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Papers about prolonged antidepressant withdrawal syndrome

25 posts in this topic

Int J Neuropsychopharmacol. 2007 Dec;10(6):835-8. Epub 2007 Jan 16.

Effects of gradual discontinuation of selective serotonin reuptake inhibitors in panic disorder with agoraphobia.

Fava GA, Bernardi M, Tomba E, Rafanelli C.

 

Affective Disorders Program, Department of Psychology, University of Bologna, Bologna, ItalyDepartment of Psychiatry, State University of New York at Buffalo, Buffalo, New York, USA.

 

Abstract at http://www.ncbi.nlm.nih.gov/pubmed/17224089?dopt=AbstractPlus

 

The aim of this investigation was to explore the prevalence and features of discontinuation syndromes ensuing with gradual tapering of selective serotonin reuptake inhibitors (SSRIs), in optimal clinical conditions in patients with panic disorder and agoraphobia. Twenty-six consecutive outpatients met the DSM-IV criteria for panic disorder and agoraphobia while taking SSRIs. Twenty remitted upon behavioural treatment. Antidepressant drugs were then tapered at the slowest possible pace and with appropriate patient education. Patients were assessed with the Discontinuation-Emergent Signs and Symptoms (DESS) checklist 2 wk, 1 month and 1 yr after discontinuation. Nine of the 20 patients (45%) experienced a discontinuation syndrome, which subsided within a month in all but three patients who had been taking paroxetine for a long time. Discontinuation syndromes appeared to be fairly common even when performed with slow tapering and during clinical remission. In some cases disturbances persisted for months after discontinuation.

 

Full text at http://www.mediafire.com/?x681dok5v8er6kl

 

 

My comment:

 

Dr. Fava's research found that 9 of 20 patients systematically tapered off SSRIs suffered a discontinuation syndrome. Most resolved in a month, but 3 patients, or 15%, who happened to be long-time Paxil users, had persistent withdrawal symptoms evident at an assessment one year post-withdrawal. There were also 2 withdrawal syndrome sufferers who "relapsed." (Also see http://www.medicalnewstoday.com/releases/94224.php.)

 

This is the longest any published studies have followed unmedicated patients after withdrawal.

 

(Again, in this study, the highest and most severe incidence of withdrawal syndrome were in patients taking Paxil.)

 

About the tapering method used in this study:

 

"....Tapering of antidepressant drugs was performed at the slowest possible pace (50 mg every other week for fluvoxamine and sertraline, 10 mg every other week for paroxetine, fluoxetine and citalopram, with 10 mg every other day in the last segment).

After 15 d from discontinuation all patients were assessed with the Discontinuation-Emergent Signs and Symptoms (DESS) checklist (Rosenbaum et al., 1998). This allowed a comprehensive collection of all manifestations of discontinuation syndrome since some may become evident only in the second week...."

 

Given the dosages the patients were taking, tapering off took a month at most. 4 out of 9 of those taking paroxetine developed withdrawal symptoms.

Edited by Altostrata
added tapering information

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A documented case of prolonged withdrawal syndrome.

 

Can J Clin Pharmacol. 2006 Winter;13(1):e69-74. Epub 2006 Jan 23.

Persistent tardive rebound panic disorder, rebound anxiety and insomnia following paroxetine withdrawal: a review of rebound-withdrawal phenomena.

Bhanji NH, Chouinard G, Kolivakis T, Margolese HC.

 

Source

 

Clinical Psychopharmacology Unit, Allan Memorial Institute, McGill University Health Centre, Montreal, QC.

 

Abstract and full text at http://www.ncbi.nlm.nih.gov/pubmed/16456219 Full text here.

 

OBJECTIVE:

 

To describe tardive rebound anxiety phenomena (panic, anxiety and insomnia) following abrupt paroxetine discontinuation.

 

METHOD:

 

Case report, with comprehensive literature review on rebound and withdrawal phenomena associated with psychotropic medications.

 

RESULTS:

 

Three different discontinuation syndromes with psychotropics are described: (1) new-onset CNS-depressant type withdrawal symptoms (minor and major); (2) rebound syndromes; and (3) supersensitivity symptoms. Abrupt paroxetine discontinuation has been well described and fits the first category. Tardive rebound panic disorder-phenomena with paroxetine has some features of the supersensitivity category.

 

CONCLUSION:

 

Chronic paroxetine treatment may lead to 5-HT2-receptor down regulation, with desensitization of 5-HT1A and 5-HT2 receptors, which may contribute to tardive rebound symptoms upon abrupt withdrawal. Early reports suggest that genetic factors may also contribute to withdrawal symptoms in susceptible individuals. Cholinergic rebound may also occur and could explain tardive insomnia and anxiety in paroxetine withdrawal.

