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Dr. Bob is Robert Hsiung, MD,
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Posted by Dinah on December 11, 2005, at 9:46:00
Also a fair amount of forgetting what I was saying midway through a sentence. Admittedly the latter two come naturally to me, but lately they've started to become a problem. And of course the first is always a problem.
I'm only sort of complaining, because I'm not sure I can do without the meds for migraine and anxiety right now.
But I am curious. Those are the exact same things that happened to me on an SSRI (Luvox) and went away when I stopped Luvox. And they seem to be such very specific problems that I'm curious as to how another drug could cause the exact same symptoms without being an SSRI.
Right now I'm on
Glucophage 500 mg (supposed to be 1000 mg but I always forget my morning dose) for diabetes
Omacor (too recently for it to have caused the problem) for triglycerides
Klonopin 1 mg (been on that forever, at nighttime) for anxiety
Provigil 100 mg for what my neurologist is positive is narcolepsy although I (and the sleep test) disagree
Risperdal .25 mg - between zero and six pills per day, usually 2-4 for anxiety
Lamictal 25 mg for migraines and mood stabilization
Any guesses as to culprits (I'm thinking either Risperdal or Lamictal) and more importantly why would anything I'm taking now have the exact same side effects as an SSRI?
Posted by zeugma on December 11, 2005, at 10:53:36
In reply to Anorgasmia and word substitution, posted by Dinah on December 11, 2005, at 9:46:00
I have severe proper name name anomia (can't remember people's names, even people's names I know quite well, though weirdly this only obtains when I am dealing with with people in auditory contexts (conversations) and not say with people I talk with via computer. I know I've always had this, but it seems more evident to me lately. I take 300 mg Provigil for putative narcolepsy (sleep tests ambiguous IMO although the sleep clinician disagreed) and unambiguous severe ADHD and fatigue. I also take 1 mg clonazepam for anxiety, in divided doses am and noon. Clonazepam above 1 mg causes severe cognitive difficultiesm though I don't know how much of this is due to nonspecific effects of sedation and how much is selective impairment of memory as opposed to global impairment of functioning.
It could be that Provigil, since I tend to notice more of my environment, causes increased awareness of what was already prominent (and ridiculous- I would have extended phone conversations with people whose names I could not recall for the life of me, though I did in fact know who they were). Also, since clonazepam lets me have more normal (not normal by any stretch of the imagination, but at least not panic-inducing) interactions with others, I may fixate more n the inability to deal with proper names since I'm not feeling like death is literally impending.
My Provigil is going to run out soon, and I will have to switch to Ritalin for the bulk of the month. My impression is that ritalin did help with the anomia, although it is hardly worth it for me b/c of its other side effects (please do not get me started on irrationality of pdoc's precribing practices, it has been the cause of considerable suffering). Ritalin definitely antagonized clonazepam's effects, including anxiolytic ones. Again, not worth it, but stupidity of prescribing practices is not a subject I can easily discuss without becoming very irritated.
As for anorgasmia, that has always been a problem, not linked to any med. Buspirone did help for a while. What can I say, life is frustrating.
-z
Posted by med_empowered on December 11, 2005, at 12:08:34
In reply to Re: Anorgasmia and word substitution » Dinah, posted by zeugma on December 11, 2005, at 10:53:36
hey! Maybe the Risperdal? I read that you can't use Risperdal in people with severe LSD (or other hallucinogen) induced flashbacks. LSD is believed to operate in large part on serotonin. SSRIs sometimes cause a renewal of flashbacks. Apparently, Risperdal is kind of like the SSRIs in this regard; instead of treating the hallucinations, it can actually make them *worse*...my guess would be that at lower doses, the ratio of serotonin: dopamine antagonism boosts levels of serotonin considerably...at higher dosages, though, Risperdal is pretty comparable to Haloperdiol in terms of side effects, so I guess the higher dosages involve a more old-drug style reduction in both serotonin and dopamine. So...there you go; thats my theory.
Posted by Phillipa on December 11, 2005, at 12:13:25
In reply to Re: Anorgasmia and word substitution, posted by med_empowered on December 11, 2005, at 12:08:34
Dinah I can relate to the forgetting. But I'm like z anorgasmia has always been a problem for me unrelated to med. Hey zeugma Babblemail me and let's compare notes. Fondly, Phillipa
Posted by Dinah on December 11, 2005, at 15:32:10
In reply to Re: Anorgasmia and word substitution » Dinah, posted by zeugma on December 11, 2005, at 10:53:36
I know what you mean about prescribing. I'm so happy with my pdoc now because he listens to me and believes me.
