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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by jessers11581 on April 5, 2005, at 20:28:36
For roughly the past two years, I've felt that my mind just isn't functioning quite up to par. I find that I can't think straight, especially when I'm talking to people, or in social situations. This even applies with my famliy and my boyfriend (like my mind will go blank, or I'll forget which words to use). I'm sure that the SSRI's have lowered my creativity some, but might they also be impairing my basic cognitive abilities? It seems to get worse when I'm anxious (which is most of the time now) and, oddly, disappates when I drink alcohol. I've been very, very worried and anxious lately about not feeling right mentally (or physically for that matter--major digestive problems, sugar-cravings/overeating, etc.). So does anyone else feel...well, stupid from taking their medication? What can I do about this?
Posted by Phillipa on April 5, 2005, at 20:56:17
In reply to can't think straight...meds or anxiety?, posted by jessers11581 on April 5, 2005, at 20:28:36
Welcome to La La Land. Yes, meds can cause this. It sounds a lot like social anxiety too. Maybe a benzo could be added to help the anxiety. Fondly, Phillipa
Posted by jessers11581 on April 5, 2005, at 21:00:52
In reply to Re: can't think straight...meds or anxiety? » jessers11581, posted by Phillipa on April 5, 2005, at 20:56:17
What are the good benzos? Will they make me even dopier? I'm surprised my pdoc hasn't mentioned this option... Also, what is Cymbalta? She mentioned that one, but decided to have me try Wellbutrin first (which I quit taking after the 3rd day). Anyway, don't know much about the newer meds. I've always been on SSRI's and nothing else really. Except Xanax for about two weeks way back in the beginning.
Posted by Phillipa on April 5, 2005, at 21:06:28
In reply to Re: can't think straight...meds or anxiety?, posted by jessers11581 on April 5, 2005, at 21:00:52
There are a lot you can try. I like valium because of it's long half-life. Some people have good results on klonopin also long-acting. Some like ativan. I've taken them all and I took xanax for years until it stopped working. It also causes rebound anxiety. Post a Thread as this is a very popular subject now. Cymbalta is the new SNRI. A lot of people also like it. It just didn't work for me as none of the other SSRI's do either. Fondly, Phillipa
Posted by AuntieMel on April 6, 2005, at 9:21:37
In reply to can't think straight...meds or anxiety?, posted by jessers11581 on April 5, 2005, at 20:28:36
It could be the meds.
I like to research new meds. As well as looking at the official prescribing information and chemical makeup I go to (among others) http://www.crazymeds.org
For example, this is from their description of topomax:
Cons: If you don't have a temporal lobe dysfunction or problems with other parts of your brain that Topamax hits, or you're at the wrong dosage, it will make you dumber than a box of rocks. The kidney stones aren't much fun.
Posted by Spriggy on April 6, 2005, at 11:05:58
In reply to Re: can't think straight...meds or anxiety? » jessers11581, posted by AuntieMel on April 6, 2005, at 9:21:37
My mother has been on SSRI's for 4 years (until last week when she got switched to Cymbalta), anyway, I have noticed a very real change in her cognitive function.
She will be in the middle of sentence with me and just stop and say, " what was I saying?"She gets lost much easier while driving, etc..
She has laughed and said, " These pills are making me dumb but they make me so happy I don't care."
LOL
so it could definitely be the meds. I would also suggest a benzo if your anxiety is that bad.
You mentioned you were on Xanex before- that is a benzo, if you had success with it, maybe try it again.
Good luck!
Posted by CK1 on April 6, 2005, at 11:44:50
In reply to Re: can't think straight...meds or anxiety?, posted by Spriggy on April 6, 2005, at 11:05:58
It "might" be the SSRI's that are doing this to you. If you are having trouble finding the right word now, I'd be very reluctant to try benzos. Yes, they are miracle drugs for some and are very safe to use, BUT, for me, they are FAR WORSE than SSRI's for cognitive blunting. I took Klonopin (.25mg 2x day)(TINY dose) for 6 weeks awhile back and it was a miracle drug for the first month, then I started forgetting EVERYTHING (like my friends names) and my mind would go blank all the time. For most people, these drugs are best used for short term relief only! Although some have been taking these their whole lives with no side effects, these cases are the minority. The stimulants tend to help my focus tremendously, but aren't the best drugs for anxiety sufferers! If you do try benzos, go with one with a long half life (like Philippa said) such as Valium or Klonopin.
