Editorial Note:  This post by Stevie Lewis raises a very tricky area.  There is no doubt that SSRIs cause movement disorders and not just temporary disorders but permanent problems like atypical Motor Neurone Disorder (ALS), Steele-Richardson Syndrome, Osmotic Demyelination Sydrome (Pontine Myelinolysis) and Multiple System Atrophy.  There is also little doubt that most neurologists have a blind spot for these problems – which is bizarre. 

Various aspects of the roller coaster ride which is protracted SSRI withdrawal have been concentrated on at different times by different campaigners; akathisia, suicide, PSSD. I want to flag up another part of the jigsaw puzzle which doesn’t receive much attention – SSRI induced movement disorders.  You are going to read a bit about my movement disorder, and about Sharron’s and K’s.  You will also see short videos of me and Sharron losing control of our bodies.

Sharron, K and I would like you to share this post and encourage feedback from anyone you know who is an “expert” on the subject:

1. Expert either because he/she has developed a movement disorder after taking or going into withdrawal from an antidepressant. Doesn’t matter if the movement disorder got better – those stories are just as important, particularly any insights on how and why they got better.
2. Or expert because he/she has any thoughts or evidence on what causes some of us to develop movement disorders. And what we might do about it.

Both Sharron and K are still in the acute phase of their journey and need any help and advice that can be given.

My first movement disorder episode occurred in November 2009.  Some time in 2010 I did my first Internet search on movement disorders.  Interestingly, when I put in the same search criteria today “SSRI induced movement disorders”, three of the same papers that I read at the time have come straight up.  Which leads me to believe that not a lot of research has subsequently been done on the subject.  Here are those three;

Leo 1996

Gerber and Lynd 1998

Koliscak and Makela 2003

The writer in the third publication thinks:  “Recognizing akathisia is important because it can be very bothersome”.  Only a dispassionate scientist could put the words “bothersome” and “suicide ideation” in the same sentence.

One reason the incidences of SSRI movement disorders are hard to track down is due to the fact that they are also known in the business as Extrapyramidal Reactions (EPRs). This more recent research (2015) concludes: “Case reports associating serotonergic antidepressants with EPRs continue to be published. Practitioners are advised that monitoring for such is important. Rigorous research efforts are needed to better understand the clinical risk factors for these adverse drug reactions.”  Hawthorne and Caley 2015

It is clear that SSRIs cause movement disorders, if you look in the right places.  Equally it is clear that SSRIs cause withdrawal if you look in the right places, but we know from experience that those who prescribe them are shielded by the system from seeing such reports.  Drug companies, medical journals and medical guidelines have made sure of that.

However, the movement disorder that Sharron, K and I have doesn’t match any described in articles or research on the subject.  We don’t seem to have akathisia, dystonia, dyskinesia, tardive or otherwise, myoclonus or tics.

Stevie’s Story

My movement disorder came out of the blue.  I had been taking Seroxat for just over 12 years, and I had tried and failed many times to withdraw with worsening symptoms each time.  In January 2009 I started on alendronic acid for osteoporosis.  In September 2009 I took 3 metoclopramide tablets.    The first episode was two months later.

The movement disorder starts with a trigger, my muscles tense and tighten and I start to feel afraid.  Then my body doubles up and I lose control as my core muscles and pelvic and buttock muscles jerk violently.  I am continually flooded with waves of fear.  Afterwards I feel in shock, and my gut responds with extreme diarrhoea.  I lost a lot of weight in a short amount of time.

You can see the movements here – Stevie Lewis

Whilst writing this article I found something I had written 10 years ago. I had drawn lightening strikes all over the page.  That is what an episode feels like – constant physical bolts and shocks. It is an entirely physical experience.

In 2013 I decided I had to stop taking Seroxat whatever the withdrawal consequences in the hope that if I did, the movement disorder would eventually go.  In the early days and during the worst years of my withdrawal, the trigger for an episode could be movement (walking, bending, stretching), something I ate or drank, something I smelt or saw or unexpectedly heard, and usually as I was dropping off to sleep. I was routinely jerked and jolted awake and I hardly slept. I can’t give a set amount of time for the length of a jerking episode.  The longest was 7 hours, the shortest 30 seconds and the rest anywhere in between.   Today I am very fortunate that I jerk rarely and if I do it is related to movement or something I swallow.  Medication or supplements are still a trigger.

I have seen 3 neurologists over 5 different visits and ended up with diagnoses of Extrapyramidal Symptoms (EPS), “stress”, Medically Unexplained Symptoms (MUS), Functional Neurological Disorder (FND) and “anxiety”.

From the many stories I have read and my own experience, where neurology is involved the patient’s experience worsens.  Not because they throw additional drugs at the problem, but because they seem wilfully blind to the role that the antidepressant, or any psychiatric drugs may have played in the symptoms presented to them.  The finger is pointed at the person rather than the ingestion of a chemical.  You can imagine them having no problem saying “It’s the heroin you’ve been injecting”.

The third neurologist I saw, when I asked him if he thought that long term use of Seroxat was causing my movement disorder, said “I don’t know about those drugs, it’s psychiatry that knows about them”.  Really?  Someone whose specialism is the nervous system claims not to know about a drug whose intended function is to alter it?

I think it is time that neurology stepped up to the plate and openly acknowledged the number of patients they now see who have developed functional neurological disorders after taking antidepressant drugs. And I think it is important to point out here that, as many people who are prescribed an antidepressant end up on other drugs which are thrown at the many side effects and withdrawal effects that arise, neurology must be regularly seeing patients with what can best be described as chemical toxicity.  Which I suspect goes unacknowledged.

Sharron’s story is next.  My claim that our movement disorders seem identical is based on meeting her, watching her body jerk and holding her as she went through an episode.

