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fasoracetam for gabapentin wd???

Cosmic Trigger

Cosmic Trigger

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I've ended up dealing with polyneuropathy and some painful nerve burning. I turned to Phenibut and Gabapentin (gaba prescribed) and have had some good success over this last year and a half. I finally felt the pain was getting better so I thought I'd like to see if I could do without. I started with Phenibut which I had been using daily at up to 3400 mg per day. The Gaba was at 1800. I divided the doses so I was taking it three times a day.

Someone suggested fasoracetam for the Phenibut wd. So I did a long slow taper and when I jumped off at 300 mg I had no withdrawals. I now have kind of assumed that the Gabapentin prevented them more than the fasoracetam but I really don't know for sure. So it's been a couple of months now and after that stunning success I'd like to have a go at the Gabapentin. I plan a slow taper. What I'm wondering, is it possible the fasoracetam will help with the Gabapentin withdrawals?

Any other tips would be greatly appreciated also. I'm pretty nervous as I've heard that Gaba withdrawals can be just as nasty as Phenibut. Oh and finally I am also on 20-30 mg. per day of Oxycodone used at night for pain and sleep.
 
I think Fasoracetam for phenibut w/d is not because of phenibut being a VDCC blocker like gabapentin, but a GABAb agonist... it's supposed to help with GABAb upregulation and of course w/d are associated with downregulation (and receptor uncoupling).

Gabapentinoids / VDCCs don't all have much to do with GABA agonism so I would not expect the fasoracetam to help generally with them all.
 
Gabapentin is a GABA-B agonist at receptors containing gb1a-gb2 subunits which seem to be sparsely populated but I can't find much literature at all on it. I've really only found them in melanotrophs which are involved in hormone regulation. There are also it's effects on increasing GABA synthesis but I wish I knew how much of a role that's playing, I think wiki said that's playing a role in Gabapentin's efficacy for mania...

I am under the impression that fasoracetam is a GABA-B antagonist because of it's ability to block some effects of baclofen when other compounds with acetylcholine/glutamate properties failed to do so. But I don't know what it's actual effects will end up being if it's also blocking pre synaptic auto receptors - it's possible that depending on subunit composition of GABA b that fasoracetam is more selective for some pre synaptic receptors and therefore maybe in some brain regions you might see increased GABA signaling. It's hard to say what's going on, I wish there was more literature. I think someone on Reddit said that fasoracetam helped them with Gabapentin withdrawal.

Another possibility is that fasoracetam doesn't have much affinity for the Gabapentin receptors that have gb1a-gb2. But I think if baclofen has affinity for those receptors maybe fasoracetam will too, and if the gb1a-gb2 receptors are playing a role in baclofen's efficacy for neuropathic pain then I would assume fasoracetam would indeed block the gb1a-gb2 Gabapentin receptors.
 
A little dizzying but:

It [gabapentin] was recently reported to be a selective agonist at GABA(B) receptors containing GABA(B1a)-GABA(B2) heterodimers, although several subsequent studies disproved that conclusion.
Click to expand...

http://www.ncbi.nlm.nih.gov/pubmed/15067218

Yes gabapentin and pregabalin affect glutamate decarboxylase which shifts balance towards GABA. :) Is phenibut known to do this?
I mean, it's only since quite recently that it was even found to be a VDCC blocker... it seems in the realm of possibilities?

Another question though is: how significant is that glutamate:GABA shift compared to VDCC blocking? Seems like it would require separating those effects with selective agents and comparing.

@ what might help w/d of a gabapentinoid...

Ironically first thing that comes to mind is phenibut :\ since its a milder VDCC blocker that from what we know at the moment does not share a number of other effects gabapentinoids have, so you would expect partial tolerance and a potential way to first withdraw from part of the effect before withdrawing from the rest. But thats mostly theoretical from the overlap, I couldnt begin to suggest how to 'switch' or taper>combine and if you are relieved you got rid of that its understandable to be outraged about getting on it again.
I'm with you in this though: I am on pregabalin, only lower doses for anxiety type issues.. and I am not sure if I am gonna have problems quitting, and if so how I or my doc are gonna pull it off. Very generally I'd suggest treating symptoms if they arise with best aimed (selective) and very moderately dosed depressants. I don't know if harsh feelings can be avoided, and if prolonging the process is only pretty much making it worse.. but some possible withdrawal effects may not be too great for you (e.g. even if not dangerous, too much insomnia can mess a person up).
 
