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Thread regarding SCI and chronic neuropathic pain


[De...]

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Hey Everyone 

 

Im starting this thread, to do a follow up with my trials, also share experiences with other folks dealing with pain and protacted symptoms from the brain injury and mal-adaptations of the CNS and brain

 

Please Bear with me, or jump to the substance trials, That is highlighted.

 

From serveral withdrawals that i had sustained since i was forcefully made dependant on benzos, which I got dependant after being assaulted with neuroleptics against my will, not once but twice and developing a brain injury both times, and from the serveral withdrawals that i suatained, trying to recover even prior to benzobuddies(2010) i ended up developing chronic pain and spinal cord degeneration, as If It was a spinal cord injury, from ecxitotoxicity and the immune mediated injuries, at the last withdrawal, préviously from stopping i had no pain, just discomfort, of course, my spine was already suffering from all of the above mentioned 

Now im trying to adress it the way i can, but my life became even worst, chronic pain, and neuropathy from the nerve comrpession, as follow 

 

Often i think its cancer, because of the pain,given the possibilities, or cervical cancer from metástasis, ss im have thyroid nodules which im investigating, high thyroglobulin, and high calcium serum levels, or could be herpes or a post viral infection, or Spinal MS, and others possibilities, lung cancer, osteoblastona and so on, too many articles of medical Gaslight úntil finding that their back pain ia cancer, aside, i had very high iron levels, and other stuff, that said, It could also be mainly and only due to the neurotoxicity of several benzo withdrawals and the issues with gaba/glutamate and neurotoxic mediated harms, thyroid dysfunction and the whole immune mediated syndrome that arise from such malfunctioning of the gabaergic system, none of these makes It easier or less life ímpairing, indeed a very sad outcome ...

 

Due to medical gaslit, as It happens with many of us and other chronic ill people, i still couldnt find an conclusive diagnosis, but several indicators and possibilities in the table, úntil now nothing as a surgery tô decompress the spine, of a possibile nerve root compression was taken into account,  i have buldging disks toucinhg the dural sac showing on the MRI and osteófits and degeneration of the intravertebral disks, these could be a cause for my pain, but no surgery indication úntil now, but im seeking for It ..

 

I will bê seeking another neurosurgeon, for an  Second opnion... i was indicated by one neurosurgeon tô another, as the former is tô old tô perform surgery,  as i couldnt at first find the guy which was indicated, i ended up seeing another, this one "didnt saw anything" and took the could be anxiety take, the usual medical gaslit,

 

LIke in the beggining im on my own to try to adress it the best i can, that is what i want to discuss here and reason i'm starting this thread, to share experiences with other folks dealing with similar, any pains, 

 

 

 

 

 

 

Ongoing Trials 

 

Im waiting for some edaravone, an ALS drug to come, its already bought and i will be receiving it soon,  searching on google schoolar, you find a lot of info about its effects on gene expression, oxidative stress, AQP4 and sirtuin, mapk, and others celular Pathways as the mtor pathways, also in terma of remyelination, and pain, i will bê adding It to my stack and share how It goes

 

Aside i am using pioglitazone 30 mg daily, which I should have srarted since the beggining, while undergoing severe harm.. all these in fact

Im also taking clemastine furamate 2mg two or 3 times a day, which i will run out soon, and have to aquire more , im treating this whole thing as MS,

Raloxifene 30mg(stopped due to affecting bp)   

 

Theofyline for peripheral nerves remyelination, to promote HDAC 2 transcription 

I have to lay low on theofyline as It seems to trigger something that is probably hsv-2 which is always latent but reactivates when i use HDACs 1/2 inhibitors and or cyclic amp modulators as theofyline/bromantane , or If i supress my immune system too much, a known thing avaliable online in scientific literature

 

theofyline is being showing tô favor remyelination, in the PNS and CNS, but wont work alone, If you dont overdo, like 15 to Max 30 mg a day(taking aside several possible interactions, which you should always check) its safe, check for interactions and use caution

 

