Emergence of Intense Suicidal Preoccupation During Fluoxetine Treatment
by Martin H. Teicher, M.D., Ph.D., Carol Glod, R.N., M.S.C.S., and Jonathan O. Cole, M.D.
American Journal of Psychiatry. 1990 147:207-210.
[full text on-line]
Six depressed patients free of recent serious suicidal ideation developed intense, violent suicidal preoccupation after 2-7 weeks of fluoxetine treatment. This state persisted for as little as 3 days to as long as 3 months after discontinuation of fluoxetine. None of these patients had ever experienced a similar state during treatment with any other psychotropic drug.
"Antidepressants occasionally promote suicidal actions in severely depressed-patients by enhancing drive and counteracting psychomotor retardation. However, standard antidepressants are not known to induce severe and persistent suicidal ideation in depressed patients free of such thoughts before treatment. We have recently observed several complex patients who appear to have had serious paradoxical responses to fluoxetine that were characterized by intense, violent suicidal thoughts…"
The Akathisia being described here doesn’t happen often, but when it does occur, it’s dramatic – easily noticed from the outside as well as from within [if there’s a high index of suspicion on the part of clinician and patient]. If the problem arises and you know it, it’s very easily treated:
Correspondence: Fluoxetine and suicide
by David Healy and William Creaney
British Medical Journal. 1991 303:1058.
… The significance of the emergence of suicidality during treatment with any psychotropic compounds as opposed to during the course of a depressive episode is that during treatment it can be anticipated and forestalled by warning patients.
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Warn people about Akathisia.
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Stop the medication if it happens.
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It goes away.
In the comments section to a recent post, I’m asked the question, "SO on balance: HAVE ANTIDEPRESSANTS DONE MORE HARM THAN GOOD?" followed by a confrontation, "What is this rally against the biological psychiatry? You can dig up as much crap as you want. [actually you can do it in any field.] But unless you can address the above, all you’ve got going here is a morality play in SSRI-landia." It deserves an answer. It implies that the point of this blog is an attack on Biological Psychiatry or the antidepressants. I think that question is a false dichotomy, or maybe addressed at the intent of some other blog. I’d rather answer this question, "Have the antidepressants done more harm than they would have if they’d been used carefully, based on the honest scientific evidence?" I’d say "You’re damned straight they have! By a mile!" And as for "all you’ve got going here is a morality play in SSRI-landia." That’s pretty much exactly what I intend – morality. And if being put off by those Lilly emails from the dawn of time where people are lobbying for accurate reporting of Clinical Trial data, but then caving in, saying "Of course, at the end of the day, we will do what we are told to do" is my being a goodie two-shoes, I accept the designation gladly and wish I’d known to put them on sooner. I still practice general psychiatry in an out-patient clinic and use these medications in that practice every time I work – at least some of them. With the depressed, I mention and describe Akathisia to every SSRI/TCA naive patient I prescribe for, and give them a number to call if they have any problem [and they do sometimes – have any problem and call]. I try to paint a realistic picture of what is to be expected from the medication and stop the drug if there’s no response. When people discontinue SSRIs, I taper them slowly and warn about withdrawal symptoms [my track record treating withdrawal symptoms by adding another drug is somewhere around zero]. I never use the short-acting SSRIs because the withdrawal is often so difficult. I learned to do all those things by reading studies and writing this blog [because I didn’t know all the dangers before]. I expect by national standards, I’m a light-weight prescription writer. No apologies for that. And in the time available in a charity clinic, I have a go at finding out what’s going on in the patients’ lives that might be making them or keeping them sick, and help if I can.
It’s the process that turned a limited and fickle drug like Prozac into a blockbuster by denying and hiding its foibles…
AMEN!
And always on my high horse, I would suggest that Lilly did the same with rDNA insulin; turned limited-use product into a blockbuster via ‘spin.’ I would suggest that at least a good portion of the Prozac users can be ‘saved’ by caring physicians. The accumulation of adverse-event reporting is an important part of this process. Sadly, those who lost life-saving warning signals of hypoglycemia when they were switched to synthetic insulin often do not survive to report life-ending adverse events. Different drugs, different (sometimes) outcomes . . . brought to you by profit-before-patients Eli Lilly.
Akathisia or a type of agitated unease or at least sleep disruption while taking antidepressants is not all that unusual, as I mentioned in a comment on the prior article. Doctors are dealing with it by prescribing benzos with the antidepressant.
The patient’s health and wellbeing are not promoted by this drug combination. The benzos often add to emotional numbing, lethargy, or depression, while the underlying dysfunctional process caused by the antidepressant continues.
So much for concern about akathisia, etc.