Jump to content

Neurological changes made by SSRI


npanth
 Share

Recommended Posts

I wrote an article about the neurological changes that SSRI make. I was thinking about the differences and similarities to other drugs, and what structural mechanism in the brain causes withdrawal symptoms. I'm not an expert in neurophysiology, but I studied it as an undergrad and since I started tapering.

http://npanth.wordpress.com/2012/06/12/how-ssri-work-in-withdrawal/

Paxil/Paroxetine/Seroxat

2000 - 2011: 40mg/day

June, 2011: 30mg/day

July, 2011: 25mg/day

August, 2011: 20mg/day

September, 2011: 15mg/day

October, 2011: 10mg/day

November, 2011: 0mg/day

January, 2012: (crash), 10mg/day

April 24, 2012: 9mg/day

June 11, 2012: 8.1mg/day

July 26, 2012: 7.5mg/day

September 24, 2012: 6.8mg/day

Link to comment
Share on other sites

Great article. I wish I'd read it before I did my way-too-fast taper.

 

Thanks.

 06/12 - Tapered off Cipralex. 30mg/Lithium 600mg/Epival 500mg

Very difficult time with 3-month taper off all drugs.

11/12 - Doc prescribed clonazepam 1 mg. for insomnia

01/14 - Clonazepan taper from 1 mg to .75 mg, then liquid microtaper to .638 mg. Depersonalization, extreme fatigue, muscle aches off/on.

05/15 - Switched to dry cut at .625 mg. Ok for 2-3 weeks, then same strong symptoms. Holding .625 mg.

06/15 - Switched over to liquid dosing .3125 ml 2x/day, 11 am & 11 pm.  Symptoms mild and no sleep issues.  Holding .625 mg/day.

10/15 - down to .530 mg. clonazepam in 4 months. .265 mg 2x/ day @ 10 am/10 pm. 

11/15 - holding at .528

11/15 - started microtaper to relieve persistent w/d symptoms

01/16 - microtaper not improving things; extremely sensitive to slightest decreases 

02/16 - holding at .524. 

Link to comment
Share on other sites

  • Moderator Emeritus

Thanks for sharing.

*** Please note this is not medical advice,discuss any decisions about your medical care with a knowledgeable medical practitioner***





http://prozacwithdrawal.blogspot.com/
Original drug was sertraline/Zoloft, switched to Prozac in 2007.
Tapering from 5mls liquid prozac since Feb 2008, got down to 0.85ml 23/09/2012, reinstated back to 1ml(4mg) 07/11/2012, didn't appear to work, upped to 1.05ml 17/11/2012, back down to 1ml 12/12/2012 didn't work, up to 1.30ml 16/3/2013 didn't work, bumped up to 2ml (8mg) 4/4/2013 didn't work, in July 2013 I reinstated Sertraline (Zoloft) 50mg, feeling better now. 

A few months down the line I switched to 5ml liquid Prozac and tapered down to a compromise dose of 3ml liquid Prozac and have stayed there ever since, no withdrawals and no emotional blunting/loss of libido.

 

Link to comment
Share on other sites

  • Moderator Emeritus

nice, clear well written article

Started in 2000 - On 150mg most of the time, (but up to 225mg at highest dose for 6 months in the beginning)
Reduced off easily first time - but got depressed (not too much anxiety) 6 months later
Back on effexor for another 9 months.
Reduced off again with no immediate w/d - suddenly got depressed and anxious ++ again 3 or 4 months later.
Back on effexor - this time for 3 years
Reduced off over a month - 6 weeks later terrible anxiety - back on.
Rinse and repeat 4 more times - each time the period before the anxiety comes back got shorter and shorter
Jan - July 2012 75mg down to 37.5mg;, 8/3/12 - 35mg. 8/25/12 - 32mg. 9/11- 28mg, 10/2 - 25mg, 10/29 - 22mg, 11/19 - 19.8mg; 12/11 - 17m,
1/1- 15.5mg; 1/22 -14mg, 2/7 14.9mg, 2/18 - 17.8mg - crashed big time: back to 75mg where i sat for 2 years....

