Cochrane Review: Selective serotonin reuptake inhibitors for fibromyalgia syndrome

Bob

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Selective serotonin reuptake inhibitors for fibromyalgia syndrome.
Walitt B, Urrútia G, Nishishinya MB, Cantrell SE, Häuser W.
Online: June 5th 2015
Cochrane Database Syst Rev. 2015 Jun 5;6:CD011735. [Epub ahead of print]
http://www.ncbi.nlm.nih.gov/pubmed/26046493

AUTHORS' CONCLUSIONS:
There is no unbiased evidence that SSRIs are superior to placebo in treating the key symptoms of fibromyalgia, namely pain, fatigue and sleep problems. SSRIs might be considered for treating depression in people with fibromyalgia. The black box warning for increased suicidal tendency in young adults aged 18 to 24, with major depressive disorder, who have taken SSRIs, should be considered when appropriate.
Abstract
BACKGROUND:
Fibromyalgia is a clinically well-defined chronic condition with a biopsychosocial aetiology. Fibromyalgia is characterized by chronic widespread musculoskeletal pain, sleep problems, cognitive dysfunction, and fatigue. Patients often report high disability levels and poor quality of life. Since there is no specific treatment that alters the pathogenesis of fibromyalgia, drug therapy focuses on pain reduction and improvement of other aversive symptoms.

OBJECTIVES:
The objective was to assess the benefits and harms of selective serotonin reuptake inhibitors (SSRIs) in the treatment of fibromyalgia.

SEARCH METHODS:
We searched the Cochrane Central Register of Controlled Trials (CENTRAL; 2014, Issue 5), MEDLINE (1966 to June 2014), EMBASE (1946 to June 2014), and the reference lists of reviewed articles.

SELECTION CRITERIA:
We selected all randomized, double-blind trials of SSRIs used for the treatment of fibromyalgia symptoms in adult participants. We considered the following SSRIs in this review: citalopram, fluoxetine, escitalopram, fluvoxamine, paroxetine, and sertraline.

DATA COLLECTION AND ANALYSIS:
Three authors extracted the data of all included studies and assessed the risks of bias of the studies. We resolved discrepancies by discussion.

MAIN RESULTS:
The quality of evidence was very low for each outcome. We downgraded the quality of evidence to very low due to concerns about risk of bias and studies with few participants. We included seven placebo-controlled studies, two with citalopram, three with fluoxetine and two with paroxetine, with a median study duration of eight weeks (4 to 16 weeks) and 383 participants, who were pooled together.All studies had one or more sources of potential major bias. There was a small (10%) difference in patients who reported a 30% pain reduction between SSRIs (56/172 (32.6%)) and placebo (39/171 (22.8%)) risk difference (RD) 0.10, 95% confidence interval (CI) 0.01 to 0.20; number needed to treat for an additional beneficial outcome (NNTB) 10, 95% CI 5 to 100; and in global improvement (proportion of patients who reported to be much or very much improved: 50/168 (29.8%) of patients with SSRIs and 26/162 (16.0%) of patients with placebo) RD 0.14, 95% CI 0.06 to 0.23; NNTB 7, 95% CI 4 to 17.SSRIs did not statistically, or clinically, significantly reduce fatigue: standard mean difference (SMD) -0.26, 95% CI -0.55 to 0.03; 7.0% absolute improvement on a 0 to 10 scale, 95% CI 14.6% relative improvement to 0.8% relative deterioration; nor sleep problems: SMD 0.03, 95 % CI -0.26 to 0.31; 0.8 % absolute deterioration on a 0 to 100 scale, 95% CI 8.3% relative deterioration to 6.9% relative improvement.SSRIs were superior to placebo in the reduction of depression: SMD -0.39, 95% CI -0.65 to -0.14; 7.6% absolute improvement on a 0 to 10 scale, 95% CI 2.7% to 13.8% relative improvement; NNTB 13, 95% CI 7 to 37. The dropout rate due to adverse events was not higher with SSRI use than with placebo use (23/146 (15.8%) of patients with SSRIs and 14/138 (10.1%) of patients with placebo) RD 0.04, 95% CI -0.06 to 0.14. There was no statistically or clinically significant difference in serious adverse events with SSRI use and placebo use (3/84 (3.6%) in patients with SSRIs and 4/84 (4.8%) and patients with placebo) RD -0.01, 95% CI -0.07 to 0.05.

AUTHORS' CONCLUSIONS:
There is no unbiased evidence that SSRIs are superior to placebo in treating the key symptoms of fibromyalgia, namely pain, fatigue and sleep problems. SSRIs might be considered for treating depression in people with fibromyalgia. The black box warning for increased suicidal tendency in young adults aged 18 to 24, with major depressive disorder, who have taken SSRIs, should be considered when appropriate.
 
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Kati

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Thank you for posting this. I will send this to my GP who believes SSRI is part of the treatment.

It irks me in the beginning when they say "Fibromyalgia is a clinically well-defined chronic
condition with a biopsychosocial aetiology. " Not! You have no clue.
 
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I don't believe any of the psychological theories in regards to Fibromyalgia. However, that being said, I am taking Savella and it does help ease the stinging type fibromyalgia pain. I know several others who are taking Savella and are helped some by it also.

