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Effexor Lobotomy

effexor venlafaxine snri ssri stupid brain damage lobotomy ultram memory loss

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#1 whatdoisay

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Posted 16 November 2012 - 05:18 AM


About two years ago I foolishly took about a 4 month course of 37.5mg of Effexor/venlafaxine, came off it without withdrawal effects, then took a similar course of low-dose (25mg) Tramadol. Since then I have been generally drug-free (no chronic usage; extremely limited recreational use) and would no longer consider myself depressed, thanks in large part to major life changes/overhauls.

However, I have been very patiently waiting for now, literally, years for the negative residual effects of these two drugs to abate. I blame mostly the Effexor, as it seems heavily reinforced by anecdotal reports of similar problems/calls for class action law suits etc (though obviously the effexor is much more frequently prescribed than the tramadol).

The worst problem is the severe short term memory loss. I will regularly forget whether I completed a task or not or what task I had set myself in motion to do. More importantly, it has tremendous impact on my ability to recall facts/words/ideas which I am sure cuts my IQ in half.

My creativity, which was once quite high, has been all but eliminated and I find it extremely difficult to get "lost" in any sort of art or experience - something which was once very easy to do and a primary reason to live.

I have a general feeling that my personality, which was quite energetic, perhaps, at times, abrasive has been neutered and a sense of heightened awareness and consciousness is an extremely muffled version of what it once was.

Perhaps MOST troubling, as it reinforces the very real nature of this all (and not just a neurosis I've programmed into my head), is that many different drugs including Caffeine have completely different or muted effects on my post-effexor self. I also cannot seem to do much of anything that requires actual cognitive faculties (i.e. read, converse, write a simple forum post) without losing energy and gaining a vague pulsing headache.

And worst of all, my ability to write, for which my career and lifestyle depend upon, is severely hampered. I find it extremely difficult to form sentences in text, mostly because my memory is too weak to recall the words and then remember where they were to be organized.

All this to say I need a solution because abstinence, as was advised to me two years ago, has clearly not worked.

The horrible irony of all of this is I have tried many, many psychoactive drugs. Most left no detectable damage and though I suspected a few (an overdose prescription of amphetamines; a bit too much MDMA a decade ago), none caused anything so blatant, so crippling, and so concurrent with so many other reports as this Effexor.

I am willing to try just about anything and I have access to a great deal, prescription or otherwise.

#2 Raza

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Posted 16 November 2012 - 09:38 AM

Ideally, you'll want to research the MoA for effexor-induced memory impairment and find something matched to it.

If that doesn't seem feasible, I'd try general purpose nerve growth/brain healing stuff. Maybe read the cerebrolysin and uridine threads? ALCAR with lion's mane, noopept and physiological levels of melatonin for NGF optimization, maybe ashwagandha.


Edited by Raza, 16 November 2012 - 09:41 AM.


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#3 Turnbuckle

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Posted 16 November 2012 - 03:24 PM

The is a bit of a scare piece, but the links might be worthwhile--

SSRIs can cause brain damage: http://www.antidepre...rain-damage.htm

And Effexor side effects: http://www.antidepre...effexor-ADF.htm

#4 nowayout

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Posted 16 November 2012 - 08:02 PM

Note that tramadol is very similar in structure and (part of its) action to effexor. (Sure the OP knows this, but just a FYI for other readers of the thread). I actually find Tramadol a very fast and effective antidepressant, but I suspect that for me this is mostly due to its opioid-induced euphoria, since I get tolerant to this very fast. It does cause my libido to be depressed, but I am sure that is unrelated to T levels in my case, since my T levels on it were pretty good.

#5 whatdoisay

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Posted 22 October 2013 - 08:38 PM

I'm bumping this with an update a year later. There is marginal improvement but it is still a severe problem. Has there been any new possibilities for rehabilitation?
Interestingly, I've discovered that residual effects (i.e. days after intended effects) of MDMA restore some of the lost luster. That can't exactly be put into any sort of regimen - it's clearly not good for you - but it suggests that whatever deficiency is more related to Serotonin than to NE. I have assumed the latter, in large part since other SSRI's didn't leave me feeling a hole in my head.

