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Healing the mind from DXM-induced psychosis


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#1 Spectre

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Posted 28 April 2010 - 02:16 AM


Hello there,

First, I must apologize for this extremely long post. I came to this forum seeking advice on potential therapies for a drug-induced psychosis that I've been battling over the past 2 years. I believe the culprit is dextromethorphan, which I haven't done since August 2008, but I still notice a permanent change in my memory formation ever since doing that specific drug. It triggered an intense schizophrenia-like psychosis in me, which has caused absolutely insane, almost uncontrollable delusions and memory problems. I've only done it 4 times in my entire life, starting from March 2008 and ending in August that year..and it was easily the most damaging drug I've ever done before. I have a brief history with other substance abuse (tons of pot smoking, some opiates, adderall, coke, muscle relaxers, diphenhydramine, xanax, shrooms, salvia, MDMA, etc.) but have completely abstained from using anything for just under a year now..and I've stayed away from most of the drugs in that list for at 2 years or more.

Anyway, I was ignorant to the effects of DXM on the brain during the times that I took it, and have researched it quite thoroughly since I quit doing drugs. But what I basically know about DXM is that it's an NMDA receptor antagonist, which like other dissociative drugs, can disrupt and modify the frequency of cortical oscillations in the brain..which is used by the NMDA system for memory formation and other uses. My goal right now, and for now on, is to have a clean mind, and heal it of the damage brought on by dextromethorphan. Most of the noticeable effects have gone away since it's been almost 2 years since I've done it, but the memory problems still pop up quite frequently. (Getting deja vu occasionally still, but which was very frequent right after my DXM trips years ago).

I just want to fix the cortical oscillations in my brain and heal my NMDA receptor system. I would kill just to have a normal memory again, and it was an incredibly hard lesson to learn. I can't seem to find enough information on alternative therapies to heal my brain, and I've found nothing to make me feel normal again. I'm tired of feeling like a nutjob and just want to be normal again. I exercise frequently, and keep my body in shape (I love bodybuilding), I meditate (granted, not nearly as much as I used to), and I follow a pretty good diet. I take multivitamins everyday and have recently started to supplement with 500mg Niacin (nicotinic acid, the form that makes your skin flush), and 400mg SAMe daily. (I started taking SAMe for my recent depression, which it's been very effective at relieving). I've taken fish oil before but didn't really notice any effects from that alone.

I feel more focused and somewhat normalized since I've been taking SAMe (it's been about 10 days since I've been on it), but I don't know if that's contributed to actual brain healing/cell methylation, or it's mild stimulating effect. I talked with a guy that owns an alternative health shop in my town and he was recommending me DMG (dimethylglycine), since it's cheaper than SAMe and proven to be an apparently effective product. He told me that it would help fix the wiring in my brain and normalize my brain function. I've never taken it personally though and I wouldn't see a point to take both DMG & SAMe together (but let me know if I should anyway). He also recommended that I take Source Naturals "St. John's Positive Thoughts." He gave me a sample of it but I didn't really notice anything aside from mild calming and anxiolytic effects.

Anyway, what would you recommend I start taking or doing to normalize my mind? I've been extremely drawn towards nootropics ever since I heard about them, and I am very interested in optimizing, and maximizing my brain function (at least after my brain is normal again). Are there any supplements or nootropic agents that would help my NMDA receptor system recover? Again, sorry for the long, and probably obnoxious post..I used the search function but couldn't find anything closely-related enough to my own issue to find a solution. Thank you.

#2 Guacamolium

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Posted 28 April 2010 - 02:38 AM

Go here first: http://www.imminst.o...?showtopic=9599



I would say memantine could help as it seems you've cause quite a lot of excitotoxicity from doing that. It modulates NMDA receptor activity and you can try to get new cell proliferation with some of those NGF supplements linked above while memantine keeps your NMDA system stabilized. No guarantees though.

Edited by somethingtoxic, 28 April 2010 - 02:39 AM.


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#3 meursault

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Posted 28 April 2010 - 02:55 AM

Most of the noticeable effects have gone away since it's been almost 2 years since I've done it, but the memory problems still pop up quite frequently. (Getting deja vu occasionally still, but which was very frequent right after my DXM trips years ago).


Have faith in time. Maybe in another a year it will largely fade away.

I meditate (granted, not nearly as much as I used to)

You should pick it up again. Anyone seriously interested in advancing their cognitive abilities should be meditating:

"Simply stated, the profound improvements that we found after just 4 days of meditation training- are really surprising," Zeidan noted. "It goes to show that the mind is, in fact, easily changeable and highly influenced, especially by meditation..."Further study is warranted," he stressed, noting that brain imaging studies would be helpful in confirming the brain changes that the behavioral tests seem to indicate, "but this seems to be strong evidence for the idea that we may be able to modify our own minds to improve our cognitive processing -- most importantly in the ability to sustain attention and vigilance -- within a week's time."

http://www.scienceda...00414184220.htm


Trying investigating these further (remember, these are rat studies):
D-Serine and a glycine transporter-1 inhibitor enhance social memory in rats.
http://www.ncbi.nlm....pubmed/20198471

E-6801, a 5-HT(6) receptor agonist, improves recognition memory by combined modulation of cholinergic and glutamatergic neurotransmission in the rat.
http://www.ncbi.nlm....pubmed/20405281

Edited by czukles, 28 April 2010 - 03:01 AM.


#4 Guacamolium

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Posted 28 April 2010 - 03:01 AM

https://www.alldaych...query=memantine

That's apparently the lowest price for memantine.

czukles is right on the money about meditation. I do mantra meditation from time to time and I've read many reports about meditation and neurogenesis.

#5 Spectre

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Posted 28 April 2010 - 03:29 AM

Go here first: http://www.imminst.o...?showtopic=9599



I would say memantine could help as it seems you've cause quite a lot of excitotoxicity from doing that. It modulates NMDA receptor activity and you can try to get new cell proliferation with some of those NGF supplements linked above while memantine keeps your NMDA system stabilized. No guarantees though.


