Use of antidepressants for/with ME/CFS?

There may be few studies of tricyclics specifically for ME/CFS, that's not the same as there being no evidence for their effects on sleep in general.

e.g.
. 2017 Jun;34:126-133.
doi: 10.1016/j.sleep.2017.03.007. Epub 2017 Mar 27.
Treatment of insomnia with tricyclic antidepressants: a meta-analysis of polysomnographic randomized controlled trials
Yang Liu 1, Xiaomin Xu 1, Meixue Dong 1, Shiyu Jia 1, Youdong Wei 2
Affiliations
Abstract


Background: Insomnia represents a significant public health burden worldwide. Antidepressants have often been the insomnia treatment of choice in recent decades. Some tricyclic antidepressants (TCAs) have been shown to improve sleep efficiency.

Objective: Assess the efficacy and safety of TCAs for the treatment of insomnia using a meta-analysis of randomized control trials (RCTs).

Methods: Relevant studies were identified in electronic databases such as PubMed, Cochrane, Embase, and Web of Science, up until July 2016. We included all polysomnographic (PSG) RCTs using TCAs to treat insomnia. The primary outcome measure was the total sleep time (TST), although other polysomnographic measures were also investigated. Next-day somnolence and dropout rates were also assessed.

Results: The meta-analysis included nine RCTs. TCAs significantly improved TST compared with placebo (SMD = 0.61, 95% CI = 0.50-0.71, P < 0.00001). Participants receiving TCAs were not more likely to drop out than those receiving a placebo because of adverse side effects (1.71% vs 1.19%, RR = 1.37, 95% CI = 0.67-2.80, P = 0.39) or any other reason (7.08% vs 8.20%; RR = 0.86, 95% CI = 0.60-1.23, P = 0.42). However, the incidence of somnolence was higher in participants receiving TCAs (6.06% vs. 3.21%; RR = 1.82, 95% CI = 1.10-3.00, P = 0.02).

Conclusions: Based on our limited data analysis with two medications at particular doses (most studies included extremely low doxepin), we assert that TCAs can be an effective pharmacological treatment for insomnia. TCAs were found to improve sleep outcome measures, with the notable exception of an 82% increase in somnolence. Overall TCAs have very problematic and dangerous side effects, while TCAs were not found to increase the dropout rate compared with the placebo.

Keywords: Insomnia; Meta-analysis; Tricycle antidepressants.
 
There’s also the risks around taking tricyclics in combination with SSRIs. Which certainly weren’t mentioned to me when tricyclics were prescribed.

I have had two chronically ill relatives who were also on amitryptiline and fluoxetine at the same time. Even the NHS website mentions this as an issue.
https://www.nhs.uk/mental-health/ta...nd-psychiatry/antidepressants/considerations/

One of my relatives who was on this combination had had a heart attack so questionable whether they should have been on tricyclics at all
 
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An interesting thing I have noticed is some people who don’t take something for their sleep (like tricyclics) can’t tolerate some posited therapies as they would stimulate them too much.
 
I think many well intentioned doctors do understand that depression isn’t ME/CFS, even though some symptoms on the surface can overlap.

And many also know, and we do too, that having ME for years with non-stop symptoms, possible worsening severity, no effective treatments and little hope that this can cause what is called reactive depression/adjustment disorder/situational depression (I think adjustment disorder is a terrible name). So antidepressants can help here just like eg pain and sleep meds help with those ME caused symptoms. One is possibly indirectly caused by ME and the others directly caused, but in the end makes little difference.
 
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It’s probably been said here before, but major depressive disorder (MDD) is extremely common in multiple sclerosis patients. I think it’s one of the most common comorbidities of MS. I’m pretty positive no MS expert knows for sure whether it’s a reactive depression or over time could actually be a cumulative downstream effect of the MS disease process.

I think the same with ME. I know for sure in the beginning and for many years afterwards I didn’t have any symptoms of depression, but I couldn’t tell you if now after more years, with more disease progression and little treatment hope, if some of the depressive symptoms going on with me were caused by the cumulative disease process or simply a reactive, situational depression.

Another reason to not necessarily ignore antidepressants, they won’t solve a lot but can still be useful. Even just to cope with the fact that many of us don’t think we will have an effective treatment before we’re too old to care and will lose most of our adult lives to this.
 
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Hi,

I recently experienced a huge flare up in symptoms - an intense and scary but thankfully short-lived setback. I believe that the antidepressants I was prescribed - Venlafaxine and Mirtazapine - made me feel I had more energy than I actually had and caused me to overdo it. I had less ME/CFS symptoms such as pain and pressure in my head too which almost always serve as warning signs that I'm overdoing it.

Has anybody else on here experienced this and found an alternative antidepressant that doesn't mask ME/CFS symptoms?

I feel lucky that the setback was shortlived and I feel that if I continued with the dose of the two drugs I was on it could have been a lot worse.

I had terrible depression and anxiety back in April and May and all the usual interventions weren't working including therapy so my GP put me on Venlafaxine in early June. Before taking this drug I had a low opinion on antidepressants because they had never worked for me in the past. However, this drug immediately cured my depression and anxiety.

On top of this, I felt more like myself, more confidence, more able to engage with people and I really felt I could do more.

I started on 37.5mg Venlafaxine and upped the dose to 75mg after two weeks. After another two weeks on 75mg of Venlafaxine I started experiencing insomnia and was put on Mirtazapine, another antidepressant that helps with sleep and (so I'm told by my GP) works in synergy with Venlafaxine.