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Psychiatry on-line. 2003.

Persistent adverse neurological effects following SSRI discontinuation (PANES).

Green B.

 

Available at http://www.priory.com/psych/panes.htm

 

Dr. Ben Green collected 5 cases of prolonged withdrawal syndrome, which he called Persistent Adverse Neurological Effects (PANES).

 

This paper contains a link to another report, a letter "Venlafaxine - long term adverse effects" on difficulty withdrawing from venlafaxine, probably from 2002, at http://www.priory.com/psych/venlafax.htm

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I emailed him as he practices in my home town but he never replied

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I got the impresion he wasn't interested

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Squirrel, how frustrating!

Did you ask him outright about whether he's taking new patients (or whatever the protocol is in the UK)? I ask because I know in my low-energy state, it's very easy for me to take "no" for an answer. Maybe he could at least give you a referral?

 

I have been frustrated by how difficult it can be to get knowledgeable professional help. Well, without paying a small fortune.

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2006 Correspondence from Dr. Richard Shelton about prolonged withdrawal syndrome

 

Subject: RE: Antidepressant discontinuation syndrome

Date: Sat, 22 Jul 2006 14:31:17 -0500

From: "Shelton, Richard" <richard.shelton@[e-mail]

To: [altostrata]

 

Sorry for the delay - I have been away at a scientific meeting.

 

I actually think the discontinuation syndrome is pretty bad in some situations and truly horrible in others. Hence, why participated in a scientific focus group that wrote a series of papers teaching docs about the problem (appeared in the Journal of Clinical Psychiatry).

 

First, let's acknowledge one thing: there is a great deal of variability in response, with a lot of people experiencing bad symptoms and others little at all, but almost all resolve; that is, except for a very small group, where the symptoms become persistent. At the core, the variability is related to genetic (actually, more correctly, genomic) differences between people (one of our areas of research).

 

The receptors do down-regulate. In fact, the reaction of the majority of people is consistent with down-regulation. That is, there is an adaptation that occurs in the receptor (actually phosphorylation) that makes it less responsive to serotonin. This, by the way, is probably the serotonin 2A type receptors. When the adaptation occurs, it takes about 10-14 days to re-equilibrate (to de-phosphorylate). The receptor returns to normal, along with related proteins (like the serotonin transporter protein). That is how they work.

 

The variation between people is probably due to genomic variations in the genes coding for proteins involved in this process. However, regardless of the situation, in the average circumstance, the re-adaptation eventually occurs. This is why it can be protracted in some situations. However, even in that situation, there is a limit in time.

 

So, why do some people have these very long effects? There may be several potential causes. For example, it is possible that something has happened to destroy some neurons - either the ones containing serotonin or the others that they connect to.

 

In fact, there is a research literature that says exactly that. However, all the studies have been in cells in culture and have one essential problem that invalidate them (sorry for being so direct). The concentrations used to achieve the toxic effects are a two orders of magnitude above what can ever be found in human tissue - that is, the concentration is 100 times as much as can ever be achieved in humans. Typical concentrations don't do that. This, then, falls into the category that too much of anything is toxic (first postulated by Paracelsus in the 16th century, I think). So, too much water, salt, sun, etc., etc.

 

In fact, a strong effect of antidepressants (including paroxetine) is the opposite - that is, preservation of neurons by stimulating the production of brain derived neurotrophic hormone, and another hormone, bcl-2. Both stimulate the growth of new tissue and preserve the health of the living cells.

 

So, what then? Let's go back to our premise: The discontinuation effect is truly horrific in some people. The direct mechanisms involved in the genesis of the problem can't really be involved in it's persistance. So, what's up with that?

 

In fact, there are long-standing adaptations that can take place in the nervous system. However, as with most things in the body, the problem is a variation of a normal process (otherwise, it wouldn't be there in the first place).

 

There appear to be lots of variation in this reaction in people who develop persistent symptoms, but one salient feature that seems almost invariably present: They become intensely afraid during the experience. People may describe this in different ways, but the way the brain is reacting is an exaggeration of what the brain does during threat. The physical symptoms are consistent with that.

 

So the "threat" systems are "turned on" and don't "turn off" easily. This can happen in a few ways, but has to occur pretty fast.

 

In fact, it is a normal response. Think of a mouse living in a field somewhere. If there is an acute threat that occurs (e.g., chased by a cat) and the mouse escapes, the mouse's brain has to remember that and react. There are a couple of ways to do that. One is to synthesize proteins to "remember." That, actually, is slow (but happens). The second is to actually do something to the genes controlling the system itself: to induce chemical modifications to the genes or the supporting structure to activate some genes and inactivate others. The net effect is for the system to stay "on" so to speak. However, in this situation, it is purely adaptive.