4th  March 2015 - 67.5mg;   31st March - 60mg;  24th April - 53mg; 13th May - 48mg; 26th May - 45mg;  9th June - 41mg; 1 July- 37.5mg; 20 July - 34mg; 11 August - 31mg; 1st Sept - 28mg;  1st Dec - 25.8mg;  28th Dec - 23.2mg; 23rd Jan-21.9mg; Feb 7th- 21mg; March 1st - 20.1mg, March 30th - 18mg

Link to comment
Share on other sites

  • Administrator

Interesting. Another explanation involves downregulation or desensitization of serotonin receptors, which means that even the new neural networks are poorly equipped with receptors to absorb serotonin. See http://survivingantidepressants.org/index.php?/topic/392-one-theory-of-antidepressant-withdrawal-syndrome/

 

This makes withdrawal syndrome not a condition of too much serotonin in the brain, but a condition where the receptors cannot sense a normal production (or even excessive production, as when serotonergic supplements are taken) of serotonin and pass dysregulation down the chain of hormonal homeostasis.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

Link to comment
Share on other sites

  • Moderator Emeritus

I only skimmed it this morning, just read it properly, it is really well written. I've always found it hard to get my head round the neurological info, it is interesting about serotonin in the gut, I had terrible problems with my gut in cold turkey withdrawal which explains a lot.

*** Please note this is not medical advice,discuss any decisions about your medical care with a knowledgeable medical practitioner***





http://prozacwithdrawal.blogspot.com/
Original drug was sertraline/Zoloft, switched to Prozac in 2007.
Tapering from 5mls liquid prozac since Feb 2008, got down to 0.85ml 23/09/2012, reinstated back to 1ml(4mg) 07/11/2012, didn't appear to work, upped to 1.05ml 17/11/2012, back down to 1ml 12/12/2012 didn't work, up to 1.30ml 16/3/2013 didn't work, bumped up to 2ml (8mg) 4/4/2013 didn't work, in July 2013 I reinstated Sertraline (Zoloft) 50mg, feeling better now. 

A few months down the line I switched to 5ml liquid Prozac and tapered down to a compromise dose of 3ml liquid Prozac and have stayed there ever since, no withdrawals and no emotional blunting/loss of libido.

 

Link to comment
Share on other sites

Interesting. Another explanation involves downregulation or desensitization of serotonin receptors, which means that even the new neural networks are poorly equipped with receptors to absorb serotonin. See http://survivingantidepressants.org/index.php?/topic/392-one-theory-of-antidepressant-withdrawal-syndrome/

 

This makes withdrawal syndrome not a condition of too much serotonin in the brain, but a condition where the receptors cannot sense a normal production (or even excessive production, as when serotonergic supplements are taken) of serotonin and pass dysregulation down the chain of hormonal homeostasis.

 

I was combining what I know about the structure and function of neurons with the new theory of neuroplasticity. It's always seemed intuitively right that neural networks extend themselves and make new connections in response to thoughts or chemical changes. I think you are right that the specific mechanism could be deregulation of the new receptors.

As new Axon terminals extend into an area of the brain that has been affected by an SSRI, they either produce desensitized Serotonin receptors, or the normal receptors are blocked by the drug. My guess is that the new receptors are blocked by the drug because that would provide a physiological explanation for drug tolerance (it takes more drug to block more receptors) and withdrawal symptoms (the sudden over abundance of Serotonin absorption capacity) once the drug is removed. Desensitization would also provide a compelling explanation for tolerance and withdrawal. I'll have to ponder and read a bit more about it. Thanks.

Paxil/Paroxetine/Seroxat

2000 - 2011: 40mg/day

June, 2011: 30mg/day

July, 2011: 25mg/day

August, 2011: 20mg/day

September, 2011: 15mg/day

October, 2011: 10mg/day

November, 2011: 0mg/day

January, 2012: (crash), 10mg/day

April 24, 2012: 9mg/day

June 11, 2012: 8.1mg/day

July 26, 2012: 7.5mg/day

September 24, 2012: 6.8mg/day

Link to comment
Share on other sites

  • Administrator

Yes, researchers who have looked into this attribute it to desensitization.

 

The much-heralded neurogenesis supposedly stimulated by antidepressants, if it exists, may be of such downregulated networks.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

Link to comment
Share on other sites

Is it possible the neurogenesis seen with AD's is actually due to death of old neurons? In other words, could the SSRI be killing brain cells, so the brain has to make more to recover?