Sharron’s Story

I was prescribed Sertraline for ‘low mood’ in 2013 by a psychiatric nurse prescriber from our local Mental Health team. My first prescription was for 50mg of Sertraline and diazepam. The diazepam was for two weeks to settle me into the Sertraline. Over the coming weeks because I felt no better, my prescription for Sertraline was increased to 150mg. Which I continued to take for six years.

My prescription for Sertraline was often given with Omeprazole over the six years.  I later developed gut problems which caused prolonged vomiting and often saw me in A & E. During these bouts of vomiting I was given various drugs to rehydrate and stop the vomiting. They finally settled on Ondansetron, the only medication that would stop the vomiting.

Whilst on holiday in Mexico I started vomiting again and was taken to hospital where I was given Dexamethasone, Ondansetron, Zyprexa, Metoclopramide, Ketoralac and Pantoprazloe.  On my return home various tests, CT scans, X-rays showed nothing that would cause the vomiting.  Months later I concluded Sertraline was causing my problems, so after six years of taking it, I decided to stop. I was unaware of tapering schedules and stopped suddenly.

Within days I developed numbness and tingling in my hands and my body began to twitch and shake. Some weeks after this began my GP decided I should see a neurologist. My GP was adamant withdrawal from the Sertraline was not the cause of my shaking and jerking, saying symptoms of withdrawal usually last only a few weeks.

My GP wrote to a psychiatrist on my behalf to ask if it was possible that my problems were due to Sertraline withdrawal. The reply was No, it was more likely to be my gut causing problems and maybe I should see a gastrointestinal specialist.  I was diagnosed with dyspepsia, no known cause. My appointment with a neurologist concluded I had FND. He was certain it was nothing to do with my sudden withdrawal from Sertraline. My MRI of my neck and brain showed no problems.  I felt very strongly that FND was not the problem and that I was not being listened to.

My gut problems continued after I stopped Sertraline. But in a different way. I had no appetite. The smell of food would start me shaking and my shoulders jerking. When I could eat, I would often start shaking and vomit. This did improve over several months and I was able to eat without vomiting and shaking. The shaking and jerking continued, for months it was a daily occurrence. I struggled to find triggers. In total I have lost 5 stone.

It starts with my buttocks tensing up, I can feel it work its way up my body. Everything tightens up, my arms go rigid, my hands and fingers became distorted, my neck and shoulders tighten, and then like a sudden release, I shake and jerk violently. Often, when the violent jerking stops, I continue to shake. The shaking often goes on for hours and often leads to more of the tense jerking.   During these episodes, I experience extreme fear, terror, panic everything becomes loud and I want to get up and run. I start to cry/sob as my body slowly relaxes again.

You can see Sharron’s movements here – Sharron

For the past year I have struggled with sleep. On occasions my body will tense up and I jerk myself awake. The fear and terror this brings with it is enough to keep me awake along with a tremor/shiver, which is more like something you experience when you are cold rather than the jerking.  This tremor/shiver is external and internal and includes palpitations and heart flutterings. I have since found the cold, pain, sudden noise, or a sudden movement can bring it on. I also have episodes where I cannot pinpoint it to anything.

One year on, I still suffer with the movement disorder. The extreme episodes are more spaced out and not happening as often. But I do not know from day to day how I will be. The longest gap between episodes is about three weeks. During that time, I had sudden jerks, my body tensed but then relaxed without going into full jerking and shaking.  A year on and I feel abandoned by the medical profession. I have been told repeatedly its nothing to do with Sertraline.   My life has changed beyond recognition. I am unable to do the job I loved. I battle daily with the frustration, loss and emotions any sudden illness/disability would bring.”

K’s Story

K approached me via social media having read my story and seen my and Sharron’s videos.

My name is K and I am 51 years old. I went to see my doctor for  help sleeping when my work schedule changed.   He prescribed Xanax .25 mg at night once in a while a few times a month. I never had any problem with that but then he added in paroxetine (Paxil/ Seroxat) without any reason.  I took it for five years as prescribed by my doctor.

Three months after stopping I developed a movement disorder which is still getting worse after two years off the drug.  It happens all day and into the night so I can’t sleep longer than 1 hour because of my whole body jolting and jerking so much with waves of fear.  The symptoms calm down and then come back up in a matter of minutes or hours.  The movement disorder that I have is very like Stevie and Sharron’s – I have seen both their videos and that is what prompted me to get in touch with Stevie.

Five months after stopping paroxetine I voluntarily admitted myself to rehab due to psychosis, and because I couldn’t control my body and mind anymore.

I went to see a movement disorder specialist; he didn’t know what was wrong with me and I was told to go back on the paroxetine.  I made multiple trips to ER and they and the mental hospital treated me like a drug addict and made me feel like I was overreacting.

When my symptoms from withdrawal were so severe I was told the movement disorder look like Parkinsons.  They put me on so many antipsychotic medications I decided to not take any after I came out of the mental hospital. Nobody believed my symptoms are caused by withdrawal not a mental health issue.  I don’t want to be more damaged than I already am.

I never had a mental health problem before taking paroxetine, I never asked for this drug in the first place. Please help me, I really feel like death alive, I have lost all hope and I feel so helpless right now.

Editorial Note:  These movements look choreiform – the point is they do fit inot recognisable neurological patterns.  We are interested to get as much input as possible from people with neurological issues on or withdrawing from any drug – not just psychotropic drug and not just antidepressants.

The expert inputs Managing Efexor and SSRI Withdrawal and Protracted Antidepressant Withdrawal to and comments on H’s case Side Effexor Withdrawal have been wonderful to get and hopefully will be a resource for others.

Helping H

H’s original problem and the idea of a commentary came about because 3 of us considered her case in response to a request she sent to RxISK for a consultation and we all figured this was not a problem that had any easy answers.  Getting and giving H a range of views seemed the best way forward.  It risked leaving her more hopeless if there were no answers, but a recognition of her difficulties and that they are widely shared might help nevertheless.