 

Going by the principle, then, that people vary in their response, some people seem particularly prone to have this to occur. That is why when people are exposed to a life threatening situation, some go on to develop post-traumatic stress disorder, and others don't. Now, one important thing is that most people develop trauma related symptoms immediately after an event (e.g., insomnia, dreams of the event, anxiety, etc., etc.). In the normal situation, these symptoms resolve within a month. But some people develop long-standing responses, in which the system is turned "on" and they can't turn it "off." I think that is what is at play here.

 

People might ask, "why then do I still have some of the same symptoms?" The answer is related to the longer-term synthesis of new proteins. What happens is that the brain activates the pathways associated with that symptom (e.g., electrical sensations in the body), and it stays on. It is like a kind of memory, so to speak. But one that reactivates the sensations.

 

That is the basic story. The question, then, is what's next? There are a few ways to potentially deal with the problem. First, you could use something to directly suppress the symptoms - really not great, but often effective. Drugs related to Valium (e.g., Xanax) activate neurons related to a chemical in the brain called gamma amino butyric acid (GABA). That is an inhibitory transmitter, which can suppress the symptoms. However, it only works when it is present, and the body adapts to it with time, producing physical dependency - not ideal.

 

Another way is to use another serotonin uptake inhibitor antidepressant (probably one with a long half life). Most people don't want to do that since they believe that the first one was toxic (which, as I've described, is untrue). Serotonin is a regulatory chemical in the body, and in the stress-emotional system its primary role is inhibitory. So, it suppresses the activity of the neurons that are "turned on," suppressing the symptoms. In most (but not all) people that will work. It is an acceptible alternative.

 

Given that the mechanism involves "memory," then information processing is important. So, certain forms of cognitive behavioral therapy seem to be effective in reducing the symptoms, at least to a manageable degree. I like that option. It has to start with several ideas - your brain has not actually been "damaged;" the symptoms are not life-threatening; etc. However, a good cognitive therapy may be able to help.

 

A lot of therapists say they do cognitive therapy; however, most who do so are not really compent at the treatment. I'd advise going to the Center for Cognitive Therapy website at the University of Pennsylvania (http://www.uphs.upenn.edu/psycct/). There is a referral list at the bottom of the page (it goes to this site: http://www.uphs.upen...rral/states.htm, where you can look up your state to try to find a therapist). If you have the choice, someone that specializes in anxiety disorders is the place to start.

 

Best of luck,

 

Richard C. Shelton, M.D.

James G. Blakemore Research Professor

Department of Psychiatry

Vanderbilt University School of Medicine

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Best of LUCK?!?! Seriously, he said that??

Did he advise about the rage that surfaces? Some CBT to quell those emotions.

Is he also saying that there are 'neuroprotective' factors at work that override the damage (but we're not calling it that)?

He is going to do WHAT with this information??? List it on his CV to look like he's doing something about the neuronal death occurring? Oh, no, that's in vitro.

I love the part about 10-14 days to correct phosphorylation.

What might Dr. Shelton say about the risk:benefit ratio?

Scary.

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I like the Lathe report (linked from Green, I think). 'Duration of treatment (8 months) is longer than any clinical trials...treatment should last max of 6 months.' (Paraphrasing)

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Also see Healy 2001 testimony about prolonged withdrawal syndrome

 

In testimony for UK courts, Dr. Healy says he has seen patients with withdrawal symptoms three months after discontinuation of Paxil, cautioning against this serious adverse effect, at that time denied by its manufacturer.

 

I regret that I am under a confidentiality order in regard to this material and am not able to disclose it to this appeal. However, I can confirm, and am prepared to testify to the substance of the points raised in the following exchange (in my testimony in Tobin v SmithKline) between Mr Charles Preuss, the attorney for SmithKline, and myself.

 

Healy: Yes, but there's a withdrawal syndrome from Paxil, including agitation, abnormal dreams and nightmares that comes through in spades in these healthy volunteer studies.

 

Preuss: You're saying Paxil is still active for three months?

 

Healy: In up to 80 percent of the volunteers on this drug for only two weeks produces withdrawal syndromes in these healthy volunteers. I'm saying in my clinical experience I've seen people on this drug for short periods of time and I've seen them have troubles three months later, yes.

