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The Idea of Kindling, and the possibility of Deep Brain Stimulation


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All,

 

I know the concept and most of the mechanism of kindling pretty well.  However, ALL credit to Nov3 found a really good article that describes it pretty well, and then another concept that poses a a potential solution.

 

I am moving the posts from the Lithium thread here for further discussion.

 

As I state at the bottom, I am in a wave right now, but in teh immortal words of Douglass MacArthur:

 

I'll be baaack.

 

Ramcon1

 

(Someone cheer me up and tell me they like or even get that joke.  Please.  I need a smile.)

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https://neuro.psychiatryonline.org/doi/full/10.1176/jnp.12.3.328

 

'Sensitization Phenomena in Psychiatric Illness: Lessons from the Kindling Model'

 

There's a lot to digest here, but it's all about glutamate receptor kindling and the resulting hypersensitivity.

 

Is it possible that our glutamate-receptor issue isn't necessarily that we have too many, but the one's that we do have are kindled, hypersensitive, and dysfunctional? Could it be that simple? The article talks about alcohol withdrawal and kindling and how when the glutamate receptors are kindled, they remain hypersensitive for life; permanently dysfunctional. Each withdrawal or subsequent response to the stimuli is worse than the last. Could it be that we simply have kindled glutamate receptors and whenever some external or internal stimuli affects those receptors too much, it throws us back into that withdrawal state - and a worse one than the prior at that?

 

This is not a fun idea to entertain. As, I don't know how one would address kindled, dysfunctional receptors. It seems to be a concept that has been pretty accepted for a while though, this article is from a decade ago. And I've not seen anything written about successfully repairing kindled, hypersensitive receptors. The common consensus seems to be that the damage is permanent. Again, the article talks about this state of dysfunction in relation to alcohol withdrawal, but it's not a stretch to connect the dots to benzos? ....Correct me if I'm wrong, but kindled hypersensitive receptors and an excess of glutamate receptors as theorized in this thread are totally different neurological beasts, yeah? I don't imagine lithium or anything else could completely remove all of our damaged glutamate receptors.

 

Though, maybe it isn't 'simple' in that, I don't think the exact molecular mechanisms for a 'kindled state' are totally and completely elucidated. WHY are the receptors in a state of hyperexcitability? There was some discussion of this specific pathophysiology in the article, maybe it explained it all perfectly, but I didn't gather that. But I am also not a neuroscientist and am dead tired and in a wave. Regardless, I think it says some potentially important things and poses new questions for this thread.

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Nov3 (and All),

 

I am having a bad day, but I cannot just leave this out there.  It is too important.  Before I give you a short answer to what may be the best question asked yet, am going to ask in advance that nobody panic.

 

I only gave the article the skimming my brain would allow today.  It was not a bad skimming.  It was far from thorough, but the short answer to your question is:

 

I think this is exactly what is wrong with us.  Exactly. 

 

They only partially cover the mechanism of kindling, and again, I only partially read the authors discussion.  But it is my opinion that dysfunctional glutamate receptors are THE SOURCE of our misery, and upregulation is a known part of kindling.  And kindling is THE REASON a member was well for "x" months/years and then did "something," an antibiotic, quit smoking, started smoking, has no idea at all what he did, but whatever he did it induced a voltage on those ionotropic glutamate receptors, he kindled, and he was sick all over again.

 

This is why I think a treatment, something like a lithium, zoloft, whatever, is essential for our recovery.  We need to beat those ionotropic glutamate subunits into submission at the neurobiological level, or we will be sick for a very, very long time.

 

All cards on the table, I cannot know this for certain, but I believe it in my bones, and it is my goal in life to understand and fix this exact problem.

 

There are other schools of thought on this:

After 6-8 years you are finally done, your glutamate receptors are fully healed and life goes on.

Kindling of ionotropic glutamate receptors only happens to a small percentage of those who become dependent on glutamate modulating meds or drugs, so don't worry.

Live like a monk till you die, and you will be fine, but if you don't you will be fucked.

 

I am not willing to accept those schools, because if I do, I will lose all hope and purpose.  It is my goal in life to understand and fix this exact problem.

 

Good find.  I will read it again and again when my mind is more clear, but, I think this is THE defining moment of these research threads.

 

Please don't panic.  It does not help. Hang in there.  Do the best you can with today, and worry about tomorrow when it gets here.

 

And.