Thank you for the link. I forgot to mention that I ordered 2 bottles of a product called "Mindcare" by Himalaya Herbals. (aka "Mentat"). It'll be a couple weeks at least before it arrives at my house but it contains some of the ingredients that were listed in the post that you linked. I've never tried this stuff before, do you have any personal experience or know anyone that has tried Mindcare before?

And I did some research on memantine but it seems somewhat dangerous considering it's an NMDA receptor-antagonist as well. Couldn't that potentially cause damaging effects to my NMDA system similar to dextromethorphan? Wouldn't I need something that promotes the activation of my receptors instead? What exactly is excitotoxicity? (I've heard that term used quite a bit but never understood what it meant).

Edited by Spectre, 28 April 2010 - 03:31 AM.


#6 Guacamolium

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Posted 28 April 2010 - 03:41 AM

Go here first: http://www.imminst.o...?showtopic=9599



I would say memantine could help as it seems you've cause quite a lot of excitotoxicity from doing that. It modulates NMDA receptor activity and you can try to get new cell proliferation with some of those NGF supplements linked above while memantine keeps your NMDA system stabilized. No guarantees though.


Thank you for the link. I forgot to mention that I ordered 2 bottles of a product called "Mindcare" by Himalaya Herbals. (aka "Mentat"). It'll be a couple weeks at least before it arrives at my house but it contains some of the ingredients that were listed in the post that you linked. I've never tried this stuff before, do you have any personal experience or know anyone that has tried Mindcare before?

And I did some research on memantine but it seems somewhat dangerous considering it's an NMDA receptor-antagonist as well. Couldn't that potentially cause damaging effects to my NMDA system similar to dextromethorphan? Wouldn't I need something that promotes the activation of my receptors instead? What exactly is excitotoxicity? (I've heard that term used quite a bit but never understood what it meant).


Memantine acts much like ketamine,PCP, and DXM in that it is an NMDA antagonist, BUT, it modulates the antagonism in a way to prevent further excitotoxicity from happening. (dain bramage)

Your mindcare is just herbal cerebral enhancers and calmatives. Take it every day till it's gone and move on to stronger things. Stick around here and you'll find out what works for you and what doesn't.

#7 Spectre

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Posted 28 April 2010 - 03:46 AM

Most of the noticeable effects have gone away since it's been almost 2 years since I've done it, but the memory problems still pop up quite frequently. (Getting deja vu occasionally still, but which was very frequent right after my DXM trips years ago).


Have faith in time. Maybe in another a year it will largely fade away.

I meditate (granted, not nearly as much as I used to)

You should pick it up again. Anyone seriously interested in advancing their cognitive abilities should be meditating:

"Simply stated, the profound improvements that we found after just 4 days of meditation training- are really surprising," Zeidan noted. "It goes to show that the mind is, in fact, easily changeable and highly influenced, especially by meditation..."Further study is warranted," he stressed, noting that brain imaging studies would be helpful in confirming the brain changes that the behavioral tests seem to indicate, "but this seems to be strong evidence for the idea that we may be able to modify our own minds to improve our cognitive processing -- most importantly in the ability to sustain attention and vigilance -- within a week's time."

http://www.scienceda...00414184220.htm


Trying investigating these further (remember, these are rat studies):
D-Serine and a glycine transporter-1 inhibitor enhance social memory in rats.
http://www.ncbi.nlm....pubmed/20198471

E-6801, a 5-HT(6) receptor agonist, improves recognition memory by combined modulation of cholinergic and glutamatergic neurotransmission in the rat.
http://www.ncbi.nlm....pubmed/20405281


Thank you for the post. I used to meditate a lot more when I smoked pot, and it's been 11 months since I've ever toked, but ever since then, I've become depressed, unhappy, and feeling unfocused to the point that I don't even feel like meditating anymore. Cannabis was one of the only things that truly helped me with my depression, stress, and it shifted my perspective on life and kept me open minded. But at the same time, I was growing tired of the short-term memory loss and frequent paranoia I experienced on it, so I decided to quit. When I meditate now, it doesn't feel nearly the same as before, and I have a hard time getting my mind into a relaxed enough state to focus when I'm meditating, and I don't sleep nearly as good as when I used to smoke. (Give some take some).

I did notice a lot of positive thoughts in my mind after I had a nice meditation session. I would feel great and everything just seemed more alive and vivid. I wish I had that feeling all the time, but meditation just isn't what it used to be for me. I feel like I've lost all my mental edge.

#8 Spectre

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Posted 28 April 2010 - 03:51 AM

Go here first: http://www.imminst.o...?showtopic=9599



I would say memantine could help as it seems you've cause quite a lot of excitotoxicity from doing that. It modulates NMDA receptor activity and you can try to get new cell proliferation with some of those NGF supplements linked above while memantine keeps your NMDA system stabilized. No guarantees though.


Thank you for the link. I forgot to mention that I ordered 2 bottles of a product called "Mindcare" by Himalaya Herbals. (aka "Mentat"). It'll be a couple weeks at least before it arrives at my house but it contains some of the ingredients that were listed in the post that you linked. I've never tried this stuff before, do you have any personal experience or know anyone that has tried Mindcare before?

And I did some research on memantine but it seems somewhat dangerous considering it's an NMDA receptor-antagonist as well. Couldn't that potentially cause damaging effects to my NMDA system similar to dextromethorphan? Wouldn't I need something that promotes the activation of my receptors instead? What exactly is excitotoxicity? (I've heard that term used quite a bit but never understood what it meant).


Memantine acts much like ketamine,PCP, and DXM in that it is an NMDA antagonist, BUT, it modulates the antagonism in a way to prevent further excitotoxicity from happening. (dain bramage)

Your mindcare is just herbal cerebral enhancers and calmatives. Take it every day till it's gone and move on to stronger things. Stick around here and you'll find out what works for you and what doesn't.


So how would that react with my current brain chemistry? Wouldn't I still experience similar effects as before? I read another post stating that memantine "is like a long-lasting version of DXM". And that's the last thing I need lol. Would memantine mimic the effects I experienced before, or reverse the effects that dextromethorphan had on my NMDA system? I don't ever plan on using mind-damaging drugs again.