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Taylor D: Truth withdrawal, Open Mind (National Association for Mental Health, London E14), September/October 1999, 16

Truth withdrawal

DAVID TAYLOR EXPERIENCED SSRI WITHDRAWAL

- IT'S NOT QUITE LIKE THE STANDARD TEXTS SAY

 

The most recent edition of the British National Formulary states that withdrawal of some antidepressants, the newer specific serotonin reuptake inhibitors (SSRIs), for example, can cause headache, nausea, paraesthesia (tingling or numbness in the extremities), dizziness and anxiety. That doesn't sound too bad does it? Other standard texts assure us that antidepressant withdrawal syndrome is usually mild and short-lived. Even better, you might say.

 

While this advice is more or less true, it gives us almost no insight into the reality of withdrawing from antidepressants. I know this, not because I have read about it, but because I speak to people every day who are going through it and, perhaps most importantly, because I have experienced antidepressant withdrawal myself.

 

The real truth is that, for many people, antidepressant withdrawal syndrome is neither mild nor short-lived. For six weeks or so, I suffered symptoms which were at best disturbing and at worst torturous. This was despite following a cautious, decremental withdrawal schedule. Whilst I did not experience headache or paraesthesia, the severity of other symptoms certainly made up for it. The dizziness I felt varied from a slight wobbliness to a frightening inability to stand up without support. For most of the time, I could not turn my head without inducing a paralysing nausea. Alongside this, I endured a more-or-less continuously pounding heartbeat and a close facsimile of influenza. When all of this subsided, I was short-tempered and moody, and remained so for a further two weeks or more.

 

None of my conversations with others who have withdrawn from antidepressants leads me to believe that my experience is unique or even unusual. In fact, this severity of symptoms seems to be par for the course with some drugs (for example paroxetine and venlafaxine). Older tricyclic drugs are often very toxic and have lots of side-effects, but they don't seem to induce such severe reactions on stopping them (I have experience of this, too).

 

So why isn't this problem more widely appreciated? Why do clinicians continue to tell people that withdrawal symptoms are mild and really nothing to worry about? Maybe it's because there is a tendency for clinicians to want to believe that new drugs are innocuous panaceas. We would do well to remember that Valium and Ativan were long felt to be the answer to almost every problem. And that Prozac and similar drugs are still widely held to be the perfect cure for just about any mental health condition you care to mention. Perhaps all this wishful thinking blinds clinicians to the negative aspects of new drugs. We become so convinced that new drugs must be better in every way than the old ones they replace that we fail to see what is before us - that new therapies can have disadvantages too.

 

_____________________________________________________________

 

David Taylor is Chief Pharmacist at the Maudsley Hospital, London

 

Published at http://www.socialaudit.org.uk/4200DTAY.htm

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When I first encountered withdrawl over 6 years ago I rang the Maudsley hospital after reading this and got the stock ' its only ever for a few weeks ' stock answer !

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Perhaps you should have spoken to David Taylor.

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In this paper, Phelps 2011 Tapering antidepressants: Is 3 months slow enough?, author Jim Phelps utilizes data from another paper (abstract below).

 

According to Dr. Phelps, patients suffering cataplexy (collapse from a loss of muscle tone, a symptom of narcolepsy, a serious neurologically caused sleep disorder) were "carefully" tapered off tricyclic and SSRIs antidepressants in order to try a different kind of drug (sodium oxybate, or Xyrem) on them.

 

The tapers were accomplished in 21 days, followed by 5-18 days of "washout," determined by the half-life of the antidepressant. (Complete disappearance of the drug from the body is thought to take 5 half-lives.) Over 100-130 days, the patients returned for 4 follow-up visits.

 

The symptomology of the cataplexy patients who had been withdrawn from antidepressants was compared to that of a group of cataplexy patients who had never taken antidepressants.

 

Analyzing the follow-up data, Dr. Phelps ascertained that it took more than 3 months for the antidepressant-treated patients to recover from the effects of withdrawal. He writes: "Note this shift, whatever its molecular basis, did not peak until at least a month into the process....in at least one condition, the physiologic changes associated with antidepressant withdrawal occur over months, not weeks."

 

(For the "molecular basis," Dr. Phelps cites Harvey 2003 Neurobiology of antidepressant withdrawal.)

 

Dr. Phelps goes on to question whether increased rates of "relapse" in several studies might not have been reduced with longer, slower tapers, i.e. whatever was diagnosed as "relapse" was actually withdrawal syndrome.

 

Sleep Med. 2009 Apr;10(4):416-21. Epub 2008 Aug 26.

Exacerbation of cataplexy following gradual withdrawal of antidepressants: manifestation of probable protracted rebound cataplexy.

Ristanovic RK, Liang H, Hornfeldt CS, Lai C.