I kind of discount the klonopin since I've been on it for.... hmmmmm.... nine years? at the same dose.
I hadn't considered the Provigil. In general it's been so helpful, once I got used to the start up effects, in my work.
My neurologist also wants to keep the narcolepsy label, even though the sleep study showed some abnormalities in my sleep architecture, but ruled out narcolepsy. He wants me to take another study. I don't have huge confidence in him, which probably affects my attitude a lot, and my belief in his diagnosis. My mother's family is just full of narcoleptics and idiopathic hypersomnia. Maybe I should just look for another neurologist and get a second opinion.
Posted by Dinah on December 11, 2005, at 15:34:21
In reply to Re: Anorgasmia and word substitution, posted by Phillipa on December 11, 2005, at 12:13:25
Perhaps because my main issue has always been anxiety rather than depression, and because even my depressions are the agitated sort, anorgasmia has *never* been a problem for me except on that one medication, now two.
I actually find it a nearly intolerable side effect, and it's a measure of how much I think I need those meds that I'm willing to put up with it.
Posted by Dinah on December 11, 2005, at 15:37:02
In reply to Re: Anorgasmia and word substitution, posted by med_empowered on December 11, 2005, at 12:08:34
That sounds like a good theory!
It would seem very odd to me if two different classes of medications had such specific similar effects without something going on there.
One thing I will say is that SSRI's caused a bit of loosening of inhibitions and some increased anxiety, neither of which has been a problem on my current meds.
Posted by jrbecker on December 12, 2005, at 10:36:25
In reply to Re: Anorgasmia and word substitution » med_empowered, posted by Dinah on December 11, 2005, at 15:37:02
I have experienced word recall problems on many different meds. Probably the worst offender for me was Lamictal. Second to that was selegiline and also Wellbutrin at higher doses. Both Cymbalta and Effexor are mild offenders at times but only at the higher doses. Ironically, both stimulants and benzos also exacerbate these problems, although it's probably that the latter causes general memory recall issues rather than the more specific issue of word recall. As for the stims, I think this is partly due to the "hyperfocus" effect that this has on some users. Also, I tend to have problems when coming off a dose rather than when its having full effects. When in combo with ADs, drinking too much caffeine can also bring on this effect. A recent study highlights this phenomenon...
http://news.bbc.co.uk/2/hi/health/3909085.stm
The problem probably involves multiple chemical pathways, but dopamine seems to be highly implicated. Recent studies have pointed to an optimal window of dopamine levels where memory would function effectively (not too high or too low)...
Under the curve: critical issues for elucidating D1 receptor function in working memory.
Neuroscience. 2005 Nov 24
Williams GV, Castner SA.
It has been postulated that spatial working memory operates optimally within a limited range of dopamine transmission and D1 dopamine receptor signaling in prefrontal cortex. Insufficiency in prefrontal dopamine, as in aging, and excessive transmission, as in acute stress, lead to impairments in working memory that can be ameliorated by D1 receptor agonist and antagonist treatment, respectively. Iontophoretic investigations of dopamine's influence on the cellular mechanisms of working memory have revealed that moderate D1 blockade can enhance memory fields in primate prefrontal pyramidal neurons while strong blockade abolishes them. The combined behavioral and physiological evidence indicates that there is a normal range of dopamine function in prefrontal cortex that can be described as an "inverted-U" relationship between dopamine transmission and the integrity of working memory. Both in vivo and in vitro studies have demonstrated a role for dopamine in promoting the excitability of prefrontal pyramidal cells and facilitating their N-methyl-d-aspartate inputs, while simultaneously restraining recurrent excitation and facilitating feedforward inhibition. This evidence indicates that there is a fine balance between the synergistic mechanisms of D1 modulation in working memory. Given the critical role of prefrontal function for cognition, it is not surprising that this balancing act is perturbed by both subtle genetic influences and environmental events. Further, there is evidence for an imbalance in these dopaminergic mechanisms in multiple neuropsychiatric disorders, particularly schizophrenia, and in related nonhuman primate models. Elucidating the orchestration of dopamine signaling in key nodes within prefrontal microcircuitry is therefore pivotal for understanding the influence of dopamine transmission on the dynamics of working memory. Here, we explore the hypothesis that the window of optimal dopamine signaling changes on a behavioral time-scale, dependent upon current cognitive demands and local neuronal activity as well as long-term alterations in signaling pathways and gene expression. If we look under the bell-shaped curve of prefrontal dopamine function, it is the relationship between neuromodulation and cognitive function that promises to bridge our knowledge between molecule and mind.
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