#6 Anewlife

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Posted 23 October 2013 - 12:44 AM

Do you exercise? Have you tried Fish Oil?

#7 penisbreath

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Posted 23 October 2013 - 05:00 AM

Doesn't it have anticholinergic properties? Maybe something cholinergic?

Edited by lucky.pierre, 23 October 2013 - 05:01 AM.


#8 typ3z3r0

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Posted 23 October 2013 - 08:45 AM

I've discovered that residual effects (i.e. days after intended effects) of MDMA restore some of the lost luster. That can't exactly be put into any sort of regimen - it's clearly not good for you - but it suggests that whatever deficiency is more related to Serotonin than to NE.


You're right. It's not good for you, and it's especially important for you to avoid using it now, seeing as though it's neurotoxic to serotonergic and dopaminergic neurons, decreases SERT and is also excitotoxic. ;)

From the abstract of a study (http://www.sciencedi...9763413001127):
"Serotonergic neurotoxicity following MDMA is well-established in laboratory animals, and neuroimaging studies have found lower serotonin transporter (SERT) binding in abstinent Ecstasy/MDMA users. Serotonin is a modulator for many different psychobiological functions, and this review will summarize the evidence for equivalent functional deficits in recreational users. Declarative memory, prospective memory, and higher cognitive skills are often impaired. Neurocognitive deficits are associated with reduced SERT in the hippocampus, parietal cortex, and prefrontal cortex. EEG and ERP studies have shown localised reductions in brain activity during neurocognitive performance. Deficits in sleep, mood, vision, pain, psychomotor skill, tremor, neurohormonal activity, and psychiatric status, have also been demonstrated. The children of mothers who take Ecstasy/MDMA during pregnancy have developmental problems. These psychobiological deficits are wide-ranging, and occur in functions known to be modulated by serotonin. They are often related to lifetime dosage, with light users showing slight changes, and heavy users displaying more pronounced problems. In summary, abstinent Ecstasy/MDMA users can show deficits in a wide range of biobehavioral functions with a serotonergic component."

19 studies are linked to here:
http://www.reddit.co...se_in_a/c7mvi4i

"A prospective study of learning, memory, and executive function in new MDMA users":
http://onlinelibrary...12.03977.x/full

"Depression, impulsiveness, sleep, and memory in past and present polydrug users of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy)":
http://www.ncbi.nlm....pubmed/24114426

Here's a study in rats showing that "dosages approximating the recreational use of MDMA may impact the male reproductive axis.":
http://www.ncbi.nlm....les/PMC2753463/

Here's a study showing that neurotoxic metabolites were found in human urine after MDMA ingestion:
http://www.ncbi.nlm....pubmed/19349378

Here's a study in rats showing that "MDMA may constitute a risk factor for dopaminergic neuron degeneration":
http://www.ncbi.nlm....pubmed/24108425

Here's one study using human SH-SY5Y differentiated cells as dopaminergic neuronal model, showing that MDMA may be neurotoxic to dopaminergic neurons in relevant concentrations:
http://www.ncbi.nlm....pubmed/24101030

Edited by typ3z3r0, 23 October 2013 - 08:47 AM.


#9 Tom_

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Posted 23 October 2013 - 09:54 AM

I'd imagine the Tramadol had the worse effects of the two if it is discontinuation syndrome.

The doses you used are tiny, I really can't see doses these sizes causing a discontinuation syndrome let alone persistent problems. At that dose they are occupying well under 80-90% of SERT required for therapeutic and are unlikely to have changed 5HT/NA receptor expression much. Severe disturbance in working memory isn't consistent with SSRI discontinuation apart from in the short-term related to delirium related to acute and severe withdrawal (which is rarely seen and would have had you either admitted to a general psych or general medical ward).

Although in theory you could make an argument for down-regulation of cholinergic receptors or atypical opioid withdrawal from tramadol...again at the dose you used this seems very unlikely.

You haven't described common symptoms of SDY?