 

Source

 

Department of Neurology, ENH-Evanston Hospital, Evanston, IL 60201, USA. r-ristanovic@northwestern.edu

Abstract

 

BACKGROUND:

 

A double-blind, placebo-controlled sodium oxybate trial provided a unique opportunity to compare changes in cataplexy following gradual withdrawal from antidepressants in narcolepsy patients.

 

METHODS:

 

Of 228 enrolled patients, 71 discontinued antidepressant therapy. Data from 57 patients were available for analysis: 37 patients discontinued tricyclic antidepressants (TCAs) and 20 discontinued selective serotonin reuptake inhibitors (SSRIs). The trial included a 21-day withdrawal phase followed by 18-day washout and 14-day single-blind treatment phases. Two additional weeks were permitted for withdrawal from fluoxetine due to its long half-life. Weekly cataplexy attacks were recorded throughout the trial. No historical data on the frequency of cataplexy prior to treatment with antidepressants was available.

 

RESULTS:

 

Among the patients who were and were not withdrawn from antidepressants treatment, the median frequency of baseline weekly cataplexy was similar (17.5 vs. 14.0, respectively). As expected, significant between-group differences emerged by the end of the washout period (52.04 vs. 15.25, respectively; p<0.05); however, the frequency of cataplexy events became similar again by the end of the trial (16.5 vs. 17.5, respectively).

 

CONCLUSIONS:

 

Patients gradually withdrawn from antidepressants experienced a significant increase in cataplexy, but eventually returned to their baseline frequency, comparable to previously untreated control patients. Compared to SSRIs, discontinuation from TCAs was associated with a greater increase in cataplexy attacks.

 

 

See discussion in topic http://survivingantidepressants.org/index.php?/topic/1217-phelps-2011-tapering-antidepressants-is-3-months-slow-enough/

Edited by Altostrata
updated

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Interesting

Cataplexy
From Wikipedia, the free encyclopedia
 
 
Not to be confused with Catalepsy. Cataplexy Classification and external resources ICD-10 G47.4 ICD-9 347 DiseasesDB 16311 MeSH D002385

Cataplexy is a sudden and transient episode of loss of muscle tone accompanied by full conscious awareness, often triggered by emotions such as laughing, crying, terror, etc.[1] It is a rare disease[2] (prevalence of fewer than 5 per 10,000 in the community), but affects roughly 70% of people who have narcolepsy.[3] However, in rare cases, cataplexy occurs without the co-occurrence of narcolepsy. The exact cause of cataplexy is unknown, but the condition is strongly linked to experiencing intense emotions and reduced levels of the neurochemical hypocretin.[4] Cataplexy can also be present as a side effect of SSRI Discontinuation Syndrome.

The term cataplexy originates from the Greek κατά (kata, meaning "down"), and πληξις (plēxis, meaning "stroke").

http://en.wikipedia.org/wiki/Cataplexy

 

Presentation[edit]

Cataplexy manifests itself as muscular weakness which may range from a barely perceptible slackening of the facial muscles to the dropping of the jaw or head, weakness at the knees, trembling of mesenteric muscles, rictus, dysarthria, may drop objects held in hands or a total collapse. Usually the speech is slurred, vision is impaired (double vision, inability to focus), but hearing andawareness remain normal. The person will lie there, fully conscious, for a few seconds to several minutes. As the attack continues the patient may experience sleepiness, hallucinations, or sleep-onset REM period. A full-blown attack may occur and results in complete muscle paralysis with postural collapse and possible injury. However, most often patients with postural collapse have the capability to avoid injury because the fall is slow and progressive.[5] Cataplexy is different from narcoleptic sleep attack because it is usually precipitated by strong emotional reactions or by sudden physical effort, especially if the person is caught off guard.[6]

These attacks are triggered by strong emotions such as exhilaration, angerfearsurpriseorgasmaweembarrassment, and laughter. An effort to catch a suddenly thrown object can trigger a cataplectic attack. Guilleminault, Wilson, and Dement (1974) noted that even people who did not have cataplexy sometimes will lose muscle strength after a bout of intense laughter; explaining why people go "weak" from laughing too hard.[7]

Cataplexy can cause serious social and parenting challenges because cataplexy can occur when one is attempting to discipline their child or during sexual activity.[8]

Occurrence[edit]

In a 24-hour period, cataplectic attacks usually occur between the hours of 10 am and 9 pm and very few attacks occur between the hours of 10 pm and 9 am. Attacks can last from a few seconds up to ten minutes, and may occur up to several times per week [4-6 times]. Cataplexy is considered “typical” when it is always of short duration (< 5 minutes).[9]

[wonder if the timing has anything to do with the cortistol... ?