I was taking 7,5mg of effexor daily for pain, while It helps to mitigate, not competely, but does, i stopped because i will revisit metformin, to aid with remyelination paired with the others, and i cant mix both, It doesnt fit well, also, venlafaxine does something at the p38mapk and foxo 3, and metformin does the inverse, as does propentofyline that i will start soon, which inhibits p38 mapk in order to reverse some of the sensitization and gabaergic dysfunction at the injury site, and spinal cord 

 

 

I will be adding propentofyline on daily basis, as It does act tô inhiibit gaba transaminase, as bromantane, and to promote gaba from glutamic acid via gad65 enzyme, as an adenosine antagonist tô some extent , also acting as a phosphatidiesterase 2, 3 and 4 inhibitor, as p38 mapk inhibitor, and augmenting the clearance of glutamate trough GLT-1 transporters, to reverse some of the central sensitization and pain that develops from mal-adaptations of the CNS after such injuries that leads to chronic pain, also as an strong thiol(antioxidant) promoter, in order to promote remyelination, and to restore some how some of the gabaergic function that was lost at the spinal cord /nerve injury that i sustained,  

 

These are methyl xantines, and their literature under neuropathic pain, and neurodegenerative conditons are avaliable online, theofyline is risky regarding arrythmias, more due to toxicity, and propentofyline is not, and has a safe side effect profile, its showing tô be a good one for restoring the functions post injuries, Strokes, and alzheimer/dementia, 

 

Propentofyline also seems to modulate the SAHH, which is a Pathways responsible for the convertion of succinic acid to gaba, in other words, improoving the gabaergic system functionality

 

I also took bumetanide an nkcc1 inhibitor that restores the functions of pre and post gabaergic neurons and the homeostasis of the spinal cord neurotransmission, íon channels, took It for some time like one and a half weeks, and It did help, but my blood sugar deemed like to spike, these is a good one, and i will try to inform myself about others that have a similar mechanism of action on the nkcc1 and nkcc2 cotransporter, as If is usefull for pain 

 

Here a few about It, to a better understanding https://www.mdanderson.org/newsroom/research-findings-re.h00-159066345.html

 

 

Im also investigating and studying about other substânces, as isx-9, sephrin1 hcl and  tpso ligands, some are in development, as the etifoxine analogue which I forgot the name GSX- some number, and other avaliable at pgl chem,

 

Anything tô recover tô some point of this pain, 

 

I do my best regarding precautions, and interactions, liver enzymes check up, etc, no doctor would probably accept these buch of stuff, they wouldnt be helping like they never did..

 

I willl bê sharing my ongoing process

 

Any one dealing with protacted symptoms, mental or physical, 

 

Feel free to drop a message, 

 

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Repurposing cancer drugs identifies kenpaullone which ameliorates pathologic pain in preclinical models via normalization of inhibitory neurotransmission

https://www.nature.com/articles/s41467-021-26270-3

Abstract

Inhibitory GABA-ergic neurotransmission is fundamental for the adult vertebrate central nervous system and requires low chloride concentration in neurons, maintained by KCC2, a neuroprotective ion transporter that extrudes intracellular neuronal chloride. To identify Kcc2 gene expression‑enhancing compounds, we screened 1057 cell growth-regulating compounds in cultured primary cortical neurons. We identified kenpaullone (KP), which enhanced Kcc2/KCC2 expression and function in cultured rodent and human neurons by inhibiting GSK3ß. KP effectively reduced pathologic pain-like behavior in mouse models of nerve injury and bone cancer. In a nerve-injury pain model, KP restored Kcc2 expression and GABA-evoked chloride reversal potential in the spinal cord dorsal horn. Delta-catenin, a phosphorylation-target of GSK3ß in neurons, activated the Kcc2 promoter via KAISO transcription factor. Transient spinal over-expression of delta-catenin mimicked KP analgesia. Our findings of a newly repurposed compound and a novel, genetically-encoded mechanism that each enhance Kcc2 gene expression enable us to re-normalize disrupted inhibitory neurotransmission through genetic re-programming.