It was my error to use both most likely. Many doctors think gabapentin has little to no wds. I doubt that. I guess I'll try a long sloooow taper. I may just be stuck with it due to pain issues. What I'd like to discover is if it actually is reducing my pain from neuropathy anymore. I guess a long taper would show that over time. Fortunately I'm an old man and in the end have not that much to lose if I'm stuck with it. Maybe.
 
Is your neuropathic condition considered to be likely to go in remission spontaneously? Has the feeling changed of the pain being there but the drugs helping with it to apparently not even feeling the pain underneath anymore? It hurting and being aware are often separate things are they not? Just curious.

It was my 'error' too so to speak since I chose pregabalin somewhat out of the blue for ASD, unusual but technically justifiable. And it really helped so much in the beginning, it was a 'golden era'. Now it still helps but not so magically anymore. I don't know that it is really an error since I cannot weigh how hard I will withdraw against how much it helped so far, but I am not at a very high dose and it would all have been worse without it.

I imagine neuropathic pain would also have been a worse option, I do not really know that many neuropathic painkillers.
 
Not likely but it's been known to happen. One thing I've had to consider is the emotional component of pain. When first symptoms appeared I got very frightened. I had read of others with all over body burning pain and was terrified that was where I was headed. Now, over the last year and a half I've calmed down. My pain has not lessened when I'm flaring but my perception has changed and I've gotten to where I can ignore it when distracted by something interesting. Now I think I can use my mind to deal with the pain and so want to find out if that's true. So I have to reduce or get off these drugs to find out. I'd much rather do without and in reality Kratom or Oxy seems to be the most effective but I can't be sure.

Why would opiates be effective? Well I now think it has to do with depression and fear. Kratom especially lifts my mood and depression and my pain usually recedes with each fresh dosing. I also have a pet hypothesis as to what has caused my neuropathy. Due to childhood abuse I have lived a long life of anxiety issues. I think my nervous system finally became overwhelmed and started to malfunction. So when I reduce anxiety and depression the experience of pain lessons. I want to find out.
 
Regarding the study from Taipei, I think the important thing is to use cell cultures that have gb1a-gb2 - which all they said is there are GABA-B receptors in the periaqueductal gray - I think verifying that there are these specific receptors there is very important. If there is another study that confirms cells with gb1a-gb2 are not affected then I will concede (and I am already apprehensious and also just playing the role of devil's advocate here too). So if there is another study that used some melanotroph cells where the GABA-B affinity was originally reported I would be curious...

It somewhat irks me that the sole point of studies is to make something replicable, and then you have a study that goes and uses different cell cultures, which I feel stupid if they decided to check other cells because other people had already checked melanotrophs but anyways.

OP, opiates are very well known to make neuropathic pain worse in the long run by inducing inflammation that causes sensitization. Treatments like low dose naltrexone work by binding to receptors on microglia and shutting them down, see the Stanford article from 2014 on naltrexone and chronic pain. You can find naltrexone online as well. I recommend starting out very low if you have an opiate habit, 1mg or less would be a good place to start I think.
 
Interesting info on opiates and neuropathic pain. I take lots of anti inflammatory foods and herbs. Guess that's a good idea. I'll try and locate that article and I thank you very much for that lead.
 
Low dose naltrexone combined with opioids is also a possibility isn't it? Don't know if that properly avoids the inflamation of the glial cells, but iirc it does help stave off some of the tolerance?

CT your hunch about life long anxiety having to do something with it isn't even so unscientific or farfetched, if the neuropathic pain is a result of auto-immune activity caused by stress that affected those very aforementioned glial cells? So in short, not too long ago that link was made between possible mental causes for physical illnesses - and if the reverse is true possibly also the healing power of the mind.

I don't know if the neuropathy from auto immune activity can go undetected in mild forms or always have to go Guillian-Barré style...
 
There are actually formulations of opoids and ultra low dose naltrexone approved as I recall, it is established that ultra low dose naltrexone potentiates morphine analgesia, some of this might have to do with naltrexone preferentially blocking excitatory G protein coupled mu opoid receptors but I think the attenuation of microglial activation is important too, as the microglial become more and more activated their TLR4 receptors up regulate and become more response to opiate induce inflammation, so it's important to try and curb that early on. Opoids bind to toll like receptors and activate inflammation, while naltrexone does the opposite. Eventually we will have dextro-naltrexone, which blocks TLR4 but has negligible affinity for opoid receptors.

