Electron Quantum Number Solution to Relativity Neuroscience

Magnesium Cures Migraines
So magnesium will cure migraines because migraines are caused by NMDA receptors switching back and forth between two adjacent energy levels rapidly (called quick-switching) which causes pain in people disposed to migraines and the magnesium will cause the energy level to either rise or fall gradually and then the reverse gradually, which keeps you from quick-switching, but you need absolutely mega-doses of magnesium daily to accomplish this, which will be safe because of the swift elimination rate of excess electrolytes in healthy people.
One of the main assumptions is that migraine sufferers have a malfunction in their NMDA receptors that does one or both of the following: 1) causes quick-switching activity, and 2) causes pain from quick-switching activity. Magnesium will help most migraine sufferers if they can get it into their blood, preferably through good absorption through digestive tracks but daily injections or a patch seem a reasonable treatment to prevent suffering.
We can help all migraine sufferers, however it is more complicated. If this simple treatment doesn't cure your migraines, it means that your NMDA gates have additional energy levels that are damaged, and that basically means that you will incur additional quick-switching activity at additional energy levels. So this means that as the magnesium makes your energy levels rise or fall, some of the risen or fallen energy levels will error and cause quick-switching between their adjacent levels. In one more sentence, folks not aided by the simple magnesium course suffer poor energy level switching at multiple places.
Therefore, to save these people, we will have to put their NMDA gates at a specific energy level. I am unaware of any drugs or substance that currently does this. So the only choice is to find a cocktail and schedule of substance that will hold their brain at specific energy levels.
But that's unspecific. We can do better.
If we can buffer against the effect of the magnesium, we can hold the energy level of the NMDA receptors at a specific energy level. The first place I'd suggest to look for such a buffer would be the opposite of magnesium, though I practiced no rigor to reach that conclusion.
But yes, yes, how can an element have an opposite? The electron surface of magnesium is well-defined and tiny, but that's not really the case for aqueous magnesium. The solution of the brain combines with the magnesium to create effective electron activity of a different shape than pure magnesium. I'm saying elements can be effectively mapped as drugs in aqueous solution.
So the shape of the effective molecule can be deduced or maybe even observed, or possibly figured out with an adept of chemsketch. Then we can apply pharmacological principles to deduce a buffer, eventually, and fix migraines, though the migraine sufferer would be taking pills all day, or maybe a patch?

 

Comparison of Neural Impulses Between ADD, Normal, Savant
Definition: Neural impulse - the electrical discharge that travels along a nerve fiber; "they demonstrated the transmission of impulses from the cortex to the hypothalamus"
Adjunct definition: Neural impulse is an approximation of the gross electron movement of an entire neural pathway from initiating synapse to ending synapse.
Note: This paper assumes familiarity with Electron Quantum Number Solution to Relativity Brain Science (which is all over my Facebook page).
Please scroll to the bottom and check the image to understand my hypothesis visually and get the most out of this document.
Therefore, dextromethorphan really causes ADD on the comedown if heavily abused for like a week, just like stimulants do. I can confirm both anecdotally, which is good enough for theory if you keep it a secret. The explanation is that dextromethorphan, after sufficient abuse, leaves your brain in an extra plastic state for many days afterward, and the stimulant comedown does the same because of NMDA modulation from the lack of synaptic dopamine due to down-regulation. This is validated a bit more later in the paper.
If the neural impulses are too thick, all the probabilistic-learning-simulating pipe-suction interferes with each other, causing the pertinent quantum number variables to go astray, resulting in sketchy math and often causing the variables to be straight up lost, which looks like forgetfulness or poor attention. I know, not all ADD are bad at math. In highschool, I knew an ADD kid who would smoke weed before pre-calculus so he could keep up, though he thought he was being a rebel!
So we can further surmise that stimulants harden plasticity, in other words probably agonizing NMDA receptors, which I just happens through modulation by excess dopamine instead of the actual ki for the NMDA receptors.
This would explain why tweakers get stuck in specific behaviors (and possibly the rare but oh so desired weed-stuck, though different neurotransmitters are at play there). This means we can treat tweakers with brain plasticity drugs rather than rubber rooms.
This also explains why dextromethorphan slows down or prevents stimulant tolerance. There are a few possible whys including ones I can't think of. How can I know that? Oracle school in a past life. I propose one explanation:
Thought A: simply balances out plasticity change. If we run with this idea, single line neural impulses build up probability suction for that segment or line (how could it be a line? Field Theory Neural Science, where the neural impulse is an interplay of vibrations between different lines. Geometry says lines need to be straight, but actually they just go forever. If Field Theory Neural Science is correct, we can shoot electricity from our brains.)
Back to this theory however: Dextromethorphan thus prevents/slows down probability change because low plasticity around a neural impulse increases probability for that neural impulse, and changes in probability gets you that novel learning buzz I so enjoy from meth. Makes me feel like a genius even though I just open up a bunch of browser tabs and stare out the blinds.
I should specify that change in probability can't be the same change repeated else you won't get the novel high no matter how many times you hit the pipe: you just get more tweaked.
This is part of the reason tripping in a new set and setting can bring back the magic, though not the complete why.
If you desire proof of this, abuse dextromethorphan liberally and often for a month to a year, and you should be able to get back at least one episode of MDMA magic. You should wait at least a month after the DXM dose probably. It worked the other way around for me, though I suppose it won't work for everyone.

