Jump to content

Serotonin Syndrome or Serotonin Toxicity


Recommended Posts

Okay I read some of his definition.  I am half asleep so maybe this won't be accurate so double-check this but it sounds like ST comes on rapidly after you start the offending drug(s). 

 

And I didn't know this (but am putting this here for others and as a future reference for myself) that Tramadol is an SRI.  I'll be sure to steer clear of it then...

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.

 

Link to post
Share on other sites
  • Replies 88
  • Created
  • Last Reply

Top Posters In This Topic

  • UnfoldingSky

    20

  • Altostrata

    14

  • reachingforthestars

    6

  • Barbarannamated

    6

Top Posters In This Topic

I feel like I am posting too much...

 

I am half asleep so maybe I am getting this wrong but I just wanted to point out that Dr. Gillman's definition in the link above has a very specific definition of serotonin toxicity which seems to exclude some adverse reactions. 

 

I know this is in my signature but please don't take my posts as medical advice.  To anyone reading this, if you are on a drug and feel it is causing you issues and aren't sure it it's serotonin toxicity please see a doctor ASAP and have them advise you about what to do about the drug.  And if you are not on a drug but are having serious problems and want to know if they are due to withdrawal or something else please seek a competent doctor as well.

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.

 

Link to post
Share on other sites

Hi WI,

 

Serotonin syndrome, or serotonin toxicity to my understanding is caused by serotonergic agents (certain drugs) while the person is taking them.  It's a particular kind of reaction, sometimes life-threatening, to these substances. Basically a form of poisoning.  So from what I understand you'd only have this if you were on a relevant drug, or combination of the substances that cause it.  It seems conceivable though that a person might have lingering problems from having had it; however I don't know what medical authorities would say about that (given they don't know much about protracted withdrawal, if they say this can't happen they could be wrong.) 

 

Hi Wiggle It,

 

I just wanted to note (and sorry for all the posts) that from what I have read and been told my understanding is it's supposed to be a particular kind of toxicity reaction with certain features that happens when you are on certain drugs, but it could be that what I have read or have been told isn't correct.

 

Forgive my heavy-handed warnings about this, it's just I am so tired and answered this and then realized it needed editing and now can't do that...And I don't want anyone here reading this and thinking that it's definitely the right definition and then making medical decisions based on this, nor do I want you to think I am diagnosing you, it's definitely something that you would want to talk to a competent medical professional about.

 

Maybe Alto can weigh in with what she knows too.

 

Did the doctor ever mention to you that he/she felt you had had it? 

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.

 

Link to post
Share on other sites
  • Administrator

You can get serotonin syndrome or serotonin toxicity in varying degrees while you are taking drugs. Only extreme cases are fatal, but it's wise to reduce dosage at any sign of overstimulation.

 

You can get withdrawal symptoms when you are off drugs.

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 post
Share on other sites
  • Moderator Emeritus

Okay.  Yeah, one of the early times I went to ER within the first two weeks of being off meds, the ER doc conferred with poison control.  ER doc told me that poison control said I had a mild case of it, but then ER doc wrote in my medical records that I did NOT have it, so I don't know if I ever did or not.

Plus, we all know how useless ERs are with cases like ours.

So, it's not possible that my own body could give me serotonin syndrome as levels readjust themselves now that I am off meds?  What if my body floods itself with serotonin or something now that things are out of whack?

**I'm not a doctor and don't give medical advice, merely personal experience
***Off all meds since Nov. 2014. Mentally & emotionally recovered; physically not
-Dual cold turkeys off TCA & Ativan in Oct 2014. Prescribed from 2011-2014

-All meds were Rxed off-label for an autoimmune illness.  It was a MISDIAGNOSIS, but I did not find out until AFTER meds caused damage.  All med tapers/cold turkeys directed by doctors 

-Nortriptyline May 2012 - Dec 2013. Cold turkey off nortrip & cold switched to desipramine

-Desipramine Jan 2014 - Oct. 29, 2014 (rapid taper/cold turkey)

-Lorazepam 1 mg per night during 2011
-Lorazepam 1 mg per month in 2012 (or less)

-Lorazepam on & off, Dec 2013 through Aug 2014. Didn't exceed 3x a week

-Lorazepam again in Oct. 2014 to help get off of desipramine. Last dose lzpam was 1 mg, Nov. 2, 2014. Immediate paradoxical reactions to benzos after stopping TCAs 

-First muscle/dystonia side effects started on nortriptyline, but docs too stupid to figure it out. On desipramine, muscle tremors & rigidity worsened

-Two weeks after I got off all meds, I developed full-blown TD.  Tardive dystonia, dyskinesia, myoclonic jerks ALL over body, ribcage wiggles, facial tics, twitching tongue & fingers, tremors/twitches of arms, legs, cognitive impairment, throat muscles semi-paralyzed & unable to swallow solid food, brain zaps, ears ring, dizzy, everything looks too far away, insomnia, numbness & electric shocks everywhere when I try to fall asleep, jerk awake from sleep with big, gasping breaths, wake with terrors & tremors, severely depressed.  NO HISTORY OF DEPRESSION, EVER. Meds CREATED it.

-Month 7: hair falling out; no vision improvement; still tardive dystonia; facial & tongue tics returned
-Month 8: back to acute, incl. Grand Mal seizure-like episodes. New mental torment, PGAD, worse insomnia
-Month 9: tardive dystonia worse, dyskinesia returned. Unable to breathe well due to dystonia in stomach, chest, throat
-Month 13: Back to acute, brain zaps back, developed eczema & stomach problems. Left leg no longer works right due to dystonia, meaning both legs now damaged
-4 years off: Huge improvements, incl. improved dystonia

Link to post
Share on other sites
  • Member
cymbaltawithdrawal5600

 

What if my body floods itself with serotonin or something now that things are out of whack?

 

This is not going to happen for various reasons that if you don't understand all the medical mumbo jumbo it won't do any good to post it. 'Serotonin Syndrome' is a term applied to a specific condition involving taking certain chemicals into your body, not something your body just up and does to you.

 

 

So, it's not possible that my own body could give me serotonin syndrome as levels readjust themselves now that I am off meds?

 

No.

 

The reason the ER doc said you did not have it is because of the above statement, the poison control people were misinformed. SS doesn't happen coming off meds, you were getting wd syndrome. Is very hard to accept docs and poison crtl center people as being wrong but that is what we are here for, the reason this board exists. We are documenting with every story how real wd syndrome is.

What happened and how I arrived here: http://survivingantidepressants.org/index.php?/topic/4243-cymbaltawithdrawal5600-introduction/#entry50878

 

July 2016 I have decided to leave my story here at SA unfinished. I have left my contact information in my profile for anyone who wishes to talk to me. I have a posting history spanning nearly 4 years and 3000+ posts all over the site.

 

Thank you to all who participated in my recovery. I'll miss talking to you but know that I'll be cheering you on from the sidelines, suffering and rejoicing with you in spirit, as you go on in your journey.

Link to post
Share on other sites
  • Moderator Emeritus

At this point, it's super easy for me to believe in the mistakes of either Poison Control or the doctors. I knew someone had made a mistake in this case since there was conflicting info, but just wasn't sure who had made the mistake.

 

I'm glad to know that my body can't give me serotonin toxicity on its own in absence of meds. I used be pretty good at decoding medical info and teaching myself concepts prior to wd, but right now might not be the time for me to tackle these details, so I will be comforted in the info that you have shared with me, CW and US and all!

**I'm not a doctor and don't give medical advice, merely personal experience
***Off all meds since Nov. 2014. Mentally & emotionally recovered; physically not
-Dual cold turkeys off TCA & Ativan in Oct 2014. Prescribed from 2011-2014

-All meds were Rxed off-label for an autoimmune illness.  It was a MISDIAGNOSIS, but I did not find out until AFTER meds caused damage.  All med tapers/cold turkeys directed by doctors 

-Nortriptyline May 2012 - Dec 2013. Cold turkey off nortrip & cold switched to desipramine

-Desipramine Jan 2014 - Oct. 29, 2014 (rapid taper/cold turkey)

-Lorazepam 1 mg per night during 2011
-Lorazepam 1 mg per month in 2012 (or less)

-Lorazepam on & off, Dec 2013 through Aug 2014. Didn't exceed 3x a week

-Lorazepam again in Oct. 2014 to help get off of desipramine. Last dose lzpam was 1 mg, Nov. 2, 2014. Immediate paradoxical reactions to benzos after stopping TCAs 

-First muscle/dystonia side effects started on nortriptyline, but docs too stupid to figure it out. On desipramine, muscle tremors & rigidity worsened

-Two weeks after I got off all meds, I developed full-blown TD.  Tardive dystonia, dyskinesia, myoclonic jerks ALL over body, ribcage wiggles, facial tics, twitching tongue & fingers, tremors/twitches of arms, legs, cognitive impairment, throat muscles semi-paralyzed & unable to swallow solid food, brain zaps, ears ring, dizzy, everything looks too far away, insomnia, numbness & electric shocks everywhere when I try to fall asleep, jerk awake from sleep with big, gasping breaths, wake with terrors & tremors, severely depressed.  NO HISTORY OF DEPRESSION, EVER. Meds CREATED it.