 

If you are 2 years clean, and life sucks, and/or you sound like what I described as "kindled,"  I am not a doctor, etc and so forth, but when I am clean I will definitely try some of the ideas batted around in Chewing the Fat.

 

Ramcon1

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Thanks Ramcon1,

 

You are making a positive difference. All of us that are searching and pushing forward are.

 

 

We have so much more in the way of resources available to us today compared to years previous.

 

As long as we keep asking, searching, and pushing, it’s possible to find a “cure”.

 

That same process is what led to solving problems of the past - smallpox, measles, malaria, polio, etc.

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Nov,

 

Holy $hit.  Good find again. 

 

I am in a bad wave and having a really, really tough time right now.  I might be sick for a week.I will not abandon this.  I have book marked the last two links you sent, and have moved them to the top of the reading list.

 

I will also move all of this to another thread.  You guys keep poking.  I will be back when I feel I can get my head.

 

You all do me a favor and take the discussion of kindling and Deep Brain Stimulation to that thread.

 

Ok?

 

Ramcon1

 

And here it is.

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I cant help but wonder if there are any similarities as to how a general allergy manifests..??

 

The first peanut, one might feel a bit off for some reason unknown... The second, one feels suddenly ill, -or atleast a closer relationship between the two.. The third instance, and its off to hospital... So to speak..??

 

I would imagine that through evolution our body's have developed some “responses” to cater for things that are not so good for us, or even detrimental to our wellbeing..??

 

Just a thought... -and simplisticly presented...

:)

 

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..... following...

 

 

I read the whole article.... looking for "take-aways".  "Central Sensitization" certainly sounds like what

has happened to a lot of us... but on what level?  The article opens up a Pandora's box of possibilities regarding "sensitization".... not just on the NMDA level. Good stuff.... but the deeper we

look.... the more elusive the quest becomes.  Thank everyone for all  your effort in research. Looking for answers is why I am glued to this site. 

 

Finally, postsynaptic NMDA receptors represent but one area where long-lasting functional changes may have relevance to sensitization. Sensitization, depending on the stage of progression, may be manifested on a cellular/molecular level by 1) presynaptic changes (e.g., enhanced neurotransmitter release, diminished/altered expression of autoreceptors, differential gene expression in presynaptic neurons); 2) postsynaptic changes (e.g., receptor plasticity, altered second messenger systems, differential gene expression in postsynaptic neurons); and/or 3) neural network changes (e.g., alterations in inhibitory control between brain regions, unmasking or strengthening of connections between brain regions, neurodegenerative changes “short-circuiting” neuronal connectivity, initiation of novel connectivity via sprouting mechanisms). It is simplistic to posit that one process predominates in sensitization phenomena, especially when different mechanisms may achieve similar phenotypic results or end-target modifications.

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I think this article is important because it could potentially change the way we think of 'kindling'.

 

https://neuro.psychiatryonline.org/doi/full/10.1176/jnp.12.3.328

 

In everything I've ever read on here, kindling is only used in reference to multiple withdrawals.

But, this discusses the concept more as "sensitization" or “kindling-like” phenomena.

Or, as topofthebottom recently posted, 'Central Sensitization'... I think it goes without being said that we are all extremely sensitive.

I feel like the entirety of our symptoms could be traced back to an extremely sensitive, hyper-excitable nervous system. As the nervous system obviously innervates our whole body.

 

So... 'kindled' receptors are SENSITIVE. And kindled receptors remain sensitive. That is what it is saying here. I think the perpetual hypersensitivity is the hallmark of our condition. It mentions the well-known 'subsequent withdrawals are worse than the last'. I feel like this could be any stimuli that affects the kindled glutamate receptors. So, obviously another benzo withdrawal would be worse, but something that affects or pisses off those SENSITIZED glutamate receptors could cause a 'SETBACK' as we call them, or, essentially a return of those kindled receptors to the withdrawal-like state.

 

Yes, we have heard of 'kindling' before. But, what if protracted withdrawal is just that - kindled, hypersensitive glutamate receptors that respond in crazy ways to internal, external, and chemical sensitization. Because the kindling of these receptors causes CENTRALIZED SENSITIZATION.

 

Ramcon posed a similar idea in that he also focused in on those glutamate receptors as the root cause of withdrawal. But I think this notion of kindling almost simplifies that idea in a way. As the kindling phenomena is proven, pretty well studied, and acknowledged as legitimate. And there are already studies aiming to reverse the issue.

 

......