The standard treatment for SDY is fluoxetine. Starting at 10-30mg with a very slow titration period (for protracted withdrawals) up to three years. I'm of the view serotonergic antagonists might be of more use. Trazadone in particular, starting at a dose of 150mg titrating to 250-400mg and then titrating downwards by 25-50mg every 1-3 weeks. L-tryptophan has been used usually with reports of little success.

Typically for tramadol withdrawal codeine or Naltrexone are used, when required alongside fluoxetine.

As I've said from what I've read this doesn't sound like withdrawal or SDY

The differential for these symptoms are massive. This really really needs to be assessed by a good G.P, not one that is instantly going to shout SDY and prescribe fluoxetine but someone who is willing if required to refer to a Psychiatrist with an interest in psychopharmacology (not just an adult psychiatrist) or a neuropsychiatrist if they can't find any pathology & standard treatment for SDY fails.

There are plenty of drugs that might improve the WM problems but if there is something else going on its best not to start chucking scripts at you until you know whats going on.
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#10 whatdoisay

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Posted 23 October 2013 - 02:24 PM

I'd imagine the Tramadol had the worse effects of the two if it is discontinuation syndrome.

The doses you used are tiny, I really can't see doses these sizes causing a discontinuation syndrome let alone persistent problems. At that dose they are occupying well under 80-90% of SERT required for therapeutic and are unlikely to have changed 5HT/NA receptor expression much. Severe disturbance in working memory isn't consistent with SSRI discontinuation apart from in the short-term related to delirium related to acute and severe withdrawal (which is rarely seen and would have had you either admitted to a general psych or general medical ward).

Although in theory you could make an argument for down-regulation of cholinergic receptors or atypical opioid withdrawal from tramadol...again at the dose you used this seems very unlikely.

You haven't described common symptoms of SDY?

The standard treatment for SDY is fluoxetine. Starting at 10-30mg with a very slow titration period (for protracted withdrawals) up to three years. I'm of the view serotonergic antagonists might be of more use. Trazadone in particular, starting at a dose of 150mg titrating to 250-400mg and then titrating downwards by 25-50mg every 1-3 weeks. L-tryptophan has been used usually with reports of little success.

Typically for tramadol withdrawal codeine or Naltrexone are used, when required alongside fluoxetine.

As I've said from what I've read this doesn't sound like withdrawal or SDY

The differential for these symptoms are massive. This really really needs to be assessed by a good G.P, not one that is instantly going to shout SDY and prescribe fluoxetine but someone who is willing if required to refer to a Psychiatrist with an interest in psychopharmacology (not just an adult psychiatrist) or a neuropsychiatrist if they can't find any pathology & standard treatment for SDY fails.

There are plenty of drugs that might improve the WM problems but if there is something else going on its best not to start chucking scripts at you until you know whats going on.



What is SDY? Whatever it is, the only thing more implausible than a truly "good GP" is a good psychiatrist, at least in the Canadian system....

I've told myself that the low dose should be a saving grace, that it's so small I must be blowing things out of proportion. The fact is, that low dose was pretty much as high as I could physically tolerate at the time. If you're hyper-sensitive to a drug, do the general dose guidelines really apply to you? Furthermore, the things I've lost which I'm most disturbed by are all higher-functioning capacities, aside from memory. I'm not a musician but, for example, I could always "hear music" being crafted in my head, and I used this in crafting good timing and "sound" in my writing, for which I once had considerable talent. Maybe it's an over-simplified view, but I'd imagine it's these types of things that go first and foremost in some wide-scale brain downregulation.

#11 penisbreath

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Posted 23 October 2013 - 02:37 PM

whatdoisay -- I can empathize with you, as a former semi-professional writer. Anti-depressants always shut off some higher aspect of my thinking/talent, and what you describe -- about rhythm etc. -- is a subtle aspect of the craft that would probably be lost on an MD. They'll most likely blame it on unresolved depression or anxiety, if my experience holds true; I had one exceptional therapist who admitted some of her clients had dropped out of postgraduate courses after being put on SSRIs.