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You see it here first, guys. Migraines can be cured with magnesium, though not in all cases. There are in fact energy levels to the NMDA voltage gates and migraines are caused by a malfunction in switching between the energy levels causing a back and forth flow of electrons, and when an electron switches locations back and forth consisently, this causes a quantum number to increase because otherwise it would cause a small resolution paradox in the timeline, which feels good, not bad.


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I believe consciousness can be quantified exactly by adding quantum numbers to electron. I'd bet five, though probably more.


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I'm studying neuroscience. I believe binding to GABA receptors dos not actually cause the effects profile of the benzodiazepines. This can be proved if someone will ingest a fatal dose of barbiturates while on a large dose of dextromethorphan or ketamine, as those drugs will prevent death from barbiturate overdoses if I'm correct.

 

Is PTSD a Form of Migraine?

Simplify! There are more brain diseases than actually exist.

I know from personal experience than dextromethorphan temporarily relieves PTSD, and also that praising Fe (the goddess of magic, though any will do) will temporarily relieve PTSD (it can stop the nightmares).

High arousal and high novelty release norepinephrine. High arousal and high novelty tend to be present in traumatic experiences (I know it's less traumatic to be raped after you're used to it, for example). My theory is that a high concentration of norepinephrine will damage energy level switching permanently, causing pain in the migraine fashion as explained by my previous posts and paper concerning Relativity Neuroscience. High norepinephrine also sets the neural pathway into a higher probability of occurring, increasing the chances of a neural impulse following that neural pathway again, which would be experienced as recurring PTSD symptoms. I suggest that norepinephrine lowers brain plasticity, and that lowered brain plasticity causes the probability of a specific neural impulse to increase when that neural impulse is fired.

PTSD must occur at regions where gaba and norepinephrine meet because gaba agonists help PTSD. Gaba agonists increase brain plasticity (NMDA antagonism) if you believe my idea that ADD is caused by over-plastic neural pathways creating "thicker" neural impulses that interfere with each other, which would also suggest that such interference would explain blackouts. It would also explain lowered inhibition because the probabilities for our normal behaviors aka our typical neural impulses are high, and for some reason I'm still working on, thicker neural impulses have different probabilities or higher brain plasticity also alter probabilities.

So, GABA agonists help PTSD by lowering the probability of symptomatic behavior from occurring, and it does this well temporarily and perhaps even permanently.

We can help traumatized people better by boldly prescribing the benzodiazepines post trauma, and there's plenty of good data suggesting that staying on the stuff won't help, but would suggest that benzo-medicated therapy sessions would relieve symptoms faster and more permanently.