Posted by ed_uk on April 6, 2005, at 14:36:57
In reply to Re: can't think straight...meds or anxiety?, posted by CK1 on April 6, 2005, at 11:44:50
Hi!
>Yes, they are miracle drugs for some and are very safe to use, BUT, for me, they are FAR WORSE than SSRI's for cognitive blunting.
Nothing makes me dumber than Xanax! I can't concentrate or remember the simplest things.
Ed.
Posted by Dave001 on April 8, 2005, at 1:26:42
In reply to can't think straight...meds or anxiety?, posted by jessers11581 on April 5, 2005, at 20:28:36
> For roughly the past two years, I've felt that my mind just isn't functioning quite up to par. I find that I can't think straight, especially when I'm talking to people, or in social situations. This even applies with my famliy and my boyfriend (like my mind will go blank, or I'll forget which words to use). I'm sure that the SSRI's have lowered my creativity some, but might they also be impairing my basic cognitive abilities? It seems to get worse when I'm anxious (which is most of the time now) and, oddly, disappates when I drink alcohol. I've been very, very worried and anxious lately about not feeling right mentally (or physically for that matter--major digestive problems, sugar-cravings/overeating, etc.). So does anyone else feel...well, stupid from taking their medication? What can I do about this?
SSRIs are very insidious when it comes cognition and alertness (i.e., the effects occur very gradually, so it is often difficult to identify their role as causitive)Take a look at the references below.
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Riedel, W. J., K. Eikmans, et al. (2005). "Specific serotonergic reuptake inhibition impairs vigilance performance acutely and after subchronic treatment." J Psychopharmacol 19(1): 12-20.
Subchronic treatment with the selective serotonergic reuptake inhibitors (SSRIs) fluoxetine, venlafaxine and paroxetine, but not sertraline, were previously shown to specifically impair vigilance performance. The current study was designed to compare the vigilance effects of subchronic treatment with the SSRIs sertraline and citalopram in healthy volunteers, according to a placebo-controlled, double-blind, three-way cross-over design. Twenty-four healthy subjects, aged 30-50 years, of whom 21 completed the study, underwent three treatment periods of 2 weeks in which they received sertraline (50 mg on days 1-8, 100 mg on days 8-15), citalopram (20 mg on days 1-8, 40 mg on days 8-15) and placebo. Treatment periods were separated by 14 days washout periods. Vigilance performance was assessed through a 45-min Mackworth Clock Test at days 1, 8 and 15 of each treatment period. It was found that citalopram impaired vigilance performance acutely after the first 20 mg dose and subchronically after 40 mg daily doses. By contrast, no vigilance impairment was found during sertraline treatment. Sertraline is the only SSRI studied so far with no detrimental effects on vigilance. This may be due to the affinity of sertraline for the dopamine reuptake site. Because citalopram is the most specific SSRI showing this effect, it is concluded that the SSRI-induced decrement of vigilance performance is specifically associated with serotonergic reuptake inhibition.Damsa, C., A. Bumb, et al. (2004). ""Dopamine-dependent" side effects of selective serotonin reuptake inhibitors: a clinical review." J Clin Psychiatry 65(8): 1064-8.