-Month 7: hair falling out; no vision improvement; still tardive dystonia; facial & tongue tics returned
-Month 8: back to acute, incl. Grand Mal seizure-like episodes. New mental torment, PGAD, worse insomnia
-Month 9: tardive dystonia worse, dyskinesia returned. Unable to breathe well due to dystonia in stomach, chest, throat
-Month 13: Back to acute, brain zaps back, developed eczema & stomach problems. Left leg no longer works right due to dystonia, meaning both legs now damaged
-4 years off: Huge improvements, incl. improved dystonia

Link to post
Share on other sites
  • Member
cymbaltawithdrawal5600

Okay,

 

Alto asked me to update this topic with the new information from Dr. Ken Gillman who has a website and is apparently quite an expert on "Serotonin Toxicity" as he prefers it be called. He states:

 

"Now, in 2015, a decade and more after key research and reviews that demonstrated the essentials of the interactions relevant to serotonin toxicity (ST), there remains much mis-understanding and mis-information in both medical journals, and reference sources that are usually considered, and should be, authoritative.

I have published a number of papers in this field and am a widely recognized expert. I am now in a position to update the information on this website and add new material that has previously only been available to bona fide researchers."

 

I am going to quote directly his page on "Introduction to Serotonin Toxicity". What is important to note is this: he has discovered that there is (for many reasons) a lot of misinformation about not only 'serotonin toxicity' but which drugs or combinations thereof are most likely to cause it. Because we refer people to the Drug Interactions Checker at drugs.com, the existing information may be incorrect, according to Dr. Gillman, but we still have to advise caution because that information is the current accepted wisdom and may be slow to reflect changes. Please read this information on his site, I will not be quoting it here.

 

Here is his introduction:

 

"S[erotonin T[oxicity] [herafter abbreviated as ST]only occurs after the ingestion of drugs that greatly increase brain serotonin levels. There is no disease or other natural cause for this constellation of signs and symptoms. It is poisoning caused by serotonergic drugs (a ‘toxidrome’)*. That is why most experts in the field consider it preferable to call it a form of toxicity, not a syndrome (1-3). Few people would suggest it is sensible to call poisoning with lithium a syndrome. Everybody calls it ‘lithium toxicity’ not ‘lithium syndrome’.

 

* It may also be noted that the term serotonergic drugs continues to be widely (almost universally) misused to include drugs that have little or no proven effect on brain serotonin levels. Almost all review papers containing tables or lists of supposedly serotonergic drugs are riddled with mistakes. Perhaps the most egregious example of this is mirtazapine, about which I have published a pharmacological analysis (4, 5).

 

The pathways involved in the production and control of brain serotonin are well-defined and so are the drugs that affect these pathways. Thus, current pharmacological knowledge indicates that only three types of drug are capable of elevating serotonin sufficiently to be involved in serotonin toxicity:

 

1) All monoamine oxidase inhibitors (MAOIs), (except selective inhibitors of MAO-B, e.g. rasagiline)

2) Serotonin reuptake inhibitors (SRIs). That comprises selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs), and other drugs marketed for different indications which in fact also act as SRIs (e.g. the pain killer tramadol)

3) drugs that act as serotonin releasers (e.g. ecstasy- MDMA)

 

There is no evidence that drugs working by other mechanisms are capable of precipitating serotonin toxicity. Case reports suggesting otherwise are almost certain to be erroneous. A recent case illustrating this, but which is by chance related to the emerging knowledge about metaxalone shows this well (6): for the details of this emerging and interesting story see:

 

http://www.psychotropical.com/index.php/metaxalone-skelaxin-and-st

 

The term ST should be reserved for those cases sufficiently severe to require hospital admission and medical intervention. There will sometimes be debate about whether a given clinical case is most appropriately described as ‘severe’ or ‘atypical’ side effects, or as ‘toxic’ effects. Probably the most relevant and objective criteria is body temperature. That is the main change that mediates the life threatening effects of ST.

 

A key goal of medical management is to predict those cases that may become sufficiently severe to necessitate urgent active intervention to prevent hyperthermia and severe morbidity or mortality. In other cases that are less severe (and do not involve combinations of MAOIs + SRIs) the only action that is likely to be required is reduction or cessation of one or more of the implicated drugs.

 

ST has been clearly characterized as a triad of neuro-excitatory features.

 

1) Neuromuscular: tremor, hyperreflexia, clonus and (in the advanced stage) pyramidal rigidity

2) Autonomic: hyperthermia, diaphoresis, tachycardia and tachypnoea.

3) Altered mental status: agitation, excitement and (only in the advanced stage) confusion.

 

Severe tremor, hyperreflexia, clonus (inducible, spontaneous or ocular), agitation, diaphoresis and hyperthermia are the key signs and symptoms. The Hunter criteria are the benchmark diagnostic rules (2). They demonstrate that if, in the presence of a known potent serotonin enhancing drug (see below for a list clinically significant drugs), spontaneous clonus is present then ST may be reliably diagnosed.

 

Clinically, the onset of toxicity is usually rapid, because it results from drug combinations and starts when the second drug reaches effective levels. The clinical picture is often alarming and rapidly progressive after the first or second dose of the second serotonergic drug in the patient’s regime. The patient is usually alert, orientated, excitable with tremor and hyperreflexia. Ankle clonus is usually demonstrable and as severity increases spontaneous clonus develops (which is sometimes mistaken as seizure activity). Neuromuscular signs are initially greater in the lower limbs, then become more generalized as toxicity increases. Other (early) symptoms may include shaking, shivering often including chattering of the teeth and sometimes trismus. Pyramidal rigidity is a late development in severe cases, and when it affects truncal muscles respiration is impaired. This rigidity causes decreased PaCO2, and a fever of 39ºC or higher heralds life-threatening toxicity.

 

An accurate list of drugs that have been proven to exhibit significant serotonergic potency in humans is most important. A brief table of the such drugs is below, the detailed justification of why particular drugs are included or excluded is contained in other commentaries (see menu), and has been investigated and explained in detail in various my peer-reviewed scientific publications. I have published more original research on this and closely related topics than anyone else (4, 5, 7-14).

Drugs with clinically relevant serotonergic potency Serotonin reuptake inhibitors (selective and non-selective)

  • All SSRIs and all SNRIs: Paroxetine, sertraline, fluoxetine, fluvoxamine, citalopram.
  • Venlafaxine (desvenlafaxine), milnacipran, duloxetine, sibutramine.
  • Clomipramine, imipramine (but not other TCAs).
  • Tramadol, pethidine, methadone, dextromethorphan, dextropropoxyphene, pentazocine (but not other opioids).
  • Chlorpheniramine, brompheniramine (but not other anti-histamines).
  • Monoamine oxidase inhibitors
  • Tranylcypromine, phenelzine, nialamid, isoniazid, iproniazid, isocarboxazid
  • clorgyline, methylene blue
  • moclobemide toloxatone, linezolid, metaxalone, furazolidone, procarbazine.
  • Serotonin releasers
  • MDMA (amphetamine?).

 

Table notes:

Clomipramine and imipramine do precipitate ST, but none of the other TCAs are able to because they are too weak as SRIs. Trazodone, nefazodone, mianserin, mirtazapine are neither SRIs nor significantly serotonergic. Also, they do not precipitate serotonin toxicity with MAOIs. Fatalities from ST involving opioids have been documented with pethidine, tramadol and dextromethorphan, but probably not with fentanyl."

 

Please refer back to his website for the relevant references and citations (which are not linked in even the article), I am not going to copy them here.

What happened and how I arrived here: http://survivingantidepressants.org/index.php?/topic/4243-cymbaltawithdrawal5600-introduction/#entry50878

 

July 2016 I have decided to leave my story here at SA unfinished. I have left my contact information in my profile for anyone who wishes to talk to me. I have a posting history spanning nearly 4 years and 3000+ posts all over the site.

 

Thank you to all who participated in my recovery. I'll miss talking to you but know that I'll be cheering you on from the sidelines, suffering and rejoicing with you in spirit, as you go on in your journey.

Link to post
Share on other sites
  • Administrator

Dr. Gillman is using a strict definition of serotonin toxicity that may be precipitated by a combination of drugs requiring the same liver enzymes for metabolization.

 

While only one of the drugs might be a serotonergic (by his definition), the drug combination can cause a buildup of the serotonergic in the bloodstream and symptoms of serotonin toxicity.

 

The drugs.com Drug Interactions Checker , to which we often refer, includes some analysis of liver metabolism overlaps (I believe).

 

Someone interested in this might write Dr. Gillman to clarify.

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 post
Share on other sites

You can get serotonin syndrome or serotonin toxicity in varying degrees while you are taking drugs. Only extreme cases are fatal, but it's wise to reduce dosage at any sign of overstimulation.