Which, leads me to the mention of the study that I posted on the other thread.

 

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0224834

 

'Deep brain stimulation restores the glutamatergic and GABAergic synaptic transmission and plasticity to normal levels in kindled rats'

 

The headline says it all. If the central sensitization/kindling of glutamate receptors is indeed our problem, this is, according to this publication, an actual cure. Flat out. This literally 'restores the glutamatergic and GABAergic synaptic transmission and plasticity to normal levels'. That is...pretty huge, imo. If it's our receptors that are dysfunctional, this restores them. Even if you subscribe to the old theory that it's merely the GABA receptors that need to upregulate, welp, this fixes that too.

 

Deep Brain Stimulation is a minimally invasive surgical implant that has been used successfully for a wide variety of neurological issues for several years. Recently a lot of attention has been put on its potential to address drug and alcohol addiction. Some places seem to offer this already.

 

http://discovermagazine.com/2015/may/17-resetting-the-addictive-brain

 

@toptobottom, I see what you mean by the article opening up a Pandora's box.

Though, I thought it was cool to see all of the intricacies that were mentioned as normalized in the DBS article I posted. It talked about gene expressions, post-synaptic currents, etc. all being returned to normal levels, compared to the kindled controls that were out of wack. It's all complicated, yes. But it also seems to be misfirings that could be potentially mitigated and reversed by DBS which prompts the receptors to get 'unstuck' and return to their normal homeostasis. It's like a 'reset' as the Discover article above says.

 

 

 

 

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Very interesting.  I'm reading that you would need to be put under to insert the device.  Wouldn't that just make things worse?

 

I actually read that you are awake for it! As the surgeon checks your feedback and responses while implanting the device. And it doesn't cause any pain. Seems really non-invasive, and pretty simple (as far as brain surgery goes...lol).

 

Regardless, that wouldn't inherently make things worse. I had a 3-hour abdominal operation a year and a half ago, well into my withdrawal. Being put to sleep was fine. Just gotta make sure you use only Propofol!

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[ee...]
Are there any places offering deep brain stimulation right now?  I would presume it would be a long waiting list to get this done and convincing them would be hard?
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Are there any places offering deep brain stimulation right now?  I would presume it would be a long waiting list to get this done and convincing them would be hard?

 

Yes, there are a good amount of places. I don't think there'd be any major waiting lists at all; it's a quick, routine, easy procedure.

But yeah, the convincing would be the bump in the road. They treat for drug and alcohol 'addiction' commonly. So... maybe we could hit it from that angle. It'd be awesome to find a benzo-wise psychiatrist to go to bat for us.

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Just tell them you're addicted to Benzos. Everyone thinks it anyways.

 

I mean, maybe not a bad idea actually... And not *exactly* a lie...

 

'I feel like absolute SHIT unless I take benzos'... ergo 'I NEED benzos to not feel like shit'... ergo 'my brain IS addicted to benzos'.... ergo 'I am technically addicted to benzos'.... eh. I would feel gross not telling the full extent of the truth, but I suppose the area of treatment would likely be the same? That would be the most important thing to determine. If treatment for the kindling would be in the same region as the treatment they use for 'addiction'.

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Wow you guys are really considering this, hard.  Today is a shit day, but I am going to force myself to read and absorb all of it.  I thought it could wait until I was feeling better, but even at 50% I will give it my best move it to the top of the reading list and chime in back here in 24 hours or less.

 

If it turns out that Deep Brain Stim is a "real solution,"  then HELL YES WE ARE ADDICTED TO BENZOS.  I sure as $hit would not let the semantics of addiction versus dependence or protracted withdrawal versus organic brain whatever get in the way of a cure.

 

For the record, the opening paragraph of my disability brief for the judge said, "Mr. Sadler was addicted to sleeping pills . . . "  I told my attorney I wanted to see the brief before she filed.  Disability attorneys are so overworked, she was young, and literally no one had ever made that request to her before (Just like neuroscience is what my life depends on now, disability law was what my life depended on in 2018, so yeah, I micromanaged the process) My point is, I was pissed, but even with that glaring misrepresentation, I still won my case.  It was so cut and dried, the judge granted my disability without a hearing.

 

My point is, we are obviously damaged, who cares what they call it if it gets us what we need.

 

In the immortal words of Douglass MacArthur, "I'll be baaaack."