I’ve seen almost no more correspondence from H than readers of this blog have seen. My sense is that she is a competent woman, perhaps very competent.  Her difficulties getting off Efexor, or anything that happened before leading her to be on it, don’t change my view.

I have known a lot of extraordinarily competent people have problems getting off these drugs – competent here doesn’t mean lawyers, doctors or professionals, although these can be competent too.  It means I have met people who impress me greatly who have had tremendous difficulties getting off and have taught me most of what I know about getting off – or not getting off – from using lower potency drugs, to splitting doses, using liquids and being active.

H is in her 40s. The difficulties in getting off appear worst of all for women in their 40s and 50s, who may have been put on paroxetine (Paxil/Seroxat) or venlafaxine – desvenlafaxine (Efexor/Effexor/ Pristiq) for perimenopausal issues – as a treatment for hot flashes for which these drugs have been promoted. In this case, totally normal women, with no hints of nervous problems ever, can end up suicidal, beyond agitated and in complete disbelief – facing doctors who pass their problems off as depression or anxiety and in need of a tweak to the meds.

Tardive Dependence

Another aspect of what shapes my view is that women in the same age group put on SSRIs for this and related reasons, end up with Persistent Genital Arousal Disorder (PGAD) on stopping.  This is clearly related to withdrawal in some way – it can start on treatment but usually declares itself on stopping.  The discomfort can be so intense it leads women to have ECT, have the nerves to their genital area cut, to injections of botulinum or cholecystokinin or other remedies into their vulva (injections means up to 100 at a time), and clitoridectomy.

There is or potentially is an element of PGAD and PSSD – a tardive element as in tardive dyskinesia – in every withdrawal syndrome and at present we have no answers for this element of withdrawal.

There are almost certainly other tardive components that can happen on treatment – affecting the bladder, gut, respiratory system, peripheral nerves and other parts of the body.

There are things we seem to be able to do if there is no “tardive” element to a withdrawal, but at the moment very little we can do for any tardive elements that may be present.

Central or Peripheral?

My exposure to withdrawal syndromes – including PSSD and PGAD – has left me leaning toward viewing these states as peripheral in origin rather than central.  People tend to worry that these drugs have fucked their brains – and point to very real memory, emotional and other cognitive problems as evidence of this.

These ideas are totally understandable given the heavy marketing of these drugs aimed at creating the impression they go straight to one little spot in the brain and correct a problem there – they don’t.  The serotonin in all of us is primarily in our body not our brain.

It is also not clear to me that withdrawal or at least the tardive component has anything much to do with serotonin.  Fifty years of research has failed to link tardive dyskinesia to the dopamine system on which antipsychotics act, and my hunch is the same will apply to drugs active on the serotonin system.

This seems to have implications for proposals to reduce in decrements of 10% and for hyperbolic rather than linear reductions.  These models hinge on an understanding that we are dealing with rates of separation from the serotonin reuptake site or related receptors, which might hold when there is no tardive element but seem less likely to hold when there is.

So if not serotonin, what?

RxISK has floated ideas about Transient Receptor Potential (TRP) channels/receptors here before primarily in connection with PSSD.

Someone linked to RxISK who cannot get off the SSRI he is on has been doing a lot of digging in this area and we hope to post something more soon about these bits of us that were almost completely unknown when the SSRIs were first launched.

Labels and Guidelines

One of the issues that has featured in comments is the issue of doctors prescribing off label or not keeping to guidelines or not recognising obvious withdrawal. The anger at this runs deep and seems to fit with complaints against pharma companies who push drugs for off-label use.

The actions of doctors like H’s doctors can be viewed with incomprehension.

Part of the problem here is some doctors are, or feel they are, stuck.  There is no drug licensed for the SSRI-induced toxicity that killed Stephen O’Neill – see The Perfect Killing Machine and The Death of Stephen O’Neill.  There are no guidelines for managing H’s or Stephen’s situations.  I don’t want anyone to comment saying there are NICE guidelines or there is a recognition of the problem by the Royal College of Psychiatrists – there isn’t.  There is a certain amount of fig-leafing going on but nothing worth anything to anyone having to live with these problems.

Many doctors who want to treat H or Stephen O’Neill will figure they have little option but to diagnose a case of depression or anxiety and treat accordingly – the complaints H and Stephen voice include depressed mood, anxiety and perhaps even suicidality after all.  Taking matters into their own hands, these doctors feel, could be risky – there are so many people out there from regulators to politicians to guideline makers to bioethicists to most people on Mad in America who will figure going off-label is just about the greatest sin there is.

No guidelines, no regulator, no academic, or senior clinician, no pharmaceutical company is ever going to say – here’s what you can do for withdrawal – other than perhaps mention tapering which doesn’t involve going off label.  Pharmaceutical companies could get sued or fined heavily for recommending anything that shows any originality.

SSRI dependence, withdrawal, addiction, raises profound political problems.  The system knows people with these problems are there – in their hundreds of thousands, perhaps millions – and it would prefer you die rather than recognise the issue and grapple with it.

Those affected find it incomprehensible that those in positions to help just don’t seem to listen – they really wish you would go away.  The surprising thing is “we” never get the message, or see their fingers stuck in their ears.  It needs something more drastic than nice letters or talking to them.

Pain and will power

The tardive point above seems to argue against the will-power, mind over matter, point that has come up in several comments.

It does and it doesn’t.  People who work with pain say that it can be very important for the person affected to recognise that their opioid or other analgesic is causing the problem for which they want more treatment. The same case can be made for some anxiety and depression states.