 

You can get withdrawal symptoms when you are off drugs.

During withdrawal, when Doxepin was my remaining med at a low dose, I took a vitamin with 5htp in it.  No more than 25 to 50mg.   I definitely developed some type of serotonin syndrome that seemed like nothing I had experienced before.  It felt similar to having the flu.   Once I stopped the vitamin, I was fine.

 

The moral of the story is be careful in taking so called benign supplements during withdrawal that have 5HTP or Tryptophan, particularly if you are sensitive like I am.

Drug cocktail 1995 - 2010
Started taper of Adderall, Wellbutrin XL, Remeron, and Doxepin in 2006
Finished taper on June 10, 2010

Temazepam on a PRN basis approximately twice a month - 2014 to 2016

Beginning in 2017 - Consumption increased to about two times per week

April 2017 - Increased to taking it full time for insomnia

Link to post
Share on other sites
  • Member
cymbaltawithdrawal5600

He mentions tryptophan on his website.

What happened and how I arrived here: http://survivingantidepressants.org/index.php?/topic/4243-cymbaltawithdrawal5600-introduction/#entry50878

 

July 2016 I have decided to leave my story here at SA unfinished. I have left my contact information in my profile for anyone who wishes to talk to me. I have a posting history spanning nearly 4 years and 3000+ posts all over the site.

 

Thank you to all who participated in my recovery. I'll miss talking to you but know that I'll be cheering you on from the sidelines, suffering and rejoicing with you in spirit, as you go on in your journey.

Link to post
Share on other sites

 

You can get serotonin syndrome or serotonin toxicity in varying degrees while you are taking drugs. Only extreme cases are fatal, but it's wise to reduce dosage at any sign of overstimulation.

 

You can get withdrawal symptoms when you are off drugs.

 

During withdrawal, when Doxepin was my remaining med at a low dose, I took a vitamin with 5htp in it.  No more than 25 to 50mg.   I definitely developed some type of serotonin syndrome that seemed like nothing I had experienced before.  It felt similar to having the flu.   Once I stopped the vitamin, I was fine.

 

The moral of the story is be careful in taking so called benign supplements during withdrawal that have 5HTP or Tryptophan, particularly if you are sensitive like I am.

I also think my serotonin level was increasing, especially when I took tryptan...

I read about body temperature that time, after the emergency visit, and I monitored myself carefuly...

My temperature was normal all the time. Only my blood pressure was rising but mu pulse was going down...

Decreasing escitaploram helped...

- 12.03.2021- doxepin- 50mg

- 6.11.2020- 75mg

- 16.10.2020- 100mg

- 30.09.2020- doxepin- 125mg

- May 2020, omeprazole 40mg switched to esomeprazole 20mg

- 2012 re-started Doxepin 75mg, evening. Increased to 150mg

- 2012, Atenolol 25mg, twice a day

- 2016, Low dose of HRT in evening, Sandrena and Utrogestan 

- Long term of Nasal spray Otrivine

- 2012, PPI Omeprazole 40mg-evening

24.10.2014- Started ESCITALOPRAM-first 5mg and then 10mg; due to the adverse symptoms reduced on 5.01.2015- Escitalopram- 2.5mg 22.07.2016- re-started reduction by 1% at a time. Completed tappering on  19.03.2020 😇

Link to post
Share on other sites

Okay,

 

Alto asked me to update this topic with the new information from Dr. Ken Gillman who has a website and is apparently quite an expert on "Serotonin Toxicity" as he prefers it be called. He states:

 

"Now, in 2015, a decade and more after key research and reviews that demonstrated the essentials of the interactions relevant to serotonin toxicity (ST), there remains much mis-understanding and mis-information in both medical journals, and reference sources that are usually considered, and should be, authoritative.

I have published a number of papers in this field and am a widely recognized expert. I am now in a position to update the information on this website and add new material that has previously only been available to bona fide researchers."

 

I am going to quote directly his page on "Introduction to Serotonin Toxicity". What is important to note is this: he has discovered that there is (for many reasons) a lot of misinformation about not only 'serotonin toxicity' but which drugs or combinations thereof are most likely to cause it. Because we refer people to the Drug Interactions Checker at drugs.com, the existing information may be incorrect, according to Dr. Gillman, but we still have to advise caution because that information is the current accepted wisdom and may be slow to reflect changes. Please read this information on his site, I will not be quoting it here.

 

Here is his introduction:

 

"S[erotonin T[oxicity] [herafter abbreviated as ST]only occurs after the ingestion of drugs that greatly increase brain serotonin levels. There is no disease or other natural cause for this constellation of signs and symptoms. It is poisoning caused by serotonergic drugs (a ‘toxidrome’)*. That is why most experts in the field consider it preferable to call it a form of toxicity, not a syndrome (1-3). Few people would suggest it is sensible to call poisoning with lithium a syndrome. Everybody calls it ‘lithium toxicity’ not ‘lithium syndrome’.

 

* It may also be noted that the term serotonergic drugs continues to be widely (almost universally) misused to include drugs that have little or no proven effect on brain serotonin levels. Almost all review papers containing tables or lists of supposedly serotonergic drugs are riddled with mistakes. Perhaps the most egregious example of this is mirtazapine, about which I have published a pharmacological analysis (4, 5).

 

The pathways involved in the production and control of brain serotonin are well-defined and so are the drugs that affect these pathways. Thus, current pharmacological knowledge indicates that only three types of drug are capable of elevating serotonin sufficiently to be involved in serotonin toxicity:

 

1) All monoamine oxidase inhibitors (MAOIs), (except selective inhibitors of MAO-B, e.g. rasagiline)

2) Serotonin reuptake inhibitors (SRIs). That comprises selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs), and other drugs marketed for different indications which in fact also act as SRIs (e.g. the pain killer tramadol)

3) drugs that act as serotonin releasers (e.g. ecstasy- MDMA)

 

There is no evidence that drugs working by other mechanisms are capable of precipitating serotonin toxicity. Case reports suggesting otherwise are almost certain to be erroneous. A recent case illustrating this, but which is by chance related to the emerging knowledge about metaxalone shows this well (6): for the details of this emerging and interesting story see:

 

http://www.psychotropical.com/index.php/metaxalone-skelaxin-and-st

 

The term ST should be reserved for those cases sufficiently severe to require hospital admission and medical intervention. There will sometimes be debate about whether a given clinical case is most appropriately described as ‘severe’ or ‘atypical’ side effects, or as ‘toxic’ effects. Probably the most relevant and objective criteria is body temperature. That is the main change that mediates the life threatening effects of ST.

 

A key goal of medical management is to predict those cases that may become sufficiently severe to necessitate urgent active intervention to prevent hyperthermia and severe morbidity or mortality. In other cases that are less severe (and do not involve combinations of MAOIs + SRIs) the only action that is likely to be required is reduction or cessation of one or more of the implicated drugs.

 

ST has been clearly characterized as a triad of neuro-excitatory features.

 

1) Neuromuscular: tremor, hyperreflexia, clonus and (in the advanced stage) pyramidal rigidity

2) Autonomic: hyperthermia, diaphoresis, tachycardia and tachypnoea.

3) Altered mental status: agitation, excitement and (only in the advanced stage) confusion.

 

Severe tremor, hyperreflexia, clonus (inducible, spontaneous or ocular), agitation, diaphoresis and hyperthermia are the key signs and symptoms. The Hunter criteria are the benchmark diagnostic rules (2). They demonstrate that if, in the presence of a known potent serotonin enhancing drug (see below for a list clinically significant drugs), spontaneous clonus is present then ST may be reliably diagnosed.

 

Clinically, the onset of toxicity is usually rapid, because it results from drug combinations and starts when the second drug reaches effective levels. The clinical picture is often alarming and rapidly progressive after the first or second dose of the second serotonergic drug in the patient’s regime. The patient is usually alert, orientated, excitable with tremor and hyperreflexia. Ankle clonus is usually demonstrable and as severity increases spontaneous clonus develops (which is sometimes mistaken as seizure activity). Neuromuscular signs are initially greater in the lower limbs, then become more generalized as toxicity increases. Other (early) symptoms may include shaking, shivering often including chattering of the teeth and sometimes trismus. Pyramidal rigidity is a late development in severe cases, and when it affects truncal muscles respiration is impaired. This rigidity causes decreased PaCO2, and a fever of 39ºC or higher heralds life-threatening toxicity.

 

An accurate list of drugs that have been proven to exhibit significant serotonergic potency in humans is most important. A brief table of the such drugs is below, the detailed justification of why particular drugs are included or excluded is contained in other commentaries (see menu), and has been investigated and explained in detail in various my peer-reviewed scientific publications. I have published more original research on this and closely related topics than anyone else (4, 5, 7-14).