#9 haha

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Posted 28 April 2010 - 04:16 AM

DXM causes quite intense stimulation through the cingulate, this could have resulted in neurodegeneration particularly if the dose was high or was mixed with another drug,erowids has info on this. The good thing is that the body has amazing ability to regenerate functional circiuts,so dont despair.

I have quite a bit of experience understanding the gluatmate system and in particular the NMDA receptor subtypes. NMDA receptors are a highly complex system, which effect neuro function in multipule and often opposite ways. NMDA receptors modulate virtually the location,composition and activity of almost all receptor types this is because they have heavily implicated in Long term potentiation and Long Term depression, which are terms to describe the strengthing and weakening of the interactions between neurons,The wikipedia articles have a good basic cover of this concept.
Nmda receptors are composed of multipule subunits that each have there own pore, THe main three are NR1A,NR2A NR2B. NR1a. NR1a is rather simple it is similar to an cAMP recetpor in that it only allows monovalent cations to enter, this means that this receptor is not involved with a change in LTP or LTD although it fasiclitates LTP and LTD via the other subunits, in other words it passes a signal, and in adults it plays an important role in keeping neural circiuts connected, piracetam enhance phosphorlation of this subunit increasing activity, which maybe a major contributor to its nootropic effects, DMX damage maybe mediated through decreased activity and expression of this subunit.There are many agents that act on NR1a.


The NR2(x)s play a different role, and that role depends whether or not there expressed on a synapse. For this discussion I shall limit talk to those NMDA receptors that are expressed on the syanpse.
The NR2A activity mediates quick actting and long term depression of the connection between neurons, From how I understand it thought is the turning off of particular connections on usually a short term basis. So the product of a thought and how it is expressed, is expressed by what in the system is still running after the said thought(this is grossly simplified). Therefore blocking the NR2a reduces the ability to hold a thought, and unfortunately the body doesnt upregulate NR2a activity in response to antagonists. Other systems do move them back and slowly they will reform.THis is the heart of the Neurodamage of DMX and PCP. For PCP i know donepezil maybe used, with pregenelonone and particular its sulfates achieving a similar end through sigma-1 receptors, if you know someone with access sciencedirect or u are affluent,or if someone else will show this paper, then we could come up with some ideas

Phencyclidine-induced cognitive deficits in mice are ameliorated by subsequent subchronic administration of donepezil: Role of sigma-1 receptors

sam-e is great, I cant afford it at present, so if you can afford it stay on it, maybe add some DMG but keep the dose low as overmethylation cause schizophrenia like traits.
THe NR2B cause LTP at the sypnase,important in memory formation and building the system but by adulthood they are less important.
Theres lots things that could be worthwhile, exercise being one, did the symptoms come on just after use? there are many things that could have caused contributed to it, even back in your childhood

#10 haha

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Posted 28 April 2010 - 04:56 AM

Memantine has a strong affinity for NR2Bs over NR2a, at the right dose it can be real good through nmda extrasynaptic block. I think keeping away from nmda antagonist is essential for you. Huperzine might be a different story as may behave like donepezil.

#11 Guacamolium

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Posted 28 April 2010 - 05:26 AM

Memantine has a strong affinity for NR2Bs over NR2a, at the right dose it can be real good through nmda extrasynaptic block. I think keeping away from nmda antagonist is essential for you. Huperzine might be a different story as may behave like donepezil.


I apologize if suggesting memantine was a wrong choice. I've been sick and up for too long, so perhaps FunkOdyssey can shed more light on this specific situation. Your knowledge of NMDA receptor subtypes outweighs mine, I'm more catecholeamine and AMPA informed. Night guys.

#12 Spectre

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Posted 28 April 2010 - 05:50 AM

DXM causes quite intense stimulation through the cingulate, this could have resulted in neurodegeneration particularly if the dose was high or was mixed with another drug,erowids has info on this. The good thing is that the body has amazing ability to regenerate functional circiuts,so dont despair.

I have quite a bit of experience understanding the gluatmate system and in particular the NMDA receptor subtypes. NMDA receptors are a highly complex system, which effect neuro function in multipule and often opposite ways. NMDA receptors modulate virtually the location,composition and activity of almost all receptor types this is because they have heavily implicated in Long term potentiation and Long Term depression, which are terms to describe the strengthing and weakening of the interactions between neurons,The wikipedia articles have a good basic cover of this concept.
Nmda receptors are composed of multipule subunits that each have there own pore, THe main three are NR1A,NR2A NR2B. NR1a. NR1a is rather simple it is similar to an cAMP recetpor in that it only allows monovalent cations to enter, this means that this receptor is not involved with a change in LTP or LTD although it fasiclitates LTP and LTD via the other subunits, in other words it passes a signal, and in adults it plays an important role in keeping neural circiuts connected, piracetam enhance phosphorlation of this subunit increasing activity, which maybe a major contributor to its nootropic effects, DMX damage maybe mediated through decreased activity and expression of this subunit.There are many agents that act on NR1a.


The NR2(x)s play a different role, and that role depends whether or not there expressed on a synapse. For this discussion I shall limit talk to those NMDA receptors that are expressed on the syanpse.
The NR2A activity mediates quick actting and long term depression of the connection between neurons, From how I understand it thought is the turning off of particular connections on usually a short term basis. So the product of a thought and how it is expressed, is expressed by what in the system is still running after the said thought(this is grossly simplified). Therefore blocking the NR2a reduces the ability to hold a thought, and unfortunately the body doesnt upregulate NR2a activity in response to antagonists. Other systems do move them back and slowly they will reform.THis is the heart of the Neurodamage of DMX and PCP. For PCP i know donepezil maybe used, with pregenelonone and particular its sulfates achieving a similar end through sigma-1 receptors, if you know someone with access sciencedirect or u are affluent,or if someone else will show this paper, then we could come up with some ideas