I am going to be honest and tell you that it really pisses me off that Savella works some because doctors use that against me all the time. "If it's not psychological then how come you are taking Savella?

I have heard and read that Savella works a bit differently and actually blocks pain receptors, but I currently can't find the study. If anyone knows of why it really works to ease the pain some and could give me some good evidence I could bring to my doctor, I would appreciate it. I'm going to do some thorough searching on google scholar.
 

JaimeS

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That same drug for straight up sciatica

Lysophosphatidic acid effects (the chemical that may cause neuropathic pain)

Antidepressants can work as opioids

Still, if a doctor is challenging you like that - "if you're not depressed, why are you taking antidepressants, huh?" - I regret to say that I don't believe they can be convinced. You can't prove you're not depressed. It's one of those wrestling-with-the-pig scenarios. It's a waste of time and there's a good chance you'll feel awful afterwards.

Basically, I fear that every study you produce that shows non-antidepressant effects for milnacipran will be used as further evidence of how deeply you're in denial. This isn't logical, since the articles here should help you prove the point that the drug you're taking is used for plenty besides depression, but someone who behaves that way has already made up his/her mind and further evidence will entrench the belief, not remove it.

I apologize for saying it. I know that's difficult to hear. Think about how important it is to you to 'prove your point' and think about how you'll feel if your doc responds by pandering or continuing to challenge you rather than going, "huh! I didn't realize that!" like a sensible creature. Then make the decision as to whether you want to pursue.

-J
 

Effi

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"If it's not psychological then how come you are taking Savella?
I asked my doctor once why they prescribe anti-depressants to people with no depression (it was about Cymbalta - also prescribed for fibromyalgia I think). He said that it's because one side effect of this medication works on the pain receptors in the body. So it's not prescribed for the mood-enhancing effect of this medication, but I can imagine other (clueless) doctors would jump to the wrong conclusion. (I read a study about this, I'll try to post later if I can find it.)

If it really bothers you that they make these remarks you could always get a psychiatrist who knows me/cfs to state that you are not depressed. Other doctors are usually impressed by that. ;) (I know it sounds strange, but that's how their little world works!)
 

Effi

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@Mya Symons I found it but it wasn't a study, it's handouts from a symposium about this, but it's in Dutch. I don't think that's gonna help... sorry!
 

PeterPositive

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"If it's not psychological then how come you are taking Savella?
This is really fun... dualism is still alive and well.
If we can't find a physiological mechanism then it must be the ghost in the machine :D

Without opening philosophical threads that are off-topic, isn't modern medicine driven by the materialistic / reductionist approach? If so, isn't the psyche just a product of the physical?

Since this model doesn't even allow for free will what the heck is a psychological illness?? :rolleyes:

It'd be fun to hear what your doc has to say ;)
 

JaimeS

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@PeterPositive , I always wondered about that one:

isn't modern medicine driven by the materialistic / reductionist approach? If so, isn't the psyche just a product of the physical?
Right now, this is allowing docs to say, "I know a bunch of physical stuff is off and labwork is sending up red flags, but that's because you're depressed." Depression has an effect on the body, but is somehow neither caused by physiological changes or illness? It causes illness but cannot be caused by it?

I really wish docs would abandon this idea of depression as its own, discrete entity and start treating it like a symptom of many different infections, inflammatory states, and endocrine dysregulations. And if they do continue to view it as its own, discrete entity, I wish they would treat it like a 'real' illness by paying attention to what's 'off' in depression, biologically (inflammatory cytokines, for sure) and maybe treat it like, I don't know, an inflammatory illness? Instead, it's SSRIs, despite the fact that there's no reliable way to measure serotonin or serotonin receptor activity.

Sorry, this topic is a full-blown rant-in-the-making, and will eventually develop into a blog post at some point I think!

-J
 
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f
That same drug for straight up sciatica

Lysophosphatidic acid effects (the chemical that may cause neuropathic pain)

Antidepressants can work as opioids

Still, if a doctor is challenging you like that - "if you're not depressed, why are you taking antidepressants, huh?" - I regret to say that I don't believe they can be convinced. You can't prove you're not depressed. It's one of those wrestling-with-the-pig scenarios. It's a waste of time and there's a good chance you'll feel awful afterwards.

Basically, I fear that every study you produce that shows non-antidepressant effects for milnacipran will be used as further evidence of how deeply you're in denial. This isn't logical, since the articles here should help you prove the point that the drug you're taking is used for plenty besides depression, but someone who behaves that way has already made up his/her mind and further evidence will entrench the belief, not remove it.

I apologize for saying it. I know that's difficult to hear. Think about how important it is to you to 'prove your point' and think about how you'll feel if your doc responds by pandering or continuing to challenge you rather than going, "huh! I didn't realize that!" like a sensible creature. Then make the decision as to whether you want to pursue.

-J
I agree with this completely. Once they have their mind set, there is no changing it. I did see a rat study under your link where rats had reduced allodynia and nerve pain with Savella. I wonder if rats get depressed?:D

Effi, I like your doctor's response. Where did you find a doctor like that? I want one!