Drugs with clinically relevant serotonergic potency Serotonin reuptake inhibitors (selective and non-selective)

 

  • All SSRIs and all SNRIs: Paroxetine, sertraline, fluoxetine, fluvoxamine, citalopram.
  • Venlafaxine (desvenlafaxine), milnacipran, duloxetine, sibutramine.
  • Clomipramine, imipramine (but not other TCAs).
  • Tramadol, pethidine, methadone, dextromethorphan, dextropropoxyphene, pentazocine (but not other opioids).
  • Chlorpheniramine, brompheniramine (but not other anti-histamines).
  • Monoamine oxidase inhibitors
  • Tranylcypromine, phenelzine, nialamid, isoniazid, iproniazid, isocarboxazid
  • clorgyline, methylene blue
  • moclobemide toloxatone, linezolid, metaxalone, furazolidone, procarbazine.
  • Serotonin releasers
  • MDMA (amphetamine?).
 

Table notes:

Clomipramine and imipramine do precipitate ST, but none of the other TCAs are able to because they are too weak as SRIs. Trazodone, nefazodone, mianserin, mirtazapine are neither SRIs nor significantly serotonergic. Also, they do not precipitate serotonin toxicity with MAOIs. Fatalities from ST involving opioids have been documented with pethidine, tramadol and dextromethorphan, but probably not with fentanyl."

 

Please refer back to his website for the relevant references and citations (which are not linked in even the article), I am not going to copy them here.

Thank you for this.

I wonder how it all relates to an individaul sensitivity?

- 12.03.2021- doxepin- 50mg

- 6.11.2020- 75mg

- 16.10.2020- 100mg

- 30.09.2020- doxepin- 125mg

- May 2020, omeprazole 40mg switched to esomeprazole 20mg

- 2012 re-started Doxepin 75mg, evening. Increased to 150mg

- 2012, Atenolol 25mg, twice a day

- 2016, Low dose of HRT in evening, Sandrena and Utrogestan 

- Long term of Nasal spray Otrivine

- 2012, PPI Omeprazole 40mg-evening

24.10.2014- Started ESCITALOPRAM-first 5mg and then 10mg; due to the adverse symptoms reduced on 5.01.2015- Escitalopram- 2.5mg 22.07.2016- re-started reduction by 1% at a time. Completed tappering on  19.03.2020 😇

Link to post
Share on other sites
  • 1 month later...
  • Moderator

I may be talking a country mile here, but - in light of the article I saw today on MIA (Mad In America) that antidepressants actually decrease serotonin - 

 

http://www.madinamerica.com/2015/02/antidepressants-actually-reduce-serotonin-levels/

 

I'm thinking that, other than the liver (serotonin toxicity, as evidenced by Dr. Gillman) 

 

that it really is a serotonin syndrome - a malfunctioning of the serotonin transmitters and receptors and the gap in between, and the gut, and all of those things that produce and are affected by serotonin (which is everything, really).  Not necessarily an "overload" in all cases, which is what is implied by toxicity.

 

Of course, each case is different......

"Easy, easy - just go easy and you'll finish." - Hawaiian Kapuna

 

Holding is hard work, holding is a blessing. Give your brain time to heal before you try again.

 

My suggestions are not medical advice, you are in charge of your own medical choices.

 

A lifetime of being prescribed antidepressants that caused problems (30 years in total). At age 35 flipped to "bipolar," but was not diagnosed for 5 years. Started my journey in Midwest United States. Crossed the Pacific for love and hope; currently living in Australia.   CT Seroquel 25 mg some time in 2013.   Tapered Reboxetine 4 mg Oct 2013 to Sept 2014 = GONE (3 years on Reboxetine).     Tapered Lithium 900 to 475 MG (alternating with the SNRI) Jan 2014 - Nov 2014, tapered Lithium 475 mg Jan 2015 -  Feb 2016 = GONE (10 years  on Lithium).  Many mistakes in dry cutting dosages were made.


The tedious thread (my intro):  JanCarol ☼ Reboxetine first, then Lithium

The happy thread (my success story):  JanCarol - Undiagnosed  Off all bipolar drugs

My own blog:  https://shamanexplorations.com/shamans-blog/

 

 

I have been psych drug FREE since 1 Feb 2016!

Link to post
Share on other sites
UnfoldingSky

Hmm, interesting...

 

I am not too with it at the moment, so maybe this isn't correct either, however they did write this:

 

When SSRIs are added and serotonin levels increase even more, it is actually the brain's own compensatory response to reduce the escalating serotonin levels that improves symptoms in some people. And because the brain's response takes time, that is the reason, they argued, that SSRIs are typically said to take several weeks before they have any positive impact.

 

Which makes me think it probably still is toxicity.

 

After all reactions do often occur immediately when the person takes the drug, and if it takes a while for the brain to start to compensate for the drug and to make changes to decrease serotonin then it still should qualify as toxicity. 

 

I wonder what Dr. Gillman would say?

 

Although, to further muddy the waters I think there'se an article by Joanna Moncrieff somewhere on MIA that details that neurotransmitter levels vary a lot in depression, like they may go up OR down relative to where they were before the "depression" started...Of course I could just be making this up, memory isn't my strong suit. 

 

 

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.

 

Link to post
Share on other sites
  • Administrator

There is no relationship between serotonin levels and depression. If serotonin levels are checked in "depressed" people (whatever "depressed" might mean) -- and that would have to be circulating serotonin, not brain serotonin, which would require drilling into a live brain -- they are all over the map.

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 post
Share on other sites
  • 1 year later...
UnfoldingSky

Bumping this.  I am too spaced out right now to go over this but I found some interesting things on Dr. Gillman's site that I want to put up here when I'm a bit more with it. So this is a reminder to myself...More in a bit...

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.

 

Link to post
Share on other sites
  • 2 weeks later...

Okay I'm back with what I wanted to say earlier.  Hopefully this isn't all just nonsense, my usual "I'm spaced out" caveat applies.

 

Attached to one of his pages you can find a link to videos of specific signs of serotonin toxicity.  There are two videos up, one is a video that is rather creepy to watch in which they show someone who has ocular clonus caused by ST.

 

What ocular clonus is according to this site is a sensation that your vision is bobbing.  However I can't quite figure out if they are implying from what is written there that everyone gets this who has toxicity, and if it's always visible or not. 

 

Personally after my adverse reaction I had serious difficulty focusing my eyes, they felt like they were darting around, though I'm pretty sure I was tested and no one said my eyes were moving in an odd way. I recall looking at them and it didn't seem like they were moving either, however what with the feeling they were it was pretty hard to tell what was what...  In fact for ages after that I had the hardest time seeing things properly in that if  I looked in the mirror I would not register all of my face at once...The same difficulty in seeing the whole of things showed up in some photos I took at the time as there would be problems with the photos, things I did not even see were in them.

 

To some extent I still have this too, though it's much improved over where it was.

 

Now...the second video is more interesting to me.  This other video is one that demonstrates a physical test that professionals are (supposedly) trained to do in order to elicit a particular issue that is a sign you have ST--ankle clonus.  Basically if they do it properly and you have it, your ankle should start jerking.

 

If this test really is that effective at eliciting a known marker for ST, then, it would potentially be of use in the sense that people could ask their doctor to run it if they felt they were  having an adverse reaction that maybe is ST.

 

Oops forgot to put the videos in!  Here we are:

 

http://curriculum.toxicology.wikispaces.net/serotonin_video

 

Also incidentally the eye video is a bit Clockwork Orange, while it's short it might be a bit freaky for those in severe withdrawal. 

 

Lastly can people who are reading here who had adverse reactions post whether or not a doctor did the ankle test on them?  I'd love to know how often it gets used.  I can't say I've ever heard of even one person saying they had this done. No one did this test on me and I can't recall that they checked my temperature either.

 

 

 

 

 

 

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.

 

Link to post
Share on other sites

Well there is so much more of interest on this site I'm half tempted to copy and paste most of it...but I'll try to be a bit selective here.

 

Given he's an expert in ST this is of great interest in quelling the "SSRIs don't cause suicide" agenda:

 

Agitation, suicide and serotonin toxicity

Agitation is a defining mental state characteristic of serotonin toxicity. That fact has implications for the debate concerning the increase in the risk of suicidal ideation and actions with selective serotonin reuptake inhibitors (SSRIs). Clinical experience of SSRIs over many years indicates that some symptoms of serotonin toxicity do occur at usual doses in a few patients e.g. myoclonus, sweating. Occasionally they are so pronounced that even the most determined patient is forced to cease the drug. Nocturnal myoclonus can be so severe that spouses present with multiple bruises. If the neuro-physiological substrate of agitation has anything to do with changes that increase the likelihood of suicidal behaviours that may help to explain this phenomenon (21-28)

 

 

Also, is it just me or has he just contradicted himself?  I thought he had said that it's only combinations of drugs that cause ST, now he seems to be suggesting that one drug in the "therapeutic" dose range can do it...

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.

 

Link to post
Share on other sites
  • Moderator Emeritus

I was taking 100 mg Pristiq and only BP medication and I am sure I had serotonin toxicity from too high a dose.  Symptoms, agitation, irritability, sweating, sleeping a lot.

