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Post-withdrawal nervous system hypersensitivity, hyper-reactivity and kindling


stan

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I need so much help. I took Lexapro for years with no issues. In 2016, while in grad school I had a panic attack and was put on Klonopin then Lexapro to help me off the benzo after about a month's use. The first Lexapro shot my brain to hell and I haven't been right since. Through the course of a year, I was tried on several other meds in hopes to return myself to normal. I've had every side effect and symptom in the book. I am terrified. I'm 11 mos off cold turkey but I've been sick the entire 21 mos of being on and off the meds...I'm bed ridden, confused, sick, can't function, agitated, have akathisia...I honestly think I"m going to die. I see no improvements. I stay agitated and can't take care of my own child; my mother does everything...I'm so sick and afraid.

Rx'd 1-2mg Clonazepam for anxiety April 2016 (after one panic attack); asked to be taken down off of it due to it being benzo (I didn't do my research)...Placed on 10mg Lexapro-had reaction (crying hysterically, digestive issues, mood swings) to it; taken off (May '16) ; took myself down off Clonaz from 1 1.5 to .5 (probably last of May) in relatively short time (didn't know better); threw me into tailspin-no sleep for a week, dizzy, brain fog/dp/dr; went to another doctor who knew that Lex had helped me years ago (2014; 40mg) so pushed me to get to 40mg; stayed on for three months June-Aug; sick to death; quit doctor went to Psych PA who brought it down to 10mg  (end of Aug) and added 5mg Buspar x2/day; was okay for awhile then crying spells returned-same symptoms experienced as I did when on med; pysch took me off Lex; (Sept 19th); took myself off Buspar thinking it had made heart run/tachy (latter Sept); currently only on .5 Clonaz and miserable (weakness daily, apathy, anxious, tachycardia, occasional high bp, spacey, brain fog/dp/dr.)

 

Breakdown of Escialopram use: 10mg in May for one week; discontinued due to horrible side effects;

Placed back on Escitalopram in latter May, early June by doctor who knew it had worked for me in the past...pushed me from May to August to get to 40mg; all the while symptoms and my complaining to doctor-kept pushing me. 

Went to psych PA who took me down from 40 to 10 that initial visit added Buspar 5mg x 2; felt a little clearer; then began feeling crying spells again. Doctor ct'd me -told me "Try to see how you feel after one week without it". All this time, I had been emailing him to let him know my symptoms and he basically told me to stop; quit him and found a PA who has been overseeing my care-he's an advocate of meds though...thinks there is no tolerance on Clonazepam.

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You have been poly-drugged and could be having tolerance withdrawal symptoms from Klonopin. SSRIs are not recommended during benzo withdrawal because of the potential for adverse reactions. Are you familiar with benzo withdrawal symptoms and how to taper off them safely (e.g., Ashton protocol)?

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  • 4 weeks later...

Has Anyone ever fully recovered from this? I have severe sensitivities as well.

Paxil 10mg 2004-2011

7.5mg 4months

5mg. 4months

2.5mg.8 months no wd issues

Dropped pax 4-10-12

5-9-12 started prozac to alleviate symptoms (no relief)

5-22-12 reinstated paxil 2.5mg

5-28-12 5mg pax (couldn't tolerate sides)

6-22-12 Pax 2.5

6-30-12 Pax O

Cerebrolysin to help with wd at 29 months. Horrible decision much worse.

Still suffering sever Brain fog, Confusion, slow thinking,And just feeling sick and weird (hard to explain),facial twitching, weakness, shaking and jerking

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I was the original poster. I believe that I have fully recovered since the post in 2016. It took until mid to late 2017.

Prozac 9/2015-1/2016 - Caused depression. Withdrawal symptoms - joint pain, fatigue, off balance, blurred vision, perceptual disturbances. 1 month taper.

Sam-E 1/2016- 3/2016 - Withdrawal symptoms - pins and needles in face, arms, hands, legs, feet. Joint pain and muscle twitching. Depersonalization. Brain fog and severe cognitive thinking issues(reversing the spelling of words), slowed reaction time. Hallucinations from the sides of my eyes, blurred vision. Feeling like I'm going to fall off a cliff. Fatigue, flu- like symptoms, Brain shivers. 3 week taper.

 

Had Brain MRI 4/5/16- Completely Normal

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Just now, Jenk said:

I was the original poster. I believe that I have fully recovered since the post in 2016. It took until mid to late 2017.

Are you fully recovered from everything? 

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Just wanted to add some things I've personally learned about tolerating supplements while extremely hypersensitive. 

 

