. I'm not sure how amphetamines would effect this system but if you're interested give it some reading.

Pupil dilation, or mydriasis, is not controlled by solely one system. Yes, ACh plays a role, but it is well known that serotonin, in particular the 5-HT2A receptor, causes extreme mydriasis (as is seen when one takes LSD or another psychedelic).

 

[ShaolinBomber]

Pupil dilation, or mydriasis, is not controlled by solely one system. Yes, ACh plays a role, but it is well known that serotonin, in particular the 5-HT2A receptor, causes extreme mydriasis (as is seen when one takes LSD or another psychedelic).

yes, thanks for the correction.

To seep:

HPPD'ers aren't "crazy" in the laments term of the word. I suffer from constant dissociation and i see visual disturbances but my reality check it fully intact.

When the new DSM comes out, HPPD will no longer be called HPPD, but more likely something else that i cannot tell you because i've been asked not to. The new definition will be much more accurate at targeting symptoms.

 

[jackie jones]

They are producing a new DSM?

Sweet.

 

[seep]

Shaolin, I didn't mean offense. Sorry if it was taken that way. My fascination with perception is genuine.

...i cannot tell you because I've been asked not to.

This is actually happening. There's plenty of great PsyD's and physicians that are really not liking the secrecy.

Tangent:Wow. Search Bluelight for "photosensitive" and you'll find a discussion about whether or not the Third Eye has photoreceptors.

 

[ShaolinBomber]

Shaolin, I didn't mean offense. Sorry if it was taken that way. My fascination with perception is genuine.



This is actually happening. There's plenty of great PsyD's and physicians that are really not liking the secrecy.
Tangent:Wow. Search Bluelight for "photosensitive" and you'll find a discussion about whether or not the Third Eye has photoreceptors.

Its being kept under close watch because right now the research thats going on is in a tight spot. i feel thats all i can really tell you right now because i keep in contact with one of them and he's asked me not to share any information we discuss.

 

[Bell Ringer]

I don't know how that slipped by for so long

1. the point about pupil dilation. well pupil dilation is controlled by a neurotransmitter called acetylcholine, or Ach for short. Look it up if you want. I'm not sure how amphetamines would effect this system but if you're interested give it some reading.

That makes too much sense. I'm ashamed I did not point that out. It is also reasonable for sleep paralysis which most people know. I just took the serotonin, pupil thing at face value because I did not care about that. I had a different point to make. I feel like a fool.

Glad you pointed that out,
Thx

 

[Bell Ringer]

If you are refering to OP's symptoms

Fair enough. Sounds somewhat like Huntington's, with the breakdown of inhibition leading to hyperbolic visual perception instead of motor conniptions (totally different regions of the brain, but yeah). This is interesting shit. How is it not degenerative?

I wasn't aware you had it. I've had 30-50 hits of acid and several dozen rolls and never had a single flashback. I wonder if there's a genetic precipitant, and why the positive symptoms are so much like those of SCPT. Actually, the latter is why I've been so keen on this thread. I've gotten so picqued by dealing with people who hallucinate (schizos in my case) that watching and studying their breakdown in perception is more appealling to me now than actually experiencing it firsthand again.

Maybe when the 5th DSM finally makes it to press, they won't append the word Flashbacks to the heading for HPPD. They're authoring it without peer review, so anything can happen.

Re the Ach and mydriasis: I thought so too, but I stumbled accross the photosensitive ganglion cell today and there looks like there's something to that. Haven't read up on it tho.

Thanks for putting up with my badgering.

Don't scare the hell out of him. What he described sounds very little link Huntington's disease. It be helpful to know his age.

 

[seep]

Don't scare the hell out of him. What he described sounds very little link Huntington's disease. It be helpful to know his age.

He and I have spent a good portion of this thread talking about dysfunctions of signaling pathways in specific regions of the brain. He's obviously smart enough to not be spooked into thinking he has Huntington's Chorea.