It’s not just a matter of recognising a particular drug is the source of much of the problem but that the act of turning to any drug can be a problem.  There is something about embracing the pain, or anxiety, or depression without figuring there is a magical solution somewhere that can be a help – this is not the same as mind over matter or of will-power.  I say this as someone who isn’t sure I would be able to deal with significant pain or withdrawal without a stack load of meds.

It is much more intuitive, it seems, to figure there must be something out there that can put this right.  Resigning ourselves to seemingly doing nothing doesn’t seem right – just like staying still in quicksand doesn’t seem right.  But trying to get out of quicksand by doing the obvious thing is what will kill us.

That said, the problems linked to withdrawal may be beyond willpower.  As Annie notes, the desperation of akathisia or PGAD doesn’t leave much room for the exercise of willpower.

Questions

Do you think this lady has Effexor withdrawal?

Yes

Are her “skin” difficulties anything you have come across before?

Skin issues linked to SSRIs yes but not particularly to withdrawal

When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

I don’t know what to do.  The worry is going back on treatment will cause further problems.

Do you see people who can’t increase or decrease?

Yes.  And a lot of doctors see things getting worse as the dose goes up and can’t make the link to an increased dose, leading to the prescribing cascade we see in H’s case.

How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

I’m not sure it does.

What would you do for this woman now?

When the problems get to this point there are no guidebooks.  You want someone you can work with.  This will almost certainly involve someone willing to prescribe off label and willing to give what you think might work rather than what s/he thinks, and maybe even giving something s/he is somewhat against.

There are people who have been helped by drugs I would never give in a million years, and options I can make a good case for that don’t work as well as I think they should. Some options are available in some countries and not others.

PGAD – PSSD

There should be a common interest between people with protracted withdrawal syndromes and those with PSSD and PGAD which represent very clear forms of tardive withdrawal.  Find an answer for PGAD and PSSD and we will likely be able to make a big difference for people stuck in withdrawal also.

How did we get Here?

In the 1980s, companies like GSK ran healthy volunteer trials in which it was clear volunteers exposed to these drugs could have withdrawal symptoms after only 2 weeks on treatment.  The symptoms included anxiety, depression, sexual dysfunction, suicidality, dizziness, gut and other problems.

These drugs were sold as non-dependence producing in contrast to the benzodiazepines.  There were however more reports of dependence/ withdrawal linked to paroxetine in 3 years of paroxetine being on the UK market than there were from all benzodiazepines combined in the previous 20 years. Yet regulators, politicians, guideline makers and others exhorted us to continue taking out pills. We did and now 10% of our populations are on them semi-permanently – they can’t get off.  Worse again, many of these same people claim these drugs are saving their lives because they feel so much better when they start taking them again after a brief stop.

One of the few things that may lead to increased recognition of SSRI withdrawal is a new drug –  there is growing interest it seems to me in the sexual dysfunction and suidicality linked to SSRIs that smells like premarketing for some new compound.

The company will have some experts get up on platforms to talk about the well-known sexual and suicidal problems SSRIs cause which might seem like recognition for people like H.  It won’t be recognition – it will be one last use of her distress to boost the sales of some new compound that will cause its own problems.

H and others concerned about people who are dependent on these drugs will be left barking while the pharma caravan moves on.

The worrying thing is there isn’t more interest at the moment in dependence on SSRIs which may mean that companies know these new drugs will also cause dependence.

Following H’s report of difficulties with Effexor, we asked Will Hall, Altostrata, Bob Fiddaman and Josef Witt-Doerring, all experienced in this area, how they would Manage her Withdrawal.

We also asked Peter Groot who helped develop the first Tapering Strips for Antidepressant withdrawal – who with colleagues has demonstrated that this can help many people – not all – unfortunately not all he would say.

Before answering the questions, all were asked, Peter offered some more general views that have been paraphrased here.

General Thoughts

What does H’s mild depression mean, why the increase in dose, were other treatment options discussed?

How did or can H’s doctor know that her sleep difficulties are not related to the use of Effexor?

Temazepam looks like it was prescribed indefinitely. How does this relate to what guidelines say?

H’s withdrawal was linear tapering as opposed to ‘hyperbolic tapering’, which is predicted to lead to ever larger problems at each following tapering step (1).

When she had difficulties, the tapering should have been halted, regardless of whether the problems she reported were thought to be physical or mental (2).

How many withdrawal symptoms can a patient report without them being recognised as such?

When doctors believe that certain symptoms are not related to withdrawal of a drug and do not report it, the effect will be that in the literature these symptoms will indeed not be related to the drug!  The result is a self fulfilling prophecy!

How do these doctors know, other than their gut feeling that these symptoms are probably transient? Where is the evidence?

In the case of adding gabapentin etc, H’s problem is not that Effexor does not work well enough but that it is causing major harm. Ever more medications to try to solve problems caused with wrongful prescribing of medications in the first place.

Were are the guidelines that support these solutions? If these are not there, what are these physicians doing? What is the difference with African medicine men we use to laugh at?

I don’t know what ‘Movical’ is. It is added to all the other medications in a desperate attempt to solve problems caused by previous medications without knowing if this could lead to yet more problems. This is clear example of a disastrous prescribing cascade causing iatrogenic harm

When H tries to come off again and the skin problems return so quickly (after what is essentially a rechallenge) this is strong evidence that these are withdrawal problems.

If this patient wants to taper, she should be enabled to do this very slowly and in very small steps allowing for proper self monitoring.

A huge problem for H now is that so much damage has been done to her, it is difficult to predict what approach could be successful for her current complaints.

I am not able to give good advice here, other than to do things gradually and – very important – on the basis of shared decision making in which the doctor is honest about what is known and what is not known and is willing to listen to and guide the patient.

In the case of her doctor – she ‘told me that people can experience depression in a very physical way. For example, some people get back pain even though there is nothing wrong with their back. She said my skin feeling was my version of that.’