(Someone, anyone, please tell me they like or at least get that joke.  I use it all the time.  I need benzo reassurance  :laugh: )

 

Ramcon1

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Ok my buddies,

 

Today was a tough day.  But I read the “Deep Brain Stim. . . “ paper, over and over until I got it all. 

 

Below is my best shot at a summary.  Happy reading.  But this was a tough one, and many of you are going to say “WTF?”  For those saying WTF, go to the bottom for the short version.  Either way, do not jump up and down with joy yet.  We have a major hurdle to make this viable for us. 

 

That said, let’s ride:

 

It looks fan-F-ing-tastic on paper.  Let’s remember what we are trying to do.  What is the question?  Do we have a disorder of glutamate reception, similar in expression to a dozen things, IBS, autism, etc., including epilepsy?

 

So before we say “Hooray,” we need to make that assumption.  We have a disorder of glutamate reception similar at the cellular level to epilepsy.  I have always been a proponent of this.  I cannot prove it definitively.  Yet.  But this paper is only helpful if believe this is what is wrong with us.

 

Assuming we do, let’s keep going . . .

Do we collectively have the problem of too many glutamate receptors that fire at too low a potential, letting too much Ca++ current through?

Can we also have too few GABA receptors that fire at too high a potential letting too little Cl- current through?

And if so,

Can Low Frequency Stimulation correct those two problems?

 

Abbreviations to make this easier:

LFS = Low frequency stimulation, they found the sweet spot of current for each animal that would activate a neuron juuuuuuuuuuuuuuust right, and then applied four 200 pulse at 0.1 microsecond duration 1 Hz square waves at 5-minute intervals, at various times from 30 after to 24 hours after kindling.  I do not know if that is clear, but it is the best I could do.

 

HFS = High Frequency Stimulation, the process that induces kindling over time, and also the process that induces a seizure when applied once.

eLTP = Excitory Long-Term Potentiation = voltage it takes to cause Ca2+ cationic pore to stay open.

iLTP = Inhibitory Long-Term Potentiation  = voltage it takes to cause Cl- anionic pore to stay open.

EPSP = Excitory Post Synaptic Potential (voltage)

EPSC = Excitory Post Synaptic Current

IPSP  = Inhibitory Post Synaptic Potential (voltage)

IPSC = Inhibitory Post Synaptic Current

 

So the first thing these guys do, is set up an experiment where they have taken a bunch of rats (after reading this, I could not stop thing, “those poor damn rats!” but you gotta break a few eggs . . .) so in these rats, they kindled the area of the brain responsible for epilepsy, using high frequency slowly increasing currents, until the neurons in that are responsible for epilepsy fire much more easily (at a lower LTP) and let more current thru (higher PSC).  And BTW, they did it in both the presence of and absence of an NMDA antagonist, so blocking the effects on NMDA.  When you block the effects on NMDA, nothing happens.  You can’t even induce the kindled epileptic potential on the excitory side.  But when you do not block the effects on NMDA the effect is profound.  This confirms, as I have stated, NMDA is crucial.

 

It shows that after electrically kindling, they reversed the eLTP and the EPSC with LFS, shown in the graphs on page 7.

 

Then they checked if Ca2+ was required for iLTP, and yes it is. So EXCITORY cations are involved in INHIBITORY LTP.

 

They then looked at something called Paired Pulse Index (PPI), which is a fancy way of saying did the PREsynapic voltage change after kindling (ratio of the voltage it took to open before and kindling) and the PPI did not change.  This confirms, as I have stated, it is not what we release, it is how we receive it.

 

Then they looked at the GABA neurons.  And I will admit I do not understand what they are showing.  I looked at the graphs on page 10 are for iLTP and IPSP, and they show the EXACT same types of changes as the eLTP and EPSP on page 7, only to a lesser degree.  Shouldn’t it be the opposite?  Shouldn’t inhibitory (GABA) synapses show an INCREASE in iLTP and a DECREASE in IPSP? 

 

The discussion on page 8 says, “In the control group, applying HFS . . . ” (the epileptic inducing frequency not LFS the cure) “. . . resulted in a significant increase in IPSP amplitude (% change) while the same pattern of HFS could not induce any changes in the kindled group.  LFS application in kindled animals restored the ability of iLTP induction the kindled group. . . ” So the DISCUSSION sounds like they fixed the inhibitory synapse to pre-kindled performance, but the graphs on page 10 make no sense, at least to me.  I am composing an email to the author with all of my questions.  That is #1.