  1. Starting at very low doses is often at option. For instance with d3, even if there's a negative reaction to regular doses of 1000+IU, you may be able to handle 100-200 IU or so. I was able to start at 100 IU, then build up over time.
  2. The body is much more likely to handle it if you take it every day. As time went on, I noticed my negative reaction diminished in proportion to the time I had taken the particular supplement. I think this is akin to the body initially being hypersensitive to any "intruders" and reacting defensively. But then after a while, it begins to allow/accept the supplement as benign. I think it's also due to a limited supply of what I see as "adaptive energy", the energy we use to adapt to small changes. In SSRI withdrawal, this energy is greatly reduced, so it's best to minimise energy needed to adapt to any changes so it can be directed towards healing. For instance, keeping sleep routines regular, eating at regular times, so the body is en-trained to a pattern and expects to sleep/eat/take supplements/etc at certain times. By disrupting patterns, we demand extra energy to adapt to changes, and this both intensifies symptoms and is unkind to ourselves. In this regard, regularity of taking a supplement is important, as is not stopping it suddenly once you've taken it for a while. 
  3. Hold doses steady, then try a small updose, then hold steady again. I did this to work up to 400 IU d3 per day. Moving from 200 to 400, I found I had a similar reaction to starting 200 IU, but by holding it steady I stabilised once again and began to tolerate this higher amount. 
  4. Always take supplements with the largest meal possible. Having an empty stomach or small amount in my stomach made sensitive reactions profoundly worse (even if it was previously fine before SSRI withdrawal). Meals seem to be a good buffer, and likely co-factors that are absorbed at the same time may also help (e.g. magnesium in food sources will help the uptake of d3). 
  5. The earlier in the day, the better. Aside from immediate reactions of anxiety, nausea, etc, the biggest impact of new supplements was on my sleep quality. Taking it early in the day gives a 14+ hour interval to fully absorb and return to homeostasis, and so makes it less likely to negatively impact sleep
  6. Add only one supplement at a time, and keep it simple. Adding one variable at a time and not adding anything more until stabilised gives clarity about the effects. Often multivitamins contain 50+ different ingredients, so it's hard to know what might be having a positive or negative effect. I think it's best to take supplements individually, add them one at a time, and generally keep things uncomplicated. 
  7. Where possible, always prefer food and environmental sources to supplements/medicationsThis probably goes without saying, but food sources of supplements are significantly less likely to cause negative reactions during absorption. I think supplements should only be used when out of necessary kindness to the body. For instance, in SSRI wtihdrawal I became profoundly intolerant to light and noise, which led to spending a great deal of time in a dark room. This in turn led to d3 deficiency, which I started to correct with supplements as well as being outside as and when I could. 
     

Lastly, I want to say I developed extreme sensitivity to almost every supplement, medication, and many many food sources - then recovered. 3 times. 1 x during benzo withdrawal and 2 x during severe SSRI withdrawal. During benzo withdrawal I recovered with time. Unfortunately during SSRI withdrawal twice, only reinstatement led to improvement with sensitivity. 

There were a few aspects of hypersensitivity I never really recovered from after my first severe psychiatric drug withdrawal - and that included the tolerance of alcohol, caffeine, and any powerful stimulant. But in a way, I came to view this as a blessing, since avoiding those substances led to a much cleaner and healthier lifestyle than before when I'd be a regular drinker and energy drink guzzler. 

Hope that was helpful to someone, Jay

  • 2008: Started Citalopram 30mg
  • Sept 2014: Tapered down Citalopram over 6 months and discontinued Feb 2015
  • Severe withdrawals peaked in July/Aug 2015. Totally housebound.
  • Sept 2015: Sertraline started @ 100mg on GP advice.
  • Oct to Dec 2015: Reduced to Sertraline 50mg due to side effects. 
  • Jan 2016 to March 2017: Tapered Sertraline to 2mg @ 10% per month. 
  • Severe withdrawals peaked again June 2017. Totally housebound. 
  • Diazepam: July 2017 5mg // Aug 2017 2.5mg // Sept 2017 1mg // 12th Dec 2017 0.85mg 
  • Sertraline Reinstatement: 23 Oct 2017 5mg // 15 Nov 2017 10mg // 23 Nov 2017 15mg 
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  • 2 weeks later...

I know this is old post, and I have been concerned about this a few times over the last few years.  I have drug sensitivity to a lot of drugs, not all.  I can take advil, and some antibiotics, but cannot take phenergan, benadryl, claritin, zofran, b vitamins, prednisone, and others.  My biggest concern is what if we need surgery, not elective but a needed surgery.  I am terrified of the anesthesia and since you're not awake to say "hey, something don't feel right", it concerns me more.  (Also, since in the last several years I have developed not only drug sensitivity but allergies to things I wasn't previous allergic to, and if you're allergic to an anesthetic, I'm not sure what you would do).  Am also concerned with the sedation that goes along with a colonoscopy, as a nurse I've seen so many 60 year old patients with colon cancer that could have been caught at the polyp stage if they had had a colonoscopy at 50, so I know this is an extremely important health screening tool.  These are just concerns that I think of from time to time. 

zoloft 2004-08 tapered too fast(2 weeks)
Luvox 5/08 100 mg 07/10 40mg via small reductions, 08/10 39mg, 09/10 38mg, 10/10 37mg, 11/10 36mg,2/11 35mg, 5/11 34mg, 8/11 33mg, 11/11 32mg, 01/12 31mg, 03/12 30mg, 4/12 29mg, 5/12 28 mg, 8/12 27 mg, 11/12 26 mg, 1/13 25 mg, 3/13 24 mg, 4/13 23 mg,6/13 22 mg, 7/13 21 mg, 8/13 20mg, 10/13 19 mg, 11/13 18 mg, 12/13 17 mg, 1/14 16 mg, 3/14 13 mg, 9/14 10.9 mg,  1/15 10 mg, 3/15  9 mg,  5/15 8 mg. 11/15 7.12 mg.  4/16  5 mg, 6/16   4.5 mg,  9/16 4.2 mg, 1/17 3.48 mg, 2/17  3.2 mg,  4/17 2.2 mg, 5/17 2.0 mg, 6/17  1.74 mg, 7/17 1.58 mg, 9/17 1.27 mg, 11/17 1.0 mg,  1/18 0.79 mg

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  • ChessieCat changed the title to Hypersensitivity to neuroactive substances
  • 1 month later...

Bumping as I had a question about kindling reactions. It's said that you need certain genes to code for certain enzyme pathways in order to effectively digest certain drugs and if you lack those genes you can react to the pills.

 

Is it possible or likely that what's going on when someone takes a drug, tolerates it, stops it for a long time and later reintroduces it, if they react severely like I did doing this, that something has happened to turn those genes off/alter gene expression.  And thus the person isn't digesting them properly and that is what accounts for the later reaction?