 

 

Physiology[edit]
Posted Image
Posted Image
In this simplified brain circuit, damage to orexin-secreting neurons in the hypothalamus can lead to inhibition of motor neurons, thus lowering muscle tone.

Cataplexy is considered secondary when it is due to specific lesions in the brain that cause a depletion of the hypocretin neurotransmitter. Secondary cataplexy is associated with specific lesions located primarily in the lateral and posterior hypothalamus. Cataplexy due to brainstem lesions is uncommon particularly when seen in isolation. The lesions include tumors of the brain or brainstem and arterio-venous malformations. Some of the tumors include astrocytoma, glioblastoma, glioma, and subependynoma. These lesions can be visualized with brain imaging, however in their early stages they can be missed. Other conditions in which cataplexy can be seen include ischemic events, multiple sclerosis, head injury, paraneoplastic syndromes, and infections such as encephalitis. Cataplexy may also occur transiently or permanently due to lesions of the hypothalamus that were caused by surgery, especially in difficult tumor resections. These lesions or generalized processes disrupt the hypocretin neurons and their pathways. The neurological process behind the lesion impairs pathways controlling the normal inhibition of muscle tone drop, consequently resulting in muscle atonia.[10]

Theories for episodes[edit]

A phenomenon of REM sleep, muscular paralysis, occurs at an inappropriate time. This loss of tonus is caused by massive inhibition of motor neurons in the spinal cord. When this happens during waking, the victim of a cataplectic attack loses control of his or her muscles. Where as in REM sleep, the person continues to breathe and is able to control eye movements.[11]

Studies[edit]

A study of 40 cataplectic patients (age range 13–23 years) reported that sagging of the jaw, inclined head, drooping of the shoulders, and transient buckling of the knees were the most common presentations. Slurred speech may be present. However, diaphragmatic paralysis resulting in central apneas has not been reported. There is an isolated form that involves facial muscles exclusively. Cataplexy may rapidly reoccur repeatedly, giving birth to "status cataplecticus", and to the "limp man syndrome" as described by Stalh et al. "Status cataplecticus" is rare and can be extremely disabling to the individual. Cataplexy also occurs more frequently in times of emotional stress and when patients are deprived of napping while sleepy.[12]

A survey of 100 cataplectic patients from the Stanford Sleep Disorders Clinic (age range 14–24 years) reported that 93 percent of the attacks lasted less than two minutes, 6 percent reported events lasting up to five minutes, and 0.94 percent reported events lasting longer than five minutes. There is a bimodal pattern of the age of onset of symptoms; either at 15 or 35 years. It has also been reported past the age of forty. Guilleminault et al. investigated 51 prepubertal children with narcolepsy; in 10 subjects (5 years and younger) cataplexy was the symptom first recognized. Cataplectic symptoms in general tend to decrease with age. A review of 100 patients with cataplexy at the Stanford Sleep Disorders Clinic (age range 12–20 years) reported that 62 of these patients stopped taking anti-cataplectic medications after 10 years. However, the general decrease in cataplectic symptoms with aging may be reversed after the experience of a significant emotional upset, such as a loss of spouse in older subjects.[13]

Hypocretin[edit]

The hypothalamus region of the brain regulates basic functions of hormone release, emotional expression and sleep. A study in 2006 in "Tohoku Journal of Experimental Medicine" concluded that the neurochemical hypocretin, which is regulated by the hypothalamus, was significantly reduced in study participants with symptoms of cataplexy. Orexin, also known as Hypocretin, is a primary chemical important in regulating sleep as well as states of arousal. Hypocretin deficiency is further associated with decreased levels of histamine and epinephrine, which are chemicals important in promoting wakefulness, arousal and alertness.[14]

Treatment[edit]

Cataplexy is treated pharmacologically. There are no behavioral treatments for cataplexy. The cholinergic and noradrenergic neurotransmitter systems are targeted in the treatment of cataplexy. Despite its relation to narcolepsy, in most cases, cataplexy must be treated differently and separate medication must be taken. For many years, cataplexy has been treated with tricyclic antidepressants such as imipramineclomipramine or protriptyline. The main feature of tricyclics is their ability to inhibit the reuptake of norepinephrine and serotonin at the nerve endings.[15]However these can have unpleasant side-effects and so have been generally replaced by newer drugs such as venlafaxine.