2003-2011: Paroxetine,Citalopram,Effexor; Aug/Sept 2011: Effexor to Mirtazapine; Oct 2011: C/T Mirtazapine back to Effexor; Nov/Dec 2011: Fast Tapered Effexor - w/d hell; Feb 2012: Reinstated Effexor 37.5mg; June 2012: Dropped to 35.6mg; Jan 2016: Propranolol 2.5mg per day for general anxiety; Feb 2016: Finasteride 0.25mg per week to slow hair loss; 18th May - 8th June 2019: Started Vyvanse 7.5mg and increased by 7.5mg weekly to 30mg (lowest “therapeutic” dose for adults).; 21st June 2019 - 12th July: Cross tapered from venlafaxine brand Rodomel to Efexor (1/4 > 1/2 > 3/4 weekly before ditching Rodomel); 13th July 2019: Cut Vyvanse dose to 15mg; 15th July 2019: Akathisia returned after years of being free; 16th July 2019: Went back up to Vyvanse 30mg

Supplements: Omega-3, Vitamin D, Zinc, Phosphatidylserine 

Link to comment
Share on other sites

  • Administrator

If I recall correctly, a repair reaction is one of the theories to explain this.

 

Another is that antidepressants interfere with the normal healthy pruning of neural networks that takes place during REM sleep -- they disrupt sleep architecture.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

Link to comment
Share on other sites

If I recall correctly, a repair reaction is one of the theories to explain this.

 

Another is that antidepressants interfere with the normal healthy pruning of neural networks that takes place during REM sleep -- they disrupt sleep architecture.

 

I've read this, too. I read an interesting article a while ago that focused on SSRI's affect on the Pineal Gland and described how SSRI disrupt sleep and dream patterns. The brain responds by intruding the dream state into waking life. In other words, SSRI literally makes us walk around in a dream.

Paxil/Paroxetine/Seroxat

2000 - 2011: 40mg/day

June, 2011: 30mg/day

July, 2011: 25mg/day

August, 2011: 20mg/day

September, 2011: 15mg/day

October, 2011: 10mg/day

November, 2011: 0mg/day

January, 2012: (crash), 10mg/day

April 24, 2012: 9mg/day

June 11, 2012: 8.1mg/day

July 26, 2012: 7.5mg/day

September 24, 2012: 6.8mg/day

Link to comment
Share on other sites

  • 2 years later...
  • Moderator Emeritus

 

 I read an interesting article a while ago that focused on SSRI's affect on the Pineal Gland and described how SSRI disrupt sleep and dream patterns. The brain responds by intruding the dream state into waking life. In other words, SSRI literally makes us walk around in a dream.

 

 

What can happen, when the serotonergic system isn't cycling anymore, in a natural circadian rhythm, is that daily consciousness will shift closer and closer to the "dream state". The verge between reality and dreaming will gradually become blurred. The lack of rhythm is the cause. Under the influence of an SSRI-AntiDepressant, serotonin levels won't fluctuate anymore, but remain continuously high. Many SSRI-AntiDepressant users reported that they had problems to distinguish reality from dreaming when they woke up from a dream and that it took quiet some time to realize that they had been dreaming instead of experiencing something real.

 

http://www.network54.com/Forum/182310/message/1057587694/SSRIs+and+the+PINEAL+GLAND+in+the+brain

 

(original full article with references and links here:  http://www.antidepressantsfacts.com/pinealstory.htm )

 

This was happening to me a lot when I stopped taking lexapro. It was worse during the first 6 months or so. I would have intense dreams which seemed to continue for hours after I woke up. It wasn't like I was still dreaming exactly, but it was like I couldn't seem to let go of the dream, believing that it was more real than my waking reality. The worst time was after one particular dream it took me 9 hours of being awake to finally feel like I was back into normal reality again.

 

I was still having problems transitioning between the dream/sleep state and waking consciousness 3 years later.

I'm not a doctor.  My comments are not medical advise. These are my opinions based on my own experience and what I've learned. Please discuss your situation with a medical practitioner who has knowledge of tapering and withdrawal...if you are lucky enough to find one.

My Introduction Thread

Full Drug and Withdrawal History

Brief Summary

Several SSRIs for 13 years starting 1997 (for mild to moderate partly situational anxiety) Xanax PRN ~ Various other drugs over the years for side effects

2 month 'taper' off Lexapro 2010

Short acute withdrawal, followed by 2 -3 months of improvement then delayed protracted withdrawal

DX ADHD followed by several years of stimulants and other drugs trying to manage increasing symptoms

Failed reinstatement of Lexapro and trial of Prozac (became suicidal)

May 2013 Found SA, learned about withdrawal, stopped taking drugs...healing begins.