Of course, I guess my condition has reached the point where other things have to be prioritized, but I don't know .. have you considered less typical cognitive enhancing agents like Memantine, Galantamine, Deprenyl, Bacopa (I found some aspect of my thinking improved with the latter, especially in conjunction with caffeine, though it made me more fatigued)? High-EPA fish oil was also excellent for cognition, but disturbed my sleep and made me slightly manic.

Sorry I can't be of more help. Someone I know takes stablon for depression and anxiety, in conjunction with a very low dose of geodon (10mg b.i.d.). At that dose, it basically just enhances prefrontal functioning and he said it gave him more cognitive flexibility than stimulants.

#12 Major Legend

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Posted 23 October 2013 - 05:42 PM

I am a big fan of noopept, I wonder if it can reverse some of the damage caused.

#13 Buffalo1900

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Posted 11 June 2016 - 08:35 PM

The uridine DHA choline stack (Mr. Happy) helped me with recovering from effexor use. I read it upregulates dopamine receptors as well as helps synaptic formation. From my experience both these occur with use of this stack. I combine this with bulletproof coffee and intermittent fasting. I use Jarrow uridine, GNC choline, and Carlson's liquid fish oil.

I am only able to take 250 mg of uridine a few times a week as I would get kidney pain possibly as a result of an increase in uric acid. My coffee intake helped with this as I read coffee lowers uric acid levels. I planned on using uridine sparingly anyways as it physically felt the optimal way to take it.

#14 Buffalo1900

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Posted 12 June 2016 - 04:34 AM

I forgot to mention the dosage I use: Uridine 250 mg, Choline 250 mg (I use a pill cutter to cut in half as it is hard to swallow for me), and Carlson's fish oil 2 teaspoons. I take the pills on an empty stomach, eat breakfast, then take the fish oil. Done once a day.

#15 fntms

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Posted 12 June 2016 - 03:53 PM

The memory issues can very well be because of depression, and are unlikely to be linked to the effexor or tramadol discontinuation...
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#16 Buffalo1900

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Posted 12 June 2016 - 04:41 PM

Anything can be linked to depression, but when a significant alteration in cognition is experienced after weeks or months of effexor use it's not difficult to figure out the culprit. Google "effexor reviews". Also, when people state that an antidepressant "worked" for them you have to take into account how much cognitive ability that person had prior to its use. Someone who doesn't use their mind substantially probably won't notice anything was lost outside of say an alteration in certain emotions or having a "senior moment".
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#17 Mind_Paralysis

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Posted 16 January 2018 - 03:44 PM

I’ve experienced the exact same thing after quitting effexor cold turkey: Brain zaps, terrible memory loss and concentration problems. The only time I’ve felt kinda normal again was when I took a large dose of CBD-Oil (haven’t been able to reliably reproduce this effect though). Has anyone found a way to reverse the damage?

 

"Damage" is an incorrect term, since no SNRI is neurotoxic until you reach such dosages that you'd already be DEAD from Serotonin-syndrome beforehand.

 

"State" is a more accurate term - it sounds a bit like something similar to Dissociation or Depersonalisation, ak a it's a form of protective state which your body then erroneously assumes is necessary and then prolongs indefinitely, long, long after the danger has stopped.

 

As such, it's sure to be reversible - of course, as far as we know, there is NO PROOF that SNRI's can cause permanent cognitive damage, nor SSRI's - but similar potential problems are more studies in SSRI's.

 

 

Here's some info about how the Sigma-receptors are involved in cognitive enhancement from SSRI-use:

 

Phencyclidine-Induced Cognitive Deficits in Mice are Improved by Subsequent Subchronic Administration of Fluvoxamine: Role of Sigma-1 Receptors

https://www.nature.c...rticles/1301047

 

Since SSRI's are weak Sigma-1-agonists, then, in theory, if one gets cognitive deficits from using Paroxetine or Fluvoxamine, then one should probably try some kind of Sigma-1-antagonist, just to see if it gets worse, or better. (sometimes receptors respond to agonism by shutting down much quicker than one would think, and sometimes the opposite is true for weak antagonism - the body then overreacts and increases receptor-density many-fold, to counter-act the antagonism)

 

 

 

There's also some proof that Serotonin-agonism from SSRI's eventually leads to powerful receptor-downregulation, which then accounts for their efficacy in treating anxiety. In theory, the same is true for SNRI's.