For cataplexy associated with narcolepsy, Xyrem (sodium oxybate) is often recommended.[16]

Monoamine oxidase inhibitors may be used to manage both cataplexy and the REM sleep-onset symptoms of sleep paralysis and hypnagogic hallucinations.[17]

Wise (2004) noted that people with narcolepsy will often try to avoid thoughts and situations that they know are likely to evoke strong emotions because they know that these emotions are likely to trigger cataplectic attacks.[18]

A newer class of antidepressants with selective serotonergic reuptake blocking properties known as the selective serotonin reuptake inhibitors fluoxetineparoxetinesertralinecitalopram has become popular for the treatment of cataplexy. This class of drugs has an active metabolite with norepinephrine reuptake blocking properties (such as nor-fluoxetine). Serotonin reuptake inhibitors (SSRIs) have fewer side effects compared to the tricyclics and can be used in adults and children. A side effect worth mentioning regarding tricyclic antidepressants and SSRIs is the risk of development of REM behavior disorder (RBD) due to elimination of the normal REM sleep atonia. These drugs are known to decrease stage REM sleep. They can also decrease muscle atonia associated with REM sleep and consequently dissociate REM sleep. As a consequence, the subject may act out his or her dreams and cause harm to himself/herself or others.[19]

Emerging therapies[edit]

Emerging therapies include Hypocretin Gene Therapy and Hypocretin Cell Transplantation for narcolepsy-cataplexy.[20][21]

The newest agent for the treatment of cataplexy is sodium oxybate (gamma-hydroxybutyrate [GHB]), known commercially as Xyrem. Although its mechanism is unknown, it reduces cataplectic attacks and other manifestations of REM sleep. GHB increases slow wave sleep, decreases nighttime awakenings, and consolidates REM sleep. Sodium oxybate is the only medication that will improve both cataplexy and daytime sleepiness. Cataplectic symptoms are improved much faster. Because it can cause daytime sleepiness, during this time, sodium oxybate should be taken concomitantly with a stimulant.[22]

 

Seems to contradict itself 

ssri used to treat this disorder 

and as 

side effect of SSRI Discontinuation Syndrome

 

I guess that is the same as using ssri to treat hot flashes in cancer treatment and menopause... because another withdrawal side effect is hot flashes... 

They know it has something to do with it it but are just throwing it out there to see what sticks...if ssri were used for treatment the symptoms would return on withdrawal... now they could say this is a recurrance of the original disorder... we have lived this lie long enough to see the writing on the wall.  

I did not have anxiety or depression before being treated for pain with prozac but these withdrawal affects become my life since. 

I think this needs a further look...

" Hypocretin, is a primary chemical important in regulating sleep as well as states of arousal. Hypocretin deficiency is further associated with decreased levels of histamine and epinephrine, which are chemicals important in promoting wakefulness, arousal and alertness" 

 

Wise geek: 

 

Low histamine is a chemical imbalance of the brain that occurs when excess copper accumulates and provokes overstimulation of the nervous system. Histamine regulates the release of dopamine in the part of the brain that controls sensory perception. When low histamine is present, it can induce hallucinations, paranoia, and other symptoms because the brain is not processing stimuli properly.

 

 

Copper contains an enzyme that normally balances the amount of dopamine, norepinephrine, and serotonin released by neurotransmitters in the brain. Too much copper in a person's system degrades the amount of available histamine, which controls the level of each chemical dispensed. As low histamine develops, it allows more copper to accumulate in the blood. Studies have shown that people with type A blood are more prone to collect excess copper.

 

 

Treatment for low histamine routinely includes a high protein diet. Protein contains an amino acid that converts histidine into histamine. Dietary supplements like vitamin C, zinc, andmagnesium remove copper from the body to help bring histamine levels into the normal range. Niacin, vitamin B12, and folic acid also help regulate brain chemical levels.

 

 

Those suffering from low histamine commonly complain of low sex drive, hyperactivity, and anxiety. This brain disorder can also lead to hallucinations and paranoia because the brain chemicals are skewed. Bipolar disease and manic-depressive disorder have also been linked to low histamine. Some patients with the condition have an abnormally high tolerance to pain. Hormonal changes after childbirth can also produce excess copper and might contribute to postpartum depression.

 

 

Physical symptoms of low histamine include excess facial and body hair and high blood pressure. Canker sore may develop, along with various food allergies. Low histamine can also induce depression and thoughts of suicide.

 

 

A histamine level that is too high is called histadelia. Histadelia sends neurotransmitters into overdrive with excess dopamine, serotonin, and norephinephrine released into the bloodstream. People with this disorder are commonly full of energy and driven to succeed. They can be compulsive overachievers who suffer from insomnia and exhibit a low tolerance to pain. Histadelia may increase sex drive and lead to sexual addictions.