 

Regarding toxicity and mitocôndrial effects effects https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5881471/ in rats

 

I will be trying to achieve this substance

 

 

Im doing some cotations, to see If i can get ahold of It, minimum order quantity and price,  

 

 

If you re interested, let me know,  maybe a group buy will be neeeded, which we would discuss in another place,

 

 

 

Feel free to drop a message and share your toughts

 

Thanks

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Following some recollection linking points

 

By searching i saw some folks on here speaking of nemopidine, and i will share some info that i recollected about It following,

 

i will add 15 mg of nemopidine for the spinal cord, as long term it does upregulate the nkcc2 cotransporter function, 

 

Results

Nimodipine, down-regulated lncRNA NEAT1, up-regulated miR-27a and down-regulated MAPT all improved brain damage and CI, inhibited brain tissue cell apoptosis, and enhanced brain cell activity. The common binding sites of lncRNA NEAT1 and MAPT were found on the miR-27a sequence fragment, and miR-27a could be paired with the former two. Nimodipine was found to cause the down-regulation of lncRNA NEAT1 and MAPT, as well as the up-regulation of miR-27a.

Conclusion

Nimodipine can improve CI after SAH in rats through the lncRNA NEAT1/miR-27a/MAPT axis

 

excess NEAT1 leads to re-localization of SFPQ (splicing factor proline/glutamine-rich) from the IL-8 promoter, resulting in transcriptional activation of IL-8 (Imamura et al., 2014). RN7SK RNA is involved in the regulation of CD4+ T lymphocytes and contributes to inflammation

 

Specifically, P2X7 receptors function as ligand-gated ion channels [44], while P2X3 receptors are preferentially expressed in DRG neurons and are upregulated under neuropathic, inflammatory, and visceral pain hypersensitivity conditions [45].

 

Upregulating miR-27a-3p inhibits cell proliferation and inflammation of rheumatoid arthritis synovial fibroblasts through targeting toll-like receptor 5

 

MiR-27a ameliorates inflammatory damage to the blood-spinal cord barrier after spinal cord ischemia: reperfusion injury in rats by downregulating TICAM-2 of the TLR4 signaling pathway

 

Our working hypothesis is that regulation of intracellular Ca2+ in the hippocampal system is impaired by aging, and nimodipine reduces this impairment by blocking calcium entry through voltage-dependent calcium channels. In effect, nimodipine restores important biophysical properties in aging hippocampal neurons so as to mimic those observed in neurons from young animals.

 

https://link.springer.com/chapter/10.1007/978-1-4615-3432-7_19

 

L-type of calcium channels are commonly spread throughout the brain. L-type of calcium channels control neuronal excitability and combine neuronal activation with gene transcription L-type of calcium channels triggered by De Novo CACNA1D mutations in ASD have been identified [14]. Calcium-channel subunit mutations in CaVβ2 is associated with autism [15]. Nimodipine is an antagonist of calcium dihydropyridine L-type channels with a long record and a high safety score. Nimodipine binds to the pore and transmembrane of voltage receptor alpha-1 subunits and serves as a modulator for the negative allosteric channel role. Nimodipine play significant roles in dendritic and somatic calcium accumulation, gene expression and excitability [16]. Nimodipine is well described for the treatment of subarachnoid hemorrhage documented to encourage improved outcomes and less severe ischemic neurological symptoms. Nimodipine has been found to be neuroprotective in many other disorders in the brain, such as ischemic stroke, traumatic brain injury, migraine [17]. Being an antagonist of calcium channel, Nimodipine is also a strong cerebral vasodilator which act on cell membranes. It is also a molecule that is more lipophilic than nifedipine, which is also a calcium channel antagonist [17]. The neuroprotective effect of nimodipine in inflammation-mediated neurodegenerative disease was attributed to the inhibition of microglial activation, since nimodipine significantly inhibited the production of nitric oxide and further cytokines from lipopolysaccharide-stimulated cells.

