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Originally Posted by
mct
When switching to escitalopram he wanted me to simply stop the mirtazepine. I had read all the horror stories of withdrawal
Big mistake. Relatively few people experience 'horror' withdrawal, but the many more that don't do not often post about it. Plus, there is considerable debate as to how much of the 'horror' is due to biology and how much psychology. Come to believe you will suffer greatly and an anxious mind is very capable of creating your worst nightmare even with a placebo.
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I was taking 20mg paroxetine for nine months 20 years ago for a specific phobia related to performing tasks under public scrutiny. It seemed to work quickly then, although this may have been placebo effect.
Anxiety disorders (also depression) are the emotional expression of an underlying physical brain deficit, atrophy of segments of the two hippocampal regions of the brain caused by high stress hormone levels in the brain killing neurons and inhibiting the growth of new ones. It is essentially a type of autoimmune disorder (which is why these disorders often worsen during infections). Both ADs and the cognitive/behavioural (CBT, REBT, etc) and mindfulness therapies work by stimulating the growth of new brain cells in the hippocampi. It is the new cells and the connections they forge which produce the therapeutic response. It takes about 7 weeks for neurons to bud, grow and mature, however, some improvement may be noticed a little earlier.
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Apart from a few dizzy episodes I did not have any problem stopping Paxil and I think I probably only tapered it over a couple of weeks.
Which was a good demonstration that withdrawal horror stories need to be taken with more than a grain of salt for paroxetine (Paxil) has quite a reputation for producing severe withdrawal symptoms due to its short half-life and lack of an active metabolite to extend its activity. Only venlafaxine (Effexor) has a worse reputation.
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I should mention that before starting the escitalopram he did prescribe Paxil in view of its previous success but after a few days at 5mg I was getting urinary hesitancy. I am surprised that I experienced that at such a low dose (?anxiety because I read of the side -effect) but I also wonder whether the 15mg mirtazepine might have had some additive anti-cholinergic effect?
Most SSRIs/SNRIs and TCAs list urinary hesitancy as a potential side-effect, so it may have been the med, but reading up on side-effects can be a sure way of experiencing them all too. Mirtazapine doesn't impact muscarinic acetylcholine receptors much.
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I was taking ondansetron periodically till about a month ago - I wonder whether this might actually delay the development of tolerance to the elevated serotonin?
Did you notice any reduction in anxiety when taking ondansetron? Back in the 1980s drug trials pointed to it having potent anti anxiety properties, but GlaxoSmithKline opted to target the more lucrative antiemetic instead. :sad:
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I still take the 3.75mg mirtazepine at bedtime and have no difficulty falling asleep. I wake in the middle of the night and take just 1.25mg zopiclone, sleep till about 5am and then take another 1.25mg which may or may not give me another hour of sleep. Then the anxiety/panics kick in and eventually I get up.
This suggests that the insomnia is not from the escitalopram. I'd also be wary of taking zopiclone daily as tolerance tends to build quite quickly. I think you would benefit from seeing a sleep specialist.
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If switching he is thinking of Paxil again (in case the urinary problem was imaginary) or venlafaxine.
Venlafaxine may be as likely to cause urinary problems as paroxetine. I'm not a venlafaxine fan (or of the other common SNRIs). Despite being classified as a SNRI, venlafaxine is really only a SSRI and has a number of potential issues such as a very short half-life and the difficulty many have with withdrawal. Imo, its active metabolite desvenlafaxine (Pristiq) would be a better option if a SNRI is preferred.
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As for other medications, I am worried about the GI side-effects of sertraline in view of my nausea predisposition and the activating effects of sertraline,fluoxetine and venlafaxine.
Sertraline is more likely to affect the gut than the other SSRIs, although, as with everything about ADs your YMMV, but I'd be less concerned about the potential activating effects of the three.
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as I suspect that I may be overthinking all this. Thanks!
I think you are. Everyone's response to ADs is individual to them. It all comes down to how the med meshes with their biology and there is no way of predicted this other than by sucking and seeing.