NEW!!!     INTERVIEW with Altostrata, SA's founder    NEW!!! 

 

Plodding along inch by inch:  12" = 1',  3' =  36 " or 1 yard,  1760 yards  = 63,360" or 1 mile

Current from 27 Mar 2021:  Pristiq 0.295 mg

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 Oct 2015 

My tapering program   My Intro (goes to my tapering graph)  My website

PLEASE NOTE:  I am not a medical professional.  I provide information and make suggestions.

Link to post
Share on other sites

I was taking 100 mg Pristiq and only BP medication and I am sure I had serotonin toxicity from too high a dose.  Symptoms, agitation, irritability, sweating, sleeping a lot.

 

Is that in the supposedly therapeutic range or did they exceed it?

 

Stands to reason too much of just one drug should do it but I swear I just read him state that it's only combos.  Weird.

 

Also did you look up to see if you had an interaction with the BP med that maybe made it worse/caused it? 

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.

 

Link to post
Share on other sites

Okay last few quotes, taken from here: http://www.psychotropical.com/1-introduction-to-st

 

I know this may not interest that many here but, I often find the term "non-linear pharmacokinetics" when reading about drugs, and, thinking it would be too complicated for my poor foggy brain to comprehend I never bothered to look it up.

 

Well seems he made it easy to understand:

 

There is variation between individuals in the susceptibility to various typical side effects, and also the actual blood level (and therefore ‘end-effect’) goes up more rapidly with some drugs than with others as the dose is increased. This is because some drugs have ‘non-linear’ pharmacokinetics (they inhibit their own metabolism, so that their blood level increases out of proportion to the increase in dose — not a desirable characteristic).

 

 

Not that I want more drugs but, if I have to take them for a physical health problem I will be looking into if they have this issue before taking one now.  I think Rx List usually will say if a drug has this issue or not.

 

And also of note, he gets to the point about the term "side effect" and how it's used to minimize primary negative effects of pills..I knew that but it's nice to hear a doctor say it, they so very seldom seem to where I live.

 

NB. The notion of what constitutes side effects (especially for SSRIs) is ‘context-dependant’, because the effects being referred to are an inevitable consequence of the drugs main intended mechanism of action, i.e. reuptake inhibition of serotonin, resulting in increased intra-synaptic serotonin levels. These inevitably cause, for instance, tremor, diarrhoea, retarded orgasm etc. Whether retarded orgasm is regarded as a side-effect or a benefit depends on degree, gender and what effect was sought. The general pattern is that side effects gradually become worse with increasing dose and some may reach a degree of severity which justifies calling them toxic effects.

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.

 

Link to post
Share on other sites

Can't seem to leave this thread...

 

I wonder what Dr. Gillman means by agitation (in the above quote regarding suicide)?  Does anyone speak to him?  Is he meaning akathisia? 

 

I really need to write him...

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.

 

Link to post
Share on other sites
  • Moderator Emeritus

No interaction between perindopril and Pristiq.

 

My diastolic blood pressure went up very high but the doctor never mentioned that it might be the Pristiq.  I can remember that at times my heart felt like it had "flipped".  That doesn't happen any more, thankfully.

 

Pristiq is available in 50 mg & 100 mg.  Found Product Monograph Pristiq (Canada) and testing was done on doses from 50 mg to 400 mg.

NEW!!!     INTERVIEW with Altostrata, SA's founder    NEW!!! 

 

Plodding along inch by inch:  12" = 1',  3' =  36 " or 1 yard,  1760 yards  = 63,360" or 1 mile

Current from 27 Mar 2021:  Pristiq 0.295 mg

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 Oct 2015 

My tapering program   My Intro (goes to my tapering graph)  My website

PLEASE NOTE:  I am not a medical professional.  I provide information and make suggestions.

Link to post
Share on other sites
  • 2 weeks later...

Unfolding sky… I believe agitation that he refers to is emotional reactivity -- like people who end up in the ER and become so agitated they start ripping out their IV's etc. It encompasses physical and emotional distress…

 

From Wikipedia:
Psychomotor agitation
 is a set of signs and symptoms that stem from mental tension and anxiety. The signs are unintentional and purposeless motions; the symptoms are emotional distress and restlessness. Typical manifestations include pacing around a room, wringing the hands, uncontrolled tongue movement, pulling off clothing and putting it back on, and other similar actions. In more severe cases, the motions may become harmful to the individual, such as ripping, tearing, or chewing at the skin around one's fingernails, lips, or other body parts to the point of bleeding. https://en.wikipedia.org/wiki/Psychomotor_agitation

2002 to 2016 Venlafaxine ER 225mg.  2013 TMS treatments triggered nerve pain in face, arm, back.  2016 TMS round ending Feb 1 Central Nerve Pain and and sub-acute serotonin toxicity compounded by Imitrex.  April-June tapered over 3 months from 225 to 0. Reinstated 6/20/16 21.5 nonER 2x day. 7/7/16-37.5mg; 7/17/16-36.6; 7/22/16-33.75; 8/22/16 32.6mg, 9/11/16-28.9mg, 9/25/16-25mg, 12/3/16-19.4mg, 12/18/16-18.5 holding.  OTHER DAILY PHARMACEUTICALS:   *Oxcarbazepine 150 mg 2x/day since mid 2015, *Naproxen 220mg 3x/day as an antidepressant and for pain since 2012, *Levothyrozine 75mcg since 2008 (hypothyroid), *Levothyronine 5 mpg 2x/day since 2012 (hypothyroid) *montelukast SOD 10 mg for asthma since 2014, Advair 250/50 2x daily, [DX 11/16 Felodopine 5mg since 2006,DX combivent 8/1/16] *MEDICAL MARIJUANA for neuropathic pain:CBD oil 25 mg 3-4 x day, THC tincture a few drops: 1/4 tsp 0-3x/day, vaporize CBD for breakthrough pain, CBD concentrate for severe pain.  PRN MEDS *Valium 5 mg PRN up to 4/day for muscle spasms, usually 1-2 x/ day. *Low dose Ketamine nasal spray for severe pain, and also finding 1 dose calms bad WD quickly. HERBAL TINCTURES: burdock, lobelia, turmeric, white willow. CURRENT SUPPLEMENTS:  *Methylated B vitamins, *Vitamin D 5000 iu, Alpha Lipoid Acid, Neti pot. [DX 6/13/16 promethazine suppository + 2 OTC Benadryl for severe pain N Acetyl Cytine for asthma1992-2002, over 20 different psych meds. 2012-2016 Eliminated 7 meds 1 at a time DX Plaquenil DX Spironolactone DX Lunesta, DX Ativan,  + others

Link to post
Share on other sites

Then, on to my reflections on Dr. Gillman's description…

 

 

ST has been clearly characterized as a triad of neuro-excitatory features.

 

1) Neuromuscular: tremor, hyperreflexia, clonus and (in the advanced stage) pyramidal rigidity

2) Autonomic: hyperthermia, diaphoresis, tachycardia and tachypnoea.

3) Altered mental status: agitation, excitement and (only in the advanced stage) confusion.

 

Severe tremor, hyperreflexia, clonus (inducible, spontaneous or ocular), agitation, diaphoresis and hyperthermia are the key signs and symptoms. The Hunter criteria are the benchmark diagnostic rules (2). They demonstrate that if, in the presence of a known potent serotonin enhancing drug (see below for a list clinically significant drugs), spontaneous clonus is present then ST may be reliably diagnosed.

 

I'd like to comment on these in my personal experience. Noting that Dr. Gillman speaks of serotonin toxicity occurring on a spectrum, as does Wikipedia. I believe I had chronic mild serotonin toxicity for years and then "moderate" toxicity for about 6 months of pure  hell.  Currently I continue to have neurotoxic effects from venlafaxine, but am stuck in the slow taper to avoid what can only be described and neurotransmitter and autonomic nervous system chaos of withdrawal.

 

"1) Neuromuscular: tremor, hyperreflexia, clonus and (in the advanced stage) pyramidal rigidity"

I had hyperreflexia as long ago as 2008 -- doctor's would note it on exam. Rubber mallet below the knee -- better jump out of the way my lower leg would fly up! I was told it was a symptom of Lyme disease by one doc and thyroid issues by another.

 

I had chronic muscle rigidity since shortly after I started on psych meds in 1992. And lasting up to this very day. I was told the time that stress had induced fibromyalgia. The stress of my situation was dire, a 3 month hospital stay followed by a 3 month period of being homeless while having severe PTSD and dissociation. I figured my whole health was falling apart. 

The muscle spasms and rigidity escalated this winter with Transcranial magnetic stimulation (a treatment for depression) to the point where every muscle on the right side of my body was in spasm -- completely locked down. Excruciating. This was the beginning of a 5 month period  Jan - May 2016 during which I had severe muscle spasms in various parts of my body daily, continuously along with nerve pain. ******* hell. 