As far as half assed neuropathy - I think we are only good at identifying the full blown MS type stuff. I think there are other minor kinds of nerve inflammation and of course lots of nerve compression type stuff that slips through the radar. There is stuff like CIDP and I think there are half assed forms of that. After all there is stuff like Bell's palsy, although that is mostly related to viruses infecting the nerves (which we also really suck at detecting).
 
Cosmic, can you tell us about the original cause of the neuropathy? Was there an injury or was it idiopathic? If it's mainly pain I think at some point something in complex regional pain syndrome spectrum should be considered - I have had mild forms of that and focusing on immunosuppressant and anti inflammatory treatments has helped.
 
No cause has been found to this point and I don't have the money to find the kind of doctors that might be of help. I get free healthcare at the bottom rung of the latter and the two neurologists I have been to were of very little help or empathy for my situation.

Would you be willing to go into more depth about your treatments?
 
Is it systemic or is there a distribution pattern with some areas unaffected?

Most of my neuropathy was from nerve compression but for the pain amplification type stuff Gabapentin and low dose naltrexone are what have helped. I think baclofen and Gabapentin are both promising for nerve pain as well as nerve damage regarding baclofen.
 
Cotcha Yankinov said:
Is it systemic or is there a distribution pattern with some areas unaffected?

Most of my neuropathy was from nerve compression but for the pain amplification type stuff Gabapentin and low dose naltrexone are what have helped. I think baclofen and Gabapentin are both promising for nerve pain as well as nerve damage regarding baclofen.
Click to expand...

Distribution pattern.

I actually have a few Baclofen around that I've never used. My doc gave them to me for Phenibut wds but I never used them. Would they work pretty fast or do they need to build up in my system? I only have twenty but if they worked my doc would give me more. I could try it along with the Gabapentin next time I've got a heavy flare going on.

Thanks for all your help btw.
 
Describe in detail the distribution pattern please.

I don't mean to give you false hope in case this is a demyelinating disease but I'll be honest - compression neuropathy is very common.

Do you have a history of MDMA or other psychostimulant use? Any joint hyper mobility? Any spine issues or neck pain? Ever any trouble with vision such as grey-ish vision or darker vision, which is sometimes worse in one eye? (or have they checked to see that your color is intact? If not I'll find a test online that you can self administer when I get a chance to check for signs of optic neuritis).

If you do have a demyelinating disease I think minocycline would definitely be something to try, for example you can read about it's use in MS on wiki's minocycline page.

Try the baclofen and see how it goes, even if it doesn't alter the course of the disease it could be worth it to try them just for symptomatic relief and quality of life if they help enough. They are underwhelming for me personally. Let me know about your experience and dosages used.

And of course you are welcome :)
 
Cotcha Yankinov said:
Describe in detail the distribution pattern please.

I don't mean to give you false hope in case this is a demyelinating disease but I'll be honest - compression neuropathy is very common.

Do you have a history of MDMA or other psychostimulant use? Any joint hyper mobility? Any spine issues or neck pain? Ever any trouble with vision such as grey-ish vision or darker vision, which is sometimes worse in one eye? (or have they checked to see that your color is intact? If not I'll find a test online that you can self administer when I get a chance to check for signs of optic neuritis).

If you do have a demyelinating disease I think minocycline would definitely be something to try, for example you can read about it's use in MS on wiki's minocycline page.

Try the baclofen and see how it goes, even if it doesn't alter the course of the disease it could be worth it to try them just for symptomatic relief and quality of life if they help enough. They are underwhelming for me personally. Let me know about your experience and dosages used.

And of course you are welcome :)
Click to expand...

bottom of feet worse on right foot where it all started
top and back of thighs and butt
back of hands
top of forearms
outside top of shoulders where tats are
upper back along shoulders and forehead

Yeah MDMA maybe 60 times or more
Total psychonaut since 18 although nothing since disease. Hundreds of LSD, Mushrooms, Peyote trips. Such fun.=D

Eyes are good except for a lot of floaters in right eye that came on suddenly about a year ago but then never got any worse

No joint hypermobility but lifetime athlete and ex Martial Arts Instructor. Occasional small of back spasms.
 
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