Huntington's involves the severance of an inhibitory loop, causing excess DA to accumulate in the basal ganglia (where ACh pathways have also been eliminated). It's the first thing I thought of when Shaolin help me disentangle the wiring he'd been talking about.

I hope you're not like pissed or anything, because I was wanting to PM you for those articles you mentioned. The only thing biological I can find with my library account is a paper from 1993.

 

[Bell Ringer]

This seems relivent...

however I don't have time to read the entire article ATM. I only read the abstract but I do plan on making time to properly check it out.

I guess I can't post attachments

http://www.bluelight.ru/vb/blog_attachment.php?attachmentid=20&d=1253861858

 

[ShaolinBomber]

He and I have spent a good portion of this thread talking about dysfunctions of signaling pathways in specific regions of the brain. He's obviously smart enough to not be spooked into thinking he has Huntington's Chorea.

Huntington's involves the severance of an inhibitory loop, causing excess DA to accumulate in the basal ganglia (where ACh pathways have also been eliminated). It's the first thing I thought of when Shaolin help me disentangle the wiring he'd been talking about.

I hope you're not like pissed or anything, because I was wanting to PM you for those articles you mentioned. The only thing biological I can find with my library account is a paper from 1993.

i can get you plenty of articles from Dr. abraham and halpern who were the first HPPD psychiatric researchers. This research took place awhile ago, i think maybe back in the late 80's and early 90's, so what they discuss is probably off compared to the current research.

 

[Bell Ringer]

You realize that monamines and monamine receptors are 2 different things.

To OP: the system of cognitive, neurological and electrophysiological events that leads to perceptual disturbances is complex, ouroboric and poorly understood, but it seems counterintuitive that a psychostimulant would ameliorate perceptual disturbances. Vigilance is heightened. The fight/flight/fright response is amplified.

Exactly what I have been saying (well close enough).

Amphetamine and its analogs weakly inhibit MAO-A and are ineffective at MAO-B.n 2* Human platelets contain only MAO-B.n 3* Even if phentermine were to inhibit platelet MAO-B, the enzyme does not metabolise serotonin and MAOIs do not affect platelet serotonin.n 3* Thus, some explanation other than MAO inhibition must be sought to explain how oral phentermine increases platelet serotonin.

Neurochemical experiments show that MAO-A inhibition increases brain serotonin and decreases its metabolite, 5-hydroxyindoleacetic acid. If phentermine blocks MAO-A, then it too should increase extracellular serotonin. Experimental data show that phentermine has little effect on neuronal serotonin or 5-HIAA. Zametkin et aln 4* measured urinary monoamines and metabolites in man after treatment with dextroamphetamine or MAO inhibitors. They concluded that dextroamphetamine did not show "even a minor degree of monoamine oxidase A inhibition". Daily administration of phentermine (37 mg/day) produces plasma concentrations of about 0.7 mumol/L,n 5* well below its Ki of 75 mumol/L for MAO-A.

Phentermine produces a spectrum of concentration-dependent neurochemical effects. It interacts with norepinephrine transporters at 0.1 mumol/L, dopamine transporters at about 1 mumol/L, serotonin transporters at 15 mumol/L and MAO-A at about 100 mumol/L. When given at typical anorectic doses, it mainly interacts with dopamine and norepinephrine transporters. The work reviewed here clearly shows that phentermine does not inhibit MAO-A at therapeutic doses. Clinical observations that co-administration of phentermine with fluoxetine, or with other SSRIs, does not characteristically produce the adverse effect known as the serotonin syndrome, which does occur when SSRIs are combined with MAOIs, is further evidence that phentermine does not block MAO at therapeutic doses.

Yes amphetamines are ,weak MAOI-A inhibiters. They also increse extacelluar serintonine, however to focus on this is misleading because one is jumping the gun.

Amp's enhance noreinephrine, cause a signifcant increase corticossteroid levels, and are dopamine agonist.

Some dopamine breaks down into norinephrine and adrenline.

Consider how such actions would affect the PNS and the CNS.