 

 

It can also produce extra body heat that produces frequent sweating. In some patients, the ears, feet, nose, and hands may grow larger to disperse the additional body heat. Often, the second toe is longer than the big toe in people with the condition. People with high levels of histamine may produce very little body and facial hair.

 

 

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I certainly has some of these symptoms in early withdrawal.  google search "Cataplexy as a side effect of ssri withdrawal"

online tidbits

The peptide hypocretin (orexin) may be involved. This is derived from the hypothalamus and is thought to be involved in sleep/wake cycles, food intake and pleasure-seeking behaviour. Narcolepsy may be caused by the loss of a relatively few neurons that are responsible for producing the neuropeptide hypocretin in the CNS. Possibly, immunological mechanisms may lead to loss of hypocretin

"

  • A sudden increase in narcolepsy was seen in Finland and other European countries in 2010. This was linked to Pandemrix® H1N1 influenza vaccine.[7] The Vaccine Adverse Event Surveillance and Communication (VAESCO) Consortium undertook to investigate the link and case gathering is still ongoing.[8] A recent study has also identified a small number of cases in the UK.[9]

http://www.patient.co.uk/doctor/narcolepsy-and-cataplexy-pro

Head drops and facial slackness are two things I had for sure. 

 

Weakness for sure... 

even as I think of the possibilities of a treatment option I am scared to death to actually put a pill in my mouth.  

Still after all these years of withdrawal I just might over come that fear in order to make a move towards wellness that is not coming on its own.. we will see. 

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Int J Neuropsychopharmacol. 2007 Dec;10(6):835-8. Epub 2007 Jan 16.

Effects of gradual discontinuation of selective serotonin reuptake inhibitors in panic disorder with agoraphobia.

Fava GA, Bernardi M, Tomba E, Rafanelli C.

 

Affective Disorders Program, Department of Psychology, University of Bologna, Bologna, ItalyDepartment of Psychiatry, State University of New York at Buffalo, Buffalo, New York, USA.

 

Abstract at http://www.ncbi.nlm.nih.gov/pubmed/17224089?dopt=AbstractPlus

 

The aim of this investigation was to explore the prevalence and features of discontinuation syndromes ensuing with gradual tapering of selective serotonin reuptake inhibitors (SSRIs), in optimal clinical conditions in patients with panic disorder and agoraphobia. Twenty-six consecutive outpatients met the DSM-IV criteria for panic disorder and agoraphobia while taking SSRIs. Twenty remitted upon behavioural treatment. Antidepressant drugs were then tapered at the slowest possible pace and with appropriate patient education. Patients were assessed with the Discontinuation-Emergent Signs and Symptoms (DESS) checklist 2 wk, 1 month and 1 yr after discontinuation. Nine of the 20 patients (45%) experienced a discontinuation syndrome, which subsided within a month in all but three patients who had been taking paroxetine for a long time. Discontinuation syndromes appeared to be fairly common even when performed with slow tapering and during clinical remission. In some cases disturbances persisted for months after discontinuation.

 

Full text at http://www.mediafire.com/?x681dok5v8er6kl

 

 

My comment:

 

Dr. Fava's research found that 9 of 20 patients systematically tapered off SSRIs suffered a discontinuation syndrome. Most resolved in a month, but 3 patients, or 15%, who happened to be long-time Paxil users, had persistent withdrawal symptoms evident at an assessment one year post-withdrawal. There were also 2 withdrawal syndrome sufferers who "relapsed." (Also see http://www.medicalnewstoday.com/releases/94224.php.)

 

This is the longest any published studies have followed unmedicated patients after withdrawal.

 

(Again, in this study, the highest and most severe incidence of withdrawal syndrome were in patients taking Paxil.)

 

About the tapering method used in this study:

 

"....Tapering of antidepressant drugs was performed at the slowest possible pace (50 mg every other week for fluvoxamine and sertraline, 10 mg every other week for paroxetine, fluoxetine and citalopram, with 10 mg every other day in the last segment).

After 15 d from discontinuation all patients were assessed with the Discontinuation-Emergent Signs and Symptoms (DESS) checklist (Rosenbaum et al., 1998). This allowed a comprehensive collection of all manifestations of discontinuation syndrome since some may become evident only in the second week...."

 

Given the dosages the patients were taking, tapering off took a month at most. 4 out of 9 of those taking paroxetine developed withdrawal symptoms.

 

Hi, have you found any new papers since posting this and th others in this thread?

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Sorry, no. I would have posted them.

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Thanks Alto. Great thread!

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Sorry, no. I would have posted them.

 

Aw too bad, well thanks for what you have posted so far.

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I join with Lex in saying great thread.

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