 

The spasms -- especially the ones in my neck (for which I went to physical therapy repeatedly) apparently, according to my current neurologist cause nerve compression, which results in neuropathic pain. Spasms and neuropathic pain go together for me, a daily struggle. I personally believe that venlafaxine is a neurotoxin for me and it's the other way around, but why try to sort that chicken 'n egg? I have to continue to try to get off this poison.

 

I do have fasciculation's and have had them on and off. I have had jerking movements of my limbs -- but was told in 2010 I was "doing that" and to stop "Doing that" by an infectious disease doctor who was vigorously attempting to not treat me for Lyme disease. 

 

"2) Autonomic: hyperthermia, diaphoresis, tachycardia and tachypnoea."

Hyperthermia is a weird one for me.  Since I have hypothyroid my normal temperature is about 96.6ºF (2.8º below normal 98.6ºF)  So when I reach a temperature of 99 -- for me that is having a temperature 2.2 degrees above normal. 100º is 3.2º above normal.  -- So, if a person with a "normal body temperature of 98.6 had a 3.2º elevation in temp it would be 101.8ºF 

During my ordeal this past Jan-May I had temperatures up and down all day long ranging from 96.6 to 100, occasionally to 101. Meaning adjusted temps up to 104.2 if one were to regard my normal temperature as part of the equation.
I had temperatures in the ER --- and I tried in my agony to explain this, but it always went unheard. At least due to my normal low body temperature I wasn't getting near fatal levels, but none the less it was a sign of serotonin toxicity. 

 

Sweating. I started sweating profusely from my head when I started Venlafaxine -- upon any level of exertion.

During the ordeal, I had daily body drenching sweats, explosive heat, shivering cold. Both sweating and feeling chilled simultaneously.  I still get very hot very quickly for no particular reason.

 

Tachycardia. In 2006 I was admitted to the ER for RVOT a heart arrhythmia that can be fatal. It was "idiopathic" meaning no known cause. I was in hospital for 10 days before it got under control with medications. I had the experience of being pulled off the toilet, dragged to bed, and having 5 medical staff surrounding me, one holding the electric shock paddles waiting for my heart to completely stop. Fortunately it did not. 

This ventricular tachycardia went on for over a year, with me needing ever higher levels of meds to control it, until there was no higher level I could safely go to. So I had a cardiac catheter ablation, which I would certify as a form of torture as I  had to lay perfectly still while they burned 21 cigarette size burns in my heart wall every one of which I felt, while being pumped full of adrenaline to make my heart misbehave and enduring excruciating jaw pain and chattering. At least it worked.

 

This year I had bouts of racing heart, that came and went.

 

Oh and i have long QT interval which is a "side effect" of venlafaxine and comes with risk of sudden death. Currently waiting to see a cardiologist in November to see how that is progressing. Perhaps it went away. Perhaps it's worse. No idea. 

 

No awareness of tachypnoea -- but I do practice breath control as a yogi and have used it extensively to calm my nervous system during this ordeal.

 

3) Altered mental status: agitation, excitement and (only in the advanced stage) confusion.

 

Agitation -- oh yes, oh yes, but really I've had that all my life from the PTSD. Raging agitation -- breaking ****, hitting myself. It definitely comes on with severe withdrawal. 

 

Excitement? How about dread? I really thought I was going to die this year. 

 

Confusion. My head hasn't been clear since I started psych meds. And it's slowly gotten worse over the years. I used to be intellectually brilliant. Not boasting,  just truthfully gifted with ease of learning, ease of writing, attention to both global and detail all at once. Creative. Needless to say the situation this year was confusing and my ability to understand and learn about my situation has been very challenging.

 

Regarding Emergency room visits

 

I was in ER three times during this period. In incapcitatingly severe pain, fever (99 - 100), sweating, unable to stand up or walk-- literally falling down in the admissions area, High blood pressure, muscle spasms, (no one tested my reflexes that I recall) I thought it was migraine and neuropathic pain, so that's what I said, they treated it as such and gave me IV benedryl and compazine, a tortuous combination -- unable to sit up from benedryl, unable to stop jerking about with akathesia from compazine. Did stop the pain though. And later benedryl and phenergan (less akathisia), both of which increase serotonin. So though they stopped the pain it ma de the situation worse. My neurologist ended up giving my phenergan suppositories and OTC benedryl as home treatment for times when I felt I should go to the ER. So making it worse and worse.

At any rate, don't count on ER folks to see what's happening. 

 

At least my psychiatrist finally figured it out. 

I write this tale of woe to hopefully shed light on the situation of "moderate" serotonin toxicity and those of you who may be or have been affected by it.

 

Now  during the long slow taper

 

Increase in neuropathic pain means it's time to go down on the dose, as long as the withdrawal stuff isn't too severe. I drop the dosage 10% down, the pain goes down. I get cranky, agitated, wobbly, headache, mild flu symptoms, and then I wait till I feel somewhat better. If a prolonged spike in neuropathic pain comes I'll go down in dose again.
 

I have anger whenever I think of this mess. So I try not to think about it.

 

So this post is going to be followed by a meditative nap.

 

I hope this is in some way useful to someone here. Otherwise it feels like a long self-indulgent complaint. 

 

 

 

2002 to 2016 Venlafaxine ER 225mg.  2013 TMS treatments triggered nerve pain in face, arm, back.  2016 TMS round ending Feb 1 Central Nerve Pain and and sub-acute serotonin toxicity compounded by Imitrex.  April-June tapered over 3 months from 225 to 0. Reinstated 6/20/16 21.5 nonER 2x day. 7/7/16-37.5mg; 7/17/16-36.6; 7/22/16-33.75; 8/22/16 32.6mg, 9/11/16-28.9mg, 9/25/16-25mg, 12/3/16-19.4mg, 12/18/16-18.5 holding.  OTHER DAILY PHARMACEUTICALS:   *Oxcarbazepine 150 mg 2x/day since mid 2015, *Naproxen 220mg 3x/day as an antidepressant and for pain since 2012, *Levothyrozine 75mcg since 2008 (hypothyroid), *Levothyronine 5 mpg 2x/day since 2012 (hypothyroid) *montelukast SOD 10 mg for asthma since 2014, Advair 250/50 2x daily, [DX 11/16 Felodopine 5mg since 2006,DX combivent 8/1/16] *MEDICAL MARIJUANA for neuropathic pain:CBD oil 25 mg 3-4 x day, THC tincture a few drops: 1/4 tsp 0-3x/day, vaporize CBD for breakthrough pain, CBD concentrate for severe pain.  PRN MEDS *Valium 5 mg PRN up to 4/day for muscle spasms, usually 1-2 x/ day. *Low dose Ketamine nasal spray for severe pain, and also finding 1 dose calms bad WD quickly. HERBAL TINCTURES: burdock, lobelia, turmeric, white willow. CURRENT SUPPLEMENTS:  *Methylated B vitamins, *Vitamin D 5000 iu, Alpha Lipoid Acid, Neti pot. [DX 6/13/16 promethazine suppository + 2 OTC Benadryl for severe pain N Acetyl Cytine for asthma1992-2002, over 20 different psych meds. 2012-2016 Eliminated 7 meds 1 at a time DX Plaquenil DX Spironolactone DX Lunesta, DX Ativan,  + others

Link to post
Share on other sites
  • 3 weeks later...

Dr Gillman has interesting things to say about Mirtazapine. He argues that it has no effect on seratonin/noradrenalin and that the data supporting its use as a AD is false. He basically said there is no data supporting seratonin toxicity for Mirtazapine in high doses and therefore the proposed mechanism of action is B***hit. On this basis, any beneficial outcomes are probably the result of the antihistamine effects on sleep - more sleep, feel better than you did before.

I am about to taper off of Mirtazapine, so will be a little more aggressive with my taper percentage and see how it goes.....just unreal how much BS is out there.

I was prescribed Effexor 150 mg for 15 yrs ending 2014 when I titrated slowly down, using Prozac the last month to stop.  The whole titration took about 1 year.  I had been lowered to 75 mg Effexor for the last 3 yrs before the titration began.

I used the counting beads method, and gained great help from supplementling with  Prozac the last month. 

 

In Jan 2016 I began ingesting strong skunk weed, in the form of edibles, and then stopped abruptly July 1, 2016. My daily dose of weed was a dash (spoon size of the measuring spoon I have) daily.   My reaction was acute anxiety.  July 5th I was prescribed Remeron 7.5 mg in the evening and Xanax 1mg twice per day ... 

 

August 4th my Xanax was replaced by Clonazepam .5 mg twice per day as the goal was to titrate, using a longer

acting benzo.  Titration on Clonazepam is expected to begin August 10th.