The patient is told that she has a major depression and this explains her complaints away by saying that the complaints of the patients can occur ‘even though there is nothing wrong‘.  If there is nothing wrong, how can the patient be diagnosed with ‘major depression’?  How is this helpful?

Increasing the dose so quickly:

• is asking for problems, because this goes way too fast, especially given the precious problems the patient had when she tried to taper
• makes it impossible to determine what could be a helpful dose for the patient (if there is one)

Increasing the dose to 375 mg:

• is irresponsible and wrong, given the fact that the patient functioned on 75 mg for 2 years and 150 mg for 8
• What reason could there be to increase the dose to 375 mg? This is iatrogenic damage

In conclusion:

I find this case a very sad example of a prescribing cascade leading to iatrogenic harm, which could have been prevented if her doctors had been willing to listen to her and had taken seriously what she was telling them, instead of relying on beliefs or even prejudices for which there is little or no proof at all, which are often called ‘expert-opinion‘

I hope it will be possible to help her to improve her situation, but I suspect this may take a long time.

Specific Questions

1.     Do you think this lady has Effexor withdrawal?

She suffered from withdrawal at the very beginning. Because the withdrawal was handled so badly, she now suffers from the iatrogenic consequences of overmedication which is the result of a terrible prescribing cascade. This makes it much more difficult to deal with than the withdrawal problems she had at the beginning.

By at the beginning, I mean the moment during the tapering when she experienced the first problems: ‘When I dropped to 75 mg problems started‘. Patients who are currently being prescribed tapering strips or the stabilisation strip we developed in the Netherlands will see that they come with a simple self monitoring form which patients are asked to fill in. We ask them to do this to help themselves and their doctor to guide the tapering.

What they are asked to do is to fill in how they rate there own subjective experiences about possible complaints they might have on a scale of 1 (no complaints) – 7 (severe complaints). They are asked to describe their complaints especially when they are new or when they suddenly become much worse or improve. But they are not obliged to do this. Our primary motivation is to help the patient because we consider this to be more urgent than trying to answer scientifically interesting questions. We explain this is the review which is about to appear  (3).

The reason to ask for subjective experiences is that these are what matter for the patient. Whether their complaints have been recorded previously by other patients may be scientifically interesting but is not the first concern of the patient. As this case demonstrates, making clinical decision based on whether certain symptoms have been reported previously can harm patients. In this particular case doctors have telling the patient fairy tales – that the complaints the patient had had nothing to do with (tapering of) the venlafaxine – without knowing if these fairy tales were true. But my main criticism is that such an approach does not help the patient.

To go back to the tapering. The way we feel this should be done – which is actually in agreement with all the not concrete advice in guidelines and patient leaflets – is to taper at a rate which helps the patient. In this particular case, the fact that this lady was experiencing problems when she reduced the dose from 112,5 mg to 75 mg very strongly predicted that the perhaps still manageable withdrawal problems she experienced would become much worse if she continued to taper further to 37,5 mg and even much much worse after that. Which is precisely what happened.

With the knowledge we have – and already had – this could have been prevented by halting the tapering at 75 mg. Or perhaps by increasing the dose, perhaps even a little bit. And by continue tapering when the patient felt better and up to it. And without prespecifying how long the taper should last. Because we must accept that we are not able – and perhaps never will be – to predict this for an individual patient.

Patients are much better helped if a doctor guides the tapering on the basis of the information the patient provides and by listening to what the patients wants. If that would have happened in this case, a lot of the damage that has now been done could – and should – have been prevented.

2.     Are her “skin” difficulties anything you have come across before?

Complaints from patients when coming off patients can be very different from each other and I doubt if a really good inventory has ever been made. A problem here are circular arguments that are often being used. Doctors who say “that’s not something which is normally reported as an Effexor withdrawal symptom” may be inclined not to ascribe these symptoms not normally reported to (withdrawal of) Effexor. As a result the symptoms may not be reported as a possible side effect. And this will lead future doctors to conclude “that’s not something which is normally reported as an Effexor withdrawal symptom”. Leading to harmful self fulfilling prophecies.

It is my view that the attitude of the medical profession in cases like this should change. Doctor should telling something completely different to their patient: ‘I do not know if your complaints have been reported before, but because you started having them while you were tapering I consider this as a signal that your tapering is going too fast for you’.

This leaves a scientific question open which is not really relevant for the patient in the first place. Because the first concern of the patient is to be helped properly. Such an helpful approach is in strong contrast with what sadly often still happens, where patients are being treated badly on the basis of theoretical considerations and ‘expert-opinion‘, which in this particular this case clearly was not worth very much.

3.     When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

This depends on the situation. The sooner a patient reports complaints, the easier it is to help them. Therefore it is so important that a patient self monitors and reports upcoming complaints during tapering to the doctor as soon as they start occurring. In such cases the advice can be relatively straightforward. The doctor can then ask the patient if the complaints are still bearable and if the patient wishes to stay on the same dose (stabilise) for a while or perhaps to increase the dose again, perhaps even a little bit in order to let the complaints go away. Outcomes will differ depending on the situation and patient, but changes to help the patient are much better if this approach is followed than based on the doctor’s beliefs or prejudices.

The longer a patient waits before asking for help, the more difficult it will become to determine what will be the best approach to continue. Because the more harm will have been done.

Whatever the advice of a doctor will be, it is crucially important that the doctor honestly discusses the uncertainties of different approaches and really listen to what a patient tells and what a patient wants. Clearly, in this particular case none of this has happened.

4.     Do you see people who can’t increase or decrease?

For me this question is too open to give a straightforward answer. Patients differ from each other as do their circumstances. Depending on these circumstances a patient may be able to increase or decrease in certain circumstances and not in other circumstances. Generally speaking we can say that until now tapering has never been done and could not be done properly. Because the medication to do this has never been made available. I think we have changed this by developing tapering medication. We are now gathering data about their use in daily clinical practice from as many patients as we can. And are working hard to publish about this in the near future. I hope this will help us to give meaningful answers to questions like this. But at this point in time I find this difficult.