Phencyclidine-induced cognitive deficits in mice are ameliorated by subsequent subchronic administration of donepezil: Role of sigma-1 receptors

sam-e is great, I cant afford it at present, so if you can afford it stay on it, maybe add some DMG but keep the dose low as overmethylation cause schizophrenia like traits.
THe NR2B cause LTP at the sypnase,important in memory formation and building the system but by adulthood they are less important.
Theres lots things that could be worthwhile, exercise being one, did the symptoms come on just after use? there are many things that could have caused contributed to it, even back in your childhood


Wow, awesome post..very informative :)

The first time I noticed any sort of "deja vu" was right after I smoked Salvia for the first time, but that sensation was multiplied but 5 after I had dextromethorphan. I'm sure that effect was contributed to both substances but I noticed it a lot more after I had DXM. I've had considerably lower doses than many other users of the drug. I've only had 4 psychoactive experiences on DXM, 2 of them being at 300mg (DXM Hydrobromide), one at about 450mg (DXM Polistirex), and the last at 450mg as DXM HBr again. I had extremely profound after effects right after the last time I had DXM, and I was experiencing deja vu at almost every moment in the day, every day, for almost 3 months. Then it would phase in and out, being extremely profound one day, then almost unnoticeable the next, and vice versa. I was getting absolutely insane delusions during that time period, thinking that Salvia & DXM must have unlocked a part of my mind that people aren't supposed to experience. I felt clairvoyant, as if I could predict the future on some level (and it seemed very real, as a lot of my pre-meditated thoughts played out in reality on the dot a few minutes later, it was crazy), but at the same time, I was extremely delusional, thinking that the universe was repeating itself, and that I'm just re-experiencing the same events in my life.

When I had Salvia, it was as if I was shown my entire life go by in just 5 minutes. Words can't express the level of insanity I was feeling. I continued to smoke it a couple times after the last time I did DXM, but it was used in low doses, with standard leaves, not powerful at all (barely noticeable psychoactive effects while on it). But the effects persisted long after I quit both. I know that Salvia also has dissociative effects on the brain, but I'm not aware of it's mechanism of action. I just know that they both made me crazy as hell and I never want to experience anything like that again.

I'm curious to know if donepezil could work on me, I'll have to research this compound some more and maybe talk to a doctor about it (I've never went to a psychiatrist or physician about this issue, surprisingly, but I felt too crazy to even talk to them before, and wasn't in the mindset to explain in detail what I was going through).

What all do you know about SAMe? Does it have brain-repairing effects? I do feel better since I've been taking it, but I'm sure it will take a while to work completely. Would you recommend DMG or TMG instead? I've never taken DMG before but I've heard good things about it. What exactly does it do to the brain? Thanks again for the feedback :p

Edited by Spectre, 28 April 2010 - 05:55 AM.


#13 haha

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Posted 28 April 2010 - 06:24 AM

Anyone who attends a university can get this article for free, its easy to sign up to imminst, so can we please get....Phencyclidine-induced cognitive deficits in mice are ameliorated by subsequent subchronic administration of donepezil: Role of sigma-1 receptors

Ill reply to the rest later today

#14 Spectre

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Posted 28 April 2010 - 07:35 PM

Salvia Divinorum long-term & pharmacology effects information from Wikipedia:

Differing studies suggest no overall consensus so far with regard to the long-term effects of Salvia divinorum on mood. It is well-established that some k-opioid agonists can cause dysphoria in humans,[79] and research using rats in forced-swim tests (where they're forced to swim in a narrow cylinder from which they cannot escape) has been used to suggest that Salvia divinorum may have "depressive-like" effects.[80] However, a report has been published detailing an individual case of Salvia divinorum use as self-medicated treatment for depression,[81] and Baggott's survey of 500 people with firsthand experience of salvia found that 25.8% of respondents reported improved mood and "antidepressant-like effects" lasting 24 hours or longer. Only 4.4% reported persisting (24 hours or more) negative effects (most often anxiety) on at least one occasion.[73]

There has been one report of salvia precipitating psychosis. However, the authors suspected that their patient was already genetically predisposed to schizophrenia.[82]

It has been suggested that the long-term effects of salvia use may include feelings of déjà vu.[83]

The Baggott survey found little evidence of addictive potential (chemical dependence) in its survey population. 0.6% percent of respondents reported feeling addicted to or dependent on salvia at some point, and 1.2% reported strong cravings. About this the researchers said "there were too few of these individuals to interpret their reports with any confidence".

Most users report no hangover or negative after-effects (e.g. withdrawal, comedown or rebound effect) the next day. This is consistent with the apparent low toxicity of salvia indicated by research conducted at the University of Nebraska.[13]


Potency

By mass, salvinorin A is the most potent naturally-occurring psychoactive compound known.[52] It is active at doses as low as 200 µg.[24][48][52] Research has shown that salvinorin A is a potent and selective κ-Opioid (kappa-Opioid) receptor agonist.[48][53] It has been reported that the effects of salvinorin A in mice are blocked by κ-Opioid receptor antagonists.[11] However, it is an even more potent D2 receptor partial agonist, and it is likely this action plays a significant role in its effects as well.[12] Salvinorin A has no actions at the 5-HT2A serotonin receptor, the principal molecular target responsible for the actions of 'classic' hallucinogens, such as mescaline and LSD, nor is it known to have affinity for any other sites to date.[11]

Salvinorin's potency should not be confused with toxicity. Rodents chronically exposed to dosages, many times greater than those to which humans are exposed, did not show signs of organ damage.[13]

Other terpenoids
Main article: Salvinorin A#Salvinorins A - F, J

Other terpenoids have been isolated from Salvia divinorum, including other salvinorins and related compounds named divinatorins and salvinicins.[54] None of these compounds has shown significant (sub-micromolar) affinity at the κ-Opioid receptor, and there is no evidence that they contribute to the plant's psychoactivity.[55][56]

Other pharmaceutical action

Salvinorin A is capable of inhibiting excess intestinal motility (e.g. diarrhea), through a combination of κ-opioid and cannabinoid (mainly CB1 receptor) receptors in inflamed but not normal gut in vivo. The mechanism of action for Salvinorin A on ileal tissue has been described as 'prejunctional', as it was able to modify electrically-induced contractions, but not those of exogenous acetylcholine[57] Results from a small study by an assistant professor at the University of Iowa indicate that it may have potential as an analgesic and as a therapeutic tool for treating drug addictions.[58][59]

A pharmacologically-important aspect of the contraction-reducing (antispasmodic) properties of ingested Salvinorin A on gut tissue is that it is only pharmacologically active on inflamed and not normal tissue, thus reducing possible side-effects.[60]


Do you know anything about Salvia Divinorum and it's effects on the brain? From what I have researched, there is no documented evidence of Salvia causing brain damage but the memory lapses and dysfunctions that I've experienced from Salvia (and presumably DXM) must mean something..maybe the combination of the 2 disrupted certain receptor systems in my brain, and hasn't completely healed yet. I need to be evaluated by a neurosurgeon and see what's exactly wrong with my brain lol. But unfortunately I'm in absolutely no financial position to do that.