OBJECTIVE: Neurophysiologic findings indicate an inhibition of dopaminergic neurotransmission by selective serotonin reuptake inhibitors (SSRIs). This article highlights the relationships between changes in dopaminergic neurotrans-mission induced by SSRIs and the occurrence of certain side effects such as hyperprolactinemia, extrapyramidal symptoms, sexual and cognitive dysfunction, galactorrhea, mammary hypertrophy, and, more rarely, gynecomastia. DATA SOURCES AND SELECTION: A systematic search of the literature in English, French, and German from 1980 to 2004 was performed in MEDLINE, EMBASE, and the Cochrane Library using the keywords SSRI, dopamine, serotonin, side effects, antidepressants, citalopram, escitalopram, sertraline, paroxetine, fluoxetine, fluvoxamine, and nefazodone. References cited in all trials were searched iteratively to identify missing studies. All studies concerning inhibition of dopaminergic neurotransmission by SSRIs and SSRI-related side effects were considered. We retained 62 significant articles debating the subject. DATA EXTRACTION AND SYNTHESIS: We critically reviewed the studies, depending on the methodologies (case reports, clinical reports, randomized studies), and assessed the pertinence of "dopamine-dependent" SSRI-related side effects. The analytic review of these articles suggests that some specific SSRI-related side effects be classified as dopamine-dependent. CONCLUSIONS: At a clinical level, it could be useful to underline dopamine-dependent characteristics of some SSRI-related side effects. This approach would allow clinicians the opportunity to search other dopamine-dependent side effects systematically. At a pharmacologic level, this approach could stimulate the development of molecules with a "corrective" function on dopamine-dependent side effects of SSRIs by facilitating dopaminergic neurotransmission.Schmitt, J. A., J. G. Ramaekers, et al. (2002). "Additional dopamine reuptake inhibition attenuates vigilance impairment induced by serotonin reuptake inhibition in man." J Psychopharmacol 16(3): 207-14.
There is evidence for a specific impairment of human vigilance following enhancement of serotonergic activity by antidepressant drugs. In the present study, we investigated the putative role of serotonergic-dopaminergic interactions in diminished vigilance by comparing the attentional effects of sertraline, a selective serotonin reuptake inhibitor (SSRI) with additional mild dopamine stimulating effects, with those of paroxetine, a SSRI without dopamine activity, using a placebo-controlled, double-blind, three-way cross-over design. Twenty-one (of 24) healthy middle-aged subjects completed the three treatment periods of 2 weeks in which sertraline (50 mg, days 1-7; 100 mg, days 8-14), paroxetine (20 mg, days 1-7; 40 mg, days 8-14) and placebo were administered. Vigilance (Mackworth Clock Test), selective (Stroop, Dichotic Listening) and divided attention (Dichotic Listening) were assessed at baseline and on days 7 and 14 of each treatment period. Selective and divided attention were unaffected by SSRI treatment. Subchronic administration of paroxetine impaired vigilance performance at each investigated dose. Sertraline did not produce a significant decline in vigilance performance, presumably due to its concomitant effects on dopamine activity, counteracting the negative effects of serotonin on dopamine neurotransmission. It is concluded that a serotonergically mediated reduction of dopamine activity plays an important role in the reduction of human vigilance following SSRI administration.Gardier, A. M., E. Lepoul, et al. (1994). "Changes in dopamine metabolism in rat forebrain regions after cessation of long-term fluoxetine treatment: relationship with brain concentrations of fluoxetine and norfluoxetine." Life Sci 54(4): PL51-6.
We examined the effects of repeated administration of the selective serotonin uptake inhibitor (SSRI) fluoxetine (Flx) (5, 10, or 15 mg/kg i.p., twice daily for 21 days) on brain and plasma concentrations of the parent drug and its active desmethyl metabolite, norfluoxetine (NFlx), in rats during the 21-day regimen as well as after cessation of drug treatment. We also measured dopamine (DA) levels in 2 midbrain regions (the striatum, St and nucleus accumbens, NAc) in rats killed 1-14 days after the last dose. NFlx concentrations in plasma and brain were ten times higher than those of Flx during the period of drug treatment. Although Flx accumulated more markedly in the rat brain than NFlx, it disappeared completely from plasma and brain after treatment stopped, while NFlx persisted up to Day P7. Chronic Flx treatment caused a persistent decrease in brain DA levels of -60% to -70% in St and NAc; this lasted for 7-14 days after cessation of treatment, depending on the dose used. The levels of DA metabolites decreased by 20-40%, and, except for 3-MT, tended to overshoot during the recovery period. Our data suggest that the long-term inhibition of DA neurons after cessation of Flx treatment parallels the inhibition previously observed for 5-HT neurons. Thus, besides blocking 5-HT uptake, Flx is likely to also inhibit in vivo DA uptake in forebrain regions, following prolonged administration.
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