5.     How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

It fits more or less, but certainly not completely. Things are definitely more complicated than that. For instance, the way people try to come off benzo’s using the Ashton protocol in which very slow tapers are shown to be helpful for some patients, cannot be explained by looking at the receptor occupancy only. The same is true for tapering of fluoxetine, where there are people who experience severe withdrawal symptoms who are being helped by gradual tapering using tapering strips. Which cannot be explained on the basis of receptor occupancy.

It is my strong view that for the time being it is most helpful to leave aside all sorts of theoretical considerations and agree that the most helpful approach for helping patients is to listen to them and to allow them to taper at a speed they agree with.

6.     What would you do for this woman now?

I am afraid I have no clear answer here. I can only hope she finds a doctor who is helpful and willing to guide her in a probably difficult and perhaps long process to recover from all the iatrogenic damage that has been done to her.

References:

1. Horowitz, M.A. & Taylor, D. Tapering of SSRI treatment to mitigate withdrawal symptoms. Lancet Psychiatry 6, 538-546 (2019).
2. Chouinard, G. & Chouinard, V.A. New Classification of Selective Serotonin Reuptake Inhibitor Withdrawal. Psychotherapy and Psychosomatics 84, 63-71 (2015).
3. Groot, P.C. & van Os, J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Therapeutic Advances in Psychopharmacology. Accepted for publication. Preprint available at https://iipdw.org/user-knowledge-psychotropic-drug- withdrawal/. (2020).

To be continued with a final entry next week

H’s nightmare with Effexor withdrawal was laid out in last week’s post.  Experts on antidepressant withdrawal were asked to comment – Will Hall, Altostrata, Peter C Groot, Bob Fiddaman, Josef Witt-Doerring have generously given time to do so.  James Moore, Stevie Lewis and Ed White, administrator for a Facebook venlafaxine withdrawal group, who have substantial international profiles on withdrawal have also added comments to last week’s post.

Most of those commenting have had lives touched by withdrawal. I’ve designated them as experts but they would likely see themselves as ordinary people who have had to grapple with two awful problems – the effects of a drug and a betrayal by the medical profession and the pharmaceutical industry – and they would likely say to any readers going through similar problems that your motivation is more likely to lead to answers than waiting for expertise to ride to the rescue.

The issues in these posts apply to all SSRI and SNRI antidepressants, but also antipsychotics, gabapentinoids and other drugs.  The withdrawal button beside the RxISK blog brings up 50+ posts on withdrawal issues with some on Sertraline and Prozac having hundreds of comments.  RxISK also has a Complex Withdrawal panel with more information.

Will Hall

Will has long been regarded as one of the leaders in the Recovery Movement and researchers on withdrawal. 

A few quick thoughts – skin rash is associated with venlafaxine and is considered very serious; she’s also on a high dose, I think this might need urgent addressing even if the risk and struggle of withdrawal is high given past experience.

She mentions a number of other drugs but it’s unclear whether still on them or not.

Doctors are consistently dismissing the role the drugs might be playing.

Sounds like she is long term benzo user which can have big implications.

Because a drug reaction isn’t reported in the clinical literature doesn’t mean it couldn’t be drug related.

Her self report is very limited and I’d want to know more about the rest of her life. Tolerance of withdrawal, like tolerance of pain, varies widely between people.

People frequently have physical ailments that are best addressed psychosocially – doesn’t mean they aren’t “real” only that we are humans and our entire lives come to play in our physical health.

Because of skin rash being associated with venlafaxine I’d consider it likely this is effexor related even if unusual.

I think the withdrawal process has to be understood and approached specific to the person’s life in general and ways for them to gain greater control and connection; many people have used 12 step and addiction groups for example to endure withdrawal. We know from addictionology and placebo studies that the body is extremely responsive to larger life context and so addressing that could be key, for example, is she alone with this.

1. Do you think this lady has Effexor withdrawal?

Yes

2. Are her skin difficulties anything you have come across before?

Skin problems, akathisia in general absolutely, not sure specific venlafaxine and these specific symptoms, but I consider it plausible

3. When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

I present pros and cons and advise them outcome is unpredictable. She’s on a very high dose right now that would be a concern. She’s gotten bad direction from professionals so I’d steer her towards finding her own leadership in all this.

4. Do you see people who cant increase or decrease?

Yes of course, I don’t know a biological standard for this but it’s consistent with the idea that there are people who can and can’t make changes in life

5. How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

I think the role of the benzos and the sleep suggest to me that there is far reaching toxic impact in her body. nobody is really modeling this bc so complicated and existing models too rudimentary

6. What would you do for this woman now?

With the rash I’d encourage her to consider significant dosage reduction, soon, despite discomfort. The rash is very troubling and would indicate abrupt withdrawal. Then I’d find out more about her life and emotional state and work on gaining more power to ease relaxation and “letting go” during a time of difficulty. I’d work with how to proceed best you can given a life out of control. I’d try to focus on areas of her life where she can get satisfaction and empowerment outside of the drug process. This would then allow the drug process to become more clear, her decision making to get clearer, and to be more tolerable. I’m especially concerned if she is alone and who is on her side, where does she go with her emotional inner world – people often just export all this onto a drug struggle.

Here is a paper I wrote that presents some of my overall learning and how it applies to how we think about drug research.

Altostrata

Altostrata set up Surviving Antidepressants – the best known website for people grappling with antidepressant dependence.  She has probably linked with more people about withdrawal than anyone else.

It’s not common, but we have a cohort of people who got skin symptoms and sensitivities as this woman describes, while tapering or after going off antidepressants. Itching is not uncommon. She may always have had a lurking allergic reaction to Effexor that tipped over when she was hypersensitized by withdrawal.