 

I am not a medical professional and nothing I say is a medical opinion or meant to be medical advice, please seek a competent and trusted medical professional to consult for all medical decisions.

 

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Has anyone found that re-instating their SSRI / SNRI has reversed the hyper sensitivity to other medications?? I was taking effexor 4 months ago before i stopped. I Took 150mg of panadol a few days back and felt like rubbish for 2-3 hours afterwards =( I can take small amounts of ibuprofen but it feels like the effects are amplified.

Am thinking of re-instating in the hope that the hyper sensitivity will improve as well. I don't want to be in a situation (not saying i will be for a while) where i have an op in hospital and have a terrible reaction to the pain killers. Any advice in this would be great =)

Paroxatine - 2004-2006

Effexor XR 75mg 2006 - 2016 (Discontinued Feb 2016) - Withdrawal for 6 months.

Effexor XR 75mg Re-instated June 2017 (Discontinued Dec 2017)

Effexor XR 2-3 mg Re-instated March 10 2018 - 1 day (Didn't work)

Effexor XR 2mg Reinstated (Again) May 11 2018. 6 Beads

July 2018 - 0.0mg of Effexor. Zilch

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  • 1 month later...

Hi I was in for a procedure on Monday and had to have sedation profonol. I took severe headache that evening and it has continued, I then took numbness down my left side that last 5 hrs. I have continued to have the headaches which are debilitating. I don't tolerate any medication or supplements and haven't for 2

and  a half years.

does this sound more like neurotoxcity than withdrawal? Replies very much appreciated as I'm petrified with what I'm feeling. Thank you

Prozac for 18years with break in 1999 for pregnancy. Started to feel unwell with numerous problems 2015 and think I was in a tolerance to drug. Started to come off May 2016 and by June 2016 wasn't able to tolerate any medications at all. Was on Lansoprazole as and when need from 2001 but haven't had to take and wldnt have been able to take since June 2016

 

GP gave sertraline 25mg 6/04/17 loss of appetite, gut pain and then following morning whole body shaking and vomiting. Stopped tablet.

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On 2/20/2018 at 9:12 AM, IrishMonkey92 said:
3 hours ago, Bluebird2009 said:

Hi I was in for a procedure on Monday and had to have sedation profonol. I took severe headache that evening and it has continued, I then took numbness down my left side that last 5 hrs. I have continued to have the headaches which are debilitating. I don't tolerate any medication or supplements and haven't for 2

and  a half years.

does this sound more like neurotoxcity than withdrawal? Replies very much appreciated as I'm petrified with what I'm feeling. Thank you

I would call your healthcare provider to ask if it’s a side effect from propofol.

Prozac 9/2015-1/2016 - Caused depression. Withdrawal symptoms - joint pain, fatigue, off balance, blurred vision, perceptual disturbances. 1 month taper.

Sam-E 1/2016- 3/2016 - Withdrawal symptoms - pins and needles in face, arms, hands, legs, feet. Joint pain and muscle twitching. Depersonalization. Brain fog and severe cognitive thinking issues(reversing the spelling of words), slowed reaction time. Hallucinations from the sides of my eyes, blurred vision. Feeling like I'm going to fall off a cliff. Fatigue, flu- like symptoms, Brain shivers. 3 week taper.

 

Had Brain MRI 4/5/16- Completely Normal

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15 hours ago, Jenk said:

 

Thank you, I did this morning and was told the drug wld only last 24hrs and wldnt cause these symptoms but it started after the use of the drug so it was the drug that caused it. Then I was told I must have high blood pressure which I don't. The usual, this doesn't happen nonsense l. But something has. 

Prozac for 18years with break in 1999 for pregnancy. Started to feel unwell with numerous problems 2015 and think I was in a tolerance to drug. Started to come off May 2016 and by June 2016 wasn't able to tolerate any medications at all. Was on Lansoprazole as and when need from 2001 but haven't had to take and wldnt have been able to take since June 2016

 

GP gave sertraline 25mg 6/04/17 loss of appetite, gut pain and then following morning whole body shaking and vomiting. Stopped tablet.

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I read of an individual who took Choline and it helped clear his sensitivies. I keep trying to find the article but now I can't. Don't recall where I saw it first.

Paxil 10mg 2004-2011

7.5mg 4months

5mg. 4months

2.5mg.8 months no wd issues

Dropped pax 4-10-12

5-9-12 started prozac to alleviate symptoms (no relief)

5-22-12 reinstated paxil 2.5mg

5-28-12 5mg pax (couldn't tolerate sides)

6-22-12 Pax 2.5

6-30-12 Pax O

Cerebrolysin to help with wd at 29 months. Horrible decision much worse.

Still suffering sever Brain fog, Confusion, slow thinking,And just feeling sick and weird (hard to explain),facial twitching, weakness, shaking and jerking

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Been taking 6 beads of effexor (about 2.0mg) for about 3.5 weeks now. Ultra sensitive to it - even a jump of 2 beads is enough to knock me around. Have had problems taking panadol. Can take ibuprofen but only small ammounts as the effect seems to be amplified. Havent tried any opiate medications as been way too afraid.

Do doctors recognise broad range medication sensitivity as an actual condition?

Paroxatine - 2004-2006

Effexor XR 75mg 2006 - 2016 (Discontinued Feb 2016) - Withdrawal for 6 months.

Effexor XR 75mg Re-instated June 2017 (Discontinued Dec 2017)

Effexor XR 2-3 mg Re-instated March 10 2018 - 1 day (Didn't work)

Effexor XR 2mg Reinstated (Again) May 11 2018. 6 Beads

July 2018 - 0.0mg of Effexor. Zilch

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3 hours ago, Lloyd said:

Been taking 6 beads of effexor (about 2.0mg) for about 3.5 weeks now. Ultra sensitive to it - even a jump of 2 beads is enough to knock me around. Have had problems taking panadol. Can take ibuprofen but only small ammounts as the effect seems to be amplified. Havent tried any opiate medications as been way too afraid.