Link to post
Share on other sites
reachingforthestars

Here's a story of drug toxicity:

 

https://www.madinamerica.com/2016/10/pills-steal-generations-lives/

 

 

The question is how do we know one is having toxic reaction to psyche drug? I was on 40mg Citalopram without side effects for 12 years but last autumn when I came down to 4mg and updosed to 5mg I had similar symptoms of serotonin syndrome. Could it be possible that my receptors have become so sensitized that they just take all in like they have lost the ability to regulate SSRI or serotonin the way they used to and that's why I ended up on toxic levels of serotonin? 

 

Could it be the reason why so many have had a bad reaction to updosing or reinstatement after long hold or being off of the drug for long time

Citalopram 40mg from 2003-2015

Jan 2015 started tapering first dropped to 35mgFeb 30mg, March 25mgApril 20mg, May 17,5mg, June 15mgJuly 12,5mg, Aug 12,5mg,

Sep 0mg for 5 days because of stomac flu and after I raised to 7,5mg. All the symptoms of acute WD shaking, diarrhea, vomiting, barely could walk ect. Still didn't realize that it wasn't only stomac flu but I was also going through WD.

Oct 2,5mg and crashed again badly and quickly raised to 4mg. It was then when I knew my symptoms were due to WD.

Then in November after a month holding on 4mg raised to 5mg due to muscle weakness and had a VERY BAD reaction to reinstatement: akathisia(lasted for one or two weeks), insomnia, anhedonia... Drop quicly back to 4mg, Dec 3mg

Jan 2016 2,6mg( in the middle of Jan after I had been on 2,6mg for a week I tried to updose to 2,8mg and immediately had bad reaction to it: akathisia for a day, andehonia got worse. The next day dropped back to 2,6mg), Feb 2,4mg( a new symptom PGAD lasted 24/7 for 2 months after that on and off), March 2,4mg, April 2,3mg, May 2,2mg, June 2,1mg, July 2,0mg( Pgad almost nonexisting, sleeping pretty good, still some anhedonia but there has been a lot of gradual progress), Aug 1,97mg-1,89mg, Sep 1,88mg-1,49mg, Oct 1,48mg- 1,70mg,

Nov 0,65mg- current dose 0,5mg

 

Link to post
Share on other sites
reachingforthestars

Here's a story of drug toxicity:

 

https://www.madinamerica.com/2016/10/pills-steal-generations-lives/

 

 

The question is how do we know one is having toxic reaction to psyche drug? I was on 40mg Citalopram without side effects for 12 years but last autumn when I came down to 4mg and updosed to 5mg I had similar symptoms of serotonin syndrome. Could it be possible that my receptors have become so sensitized that they just take all in like they have lost the ability to regulate SSRI or serotonin the way they used to and that's why I ended up on toxic levels of serotonin? 

 

Could it be the reason why so many have had a bad reaction to updosing or reinstatement after long hold or being off of the drug for long time

 

Before 1mg updose from 4mg to 5mg I was very emotional like I didn't have filter and just took it all in good and bad and just felt it all very deeply. Long term result from bad reaction has been anhedonia. Experiencing serotonin syndrome or toxicity also make people anhedonic.  

 

Long term result from bad reaction has been anhedonia.

Citalopram 40mg from 2003-2015

Jan 2015 started tapering first dropped to 35mgFeb 30mg, March 25mgApril 20mg, May 17,5mg, June 15mgJuly 12,5mg, Aug 12,5mg,

Sep 0mg for 5 days because of stomac flu and after I raised to 7,5mg. All the symptoms of acute WD shaking, diarrhea, vomiting, barely could walk ect. Still didn't realize that it wasn't only stomac flu but I was also going through WD.

Oct 2,5mg and crashed again badly and quickly raised to 4mg. It was then when I knew my symptoms were due to WD.

Then in November after a month holding on 4mg raised to 5mg due to muscle weakness and had a VERY BAD reaction to reinstatement: akathisia(lasted for one or two weeks), insomnia, anhedonia... Drop quicly back to 4mg, Dec 3mg

Jan 2016 2,6mg( in the middle of Jan after I had been on 2,6mg for a week I tried to updose to 2,8mg and immediately had bad reaction to it: akathisia for a day, andehonia got worse. The next day dropped back to 2,6mg), Feb 2,4mg( a new symptom PGAD lasted 24/7 for 2 months after that on and off), March 2,4mg, April 2,3mg, May 2,2mg, June 2,1mg, July 2,0mg( Pgad almost nonexisting, sleeping pretty good, still some anhedonia but there has been a lot of gradual progress), Aug 1,97mg-1,89mg, Sep 1,88mg-1,49mg, Oct 1,48mg- 1,70mg,

Nov 0,65mg- current dose 0,5mg

 

Link to post
Share on other sites
  • 4 weeks later...
reachingforthestars

Daisy, Your experience when on citalopram was likely due to adverse effects from the medication.

 

How can you know that what Daisy experienced was likely this or that? Serotonin syndrome or wd syndrome cannot be measured but it doesn't mean they don't exist. Noticing the difference between adverse effects or serotonin toxicity also is hard. Maybe an adverse reaction and serotonin syndrome are the same thing? How can you tell the likeliness of what Daisy experienced? Do you have some statistics? 

 

Daisy had kidney issues which indicates to having higher levels of citalopram in circulation bc when kidneys don't function properly citalopram reabsorbs more from the urine to circulation. 

 

About serotonin syndrome:"Serotonin syndrome is an increasingly common adverse drug reaction, which can be life-threatening.[/size]1[/size] Despite the common use of medications with direct or indirect serotonergic effects, many physicians are not aware of the presentation and management of serotonin excess.[/size]2[/size] This is particularly true of less severe presentations of serotonin syndrome, which still contribute to patient morbidity.[/size]3"[/size]

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2464814/

Edited by scallywag
moved from Daisy1's intro

Citalopram 40mg from 2003-2015

Jan 2015 started tapering first dropped to 35mgFeb 30mg, March 25mgApril 20mg, May 17,5mg, June 15mgJuly 12,5mg, Aug 12,5mg,

Sep 0mg for 5 days because of stomac flu and after I raised to 7,5mg. All the symptoms of acute WD shaking, diarrhea, vomiting, barely could walk ect. Still didn't realize that it wasn't only stomac flu but I was also going through WD.

Oct 2,5mg and crashed again badly and quickly raised to 4mg. It was then when I knew my symptoms were due to WD.

Then in November after a month holding on 4mg raised to 5mg due to muscle weakness and had a VERY BAD reaction to reinstatement: akathisia(lasted for one or two weeks), insomnia, anhedonia... Drop quicly back to 4mg, Dec 3mg

Jan 2016 2,6mg( in the middle of Jan after I had been on 2,6mg for a week I tried to updose to 2,8mg and immediately had bad reaction to it: akathisia for a day, andehonia got worse. The next day dropped back to 2,6mg), Feb 2,4mg( a new symptom PGAD lasted 24/7 for 2 months after that on and off), March 2,4mg, April 2,3mg, May 2,2mg, June 2,1mg, July 2,0mg( Pgad almost nonexisting, sleeping pretty good, still some anhedonia but there has been a lot of gradual progress), Aug 1,97mg-1,89mg, Sep 1,88mg-1,49mg, Oct 1,48mg- 1,70mg,

Nov 0,65mg- current dose 0,5mg

 

Link to post
Share on other sites
  • Moderator
https://www.ncbi.nlm.nih.gov/.../PMC24...
National Center for Biotechnology Information
by C Frank - ‎2008 -

It is important to note that symptoms of serotonin syndrome usually present within 6 to 8 hours of initiating or increasing serotonergic medications. The onset tends to be more acute than in a condition such as neuroleptic malignant syndrome, which shares some other features with serotonin toxicity.

 

Serotonin Syndrome is an acute IMMEDIATE reaction to taking to high a dose of ADs ans APs. It does not happen many weeks or months after the fact and it does not happen when reducing the amount of drug taken.

Edited by scallywag
moved from Daisy1's intro

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.

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

Link to post
Share on other sites
reachingforthestars

 

https://www.ncbi.nlm.nih.gov/.../PMC24...
National Center for Biotechnology Information
by C Frank - ‎2008 -

It is important to note that symptoms of serotonin syndrome usually present within 6 to 8 hours of initiating or increasing serotonergic medications. The onset tends to be more acute than in a condition such as neuroleptic malignant syndrome, which shares some other features with serotonin toxicity.

 

Serotonin Syndrome is an acute IMMEDIATE reaction to taking to high a dose of ADs ans APs. It does not happen many weeks or months after the fact and it does not happen when reducing the amount of drug taken.

 

 

"It is important to note that symptoms of serotonin syndrome usually present within 6 to 8 hours of initiating or increasing serotonergic medications." 

 

"Although the exact mechanism of action of SSRIs is not fully understood, it is believed that they inhibit the reuptake of serotonin at the neuronal synapse." 