I don't know if my memory problems are from the use of either specific drug, or the combination of them both. I just know that I've gotten horrible effects from both and I need to find a way to heal my mind and restore normal brain function. I'll pick up some dimethylglycine sometime soon and stack it with SAMe for a few months, hopefully I won't start exhibiting schizophrenic-like symptoms from taking them but I won't know until I try.

Edited by Spectre, 28 April 2010 - 07:41 PM.


#15 Spectre

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Posted 28 April 2010 - 08:25 PM

I found a report of an individual that suffered long-term mental damage from Salvia Divinorum, which doctors believe triggered a schizophrenic-like psychosis in the individual. He's apparently the only documented person to have such a case, but I'm sure this has happened to a lot more people. I believe I might be dealing with the same issue, but to a lesser degree:

http://ajp.psychiatr...t/166/7/832.pdf

Persistent Psychosis Associated With Salvia
Divinorum Use


TO THE EDITOR: Salvia divinorum (salvia) is a sage plant that
is easily obtained in the United States. Its active ingredient,
Salvinorin A, is a novel and highly selective pure kappa opiate
receptor agonist with rapid onset and powerful hallucinogenic
properties (1). Salvia has become increasingly popular
as a drug of abuse when smoked. No long-term negative outcomes
have been reported from the use of salvia. We present
a case in which salvia precipitated persistent psychosis.

“Mr. J” was a 21-year-old man with no family or personal
psychiatric history or laboratory abnormalities. He
was reported to have normal social interactions, behavior,
and cognitive skills. He was transferred to our psychiatric
unit for acute psychosis and paranoia, which occurred
shortly after smoking salvia. In transport, the patient became
suspicious and attempted to jump from the vehicle.
Upon presentation, he demonstrated echolalia, paranoia,
flight of ideas, and psychomotor agitation. The patient remained
agitated for the first 2 days of hospitalization. He
attempted to barricade himself in his room. Risperidone
(3 mg by mouth/three times per day) was administered,
and the patient was eventually stabilized. The dosage,
however, resulted in the parkisonian features of rigidity,
bradykinesia, and masked facies.

Mr. J was transferred to the chemical dependency unit
for further treatment. He was stabilized, and treatment
with risperidone was slowly tapered. During the taper
from risperidone, the patient continued to improve and
manifested better insight and logical thought processes.
He participated in group therapy and interacted with
peers, and the parkinsonian features subsided. One day
after risperidone was withdrawn, the patient’s symptoms
abruptly returned. He became agitated, paranoid, and aggressive
and believed he was able to project and receive
thoughts. He returned to the inpatient psychiatry unit
where risperidone (3 mg by mouth/twice daily) was reinstated.
He was once again stabilized and transferred to
the referring psychiatric facility for further treatment. At
the 4-month follow-up, the patient exhibited no perceptible
improvement.

To the best of our knowledge, this is the first reported case
of a persistent negative outcome from the use of salvia. We
suspect that our patient was genetically predisposed to
schizophrenia, and salvia precipitated the clinical manifestations.
This may relate to the drug’s ability to influence dopamine
levels in the brain and potentiate plastic changes in
frontal lobe networks (3).

Previous studies have cited salvia as a potential treatment
option for CNS illnesses (2). This is surprising, considering the
paucity of research regarding its efficacy. Salvia’s ability to increase
dopamine levels in the nucleus accumbens increases
its potential for dependence. Consistently, patients at our
clinic who have used the drug report that its psychological effects
are abrupt and frightening. Clinicians should be aware
that salvia use can be associated with psychiatric illness.


Experts on the subject, what do you think about this? Both Salvia & DXM have caused long-term negative effects in my brain, that I know..but I have no clue which parts of my brain need to be repaired (except the NMDA system). It's unfortunate that science doesn't know exactly how Salvia works on the brain. I should have never been so naive and used this crap.

Edited by Spectre, 28 April 2010 - 08:25 PM.


#16 haha

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Posted 28 April 2010 - 08:54 PM

Hey for my money i would run a low dose of piracetam.huperzine and sam-e, I would also add caffeine free green tea extract, alpha lipoic acid and curcumin(tumeric search other threads), magnesium. Throw some tmg or dmg in if you want, but do it in the morning, because methylation is involved with gene expression and you want your genes to be expressing a high energy, functional state.

Then you should forget you have any problems and go be the best you can be at what ever you want.the mind has the power to overcome many things, given sucess your problems will fade away. Obessing about the problem usually is the problem. Anyway sterotypical values of society say its psychosis, maybe its your spirituality.
Chasing MJ and dmx is a sign that your LTP system is dominating your LTD system btw

#17 Spectre

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Posted 28 April 2010 - 09:35 PM

Hey for my money i would run a low dose of piracetam.huperzine and sam-e, I would also add caffeine free green tea extract, alpha lipoic acid and curcumin(tumeric search other threads), magnesium. Throw some tmg or dmg in if you want, but do it in the morning, because methylation is involved with gene expression and you want your genes to be expressing a high energy, functional state.