Do doctors recognise broad range medication sensitivity as an actual condition?

No they don't, they say it isn't possible, but my fast yo surgeon has said I have a dysregulated nervous system from stress and that's what is causing it. I think he is right and I don't think mine is withdrawal any longer.

Prozac for 18years with break in 1999 for pregnancy. Started to feel unwell with numerous problems 2015 and think I was in a tolerance to drug. Started to come off May 2016 and by June 2016 wasn't able to tolerate any medications at all. Was on Lansoprazole as and when need from 2001 but haven't had to take and wldnt have been able to take since June 2016

 

GP gave sertraline 25mg 6/04/17 loss of appetite, gut pain and then following morning whole body shaking and vomiting. Stopped tablet.

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3 hours ago, Lloyd said:

Been taking 6 beads of effexor (about 2.0mg) for about 3.5 weeks now. Ultra sensitive to it - even a jump of 2 beads is enough to knock me around. Have had problems taking panadol. Can take ibuprofen but only small ammounts as the effect seems to be amplified. Havent tried any opiate medications as been way too afraid.

Do doctors recognise broad range medication sensitivity as an actual condition?

One psychiatrist has told me my nervous system is primed due to withdrawal and that's the problems others say ptsd. I don't know.

Prozac for 18years with break in 1999 for pregnancy. Started to feel unwell with numerous problems 2015 and think I was in a tolerance to drug. Started to come off May 2016 and by June 2016 wasn't able to tolerate any medications at all. Was on Lansoprazole as and when need from 2001 but haven't had to take and wldnt have been able to take since June 2016

 

GP gave sertraline 25mg 6/04/17 loss of appetite, gut pain and then following morning whole body shaking and vomiting. Stopped tablet.

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3 hours ago, fj929 said:

I read of an individual who took Choline and it helped clear his sensitivies. I keep trying to find the article but now I can't. Don't recall where I saw it first.

Thank you

Prozac for 18years with break in 1999 for pregnancy. Started to feel unwell with numerous problems 2015 and think I was in a tolerance to drug. Started to come off May 2016 and by June 2016 wasn't able to tolerate any medications at all. Was on Lansoprazole as and when need from 2001 but haven't had to take and wldnt have been able to take since June 2016

 

GP gave sertraline 25mg 6/04/17 loss of appetite, gut pain and then following morning whole body shaking and vomiting. Stopped tablet.

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I have went back to the way I was in first withdrawal I can't sleep, system going crazy, head pain and restless legs. Will this did as long to recover from as first withdrawal. I have reacted badly

Prozac for 18years with break in 1999 for pregnancy. Started to feel unwell with numerous problems 2015 and think I was in a tolerance to drug. Started to come off May 2016 and by June 2016 wasn't able to tolerate any medications at all. Was on Lansoprazole as and when need from 2001 but haven't had to take and wldnt have been able to take since June 2016

 

GP gave sertraline 25mg 6/04/17 loss of appetite, gut pain and then following morning whole body shaking and vomiting. Stopped tablet.

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Anyone reacted badly to something like over the counter paracetamol?

Paroxatine - 2004-2006

Effexor XR 75mg 2006 - 2016 (Discontinued Feb 2016) - Withdrawal for 6 months.

Effexor XR 75mg Re-instated June 2017 (Discontinued Dec 2017)

Effexor XR 2-3 mg Re-instated March 10 2018 - 1 day (Didn't work)

Effexor XR 2mg Reinstated (Again) May 11 2018. 6 Beads

July 2018 - 0.0mg of Effexor. Zilch

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  • Moderator Emeritus

* NO LONGER ACTIVE on SA *

MISSION ACCOMPLISHED:  (6 year taper)      0mg Pristiq  on 13th November 2021

ADs since ~1992:  25+ years - 1 unknown, Prozac (muscle weakness), Zoloft; citalopram (pooped out) CTed (very sick for 2.5 wks a few months after); Pristiq:  50mg 2012, 100mg beg 2013 (Serotonin Toxicity)  Tapering from Oct 2015 - 13 Nov 2021   LAST DOSE 0.0025mg

Post 0 updates start here    My tapering program     My Intro (goes to tapering graph)

 VIDEO:   Antidepressant Withdrawal Syndrome and its Management

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Bluebird,  I just read Brassmonkey’s introductory post regarding withdrawal symptoms on the home screen.  One of the post describes the reemergence of withdrawal symptoms after different periods of time, particularly at three month and again at ten months after completely stopping the drug.  It’s seems the symptoms return, but generally pass faster  than the first time around.  The posts also caution that sometimes certain substances like alcohol can trigger the withdrawal sympyoms.  

        I recommend that you look at introductory posts again for reassurance.

Paxil 25 mg — January 2010 — June 2012

 

Wellbutrin 300 mg — December 2012 — September 2016

Prozac 20 mg — December 2012 — September 2016

Trazadone — 100 mg December 2012 — September 2016

 

10 mg Prozac — October 2016 — November 2017

25 mg Trazadone — October 2016 — present

 

8 mg Liquid Prozac November 2017 — present

 

 

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Are We There Yet? How Long is Withdrawal Going to Take?

 

Here's the link to that thread. It's in the Symptoms and Self Care Forum. Ruth is talking about the section "It Doesn't end at "0" (12)".  

20 years on Paxil starting at 20mg and working up to 40mg. Sept 2011 started 10% every 6 weeks taper (2.5% every week for 4 weeks then hold for 2 additional weeks), currently at 7.9mg. Oct 2011 CTed 15oz vodka a night, to only drinking 2 beers most nights, totally sober Feb 2013.