Protracted withdrawal, with a very sensitized nervous system, slowly recovering as time passes

Supplements which have helped: Vitamin C, Magnesium, Taurine

Bad reactions: Many supplements but mostly fish oil and Vitamin D

June 2016 - Started daily juicing, mostly vegetables and lots of greens.

Aug 2016 - Oct 2016 Best window ever, felt almost completely recovered

Oct 2016 -Symptoms returned - bad days and less bad days.

April 2018 - No windows, but significant improvement, it feels like permanent full recovery is close.

VIDEO: Where did the chemical imbalance theory come from?



VIDEO: How are psychiatric diagnoses made?



VIDEO: Why do psychiatric drugs have withdrawal syndromes?



VIDEO: Can psychiatric drugs cause long-lasting negative effects?

VIDEO: Dr. Claire Weekes

 

 

 

Link to comment
Share on other sites

  • 2 weeks later...

I wrote an article about the neurological changes that SSRI make. I was thinking about the differences and similarities to other drugs, and what structural mechanism in the brain causes withdrawal symptoms. I'm not an expert in neurophysiology, but I studied it as an undergrad and since I started tapering. http://npanth.wordpress.com/2012/06/12/how-ssri-work-in-withdrawal/

 

So from what you're describing, the brain doesn't down regulate serotonin receptors in response to the flood of serotonin in the synapse, instead, it synthesizes entire new neuronal networks that are meant to absorb this excess serotonin.  Wouldn't it seem energetically less expensive for the cells to just change protein synthesis pathways and downregulate serotinin receptors in pre existing neuronal networks rather than synthesize an entire new network of cells?

 

I'm also not sure that I understand how these changes can produce the wide range of symptoms that individuals experience when withdrawing or having an adverse reaction to these medications.  Why would someone have tingling, burning, and numbness of limbs and extremities if there was just a simple chemical imbalance of serotonin?  It seems to me like there's more nefarious actions taking place in some people that produce a toxic neuropathy of sorts.  This idea of neuropathy has been echoed by experts in the field, including David Healy.

 

Many of the symptoms, such as flattened mood, anhedonia, mood swings, sleep disturbances, anxiety, depreonslization, etc would be very much consistent with your theory and I find it consistent with what you're describing - but other symtpoms, such as the numbness of the face, the involutnary twiches, the burning in the hands and feet, and genetilia seem like something entirely different.

 

Moreover - how could this explain the hypersensitivity?  From what I can garner, the hypersensitivity is a result of some sort of neuronal inflammation or damage - something akin to the swelling and twisting of neurons that has been described in the literature.  How else could someone who had no problems drinking or eating a variety of substances suddenly experience sensitivity to these substances?  I have a hard time believing that a too little seritonin in the synapses is causing a sudden intolerance of fast food, alcohol, drugs, supplements, etc - that doesn't really make too much sense.  It would seem to me, in my opinion, that this hypersensitivity goes along the lines with the neuropathy that has been posited by Dr. Healy.

 

So I'd argue that IN ADDITION to some of the changes that you are describing, there are also other changes occurring simultaneously in some people.  Especially in those who have had adverse reactions to the medications themselves, or an adverse reaction during tapering (etc).

Link to comment
Share on other sites

  • Administrator

I don't believe npanth's description is correct. You would have to correspond with npanth on his blog to find out his sources.

 

That SSRIs cause downregulation or depopulation of serotonin receptors is well-documented.

 

The nervous system tries to compensate for dysregulation of the serotonergic receptors with changes in other neuronal networks -- this is the alternative homeostasis postulated by Giovanni Fava and Paul Andrews -- but it's not to absorb serotonin.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

Link to comment
Share on other sites

I don't believe npanth's description is correct. You would have to correspond with npanth on his blog to find out his sources.

 

That SSRIs cause downregulation or depopulation of serotonin receptors is well-documented.

 

The nervous system tries to compensate for dysregulation of the serotonergic receptors with changes in other neuronal networks -- this is the alternative homeostasis postulated by Giovanni Fava and Paul Andrews -- but it's not to absorb serotonin.

 

Thank you for clarifying.

Link to comment
Share on other sites

  • 3 months later...

Can I still heal if I quit CT?

CD off meds in July 2015, not on any medication since. Went through WD nightmare, now dealing with normal anxiety, but decided not to leave this forum yet because I want to support and give hope to others. ♡

Link to comment
Share on other sites

 Share

×
×
  • Create New...

Important Information

Terms of Use Privacy Policy