 

They did the exact same thing for EPSC and IPSC (currents).  Seemingly wrong in the graphs on page 12, but clear as curative in the text on page 11 and 13.  That is question #2.

 

Page 13 discusses measuring gene expression by measuring mRNA activity, the encoding of proteins to make NMDA, AMPA and GABA subunits.  All ruined by kindling, NMDA AMPA up, GABA down, and righted by LFS.  This is shown in the graph on page 12 Figure 5(D) for NMDA and AMPA, and Fig 6(D) for GABA.  So this is measuring, as best we can, receptor count and finding too many glutamatergic subunits, not enough GABAergic subunits. And even this was corrected by LFS.

 

The “Discussion” is very long, and has a lot of intermediate conclusions, but a very good summary is in the sentence mid page 15 which states, “Although the exact mechanism of the LFS anticonvulsive effects has not been completely determined, this phenomenon is accompanied by returning the glutamatergic and GABAergic transmission to normal.”  Also a top page 16, NMDA receptors had an essential role in eLTP induction.” And from page 16-17 the same statement about GABA correction.

 

OK now, WTF?

This paper demonstrates, matter of factly, that “kindling” occurs when you apply currents to neurons over time.  They state they can do it slowly, or they can do it quickly.  They choose quickly just to get it done.  It does not say anywhere in this paper,  but the “slow” method is exactly what happens to us while we took/take benzos.  We poke those GABA receptors to release Chloride anions (Cl-) and induce a current over our neurons.  The paper does make a few references to the applicability of the receptor dysfunction to other diseases, page 17, “associated with the etiology of several neurological and mental disorders . . .”

 

The paper goes on to discuss how kindled rats have:

1. NMDA receptors that respond to lower voltage than normal and stay open longer than normal.

2. GABA receptors that behave abnormally. The way they are abnormal is unclear in the graphs, and I will email the authors, but the gist at least in the discussion is they do not release the same amount of inhibitory current as normal.

3. And by looking at the mRNA which is how our DNA encode proteins, they can tell these kindled rats have too many glutamate receptors, and too few GABA receptors.

 

But that Low Frequency Stimulation, LFS, fixes ALL of that, at least in rats kindled to have epilepsy.

 

More good news, you can forget “Deep Brain” Stimulation.  This has nothing to do with Deep Brain.  Throughout the experiment, the authors only refer to their technique as Low Frequency Stimulation (LFS) the “deep brain” part is only because that is the area of the brain that causes epilepsy.

 

I said in order for this to apply to us, we have to make the assumption that what we feel, what is wrong with us, is exactly what the authors lay out in points 1 thru 3 above.  Then we have to make the other assumption that what worked in the rat hippocampal neuron will work in any mammalian neuron, in other words, a benzo damaged neuron anywhere in the human body, or in “other other” words, us.

 

Then the MAJOR hurdle is, how in the world can we apply LFS to every neuron in a benzo damaged human?  I don’t know about you, but at least 50% of my symptoms are physical, most notably my stiff as hell spine and irritable as hell bowel.  That is another question I will pose to the authors, question #3 if you have read this from the top.

 

Now I am completely spent.  I hope you all found this worthwhile.  I needed to do it anyway, and it was a good distraction.

 

Honestly, I also had something to prove.  Probably not here in the research threads, but elsewhere on the board, members have questioned my ability as “self-taught neuroscientist.”  And in fairness, I have met a few self-taught engineers.  Some were really good.  Some not so much.  I know I still have A LOT to learn (the more I learn the less I know,) but I needed to gain your confidence that I can hold my own with the caliber of people that wrote this paper.

 

I hope I have done so.

 

I will come back when I email the authors and get a reply.

 

Good night,

 

Ramcon1

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PS I would not have written the part about needing to prove myself on a better day.  That is my scientist's equivalent to the benzo need for reassurance. :(
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Ramcon1 - thank you so much. And especially for reaching out to the authors.

 

It’s reassuring to understand that what we might be looking at as a remedy isn’t so much Deep Brain Stimulation as it is a body wide reset process.

 

 

Have you read Dr. Norman Doidge’s book The Brain’s Way of Healing?

 

Chapter 7 is A Device That Resets the Brain, Stimulating Neuromodulation to Reverse Symptoms - which is about the PoNS device. (I think we’ve talked about that before.)

 

Reading right now about all the successes with the device - stroke, Parkinson’s, vestibular issues, etc.