Then you should forget you have any problems and go be the best you can be at what ever you want.the mind has the power to overcome many things, given sucess your problems will fade away. Obessing about the problem usually is the problem. Anyway sterotypical values of society say its psychosis, maybe its your spirituality.
Chasing MJ and dmx is a sign that your LTP system is dominating your LTD system btw


Cool, thanks for the advice. I'll start using Himalaya Herbs Mindcare in a couple weeks as well, finish out those bottles, and see how my mind is at that point. If I don't notice an improvement, I'll try out Piracetam and Huperzine. I've never tried these compounds before and don't know anyone with personal experience with them either. I'll continue taking SAMe and will more than likely incorporate DMG pretty soon as well. I haven't done any drugs for a long time and I don't plan on doing them again (aside from nootropics).

What exactly are the LTP and LTD systems? I have never heard of these before.

Edited by Spectre, 28 April 2010 - 09:35 PM.


#18 haha

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Posted 28 April 2010 - 10:38 PM

Long Term potention and long term depression, I talked about them in my orginal post regarding NMDARs, wikipedia has alot more info, most recreational drugs increase LTD, and it might even be the main reason people take them. Huperzine and piractam should increase the distance messages can be carried free of nosie in the neural system, this should really help with dissasoiative damage but keep the dosage low moderate to begin with.

#19 Spectre

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Posted 28 April 2010 - 11:27 PM

Long Term potention and long term depression, I talked about them in my orginal post regarding NMDARs, wikipedia has alot more info, most recreational drugs increase LTD, and it might even be the main reason people take them. Huperzine and piractam should increase the distance messages can be carried free of nosie in the neural system, this should really help with dissasoiative damage but keep the dosage low moderate to begin with.


I did a little reading and found that Huperzine is also an NMDA receptor antagonist, but it's related to Donepezil, which was recorded to be useful in repairing PCP-induced schizophrenia. I don't understand how one NMDA receptor antagonist can be useful in repairing damage from another NMDA receptor antagonist..that seems completely contradictory, but I'm not educated on Huperzine's mechanism of action.

Huperzine A, is a naturally occurring sesquiterpene alkaloid compound found in the plant firmoss Huperzia serrata.[1]

Huperzine A is an Acetylcholinesterase inhibitor similar to other compounds donepezil, rivastigmine, and galantamine.

In the US Huperzine A is sold as a dietary supplement for memory support. The botanical has been used in China for centuries for the treatment of swelling, fever and blood disorders. Clinical trials in China has shown it to be effective in the treatment of Alzheimer's disease,[2] and has been shown to enhance memory in healthy young students in one study. [3]
[edit] Pharmacological effects

Acetylcholinesterase inhibition[4] and NMDA receptor antagonism.[5]

Huperzine A has also attracted the attention of US medical science. It is currently being investigated as a possible treatment for diseases characterized by neurodegeneration – particularly Alzheimer’s disease.[6][7] It has been found to be an inhibitor of the enzyme acetylcholinesterase.[8] The structure of the complex of huperzine A with acetylcholinesterase has been solved by X-ray crystallography (PDB code: 1VOT; see the 3D structure).This is the same mechanism of action of pharmaceutical drugs such as galantamine and donepezil used to treat Alzheimer's disease. Huperzine A is also a NMDA receptor antagonist[citation needed] which protects the brain against glutamate induced damage, and it increases nerve growth factor levels.[citation needed]

Clinical trials in China have shown that huperzine A is comparably effective to the drugs currently on the market, and may even be a bit safer in terms of side effects.[citation needed] Currently, the National Institute on Aging is conducting a Phase II clinical trial to evaluate the safety and efficiency of huperzine A in the treatment of Alzheimer's disease in a randomized controlled trial of its effect on cognitive function. Recently, it has been investigated for its effectiveness against epilepsy in an initial 20-person clinical study by Harvard University neuroscientists examining its worth and side effects in those who are not satisfactorily treated by existing pharmaceuticals.[citation needed]

Possible side effects may include breathing problems, tightness in the throat or chest, chest pain, skin hives, rash, itchy or swollen skin, upset stomach, diarrhea, vomiting, hyperactivity and insomnia.[9] Most adverse events were cholinergic in nature and no serious adverse events occurred. Huperzine A is a well-tolerated drug.[10]



#20 haha

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Posted 29 April 2010 - 05:13 AM

Huperzine should potentiate NR1a(nmdar)of the nmda receptor, while it mediates low level antagonism of the NR2x's(nmdar). At a sufficiently low dose this should really help you as it is quite similar to donepezil. taper up real slow. Read around some ppl say these shouldnt be taken by the young(but you might have more reason)
, nicotine patchs are another possability, again read around.
THese receptor display some interesting dynamics, simple more less doesnt help

#21 Spectre

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Posted 30 April 2010 - 05:50 AM

Huperzine should potentiate NR1a(nmdar)of the nmda receptor, while it mediates low level antagonism of the NR2x's(nmdar). At a sufficiently low dose this should really help you as it is quite similar to donepezil. taper up real slow. Read around some ppl say these shouldnt be taken by the young(but you might have more reason)
, nicotine patchs are another possability, again read around.
THese receptor display some interesting dynamics, simple more less doesnt help


Thank you :p Do you know the best place to get some Piracetam online? (In terms of price & quality). I read some pretty good things about it, and since you recommended it then why not give it a try. I'm still sort of apprehensive on taking the Huperzine, but once I'm able to find some I'm sure I'll give it a test run as well..I just don't want to overload my mind with too much stuff haha.

I also did some more research regarding the pharmacological effects of salvinorin and dextromethorphan. They are both apparently D2 dopamine receptor agonists, which has been linked to cases of schizophrenia. I think that both of these drugs may have overstimulated those receptors in my brain, causing similar abnormalities in my memory function. I found that there are some antipsychotics that antagonize the D2 receptors but I'm not sure if that would be an intelligent or safe idea.