Since I wrote this I have continued to decrease my dose by 10% every 6 weeks (2.5% every week for 4 weeks and then hold for an additional 2 weeks). I added in an extra 6 week hold when I hit 10mg to let things settle out even more. When I hit 3mgpw it became hard to split the drop into 4 parts so I switched to dropping 1mgpw (pill weight) every week for 3 weeks and then holding for another 3 weeks.  The 3 + 3 schedule turned out to be too harsh so I cut back to dropping 1mgpw every 4 weeks which is working better.

Final Dose 0.016mg.     Current dose 0.000mg 04-15-2017

 

"It's also important not to become angry, no matter how difficult life is, because you can loose all hope if you can't laugh at yourself and at life in general."  Stephen Hawking

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  • Altostrata changed the title to Post-Withdrawal Nervous System Hypersensitivity or Kindling
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Neurobiol Dis. 2014 Mar;63:194-200. doi: 10.1016/j.nbd.2013.11.020. Epub 2013 Dec 7.

Chronic antidepressant treatment accelerates kindling epileptogenesis in rats.

Cardamone L1, Salzberg MR2, Koe AS1, Ozturk E1, O'Brien TJ1, Jones NC3.

 

Abstract at https://www.ncbi.nlm.nih.gov/pubmed/24321434

 

OBJECTIVES:

Due to the high comorbidity of epilepsy and depression, antidepressant treatment is commonly indicated for patients with epilepsy. Studies in humans and animal models suggest that selective serotonin reuptake inhibitors (SSRIs) may reduce seizure frequency and severity, and these drugs are generally considered safe for use in epilepsy. No studies have investigated the effects of SSRIs on epileptogenesis, the neurobiological process underlying the development of the epileptic state.

METHODS:

The effect of continuous infusion of the SSRI, fluoxetine (10mg/kg/day sc), versus vehicle control on amygdala kindling was examined in adult male Wistar rats. Seizure threshold and kindling rates were compared between SSRI-treated rats and controls. The study was then repeated examining the effect of a different SSRI, citalopram (10mg/kg/day sc), versus vehicle control. Hippocampal mRNA expression of the serotonin transporter (SERT) and the 5-HT1A receptor was examined in the brains of the rats post-mortem.

RESULTS:

Treatment with either fluoxetine or citalopram significantly accelerated kindling epileptogenesis, as evidenced by fewer stimulations to reach Class V seizures compared to their respective vehicle-treated group (p<0.01 for both drugs). Seizure duration was also increased in fluoxetine-treated rats. No differences in seizure threshold were observed between treatments (p>0.05). mRNA analysis did not reveal any molecular changes which were common to both treatments.

CONCLUSIONS:

The rate of epileptogenesis in rats is enhanced by chronic treatment with SSRIs. This could potentially have implications regarding the effect of SSRIs on the development or progression of human epilepsy.

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.

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Br J Psychiatry. 1978 Jul;133:1-14.

Kindling as a model for alcohol withdrawal syndromes.

Ballenger JC, Post RM.

 

Abstract at https://www.ncbi.nlm.nih.gov/pubmed/352467

 

Periodic brain stimulation, particularly in the limbic system, at stimulus intensities initially too low to produce any behavioural or EEG effects, progressively produces EEG changes, motor automatisms, and eventually convulsions, an effect called kindling. Data are presented and reviewed that suggest that the severity of alcohol withdrawal symptoms progressively increases over years of alcohol abuse in a stepwise fashion similar to the kindling process. The model is presented that the limbic system hyperirritability which accompanies each alcohol withdrawal serves over time to kindle increasingly widespread subcortical structures. These long-term changes in neuronal excitability might relate to the progression of alcohol withdrawal symptoms from tremor to seizures and delirium tremens, as well as the alcoholic personality changes between episodes of withdrawal.

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.

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Toxicol Ind Health. 1994 Jul-Oct;10(4-5):343-58.

The phenomenology of limbic kindling.

Gilbert ME1.

 

Abstract at https://www.ncbi.nlm.nih.gov/pubmed/7539949

 

Kindling is a model of epilepsy whereby repeated administration of brief low-intensity trains of electrical stimulation come to elicit electrographic and behavioral manifestations of seizure. In the absence of overt tissue damage, an animal that has been kindled is rendered in a permanent state of increased susceptibility to seizures. A number of persistent biochemical and physiological alterations in function accompany kindling, some of which may impact upon behavior of the organism for a long period of time despite the absence of further seizure activation. The sensitivity of limbic structures to kindling may contribute to the behavioral categories of cognition and affect that are particularly impacted by the kindling process. The increased proclivity for seizure disorders that characterizes kindling is not restricted to the initial kindling stimulus, but generalizes to other agents with convulsive properties. This paper provides an overview of the phenomenology of kindling, describes some of the conditions necessary for its induction, and some of the functional alterations that accompany its development and endure when overt convulsive behavior has subsided. Finally, a series of studies in our laboratory is presented which provides evidence of chemically induced kindling by repeated low-level exposure to some pesticides, namely those of the chlorinated hydrocarbon class.

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.

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Ann N Y Acad Sci. 2001 Mar;933:68-91.

Does the kindling model of epilepsy contribute to our understanding of multiple chemical sensitivity?

Gilbert ME1.