She should not have continued tapering through “mild” withdrawal symptoms. Continued tapering makes mild withdrawal symptoms worse.

If she had asked me, I might have suggested a reinstatement of 5 beads of Effexor. That is correct, 5 beads. This is to evade the hyper-reactivity that seems to be almost universal in withdrawal syndrome and which she’s already evidenced. We often find a very low dose reinstatement is enough to reduce withdrawal symptoms to a tolerable level; after that, improvement is gradual over months — not days or weeks. To repeat: Very low-dose reinstatement is sufficient. (With SSRIs, particularly paroxetine, I would take the occasion to substitute perhaps 1mg fluoxetine instead.)

Currently, she clearly is suffering from an unnecessary but typical prescription cascade from her psychiatrist. Her current symptoms (Effexor and Lyrica?) may be an allergic reaction to any one or a combination of her drugs, or it could be a universal hypersensitivity reaction to the absurdly high doses of all of them. To find out which drugs are causing the problem, I would ask her to submit a daily diary over several days including when she takes each drug, the dosage, and her symptoms after each dose.

If it’s a single drug causing the reaction, symptoms will be more severe shortly after taking the dose or at peak plasma. To find a drug-drug reaction, I would map the P450 cyp requirements of each drug she’s taking.

She didn’t say how much Lyrica she’s taking, but I’ll bet it’s a lot. As she observes, it causes constipation. If she weren’t taking an unholy amount of Effexor, it’s likely a lower amount of Lyrica would help her sleep. As this woman observed, Effexor always interfered with her sleep.

My guess is that gradually reducing Effexor will help quite a bit. She may have to cope with “psychological” symptoms. I imagine she feels terrible physically and will be further traumatized when she realizes the drugs are making her sick. Feeling “depressed”, angry, helpless, and betrayed in these situations is a normal reaction.

So, overall, she’s overdrugged by a typical psychiatrist who thinks more is better and all the patient’s complaints are due to “depression”. As ever, I am disgusted and appalled at the utter cluelessness of a profession that throws psychotropics into people with wild abandon.

Would like to point out that very low dose reinstatement for post-discontinuation withdrawal symptoms conforms to theory underlying hyperbolic taper. As demonstrated in the SERT occupancy literature, you don’t need a lot of drug for partial receptor occupancy.

Shapiro, Bryan B. Subtherapeutic Doses of SSRI Antidepressants Demonstrate Considerable Serotonin Transporter Occupancy: Implications for Tapering SSRIs.

Psychopharmacology 235, 9 (2018): 2779–81. https://doi.org/10.1007/s00213-018-4995-4.

Bob Fiddaman

Bob Fiddaman is a wee known SSRI activist. Over the years, The Fiddaman Blog has discombobulated the UK regulator and many others and his account of withdrawal from Seroxat/Paxil in The Evidence However is Clear shaped perceptions of the problem – See Here. 

I suspect we may all have different opinions but I write these down as someone who has gone through a 19 month taper of Seroxat (Paxil) and three month period of cold-turkey.

1. Do you think this lady has Effexor withdrawal?

Yes

2. Are her “skin” difficulties anything you have come across before?

Absolutely. ‘Skin-itching’ is otherwise known as ‘crawling skin sensation’, which is a classic symptom of akathisia.

It’s sometimes difficult to explain. I’ve read many first hand accounts where people describe it as small worms crawling under their skin.

Even the National Alliance on Mental Health (NAMI), who are a pharma funded organisation, admit this. They write:
“The symptoms you are experiencing could be due to your medication. These types of symptoms are consistent with a side effect referred to as akathisia. Those with akathisia experience an inability to sit still and a constant urge to move. Due to a feeling of inner restlessness, a patient may experience fidgeting, pacing, rocking while standing or sitting, crossing and uncrossing legs while sitting, and constant movement of the feet. Patients have also described these feelings as “wanting to jump out of my skin” and as a “crawling skin sensation.” ~ https://www.nami.org/FAQ/Mental-Health-Medication-FAQ/I-have-recently-started-a-new-drug-I-have-been-ha

3. When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

This is a good question and, for me at least, very difficult to answer as I am not a healthcare professional. Do we tell a heroin addict going through cold-turkey to take a shot of heroin if their withdrawal gets intolerable? The advice I normally give is to taper at your own pace and not at the pace of what a prescribing physician tells you  to. I use the mantra, ‘Your body, your rules’.

4. Do you see people who can’t increase or decrease?

Decrease, yes. In my experience of increasing the dose after an initial drop, the withdrawal effects seem to disappear. Decreasing is a whole different ball game because the only crutch one has is to go back to the original dose. When a person increases, it, in essence, gives the brain what it wants because the prior dose was ‘wearing off’, or rather ‘losing its strength’. There’s a train of thought on kids who smoke weed – On first trying weed, one may get a high after four or five ‘tokes’. As they become more experienced in smoking weed, those four or five tokes barely make a dent – so they take more draws until they reach their ‘high’. – Eventually they can smoke a whole joint, then two, three, four etc. In other words, a drug doesn’t have the desired effect if a person stays on the same dose, although I’m still baffled at what a ‘desired effect’ is when it comes to drugs like Effexor.

5. How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

As I said, ‘Your body, your rules’. Nothing is set in stone regarding drug withdrawal. The 10% rule is merely a guidance. I, myself, came down ultra slowly because 10% would have been too drastic for me to tolerate. A smoker who smokes 40 cigarettes a day and wants to quit, may jump to just 20 a day – this would be too much of a drastic drop. He may then try 30, or 35 a day and still find he struggles. Cutting down to 39 a day for 7 days, then 38 a day for 7 days may be the only way he can beat his reaction to nicotine craving. This is basically the rule I used when tapering from Seroxat (Paxil)

6. What would you do for this woman now?

The electric zaps she is experiencing are what I have also experienced. I found a way to combat them – worked for me but may not work for her.