 

 

Thanks again!

 

 

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Thanks for checking it out, Ramcon.

 

More good news, you can forget “Deep Brain” Stimulation.  This has nothing to do with Deep Brain.  Throughout the experiment, the authors only refer to their technique as Low Frequency Stimulation (LFS) the “deep brain” part is only because that is the area of the brain that causes epilepsy.

 

I don't think we can forget DBS yet. They used LFS, or a frequency lower than 100 Hz, but had to use DBS to access the part of the brain they needed to, so they could actually deliver the LFS there. Similarly, benzos definitely impact parts of the 'deep' brain that would require DBS to access. I have not seen anything regarding LFS treatments that are able to access those deep brain locations without DBS. But I am happy to be corrected on this. I think DBS is needed...... Until these new, non-invasive stimulation techniques become available - such as optogenetics or temporal interference. But with all the trials and stuff, who knows how long that will be.

 

 

I said in order for this to apply to us, we have to make the assumption that what we feel, what is wrong with us, is exactly what the authors lay out in points 1 thru 3 above.  Then we have to make the other assumption that what worked in the rat hippocampal neuron will work in any mammalian neuron, in other words, a benzo damaged neuron anywhere in the human body, or in “other other” words, us.

 

 

It would certainly be great if it lined up *exactly* with this paper. And, shoot, it sounds like it really could. But, I think even with small differences there could still be a lot of hope in this. You can find other articles with mentions of the normalization of other dysfunctional receptors. Other mentions of it addressing brain disorders where there is a problem of something being 'stuck'. It's been called a potential 'reset' for addiction in the brain as shown in the other article I posted. I think it has potential to help kind of reboot receptors that aren't functioning normally. Which clearly could work if that article explains our issue to perfection, but might help us even if we have some slight variations, imo.

 

 

Then the MAJOR hurdle is, how in the world can we apply LFS to every neuron in a benzo damaged human?  I don’t know about you, but at least 50% of my symptoms are physical, most notably my stiff as hell spine and irritable as hell bowel.  That is another question I will pose to the authors, question #3 if you have read this from the top.

 

 

Do you not think the problems are mostly issues in the brain? And the brain misfirings then cause symptoms throughout the body via the brain-connected nervous system that runs through everything? ......It would be great to determine which areas of the brain are MOST affected by benzos. Which are the most prominent spots for glutamate receptors?

 

Other parts of the body are applicable to Low Frequency Stimulation as well though. I remember seeing an article discussing LFS in the stomach to treat gastroparesis. The abdomen could be treated with LFS similarly it seems. Why not other places like the spine?

 

It would be great to treat the whole body, but I have not seen something that allows for such, as you said, that would be a hurdle probably. But one could focus on problem areas, if not the brain exclusively. While it's ideal, it might not be necessary to hit everything - just the places that are flaring with symptoms.

 

.............

We should strive to learn more about low frequency stimulation in general here. Are there devices we could get access to that would provide the stimulation we need at the frequency we need? It's just 'stimulation' after all. Whether those are devices we could get access to or treatments available in medical facilities. And furthermore, how deeply would these devices penetrate? What tissues could we access? ....I still think the DBS will be necessary for accessing the places in the brain we need. And the brain is undoubtedly the most important place we must address.

 

So let's look into LFS and let's try to determine what areas of the brain are likely most affected by benzos.

 

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Transcranial Direct Current Stimulation (tDCS) may have some potential here...

It’s a noninvasive way of sending frequencies through the brain. Available and programmable to the masses.

 

It has a few notable disadvantages to DBS, such as its lack of specificity, but that might not necessarily be a deal breaker for us...though, it does have the potential to cause some off site side effects and it may be harder to deliver the frequencies to the exact places we want them. I’ve read a few contrasting statements about its ability to penetrate into areas of the ‘deep brain’, but it looks like the chances are fairly good that it does.

 

If we use the same frequency that the Iranian scientists used in the initial article I posted, strategically placed the electrodes to sufficiently reach the primary areas of concern, and fleshed out the other details and intricacies of this plan... we might actually, maybe, possibly, potentially be able to do this on our own.....

 

 

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Ramcon 1,

 

Thank you for everything you do, and thanks to those who bring forth new papers and ideas.

 

I came across Elon Musks Neuralink which aims to eradicate the use of invasive procedures like DPS with his technology.

 

I’m unsure whether this is at all relevant,  Here’s a link to his presentation.

 

 

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