 

Abstract at https://www.ncbi.nlm.nih.gov/pubmed/12000037

 

Multiple chemical sensitivity (MCS) is a phenomenon whereby individuals report an increased sensitivity to low levels of chemicals in the environment. Kindling is a model of synaptic plasticity whereby repeated low-level electrical stimulation to a number of brain sites leads to permanent increases in seizure susceptibility. Stimulation that is initially subthreshold for subclinical seizure provocation comes, over time, to elicit full-blown motor seizures. Kindling can also be induced by chemical stimulation, and repeated exposures to some pesticides have been shown to induce signs of behavioral seizure, facilitate subsequent electrical kindling, and induce subclinical electrographic signs of hyperexcitability in the amygdala. Many of the symptoms of MCS suggest that CNS limbic pathways involved in anxiety are altered in individuals reporting MCS. Limbic structures are among the most susceptible to kindling-induced seizures, and persistent cognitive and emotional sequelae have been associated with temporal lobe epilepsy (TLE) in humans and kindling in animals. Thus, a number of parallels exist between kindling and MCS phenomena, leading to initial speculations that MCS may occur via a kindling-like mechanism. However, kindling requires the activation of electrographic seizure discharge and has thus been primarily examined as a model for TLE. Events leading to the initial evocation of a subclinical electrographic seizure have been much less well studied. It is perhaps these events that may serve as a more appropriate model for the enhanced chemical responsiveness characteristic of MCS. Alternatively, kindling may be useful as a tool to selectively increase sensitivity in subcomponents of the neural fear circuit to address questions relating the role of anxiety in the development and expression of MCS.

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

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Toxicol Ind Health. 1999 Apr-Jun;15(3-4):295-304.

Neural sensitization model for multiple chemical sensitivity: overview of theory and empirical evidence.

Bell IR1, Baldwin CM, Fernandez M, Schwartz GE.

 

Abstract https://www.ncbi.nlm.nih.gov/pubmed/10416281

 

This paper summarizes theory and evidence for a neural sensitization model of hyperresponsivity to low-level chemical exposures in multiple chemical sensitivity (MCS). MCS is a chronic polysymptomatic condition in which patients report illness from low levels of many different, structurally unrelated environmental chemicals (chemical intolerance, CI). Neural sensitization is the progressive host amplification of a response over time from repeated, intermittent exposures to a stimulus. Drugs, chemicals, endogenous mediators, and exogenous stressors can all initiate sensitization and can exhibit cross-sensitization between different classes of stimuli. The properties of sensitization overlap much of the clinical phenomenology of MCS. Animal studies have demonstrated sensitization to toluene, formaldehyde, and certain pesticides, as well as cross-sensitization, e.g., formaldehyde and cocaine. Controlled human studies in persons with self-reported CI have shown heightened sensitizability in the laboratory to nonspecific experimental factors and to specific chemical exposures. Useful outcome measures include spectral electroencephalography, blood pressure, heart rate, and plasma beta-endorphin. Findings implicate, in part, dopaminergic mesolimbic pathways and limbic structures. A convergence of evidence suggests that persons with MCS or with low-level CI may share some characteristics with individuals genetically vulnerable to substance abuse: (a) elevated family histories of alcohol or drug problems; (b) heightened capacity for sensitization of autonomic variables in the laboratory; (c) increased amounts of electroencephalographic alpha activity at rest and under challenge conditions over time. Sensitization is compatible with other models for MCS as well. The neural sensitization model provides a direction for further systematic human and animal research on the physiological bases of MCS and CI.

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

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Environ Health Perspect. 1997 Mar;105 Suppl 2:539-47.

Testing the neural sensitization and kindling hypothesis for illness from low levels of environmental chemicals.

Bell IR1, Rossi J 3rd, Gilbert ME, Kobal G, Morrow LA, Newlin DB, Sorg BA, Wood RW.

 

Abstract and free full text https://www.ncbi.nlm.nih.gov/pubmed/9167993

 

Sensitization in the neuroscience and pharmacology literatures is defined as progressive increase in the size of a response over repeated presentations of a stimulus. Types of sensitization include stimulant drug-induced time-dependent sensitization (TDS), an animal model related to substance abuse, and limbic kindling, an animal model for temporal lobe epilepsy. Neural sensitization (primarily nonconvulsive or subconvulsive) to the adverse properties of substances has been hypothesized to underlie the initiation and subsequent elicitation of heightened sensitivity to low levels of environmental chemicals. A corollary of the sensitization model is that individuals with illness from low-level chemicals are among the more sensitizable members of the population. The Working Group on Sensitization and Kindling identified two primary goals for a research approach to this problem: to perform controlled experiments to determine whether or not sensitization to low-level chemical exposures occurs in multiple chemical sensitivity (MCS) patients; and to use animal preparations for kindling and TDS as nonhomologous models for the initiation and elicitation of MCS.

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Toxicol Ind Health. 1994 Jul-Oct;10(4-5):277-312.

White paper: Neuropsychiatric aspects of sensitivity to low-level chemicals: a neural sensitization model.

Bell IR1.

 

Abstract https://www.ncbi.nlm.nih.gov/pubmed/7778100

 