I don't have PTSD anymore, but if you know someone that does, experimenting on them with memantine or ketamine may be interesting. A single sub-anesthetic dose of ketamine should cure PTSD for weeks afterward. This was verified in an alternate dimension, if you're a believer!

 

We can prove my neuroscience with another animal experiment:
Blocking SERT completely in a dog should not kill it and also prevent it from understanding you, and you should be able to slap it in the face repeatedly without it ever developing a flinch response or suspecting the next strike.
My troll-casual reference-free paper on this follows:
Serotonin's Role in Psychosis and Learning
Flipping the fuck out is a mild form of dopamine psychosis (imagine the flip outs of the people we typically call bi-polar)? So I can come back from stimulant psychosis with ketamine or dextromethorphan.
Think serotonin levels increase when you hurt people? And that's what eventually shuts down the flip out.
Was pondering a serotonin releaser easing or stopping a psychotic break as well.
The amphetamines do release serotonin but not enough to prevent psychotic breaks, not even MDMA does. Dopamine's buffer, too, in terms of changing brain plasticity.
But depressed people aka people on SSRIs get addicted to drugs more often than normal, suggesting that serotonin mediates probability increases which lowers psychosis incidence and addiction rate.
Interacting with people does release serotonin I believe, suggesting that serotonin plays a role in learning from others.
So pretty sure abuse lowers serotonin levels permanently, which suggests...
So think that completely disabling SERT in a dog, presuming it doesn't die, prevents it from understanding you.
Well anyway, so then the connection between abuse depression addiction -> not just serotonin but lowerered serotonin levels lower your ability to change probability of neural impulses, thus the addict truly cannot tell how much the drug is hurting them.
Also explains why I only quit when I'm high.
But we can also see that lowered serotonin levels are a defense mechanism against abuse. So blocking serotonin may also prevent flinch reactions from building, so I'm saying that the SERT-disabled dog could be slapped repeatedly in the face and it would never flinch or suspect the next blow.
So the inverse test of this is to take PTSD vets, increase serotonin levels and play loud noises near them, presuming they got fucked up in an explosion. This should allow them to more quickly drop the flinches and the fight or flight response. This will lower military divorce rates, so really this will be standard one day.
So after butt rape sessions from my rapists, I could not bare being touched by anyone. I'd hurt and freak out.
Needing help, my rapists suggested a classic psych technique: wrap me in a heavy blanket and hold until I stopped screaming and relaxed.
I'll just finish by saying this worked and I could handle contact for short term afterward and a few repeats later in the week cleared up touch issues mostly.
Uhh, but if you have a real hard case, you could speed up re-adaption by increasing serotonin levels though a dose of ketamine would work far better.
So high serotonin hardens brain plasticity, increasing probability of probability increase of a neural impulse when neural impulse fires.
Abuse lowers serotonin levels, increasing brain plasticity and lowering probability of probability increase of a neural impulse when neural impulse fires -> effectively the abuser can't hurt you as much.
Brain plasticity increases thickness of neural impulses, causing interference of signal, therefore depression makes you forgetful and contributes to lowered motivation. Also contributing to lowered motivation is the lowered probability of probability increases from outside sources -> you can't learn that you feel better from doing things.
So 5-htp would help with jet-lag, sleep patterns being explained by probability changes of outside cues (+ other stuff).
Oh, but what to do about all the dead serotonin receptors in my and target audiences' heads?
I'm going to argue NMDA-miracle for dead serotonin receptors, because a highly plastic brain will just cave in and fold around the hole, effectively allowing different receptors to shuttle the signal.
This probably happens anyway, but I like to sell dissociatives.
Still not super ideal because you can't store as many different probabilities.

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Believe we can debunk pharmacology by soaking a squid tentacle in sarin and then inducing a neural impulse (movement) through torture.
My thoughts are that the sarin would paralyze the tentacle, but that somehow the tentacles would try to escape the pain and there'd be detectable neural impulses (movement).

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Suspense releases norepinephrine, which increases the probability that you continue watching the show (suspense activating fight or flight activating norepinephrine which hardens brain plasticity which increases the probability of the activated neural impulse of activating again).