First, in my experience, it’s best to taper during the colder months of the year – for some reason my withdrawal was worse in the summer months – I can’t quite put my finger on this, I just know it was easier during the winter.

Second, drink lots of water – I drank up to 8 pints of water a day – this may be a placebo effect – I told myself I was flushing out poison.

Thirdly, if at all possible, go for walks, really push yourself – wear loose clothing and focus on what’s in front of you. Turning your head during withdrawal can be problematic as it can cause visual problems, dizziness and a nauseous feeling.

Finally, when the zaps start run a bath or sink of cold water, the colder the better. Place a large towel in the bath, wring it out then wrap it around your head like a turban. This, for me at least, gave me immediate relief. Also, running cold water on your wrists (the pulse part).  There is something about the cold that helps. Has any study ever shown the brain to be hotter during any kind of drug withdrawal?  This may be why it’s easier, for some, to taper during the winter months.

Josef Witt-Doerring

Josef is a medical doctor who in 2018 had a feature on the front-page of Psychiatric Times with an inside spread on Antidepressant Withdrawal and the need to listen to patients and patient groups – astonishing views to see expressed in the heart of US psychiatry.  

1. Do you think this lady has Effexor withdrawal?

I believe this lady has a tardive (late onset) and chronic sensory disorder likely caused by Effexor. The descriptions of the sensory disturbance sound partially similar to akathisia and restless leg syndrome (minus the confinement to the legs of course). The sensory pain in those conditions appear to match what this woman is describing: a hard to explain, deep scaly, crawling, agonising sensation. It has become more recognized recently that antidepressants have the potential to cause these types of disturbances – tardive sensory problems.

The onset of the sensory difficulties also fits a pattern common with tardive syndromes caused by long term use of certain monoamine modulating drugs (antipsychotics and antidepressants) : onset during withdrawal and persistent for many months after discontinuation and thankfully for this lady partial remittance on reinstitution of treatment – there are reports of these syndromes persisting despite reinstitution of the causative drug.

2. Are her “skin” difficulties anything you have come across before?

I haven’t heard about the red-pin spots before as being a common symptom directly stemming from these tardive syndromes, but I have heard of emergent drug sensitivity (such as with antibiotics). If this isn’t simply a symptom of these tardive syndrome I’m yet to encounter, it may be worth looking for other exposures in her environment which, did not precipitant skin reactions in the past but may now be doing so. Perhaps, other drugs, laundry detergents etc.

3. When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

Hard to say. Depending on the experience during the withdrawal. If for example there was absolutely no improvement in 6 months, that appears to me to be a reasonable sign that the condition may be permanent. E.g the body does not appear to be capable of correcting whatever biological aberration that has been induced.  If there was a trend towards improvement, but the withdrawal failed due to the enduring difficulty of the symptoms, despite slight improvements, then I would be more hopeful in re-attempting withdrawal again in the future at a much slower pace. Additionally, in conditions such as Tardive dyskinesia which can often be permanent, old age can be a poor prognostic sign for recovery, I would be more encouraging in younger patients than older ones in reattempting withdrawal with the hope of cure. Also, the level of support someone has would be important in gauging how well they would tolerate another withdrawal.

4. Do you see people who can’t increase or decrease?

I’ve read many cases and heard from many individuals first-hand about being unable to decrease without severe symptoms. However I have not read cases like this where even dropping half a pellet from a very high dose — 375 mg, causes symptoms to emerge, typically these small drops only cause problems at the lower end of tapering.

5. How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

A good question. The idea behind reducing dosages in increasingly small amounts in order to drop receptor occupancy in a controlled linear fashion is that it will give the brain a greater chance to modulate receptor expression/sensitivity as previously modulated synaptic neurotransmitter levels return to normal. This is intuitively appealing and does appear to be the experience of many people who taper of psychiatric drugs – smaller drops confer better chance of success and reduced severity of withdrawal symptoms.

The problem here that I can see is that there does exist tardive syndromes which simply don’t improve, regardless of the time that someone is off the drug: Tardive Dyskinesia being the paradigm. Although it is very bleak and disheartening, I think there might need to be a place where some, after attempting to discontinue for long periods of time, might have to come to the conclusion that the problems will not go away. In these cases, hopefully reinstitution of the drug can improve these symptoms.

6. What would you do for this woman now?

There appears to be two options: One which manages symptoms and one which tries to cure the condition.

1)    Symptomatic Management:
Persist with the Effexor which is at least masking the sensory disturbance and work on finding a combination of therapies: pharmacologic and others which allow this lady to live as comfortable as is possible.

2)    Curative:
Proceed on the assumption that a long taper of miniscule decreases might allow this lady to come off the medication. Liquid formulations might be useful for titration, switching to fluoxetine might be useful as it could have less inter-dose fluctuations given the long half-life. Although given this patients demonstrated sensitivity to even minuscule changes in Effexor dose, this sounds frightening to attempt.

There would likely need to be pharmacologic and other therapeutic treatments to be used regularly and as needed if the withdrawal symptoms are severe during the taper.

Both are hard choices, with 1 there is always a chance the symptoms might break through in the future necessitating higher and potentially more dangerous doses of Effexor to suppress them, and with 2 there is a chance it may not work, or simply be too be excruciating.

Both plans would need a knowledgeable doctor who can be flexible as treatment proceeds. The worst-case scenario would be getting treated by someone who simply throws meds at her off an algorithm or writes these symptoms off as hysteric manifestations of her depression.

The picture above comes from Heather’s Life Moments – created by Heather to reflect her hell coming off Paxil.  Like H in this post, Heather appears to have been on a road to a prescription cascade.

To be Continued with 2 more posts…