 

"Cochrane Database of Systematic Reviews, MEDLINE, and Google were searched from January 1990 to December 2006 for articles on serotonin syndrome or serotonin toxicity. Although there are research papers related to diagnosis, there are few high-quality data on prospective treatment. No guidelines or consensus statements have been published for either diagnosis or management. Recommendations were drawn from the literature, but there is minimal high-level evidence, especially in the realm of treatment. " 

 

 

Brassmonkey, you cannot present this as a fact: "Serotonin Syndrome is an acute IMMEDIATE reaction to taking to high a dose of ADs ans APs. It does not happen many weeks or months after the fact and it does not happen when reducing the amount of drug taken." 

 

These drugs can cumulate so in that sense it sounds logic that the reaction doesn't have to be immediate and I guess the reduction can be too small after serotonin syndrome so that one can still be on toxic levels even though he/she's reducing.

 

"The original and revised criteria5,6 for diagnosis of serotonin syndrome emphasize the mental status changes and clinical findings typically observed in more severe cases. As a result, these criteria have been criticized for not highlighting the wider spectrum of toxic side effects that can be seen with this disorder. For this reason, some authors prefer to use the term serotonin toxicity to include findings of earlier or milder cases."

 

 

How to make difference between daily mild serotonin symptoms and daily side effects or an adverse effect? 

 

My opinion is that we just don't know enough about serotonin syndrome but it doesn't mean it doesn't exist. We don't know how these drugs change our brain. But we do know that serotonin syndrome can be very dangerous and lead to death in serious cases. 

 

I don't even know is there accurate data to show how long SSRI stays in ones system? Does it stay much longer if one has renal impairment or is genetically poor metabolizer? Fluexetine which has half-life of 1-3 days have been reported to interact with other SSRI up to 5 weeks after discontinuation. Even single doses of SSRI have been implicated in serotonin syndrome according to the study I linked before. So the variation is enormous. I think it doesn't sound  impossible that one can stay on a toxic level for a long time after discontinuation if she/he is having a lot of symptoms similar to serotonin toxicity since there are no possibility to take any kind of measurements and analyze the levels of serotonin in the brain.   

 

Serotonin receptors regulate the amount of serotonin in the brain and too much serotonin entering --> serotonin syndrome. ( if I have understood correctly.) I wonder is it possible that long term use of SSRI can change the ability to regulate serotonin in the way that receptors became too sensitive after discontinuation and is that the reason why on the second run many find that the reaction to SSRI is so different and can it lead to entering too high levels of serotonin in the brain and serotonin toxicity?

Edited by scallywag
moved from Daisy1's intro

Citalopram 40mg from 2003-2015

Jan 2015 started tapering first dropped to 35mgFeb 30mg, March 25mgApril 20mg, May 17,5mg, June 15mgJuly 12,5mg, Aug 12,5mg,

Sep 0mg for 5 days because of stomac flu and after I raised to 7,5mg. All the symptoms of acute WD shaking, diarrhea, vomiting, barely could walk ect. Still didn't realize that it wasn't only stomac flu but I was also going through WD.

Oct 2,5mg and crashed again badly and quickly raised to 4mg. It was then when I knew my symptoms were due to WD.

Then in November after a month holding on 4mg raised to 5mg due to muscle weakness and had a VERY BAD reaction to reinstatement: akathisia(lasted for one or two weeks), insomnia, anhedonia... Drop quicly back to 4mg, Dec 3mg

Jan 2016 2,6mg( in the middle of Jan after I had been on 2,6mg for a week I tried to updose to 2,8mg and immediately had bad reaction to it: akathisia for a day, andehonia got worse. The next day dropped back to 2,6mg), Feb 2,4mg( a new symptom PGAD lasted 24/7 for 2 months after that on and off), March 2,4mg, April 2,3mg, May 2,2mg, June 2,1mg, July 2,0mg( Pgad almost nonexisting, sleeping pretty good, still some anhedonia but there has been a lot of gradual progress), Aug 1,97mg-1,89mg, Sep 1,88mg-1,49mg, Oct 1,48mg- 1,70mg,

Nov 0,65mg- current dose 0,5mg

 

Link to post
Share on other sites
  • Moderator Emeritus

 

Daisy, Your experience when on citalopram was likely due to adverse effects from the medication.

 

How can you know that what Daisy experienced was likely this or that? Serotonin syndrome or wd syndrome cannot be measured but it doesn't mean they don't exist. Noticing the difference between adverse effects or serotonin toxicity also is hard. Maybe an adverse reaction and serotonin syndrome are the same thing? How can you tell the likeliness of what Daisy experienced? Do you have some statistics?

 

Counterpoints:

  1. Serotonin syndrome is an adverse effect from the medication.
  2. How does the neurologist know what it was -- 4 months after the last dose of citalopram?

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.
1997-1999 Effexor; 2002-2005 Effexor XR 37.5 mg linear taper, dropping same #beads/week with bad results

Cymbalta 60 mg 2012 - 2015; 2016: 20 mg to 7 mg exact doses and dates in this post; 2017: 6.3 mg to  0.0 mg  Aug. 12; details here


scallywag's Introduction
Online spreadsheet for dose taper calculations and nz11's THE WORKS spreadsheet

Link to post
Share on other sites

Do you have a problem  RFTS ?  Yes, Daisy's experience was LIKELY due to adverse effects from the medication. Do you have some statistics ?

Many SSRI's and SSNRI's over 20 years. Zoloft for 7 years followed by Effexor, Lexapro, Prozac, Cymbalta, Celexa, Pristiq, Valdoxan, Mianserin and more - on and off. No tapering. Cold turkey off Valdoxan - end of May 2014

 

                                                  Psych Drug - free since May 2014
.
         

Link to post
Share on other sites
  • Administrator

As I understand it, serotonin syndrome is an acute and potentiallly fatal reaction occurring rather quickly after ingestion of serotonergics, usually a combination of serotonergic drugs but possibly an overdose of one drug.

 

Serotonin toxicity is a lower-grade version of this adverse reaction. We have had many people come here with symptoms of serotonin toxicity over extended periods of time, even years, because their physicians did not identify it.

 

Both serotonin syndrome and serotonin toxicity are adverse reactions or adverse effects of drugs.

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 post
Share on other sites
reachingforthestars

 

 

Daisy, Your experience when on citalopram was likely due to adverse effects from the medication.

 

How can you know that what Daisy experienced was likely this or that? Serotonin syndrome or wd syndrome cannot be measured but it doesn't mean they don't exist. Noticing the difference between adverse effects or serotonin toxicity also is hard. Maybe an adverse reaction and serotonin syndrome are the same thing? How can you tell the likeliness of what Daisy experienced? Do you have some statistics?

 

Counterpoints:

  1. Serotonin syndrome is an adverse effect from the medication.
  2. How does the neurologist know what it was -- 4 months after the last dose of citalopram?

 

 

I had to check the word "an adverse effect". I confused an adverse effect with side effect. It sounded to me that you were saying that Daisy did not likely had serotonin syndrome at all. My point is how can we make difference through internet between an adverse reaction or serotonin syndrome in her case? But now I understand that you only meant that what ever Cindy had it is very difficult to diagnose. I agree.

 

Yes, neurologist cannot know anything about these drugs 100% like no one can. Serotonin syndrome is only diagnosed clinically from symptoms and no labs can measure it( if I have understood correctly). So basically I don't think it is impossible to neurologist to make a diagnosis only by listening symptoms afterwards. Of course it isn't 100% but I guess serotonin syndrome diagnose cannot anyway be 100% sure. Still I believe from my own experience that many neurologist seem to know little bit better about psych meds than most psychiatrists. 

Citalopram 40mg from 2003-2015

Jan 2015 started tapering first dropped to 35mgFeb 30mg, March 25mgApril 20mg, May 17,5mg, June 15mgJuly 12,5mg, Aug 12,5mg,

Sep 0mg for 5 days because of stomac flu and after I raised to 7,5mg. All the symptoms of acute WD shaking, diarrhea, vomiting, barely could walk ect. Still didn't realize that it wasn't only stomac flu but I was also going through WD.

Oct 2,5mg and crashed again badly and quickly raised to 4mg. It was then when I knew my symptoms were due to WD.

Then in November after a month holding on 4mg raised to 5mg due to muscle weakness and had a VERY BAD reaction to reinstatement: akathisia(lasted for one or two weeks), insomnia, anhedonia... Drop quicly back to 4mg, Dec 3mg

Jan 2016 2,6mg( in the middle of Jan after I had been on 2,6mg for a week I tried to updose to 2,8mg and immediately had bad reaction to it: akathisia for a day, andehonia got worse. The next day dropped back to 2,6mg), Feb 2,4mg( a new symptom PGAD lasted 24/7 for 2 months after that on and off), March 2,4mg, April 2,3mg, May 2,2mg, June 2,1mg, July 2,0mg( Pgad almost nonexisting, sleeping pretty good, still some anhedonia but there has been a lot of gradual progress), Aug 1,97mg-1,89mg, Sep 1,88mg-1,49mg, Oct 1,48mg- 1,70mg,

Nov 0,65mg- current dose 0,5mg

 

Link to post
Share on other sites

×
×
  • Create New...

Important Information

Terms of Use Privacy Policy