#22 haha

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Posted 30 April 2010 - 11:46 PM

Huperzine should potentiate NR1a(nmdar)of the nmda receptor, while it mediates low level antagonism of the NR2x's(nmdar). At a sufficiently low dose this should really help you as it is quite similar to donepezil. taper up real slow. Read around some ppl say these shouldnt be taken by the young(but you might have more reason)
, nicotine patchs are another possability, again read around.
THese receptor display some interesting dynamics, simple more less doesnt help


Thank you :p Do you know the best place to get some Piracetam online? (In terms of price & quality). I read some pretty good things about it, and since you recommended it then why not give it a try. I'm still sort of apprehensive on taking the Huperzine, but once I'm able to find some I'm sure I'll give it a test run as well..I just don't want to overload my mind with too much stuff haha.

I also did some more research regarding the pharmacological effects of salvinorin and dextromethorphan. They are both apparently D2 dopamine receptor agonists, which has been linked to cases of schizophrenia. I think that both of these drugs may have overstimulated those receptors in my brain, causing similar abnormalities in my memory function. I found that there are some antipsychotics that antagonize the D2 receptors but I'm not sure if that would be an intelligent or safe idea.


I would keep away from antiphycotics at all cost unless your a danger to the public.....They are designed to destroy you, not the delusions. I wouldnt believe to much of what you read on articles on the net. Piracetam is good for most, if you dont feel that its helping you then stop, it so cheap anyway. I would do either drug on its own intially, personally I would have started with the huperzine <100mcg.
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#23 Spectre

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Posted 01 May 2010 - 09:27 AM

Huperzine should potentiate NR1a(nmdar)of the nmda receptor, while it mediates low level antagonism of the NR2x's(nmdar). At a sufficiently low dose this should really help you as it is quite similar to donepezil. taper up real slow. Read around some ppl say these shouldnt be taken by the young(but you might have more reason)
, nicotine patchs are another possability, again read around.
THese receptor display some interesting dynamics, simple more less doesnt help


Thank you :p Do you know the best place to get some Piracetam online? (In terms of price & quality). I read some pretty good things about it, and since you recommended it then why not give it a try. I'm still sort of apprehensive on taking the Huperzine, but once I'm able to find some I'm sure I'll give it a test run as well..I just don't want to overload my mind with too much stuff haha.

I also did some more research regarding the pharmacological effects of salvinorin and dextromethorphan. They are both apparently D2 dopamine receptor agonists, which has been linked to cases of schizophrenia. I think that both of these drugs may have overstimulated those receptors in my brain, causing similar abnormalities in my memory function. I found that there are some antipsychotics that antagonize the D2 receptors but I'm not sure if that would be an intelligent or safe idea.


I would keep away from antiphycotics at all cost unless your a danger to the public.....They are designed to destroy you, not the delusions. I wouldnt believe to much of what you read on articles on the net. Piracetam is good for most, if you dont feel that its helping you then stop, it so cheap anyway. I would do either drug on its own intially, personally I would have started with the huperzine <100mcg.


Designed to destroy you? What do you mean by that? I have heard horror stories of antipsychotics, and the contrary as well, but I have no personal experience with them..nonetheless, I'll stay away from any pharmaceuticals.

I did some more reading on Piracetam and Aniracetam. Would your recommend Piracetam over the other? I read that Aniracetam apparently increases sensory perception in some users (increased sense of smell, taste, touch, enhanced color perception, etc.) and that seems very appealing to me. I would love to visualize the world with more saturation, but fixing my brain is my ultimate goal. Would I benefit more from Aniracetam?

#24 haha

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Posted 01 May 2010 - 09:44 AM

Im not to shore about aniracetam, Theres are recent article regarding it that should some alarming features, I thought it speed up my mind but maybe lost the higher end functions.

I really think targeting Sigma-1 is the way to go, DXM causes specific changes and sigma-1 drugs countact those negatives, Huperzine maybe a sigma-1 or very similar per other recent huperzine post. You could buy that article, any friends who study? and take it to a shrink and get donepezil, you would only want 2-4mg per day.

Most docs are paid to prescibe antiphycotics to patients even generics, without going into the details they could treat most of the individuals with drugs of opposite effect and cure the negatives(ps this doesnt mean d2 agonists) Getting healthy is key

#25 Spectre

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Posted 01 May 2010 - 10:04 AM

Im not to shore about aniracetam, Theres are recent article regarding it that should some alarming features, I thought it speed up my mind but maybe lost the higher end functions.

I really think targeting Sigma-1 is the way to go, DXM causes specific changes and sigma-1 drugs countact those negatives, Huperzine maybe a sigma-1 or very similar per other recent huperzine post. You could buy that article, any friends who study? and take it to a shrink and get donepezil, you would only want 2-4mg per day.

Most docs are paid to prescibe antiphycotics to patients even generics, without going into the details they could treat most of the individuals with drugs of opposite effect and cure the negatives(ps this doesnt mean d2 agonists) Getting healthy is key


Does Huperzine A agonize or antagonize sigma-1 receptors? DXM apparently agonizes it:

σ1 and σ2 sigma receptor agonist (Ki = 205 nM and 11,060 nM, respectively). In a comparative investigation of dimemorfan, dextromethorphan and dextrorphan in mouse cells, dextromethorpan binds with relatively high affinity to Sigma-1 receptors and with very low affinity to Sigma-2 receptors.


I seriously need to learn more about these drugs..I'm only 19 and I feel like I'm gonna make my brains wiring go crazy before it's even done developing lol.

#26 haha

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Posted 01 May 2010 - 12:40 PM

Im not to shore about aniracetam, Theres are recent article regarding it that should some alarming features, I thought it speed up my mind but maybe lost the higher end functions.

I really think targeting Sigma-1 is the way to go, DXM causes specific changes and sigma-1 drugs countact those negatives, Huperzine maybe a sigma-1 or very similar per other recent huperzine post. You could buy that article, any friends who study? and take it to a shrink and get donepezil, you would only want 2-4mg per day.

Most docs are paid to prescibe antiphycotics to patients even generics, without going into the details they could treat most of the individuals with drugs of opposite effect and cure the negatives(ps this doesnt mean d2 agonists) Getting healthy is key


Does Huperzine A agonize or antagonize sigma-1 receptors? DXM apparently agonizes it:

σ1 and σ2 sigma receptor agonist (Ki = 205 nM and 11,060 nM, respectively). In a comparative investigation of dimemorfan, dextromethorphan and dextrorphan in mouse cells, dextromethorpan binds with relatively high affinity to Sigma-1 receptors and with very low affinity to Sigma-2 receptors.