 

https://www.cpn.or.kr/journal/view.html?doi=10.9758/cpn.2022.20.4.725

 

 

fatty acid 2-hydroxylase (FA2H) upregulated by nimodipine in vitro

 

Nimodipine but not nifedipine increases FA2H protein levels and also significantly increases mRNA levels of FA2H in both undifferentiated and differentiated Neuro2a cells. Our findings indicate that higher expression of FA2H induced by nimodipine may cause higher survival of Neuro2a cells stressed with surgery-like stressors.

 

Nimodipine Promotes Functional Recovery After Spinal Cord Injury in Rats (nkcc2/calcitonin)

 

 

https://www.frontiersin.org/articles/10.3389/fphar.2021.733420/full

I Will do a follow up regarding pro-pentofyline

 

Feel free to drop a message 

 

 

 

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Propentofylline, as a vasoactive and neuroprotective drug, reduces ischaemic damage by increasing the cerebral and peripheral blood flow, attenuate brain damage and neurological dysfunction.[12–14] Propentofylline blocks adenosine transport processes and adenosine receptors[12,13] and is also capable of PDE inhibition, especially PDE4.[14] It was also reported to be a less potent blocker of PDE3, as well as PDE2, and PDE5 and to cause an increase not only in intracellular cAMP level, but also cGMP concentration.

 

Propentofylline administration induced inhibition of thymocyte maturation and an increase in Treg subset

 

might be beneficial for an inhibition of immune response.

 

propentofylline may regulate mTORC activity in spinal astrocytes partially through inhibition of the JNK pathway. Our results suggest that propentofylline inhibit astrocyte activity in a broad fashion by attenuating flux through specific pathways

 

propentofylline targets TROY

 

Propentofyline suppress activation downstream signaling effectors including AKT, NF-κB, and Rac1

 

TROY serves as an important negative regulator of oligodendrocyte development and that TROY inhibition augments the repair potential of oligodendrocyte precursor cell (OPC) graft for SCI

 

 

Propentofyline is not immune supressive, but It does something with neutrophils, paired with others is more risky, so measuring white blood cells is important for anyone mixing substânces

 

 

 

Propentofylline, an atypical synthetic methylxanthine, is capable of targeting microglial cells via inhibition of TNFRSF19 

 

 

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Raloxifene spiked my blood pressure, so i will have tô stop, controling the spike with captopril (that already sheded my hair previously) and propanolol, which seems to also have this side effect for some folks, pain ehile is constant is/was decreasing, neuropathy is better in general, but constant pinched nerve, speacially when laying, elétricity always ruining trough the spine and nerves, less but still, as mentioned above regarding the situation, nimodipine while permitted is lacking in my country, seems like i will need to import

 

Hopefully i feel better soon, regarding the hbp, several stuff comes into terms, my calcium levels are marginal high since 2022 (10,0ng/dl, 9'9 and 10,00ng/dl now a days, respectvelly) and theofyline while good for neuropathy, MS peripheral and CNS remyelination and cervical cancer, It can lead to hypecalcemia, and thats concerning, i feel my kidneys due to HBP, propanolol seems to work for hypecalcemia, will seek a doctor tomorrow, but im suffering dismissal since 2010 when first assaulted, and 2022, só on, while i was dealing with high calcium levels, hemocromatosys(iron too high) and high thyroglobulin,  probably taking metformin, pioglitazone, which I should be taking since day one could possibly bê protecting my kidneys, heart and só on from high calcium levels, dismissal sucks 

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Got my edaravone today,

 

These guys from pglchem are solid

 

I took 30 mg, It does something, but Very soon to tell, everything that i take I feel in my nerves and injured spot, my pain is under control, not good but under control, It could be many things like i mentioned above in this topic, could be intravertebral disk decease, as pregabalin is cytotoxic to the NP of the disks, def It contributed to my decline regarding this and causing me CP

 

From what im Reading, edaravone seems tô be good for OA, and nimodipine also which seems to work on nurishing Pathways of the NP aside from pain management