However, I had a bad setback mid-July after a particularly active week.

To be fair, I didn't go crazy, I was doing about 10-20% more than my normal baseline and still pacing and resting.

I've stopped Mirtazapine as I found that drug particularly risky when it comes to masking ME/CFS symptoms and I've reduced Venlafaxine to a very low dose: 18.5mg. I'm experiencing a bit of low mood again (it's manageable at the moment) but I will maintain the dose at 18.5mg until I find my new baseline and then maybe increase to 37.5mg again (no higher).

I have kept my GP in the loop and when she gets back from her holiday I'll discuss other options.

In the meantime I thought I'd check on here to see if anyone has had this experience and found other antidepressants that don't mask ME symptoms.

I am on low dose amitriptyline (10mg currently but used to be on 20mg) and trazodone (100mg currently but used to be on 300mg) for sleep. They have never done anything for my mood though. I used to be on 30mg duloxetine but that didn't do anything for my mood either and I couldn't tolerate a higher dose because it affected my sleep.

Thanks in advance for any suggestions
 
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That seems like an awful lot of antidepressants to be on at once ...

All I can say is that my caree is on mirt and I'm not aware that it masks her symptoms. Also, it is frequently reported that pwME can react excessively to standard-level increases in dosage and may need to increase by much smaller doses than "normal" individuals.
 
Wits_End said:
That seems like an awful lot of antidepressants to be on at once ...

All I can say is that my caree is on mirt and I'm not aware that it masks her symptoms. Also, it is frequently reported that pwME can react excessively to standard-level increases in dosage and may need to increase by much smaller doses than "normal" individuals.
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Ya, I haven't tried Mirtazapine on it's own yet only in combination with venlafaxine. So maybe the negative effects I'm getting when I add Mirtazapine is because of interactions with venlafaxine or other meds Im on. I'll try that next week, thanks
 
shak8 said:
Low dose Mirtazapine is used for insomnia in the US quite a lot.

Is your doctor concerned about excess serotonin (serotonin syndrome) from multiple anti-depressants? Just asking out of potential safety concerns (I'm was a nurse).
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I have an excellent doctor and she is aware of the risk of seratonin syndrome when taking multiple antidepressants but is not concerned in my case as I'm on a low dose of each one
 
I tried Mirtazapine on it's own yesterday at a small dose (7.5mg) but had awful dreams and other distressing side effects. It seems without the venlafaxine the dreams turn stressful.
The side effects may also have been due to stopping venlafaxine (which I've been reducing slowly over the last 3 weeks) too soon.
The mission to address both my mood disorders and the false energy in certain antidepressants continues...
 
celestron said:
I tried Mirtazapine on it's own yesterday at a small dose (7.5mg) but had awful dreams and other distressing side effects. It seems without the venlafaxine the dreams turn stressful.
The side effects may also have been due to stopping venlafaxine (which I've been reducing slowly over the last 3 weeks) too soon.
The mission to address both my mood disorders and the false energy in certain antidepressants continues...
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I tried mirtazapine at 7.5 mg on two occasions as a sleep aid to avoid waking up in the middle of the night. It worked exceptionally well in that I was so sedated that I could barely muster the energy to roll over in my bed, but similarly to your experience I had the most terrible, intense nightmares (
dreaming of being tortured and stabbed to death all night long
).

In hindsight I am glad that this side effect prevented me from going on mirtazapine because I have since then gotten to know people who have developed a prolonged withdrawal syndrome from it. And from venlafaxine too, unfortunately.
 
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I've been taking 10mg amitriptyline for a couple of years - it was suggested by a neurologist to reduce sound and touch hypersensitivity and migraine-like symptoms, and I think it has helped somewhat with that. But I'd like to try coming off it now. Not sure whether I'd need to taper off from such a low dose, and if so how.

Not asking for medical advice directly, but can anyone recommend a source of simple advice on this? I've tried googling it, but there's such a flood of conflicting information, and mostly directed at people on much higher doses, I can't find my way through.
 
I set my own approach to tapering off Fluoxetine the GP seemed to think a few weeks 3 I think she said. Because I’d heard other people who had problems I decided to go much slower as I didn’t want to risk it. I was taking 1 20mg a day, I started with one tablet free day a week for a month then 2 and so on. Obviously it’s not the same type of medication but I had no issues at all.

On the other hand I was also on Amitryptiline for a year or so for sleep but it had stopped helping with sleep and yet still made me sedated in mornings so I was very keen to stop asap. I can’t remember tapering in the same way I did for fluoxetine but I think I had already been missing doses if I had something important the next day.
 
Eleanor said:
I've been taking 10mg amitriptyline for a couple of years - it was suggested by a neurologist to reduce sound and touch hypersensitivity and migraine-like symptoms, and I think it has helped somewhat with that. But I'd like to try coming off it now.
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It has been suggested that the tricyclic clomipramine is useful for treating hyperacusis. Has anyone else noticed tricyclics affecting sensitivity to sound (or other sensitivities)? Has anyone experience specifically with clomipramine?

@wastwater posted a link to an article about clomipramine potentially being useful in MS, possibly protecting nerves, here: FOX genes

A small study of clomipramine reported some benefits including reducing hyperacusis in OCD patients (paywall):
clomipramine reduced skin conductance and heart rate responses to loud tones and tonic and phasic skin conductance responses in a two-flash discrimination task. This suggests that reductions in autonomic responses to important and/or aversive stimuli may be critical to clinical improvement in obsessive compulsive disorder.
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