I seriously need to learn more about these drugs..I'm only 19 and I feel like I'm gonna make my brains wiring go crazy before it's even done developing lol.

Hey good research, i knew DXM did bind to sigma-1 but i didnt realise the potency compared to NMDA, it would have to be a partial agonist at the very best otherwise it would give you a screaming headache by 1 microM which recreational users definitly exceed. Ive used donepezil which is a very clean sigma-1 agonist and it didnt seem at all like dxm....hmmmm im definitly less sure of what i said. Notice DXMs affinity of the Uopoid receptor thats pretty intense. I still think the problem is associated with the NR2a blockade similar to PCP causing a decrease in NMDA long range communication, I think that article goes into detail and huperzine may still be appropraite. What ever you do be careful

"dextromethorphan was four times more potent at NR1A/NR2A than at NR1A/NR2B "

#27 Spectre

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Posted 02 May 2010 - 01:39 AM

Im not to shore about aniracetam, Theres are recent article regarding it that should some alarming features, I thought it speed up my mind but maybe lost the higher end functions.

I really think targeting Sigma-1 is the way to go, DXM causes specific changes and sigma-1 drugs countact those negatives, Huperzine maybe a sigma-1 or very similar per other recent huperzine post. You could buy that article, any friends who study? and take it to a shrink and get donepezil, you would only want 2-4mg per day.

Most docs are paid to prescibe antiphycotics to patients even generics, without going into the details they could treat most of the individuals with drugs of opposite effect and cure the negatives(ps this doesnt mean d2 agonists) Getting healthy is key


Does Huperzine A agonize or antagonize sigma-1 receptors? DXM apparently agonizes it:

σ1 and σ2 sigma receptor agonist (Ki = 205 nM and 11,060 nM, respectively). In a comparative investigation of dimemorfan, dextromethorphan and dextrorphan in mouse cells, dextromethorpan binds with relatively high affinity to Sigma-1 receptors and with very low affinity to Sigma-2 receptors.


I seriously need to learn more about these drugs..I'm only 19 and I feel like I'm gonna make my brains wiring go crazy before it's even done developing lol.

Hey good research, i knew DXM did bind to sigma-1 but i didnt realise the potency compared to NMDA, it would have to be a partial agonist at the very best otherwise it would give you a screaming headache by 1 microM which recreational users definitly exceed. Ive used donepezil which is a very clean sigma-1 agonist and it didnt seem at all like dxm....hmmmm im definitly less sure of what i said. Notice DXMs affinity of the Uopoid receptor thats pretty intense. I still think the problem is associated with the NR2a blockade similar to PCP causing a decrease in NMDA long range communication, I think that article goes into detail and huperzine may still be appropraite. What ever you do be careful

"dextromethorphan was four times more potent at NR1A/NR2A than at NR1A/NR2B "


I just ordered some Piracetam and Huperzine A, and got an awesome deal! (500g of PrimaForce Piracetam + Source Naturals 120 Huperzine 200mcg tabs for $38.68 after shipping). I should get them in about a week I presume..I'll start off with Piracetam and see how I adjust on it for a couple weeks, then add Huperzine if I'm getting good results. I'll hold off on the mentat that I ordered since it would make more sense to maximize brain function after it was already fixed. I don't see a point in trying mentat before the other stuff. Thank you for all the great feedback, you really helped me out =)

#28 haha

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Posted 02 May 2010 - 10:08 AM

INterested in hearing how it goes for you, antioxidants(green tea extract, curcumin,pinebark extract, Cocoa) are so important to good brain function. Also Magnesium antagonisum could be real good for you as it voltage dependent and protects neurons etc.

#29 Spectre

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Posted 03 May 2010 - 07:18 PM

INterested in hearing how it goes for you, antioxidants(green tea extract, curcumin,pinebark extract, Cocoa) are so important to good brain function. Also Magnesium antagonisum could be real good for you as it voltage dependent and protects neurons etc.


Would taking Huperzine A be safe at my age though? (I'm 19, and will be 20 later this month). I've heard good and bad things about it, and read an article in Muscle & Fitness magazine supporting it's use as a strength enhancer. Should I start off at 50-100mcg and work my way up? Since Piracetam is an NMDA-modulator, would stacking it with Huperzine be a wise idea? Or would they cancel out each other's effects? Thanks.

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#30 Shifftee

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Posted 04 May 2010 - 02:20 PM

Humf. I did dxm when I was about 15. A few days after my last dose I went to shoot in the forest with my dad. When I went to bed that night as soon as I closed my eyes I would get these vivid hallucinations I was in the forest, shooting at birds. I started to hear birds singing. I got scared, got up, sat on the pc for a half a hour or so and went back and as soon as got to bed and closed my eyes I started hallucinating again (all sorts of things). The hallucinations got more and more abstract. It was as if my subconsciousness was pushing these strange and vague images that were not supposed to be conceptualized by the conscious mind. I was very scared. That night was the only night for quite a while that I visually hallucinated but I kept hearing birds singing. Oh man, those birds.. they were driving me nuts. I didn't hear them when I was awake. I didn't hear them if I closed my eyes when I was awake. But as soon as I went to bed and I closed my eyes - they were there. This got me so stressed I was afraid to go to sleep at night - I thought I was going schizophrenic, it's not a nice feeling, you should know better than me. I started listening to music as I went to sleep, so I wouldn't hear them - then I started watching movies or sth as I went to sleep. Over some months, they slowly faded away. The more I tried to get used to the problem and ignore it, the less stress it caused and eventually they stopped. Oh, and by the way, the first night I got a fucking panic attack. I thought about taking lexotan (3mg), but decided not to (I now believe that was a mistake).

Well, my problem was nothing compared to your's, but partially, I know your pain. Just wanting to be normal. I believe if you get your mindset right, take care of your health and not overemphasize on your problems, they will go away. As haha stated, the human brain has remarkable abilities to repair itself.

To the best of luck, brother.




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