 

Also, hypothetically, the 5ht2c-receptor is agonised, but does NOT downregulate, which would cause secondary antagonism, and hence increased release of DA and NE - instead it would lead to decreases in DA and NE activity in the PFC. Hence, perhaps low-dose 5ht2c-antagonism might be useful - that, or try low doses of 5ht2c-agonists, which would then lead to opposite reactions, et c.

 

SSRI-Induced extrapyramidal side-effects and akathisia: implications for treatment

http://journals.sage...988119801200212

 

 

Agomelatine is a weak 5ht2c-antagonist - give it a shot, and see what happens. If you get worse, then you'll know that your receptors are downregulated. (could also be that the day after, you suddenly get MANYFOLD better, as your body will then have decided to counteract antagonism by upregulating it, and while doing so, it dissolves the previous over-reaction deadlock in your brain)

 

 

EDIT:

 

Btw, just found this great link, with a whole review on something that sounds similar to "Effexor Lobotomy" - SSRI-induced apathy! :D

 

 

http://static1.1.sqs...FgotxAVqN F/CY=

 

 

Apparently case-reports exist wherein Buproprion, Sulpiride and Olanzapine.

 

Buproprion theoretically increases dopaminergic signalling - in the pfc, this is done by 5ht2c-antagonism...

Sulpiride is to surprisingly high doses, actually stimulating - it antagonises auto-receptors - theoretically causing dopaminergic signalling to go up - in the pfc... this is done by... 5ht2c-antagonism...

Olanzapine... is a 5ht2c-antagonist, of reasonable affinity...

 

(interesting thing to note.. in low dosages, Sulpiride also causes robust UPREGULATION OF GHB-SITES ON THE GABA-RECEPTOR! : O  Huh...)

 

 

Well... I see a certain pattern here. I don't know if you can see it as well, but I'd suggest you give 5ht2c-antagonism a shot - then you move on to the above substances.

 

Btw, final note - psychiatric researchers whom responded with hypothesis to what they had identified as SSRI-induced apathy also noted how they had yet to NOT record a single case of SNRI-induced apathy, of a similar character, from any of their patients. As such, you should probably consider that it may not be related to Venlafaxine, and if it is, then the above studies and ideas I posted... May be pointless.

 

SNRI-induced apathy could be from a completely different mechanism.


Edited by Stinkorninjor, 16 January 2018 - 04:00 PM.


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#18 Mind_Paralysis

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Posted 16 January 2018 - 04:15 PM

Anything can be linked to depression, but when a significant alteration in cognition is experienced after weeks or months of effexor use it's not difficult to figure out the culprit. Google "effexor reviews". Also, when people state that an antidepressant "worked" for them you have to take into account how much cognitive ability that person had prior to its use. Someone who doesn't use their mind substantially probably won't notice anything was lost outside of say an alteration in certain emotions or having a "senior moment".

 

You presume far, far too much here.

I smell your cognitive bias all the way down here, into my own little cave of bias, deep down in a hole in the ground.

 

You should be aware that there have been a great debate regarding if depression is far more common among people towards the higher spectrum of intelligence, or not - there's a great deal of evidence pointing towards the idea that the answer is a resounding 'YES!' - if this is true, which is very plausible at the moment, then that means that your entire argument is fundamentally flawed - as this would skew the entire spectrum of depressed people much closer towards moderately gifted - and a group that is at least slightly more talented than the norm would EASILY notice if SSRI's improved of worsened their cognitive abilities.

 

http://www.medicalda...ally-ill-270039

 

http://www.independe...n-a8005801.html

 

Do not presume so much about the abilities or failings of others.







Also tagged with one or more of these keywords: effexor, venlafaxine, snri, ssri, stupid, brain damage, lobotomy, ultram, memory loss

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