Will finsh and edit post soon but I am guessing most of you can do the math from here. The artical I ref.ed was from The Lancet and I will attactch it or upload it somewhere and link to it Gotta run

 

[Gormur]

maybe the lack of GABA would explain my natural tolerance to alcohol and benzos then..and the fact that i basically can't really take them since starting amps, as they just make me feel extremely depressed+suicidal

anxiety is getting to catatonic levels lately, even after i've been off amps for 2 weeks now. my hallucinations/dissociations have grown more intense as well

while i don't doubt that amps decrease psychotic symptoms short-term, i think for a lot of people they exacerbate them long-term..maybe not in immediately obvious ways, but over long-term use, it seems they screw a lot of people up mentally

i had a lot of visuals and such before starting amps this year, but never the dissociation, delusions, or extreme paranoia till a few months ago- after i'd been on amps for about 5 months

sorry if i went a bit off-topic... carry on

peace

 

[ShaolinBomber]

maybe the lack of GABA would explain my natural tolerance to alcohol and benzos then..and the fact that i basically can't really take them since starting amps, as they just make me feel extremely depressed+suicidal

anxiety is getting to catatonic levels lately, even after i've been off amps for 2 weeks now. my hallucinations/dissociations have grown more intense as well

while i don't doubt that amps decrease psychotic symptoms short-term, i think for a lot of people they exacerbate them long-term..maybe not in immediately obvious ways, but over long-term use, it seems they screw a lot of people up mentally

i had a lot of visuals and such before starting amps this year, but never the dissociation, delusions, or extreme paranoia till a few months ago- after i'd been on amps for about 5 months

sorry if i went a bit off-topic... carry on

peace

that sounds more like amph induced psychosis, not hppd.

 

[ShaolinBomber]

He and I have spent a good portion of this thread talking about dysfunctions of signaling pathways in specific regions of the brain. He's obviously smart enough to not be spooked into thinking he has Huntington's Chorea.

Huntington's involves the severance of an inhibitory loop, causing excess DA to accumulate in the basal ganglia (where ACh pathways have also been eliminated). It's the first thing I thought of when Shaolin help me disentangle the wiring he'd been talking about.

I hope you're not like pissed or anything, because I was wanting to PM you for those articles you mentioned. The only thing biological I can find with my library account is a paper from 1993.

Right now, for public access, this is the best i can do. But theres alot of good information in these.

http://www.nodid.net/Articles/articles.htm

That has quite a few articles relating to HPPD and HPPD related disorders.

 

[ShaolinBomber]

For those who were interested in this discussion, alterations in receptor mapping is not the only thing they are investigating for the causes of HPPD.

For Chronic forms of the disorder, they are also looking into epigenetic changes, as well as Long-term potentiation. The neocortex consists of 6 layers, all of which have a role in processing somatosensory and visual information. One proposal for chronic HPPD is that synapses that regulate late excitatory polysynaptic potentials have been reinforced through overstimulation in vulnerable people.

The 6 layers in the neocortex communicate with eachother in order to properly filter visual information before we consciously percieve what we're looking at. Layer 6 of the neocortex is the initial area that recieves all visual information and has its own process for filtering, and then projects the stimuli down circuitry columns via dendritic axons to neurons in neighboring layers. When this happens, you have a simultaneous excitation of pyramidal cells, which respond to serotonin and releases glutamate, and these signals travel down to the layers 1-5 of the neocortex.

So the proposal here is that late excitatory post-synaptic potential FREQUENCY,mediated by glutamate release via serotonin excitation, has increased to the point where it overrides much of the inhibitory tone provided by GABAb receptors, and fast spiking inhibitory currents by GABAa receptors. This would now change a persons neocortex from being in a state of equilibrium to a state of excitation, because inhibitory tone and fast acting inhibitory spikes cannot effectively stop these reinforced currents. This would give rise to a reoccuring excitation loop throughout the neocortical layers, which include the occipital, parietal, and temporal lobes.

These main lobes of the neocortex are mainly responsible for visual processing, sensory processing from various parts of the body, auditory processing, and memory.