The present paper summarizes the proposed time-dependent sensitization (TDS) and partial limbic kindling model for illness from low-level chemicals; reviews and critiques prior studies on CNS aspects of multiple chemical sensitivity (MCS); and outlines possible experimental approaches to future studies. TDS is the progressive and persistent amplification of behavioral, neurochemical, endocrine, and/or immunological responses to repeated intermittent stimuli over time. Partial limbic kindling is a progressive and persistent lowering of the threshold for eliciting electrical afterdischarges, but not motor seizures, in certain brain structures such as amygdala and hippocampus; behavioral consequences include increased avoidant behaviors. The focus of the paper is the controversial claim of altered sense of smell and illness from low levels of environmental chemicals (i.e., "cacosmia"), levels that should not have any biologically harmful effects by the rules of classical neurotoxicology. A major perspective of this paper is that the phenomenology of MCS is similar to that of time-dependent sensitization (reverse tolerance) and tolerance as studied in the substance abuse literature. The TDS model for MCS proposes that neurobiological amplification underlies the symptoms and phenomenology of these patients, including their behavioral features of heightened affective and somatic distress. It is hypothesized that MCS patients, who are mostly women, may be individuals who sensitize to substances rapidly and to the extreme, to the point of aversive symptomatology with less complete capacity for development of tolerance. Possible parallels between MCS and TDS include: (a) initiation by single or multiple intermittent stimuli; (b) lasting changes in subsequent reactivity to low levels of chemically unrelated substances; (c) cross-sensitization between the stressors and pharmacological agents; (d) greater vulnerability of individuals who are female, who have certain genetic characteristics, and/or who may be hyperreactive to novelty (cf. trait shyness); (e) lack of obvious differences between sensitized and unsensitized individuals at baseline without eliciting exposures; (f) bidirectionality (bipolarity) of sensitized responses; (g) both context-dependent (conditioned) and context-independent (unconditioned) amplification of responses. To minimize variability between studies, research in this area needs (a) consensus on a working case definition of MCS or at least of cacosmia as a specific symptom in a subset of well-defined medical and psychiatric disorders; and (b) proper design of chemical challenge studies in MCS, controlling for individual differences in sensitizability and for the properties of sensitization (e.g., repeated intermittent exposure tests) and tolerance (e.g., removal from customary ambient air exposures prior to testing).

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

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Pharmacology. 1995 Oct;51(4):205-23.

Benzodiazepine side effects: role of pharmacokinetics and pharmacodynamics.

Vgontzas AN1, Kales A, Bixler EO.

 

Abstract https://www.ncbi.nlm.nih.gov/pubmed/8577815

 

Benzodiazepines have a wide variety of indications. However, CNS and psychiatric adverse reactions, tolerance, and withdrawal effects of benzodiazepines are becoming increasingly recognized and must be better understood for proper drug use. Certain benzodiazepines are associated with memory impairment and other cognitive defects and hyperexcitability phenomena during treatment (early-morning insomnia, daytime anxiety) and following withdrawal (rebound insomnia and anxiety, seizures). Elimination half-life, receptor-binding affinity, effects on the locus coeruleus-norepinephrine (LC-NE) and hypothalamic-pituitary-adrenal (HPA) axes, and the interaction of these factors appear to be major determinants of frequency and severity of these untoward effects. Rapid drug elimination and high receptor-binding affinity were initially suggested as primary underlying factors which determine frequency, severity, and type of the side effects of benzodiazepines during administration and withdrawal. Newer data and information on triazolobenzodiazepines indicate that these psychiatric adverse reactions also relate to whether the benzodiazepine has strong direct effects on the LC-NE and HPA systems. Initial suppression of the LC-NE and HPA systems is followed, on an interdose basis, by a significant rebound and activation. This repetitive pattern of suppression followed by rebound results in a neurophysiologic and behavioral sensitization (kindling) of the limbic system and consequently contributes to central nervous system and psychiatric adverse reactions. The tendency of certain of these side effects to worsen over time supports empirically this neurophysiologic and biochemical model.

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From 2012 Current Medical Diagnosis & Treatment

Psychiatric Disorders

Stuart J. Eisendrath, MD Jonathan E. Lichtmacher, MD

page 1051

 

Quote

There is accumulating evidence that an impairment syndrome exists in many former (and current) drug users. It is believed that drug use produces damaged neurotransmitter receptor sites and that the consequent imbalance produces symptoms that may mimic other psychiatric illnesses. “Kindling”—repeated stimulation of the brain—renders the individual more susceptible to focal brain activity with minimal stimulation. Stimulants and depressants can pro- duce kindling, leading to relatively spontaneous effects no longer dependent on the original stimulus. These effects may be manifested as mood swings, panic, psychosis, and occasionally overt seizure activity.....

 

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  • 4 months later...

Can excessive stress cause kindling. I had an extreme stressful 3 week job in which I was not resting well,  body was burning, severe migraines, brain foggines(these were sx I had in early acute withdrawal). After 3 weeks I started to get vertigo for the first time in my withdrawal of 3 years. Now after all this I still continue to experience these sx and also dizziness. I am really scared of what I have done to myself. 

2008-seroxat,zoloft,olanzapine briefly for a few months. No effect no side effects. Jan 2014-  July 2015 fluvoxamine and on and off lexotanil. July 2015 left fluvoxamine after tapering 100 to 75 to 50 to 25mg and then dropped to zero this was over a period of 9 months.  Developed withdrawal sx after 2 months.  October 2015- nov 2015- mirtazapine, buspirone, rivotril quit cold turkey reinstated rivotril then cold turkeyed reinstated mirtazapine(last drug I was on) and tapered in a week  Jan2016.

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  • ChessieCat changed the title to Post-withdrawal nervous system hypersensitivity or kindling
  • 4 weeks later...

@deadbrain yes, this can happen. But, unless you have a hole in your head...you WILL heal if you treat your body, mind, spirit right. Stay positive, learn from the mistakes. I sure have. Be gentle with yourself!! 

 

XOX.

rachel 

 

Rachel - 1998-2012 Prozac 20mg

2012-2014 Prozac 40mg

Sept 17 Remeron 15mg, March ‘18 7.5mg

Jan 31 - Feb 13 1/4 - 1mg Ativan

Jan 31 - feb 5 - 2mg Prozac, 4mg feb 7

feb 10 - 10mg rem, Feb 27 - 7.5mg rem

Feb 27 - March 6th - 5mg Baclofen 

March 12th - Keppra 250mg

March 24 - 30mg phenobarbital 

 

 

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  • 3 weeks later...
On 9/20/2018 at 10:59 PM, Altostrata said:

Stimulants and depressants can pro- duce kindling, leading to relatively spontaneous effects no longer dependent on the original stimulus.