 

Bromantane also Works for pain and neuropathy in conjuntion with these, probably trough kir.21 channels, idk exactly the effects of bromantane related to the spinal cord, i got find out reading, as It modulates HDAC 1 , and erk, ras and other proteín kinases, i need to find out exactly what are the effects on the long run, https://www.researchgate.net/figure/SP6616-treatment-improved-abnormal-mitochondrial-respiration-in-DRG-neuron-from-diabetic_fig5_347576189 here is about a drug in development that also Works trough kir 2.1 like amantadine which I guess Isnt safer than bromantane, given It might cause Neuroleptic malignant syndrome If withdrawed too fast

 

Metformin

Edaravone(started today)

Pro-pentofyline (took 12.5 mg today)

Bromantane ( sometimes as too much of It reactivate viruses)

 

Nimodipine (need to import)

 

MSM, b12, biotin, 

 

Could be that theofyline was causing my hbp, or raloxifene, or both contributed, 

 

 

Now my blood pressure seems tô be comming back to normal, but still kinda elevated 13/9

im on my last 25 mg of pregabalin, from 300mg that i took for 7+ years, couldnt quit, couldnt quit faster then what i did, started at 2 years off this time, had to taper 25 mg every 2/3 months, sometimes 4, and would never be able to quit without metformin, pioglitazone, and others which didnt resolved the pain but made It less bad,  now with these i keep going to fully stop, going to wait a month and drop the last 25 mg

 

 

Feel free to drop a message or If you have any contribuition in these topics, feel free to share

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Update here, a few observations

 

 

Im almost done with pregabalin, less than 25 mg a day, im almost over with It, my mood and sleep is not good also because of this, my pain tends tô flare for some time after each cut, i would never be able to quit without this other substances

 

A note, for the ones in acute, i couldnt take a lot of stuff.. not even alfa lopoic acid, but pioglitazone helped since the start, no issues, edavarone is a good additon imo, for ones in severe also, metformin made me feel bad, as It mixed with pregabalin, lowered my glicemic levels several times due to the interaction, metformin pumped blood to my isquemic tissues from the injury i sustained from neuroinflammation, and It i should have taken It since the start, pioglitazone feels cleaner tho, and metformin imo, its of aid for those in severe pain paired with pioglitazone, for neuroinflammation, also meloxicam for s.o.s but i think its not adivesd paired with edaravone, something with the kidneys

Just as a note, venlafaxine doesnt mix with metformin for me, feels bad, due to inverse mechanisms maybe, i took venlafaxine for some time, for pain, neuropathy, and its not venlafaxine which Will remyelinate the nerves..

 

 

Im a few days in taking edaravone, 100 or 150 mg a day in two divides doses, some sublingually, i guess It hás an antivíral property, It is good stuff,t not too noticiable in terms of mentall effects, it does something, also for pain, everything that i take I feel in my nerves, too soon also, not even a week' in

 

Theofyline, i was overdoing by taking slow release beads two times a day, now taking one time a day is fine, blood pressure is fine, raloxifene was the major cause of hbp,  back to theofyline, im taking 15 to 20 mg a day, once a day 100mg weights 0.150g on a mg scale, so 0.015 is more or less 10mg, liver health, liver protective,  If you google about theofyline and remyelination, you will find research about PN, and MS, also câncer, you need like with pioglitazone, to take vitamin D for the bones paired with It, It hás a lot of interactions, dont overdo It, its risky, not needed, low doses 10/20mg once a day is enough for its effects on gene expression 

 

Propentofyline, taking 50/100 mg a day, not a strong, sublingually, doses should be 300mg 3x a day, It does something,

 

in terms of nerve conduction, roflumilast provided more relief in terms of neuropathy, ibudilast seems to be expensive and maybe ordering from a lab in a group of people which are interested, propentofyline feels better mentally 

 

Im thinking about starting a group, for people interested in propentofyline, ibudilast and maybe edaravone itself from a good lab which I have conctact,