Could this theoretically also explain derealization?

1999:  Paroxetine (20mg). Age 16. 2007-2008: Fluoxetine (Prozac) for 1.5 years (age 25) Citalopram 20mg 2002-2005, 2009: Escitalopram (20mg), 2 weeks, (age 26) (adverse  reaction)/*Valium 5mg/Temazepam 10mg 2010: Mirtazipine (Remeron)( do not remember dosage) 2010, 5 months.                     2010-2017: Citalopram (20mg) (age 27 to 34) 2016: i.1st Sept- 31st Oct Citalopram 10mg , ii.1st November 2017-30th November 2017, Citalopram 5mg iii.1st December 2017- 4th February 2018, Citalopram 0mg, iv.5th February 2018- March 2018 Citalopram 5mg (10mg every other day) 28th February- tried titration of 5mg ( some adverse effects)

2018: 1st March 2018- 1st June Citalopram 10 mg (tablet form) /started titration 8mg , then 7 mg.2018: June 15th- 10th July Citalopram 10 mg pill every other day 2018: 10th July - 13th Sept Citalopram- 0mg  (CBD oil first month of 0mg, passiflora on and off) 2018 13th Sept Citalopram  2mg ,  approx 16th Sept 4mg , approx 25th Sept 6mg held.  2019: 11 Feb 19: 7mg (instant bad rxn) 12 Feb 19 6mg held 1 May 19 5.4mg held 5 Oct 19 5.36mg 22 Oct 19 5.29mg 30 Oct 19 5.23mg 4/NOV/19 5.18mg 12 Nov 19 5.08mg 20 Nov 19 4.77mg 7 May 22 2.31mg 17/09/2023 0.8mg

(Herbal/Supplements since 1st September: Omega Fish Oil 1200mg, 663mg of EPA- 2 tablets a day, magnesium and magnesium bath salts)

I did not die, and yet I lost life’s breath
- Dante
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Kindling is usually some kind of activation, such as waves of anxiety, fast heartbeat, or sleeplessness.

 

Derealization arises from nervous system dysregulation. It is not a sign of kindling.

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

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 i have a long story  of 07 years  with kindling ,and hypersesitivity , at the begining i ignored that it was all about the adverse reactions & too late reinstatement that i have done in 2012 !i kept taking prozac 20 mg wich i was on for 10 years (2001-2011),my psychiatrist said that i have to keep eating it & it will kick in in few days as in the past ,i beleived him however every day i was experiencing worse adverse raection to it i told him what was hapening to me but he didnt beleive in kindling or neurotoxicity or anything else ,for him the drugs were safe all of them !i was not knowing or discovred this best website SA ,wich i found it 5 years later ,& when i read topics & discovered files on here ,it help me a lot !so i was damaging my brain over 6 years after 2012 ,during them i have uped ,lowed,gone back & forth ,cold turkyed went through serotonin syndrome ,panic attacks , switched to lexparo for a short period  too! i have also went through a horrific protracted withdrawals with hundreds of uncredible symptoms every day , later in 2017 i learned all from this wonderful site that i have to taper slowly & that the antidepressants are no longer the answer for me !so i started tapering 5 mg of lexapro  for 01 year & last summer i was off of it (august 2018) i was verry sick during the adverse reactions & kindling years almost 06 years in 2018 ,after that i was stabilized a bit (symptoms were present 24/7) three months later (december 2018) withdrawals started to rise again & hit stronger ,i said that i wont reinstate ,i said no it wont help ,i did it before & i was damaged a lot (two decades 1997-2018),this time i wont take back an SSRIs  or a Benzo ! i lived through a hell every day ,there was not an other way , this last week i have experienced an other symptom wich was a pain brains,& pain /burning itching behind my neck & down to my back! wich lasted 7 days ! i was eating every thing had a lot of issues ,but now that i read this posts i ll avoid a lot of things ,i need Diet ,i steel experiencing withdrawals at 7 months off but its too early to heal, i know that it will take several months or maye be years ,is there some advices about alternatives or a Diet programm ?what shall i avoid? as you know i m hypersensible to every thing ,light,noise,some foods, hearing music,dark places, i do feel bad in winter, feeling cold,sweating, these are the a part of symptoms the others onces are the known withdrawals symptoms ! physical & psychological ! thank you 

Mars 1997- juillet 1997 Anfranil 25 mg, Tranxène 5 mg, Librium 10 mg, sulpiride 50 mg (juillet 1997)

Oct 1997-nov 1998 Anfranil 25mg, Tranxène5mg (rétabli ces deux médicaments seulement)

Nov 1998-mar 2000 Drugs off ( tapered with my psychiatrist help)

Avril 2000-juin 2001 Anfranil 25mg, Tranxène5mg (réinstatement these only drugs after 18 months off)

jul 2001-sep 2010 Prozac 20mg, Tranxène 5mg (passé de l'anafranil 25 à Prozac 20mg depuis juillet 2001)

jun 2007- jan 2010 Tapered Tranxène 5mg ( quick tapered  it while steel on Prozac 20 mg(les choses se passaient bien, pas de retraits)

sep 2010-mai 2011 Prozac 20mg conique (les choses se passaient bien sans retrait)

mai2011-mar 2012 Dugs gratuits (les choses étaient bien, pas de retraits)

mars 2012 rétabli Prozac 20mg (too late reinstatement = adverse reactions ) 

mar 2012 -apr 2016 prozac 20 mg on / off plusieurs jours cold turkeyed ( going on it back & forth )  et réintégration (effets indésirables et embrasement, neurotoxicity ) 

avril 2016-2018 lexapro 10mg on / off depuis sep 2017 lexapro tapering (effets indésirables et embrasement)

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