 

edavarone from pgl chem is good, but i guess from a lab in more quantity would be less expensive 

 

Im taking DHEA, at first It setted me back, but It helps with depression, mood and pain, is a decease modifying treatmnt for OA and intravertebral disks that suffered damage, it makes me somehow agressive, moody, emottional like Flares of toughts and regrets, but im adjustting, i gotta reach somewhere of improovment, It gives energy and its antidepressant,

 

I cant recommend for sensitive people nor anyone going trough severe wd, It messes with bp If taken too much, and It messes with your brain and perception, not Just in a good way, but I feel its necessary to my issue, pain, neuropathy, and intravertebral disks compression, im on 3mg, sometimes 5mg, It makes me remeber some of myself prior to being assaulted and killed alive by psychiatric drugs and abuse 

 

If you willing to try, i guess its an aproach to take Just one mg at first, for at least 2 weeks, It has antiviral properties, dont take It If you're too soon, you will suffer for nothing, give It time until you feel prepared enough, no need to rush, imo, focus on the other aproaches If you're to soon or to severe

 

Bromantane, helps with mood, hás its role as an HDAC, kir 2.1, umo seems as usefull as clemastine furamate, which is similar in terms of remyelination and some Pathways like, hERG, good in conjuntion , bromantane aids a little with neuropathy, more in higher doses, it mess with my sleep, which others factors are also  affecting, bromantane burns lactic acid build up helps with smoking 

 

Pioglitazone, 30 or 45 mg on occasional days, extensive research for remyelination, câncer, spinal cord and etc.. like edaravone, for OA, It promotes colagen, and protects the NP of the disks, extensive research online, will start to order from índia for cheaper, expensive drug 

 

Metformin, 500 sometimes 1000mg a day, ER, divided in two doses, or pieces trhougout the day, If you mix with some drugs, like selegiline, BPAP, losartan you get hypoglicemic, others aswell, specially If more than 500mg and like me, combined with pioglitazone, metformin hás enough research about NSC, spinal cord , rejuvenating, It builds lactic acid, bromantane burns it

 

MSM, b12, folinic acid, biotin, Selenium methionine

 

I Will add some 7keto-dhea for its effects on the mitocôndrial unhfolding proteíns(something like that), effects on fattty ácids and acyl-COA,  idk how It feels, or its effects, its a gaba antagonist like dhea, as i guess that It promotes regeneration of bones and intravertebral tissues 

 

Nimodipine, Will bê ordering from índia, to take low doses, reasons above mentioned in this thread

 

Looking also for Theobromine, for bones and health, another methyl xantine, NN, N,N-Dimethylphenethylamine (N,N-DMPEA)  as an antidepressive , forksolin, 

 

Tudca which im looking at leviathan suplements, since another source from the UK is not currently shipping due to brexit

 

And also looking at SR9011 from the UK, and a SARMs in particular, called AC 256 , for AZ, osteoporosis, others

 

My nerves pumps, ticks when i take this stuff, like wanting tô release the pressure where its compressed, my neuropathy in terms of intensity is better, 

 

Im in a process, not in a good day in terms of pain, because of the cut, also its too soon to tell the effects, it aids with pain, im in a flare due to my cut as i said above, tends to flare for some time after each cut, bad sleep doesnt help, im almost done with pregabalin, trying to adress the damages that It bringed upon me and my life, 

 

Its hard, you loose hope and keep fighting, hopefully i get somewhere able to back to living and to work

 

My liver is fine, i Will bê doing other check ups , electrolites and etc,

 

I need to check my nodules, (thyroid) but doctors are always not of help (they are never concerned enough) 

 

I will be updating as time goes by

 

 

 

 

 

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https://www.sciencedirect.com/science/article/abs/pii/S0022510X10000596

 

Wanted to post this here, regarding nerve excitability, and how IVG, which seems to help folks with neuropathy from antidepressants works

 

not by just damping down inflammation,and helping with remyelination but changing the celular/nerve membrane potential , that has to do with the sodium/potassium ions pump, also the nkcc2 cotransporter that plays a role in nerve excitability and promoting efflux of chloride íons from intracelular space, making the membrane potential to go from hyperpolarized(excitatory) to depolarized(inhibitory)

 

Idk exactly about the mechanisms of IVg on this íon pump exchange, or If It affects the nkcc2 cotransporter, bumetanide does and help with nerve  pain and neuropathy (already took It) doesnt feel good for me, mess with glicemic levels and maybe something else, nimodipine also does act on the nkcc2 in as above mentioned, reason i'm going to import the latter 

 

If anyone hás something interesting to add, a substance or scientific literature about this, feel free to share ..

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Uploading this here

It Will take some time to come from india, nimodipine is lacking in my country, but aside from the effects on the nkcc2 cotransporter expression, which extrudes cloride depolarizing the membrane potential (towards more inhibitory, restoring the inhibitory potential), It h@s an effect on facial nerves, i dont have pain in my face, but anyway, pain is terríble anywhere

https://onlinelibrary.wiley.com/doi/abs/10.1111/fcp.12827

 

Bromantane acts on kir2.1 channels, and as an HDAC1 promoter or inhibitor, i have this information here, Just need to dig in my scihub archieves, It helps with pain paired with the others, hopefully its safe to mix all that stuff, bromantane, theofyline, propentofyline all are liver protectors, i will move bromantane for the morning/ mid day, paired with theofyline and a drop of vitamin D, regarding my blood pressure is fine, carefull is needed with theofyline.. It could deplete b6, so its a good measure to take the Active form of b6 that has no such toxicity to nerves

 

pro pentofyline is not as pain reliving as  roflumilast, ibudilast must be good, but just possible tô achieve with a group buy, to get It for a cheap price.. roflumilast is expensive and its not a liver protective substance, soon i will try low doses of Theobromine, which is good for the spine and also a xhantine molécule, probably safe If low dosing even paired with the others, which are also on the lower end regarding dose, 25mg Max of theofyline an HDAC 2 promoter 

 

Im doing more or less given the pain flare from finally quitting pregabalin..

 

I was also reading about indol propionamide and how It acts on the mitocôndrial complex 1 and 4 , augmenting its function, i guess that could be something for nerve pain and neuropathy, Very little information and no much reports, Its similar to melatonin in terms of Its chemical molecule, but longer half life and no pro oxidant function, avaliable on everychem and from pglchem ukraine 

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  • 2 months later...

 

Nimodipine-Dependent Protection of Schwann Cells, Astrocytes and Neuronal Cells from Osmotic, Oxidative and Heat Stress Is Associated with the Activation of AKT and CREB

https://www.mdpi.com/1422-0067/20/18/4578

 

It seems to have an effect on facial nerves, possibly help with TN

 

I guess that, in my case, paired with a low dose of SR9009 or SR9011 to manage the auto-imune disorder, a low dose of nimodipine could aid with nerve recovery and intracellular calcium homeostasis, nimodipine is a drug and might have dose dependant possible side effects

 

Nimodipine protects cultured spinal cord neurones from depolarization-induced inhibition of neurite outgrowth

 

https://www.sciencedirect.com/science/article/abs/pii/014341609390050G

 

Nimodipine Activates TrkB Neurotrophin Receptors and Induces Neuroplastic and Neuroprotective Signaling Events in the Mouse Hippocampus and Prefrontal Cortex

 

https://link.springer.com/article/10.1007/s10571-014-0110-5

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As a note, carefull with sr9009 or sr9011 If in acute or having a bad time, even 0.02 g from 0.500/10mg of sr9009 already relives pain,

 

 

still, i had a bad time with it from taking too much at 2 and a half years off, at 0.02g It already cause some anxiety later on the day, It inhibits gaba, sr9011 doesnt cause the same sort of anxiety for me, but Its more selective and doesnt relieve pain the same way, could bê that my source Isnt good, or that i took too little.

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