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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 12 of 12. This is the beginning of the thread.
Posted by linkadge on July 12, 2004, at 17:34:57
Was it you who was on a trial of trileptal ?? How is that going. I have my reserves about anticonvulsants but I really want to know what others thing. Havn't heard from you in a while.
Linkadge
Posted by chemist on July 12, 2004, at 19:15:05
In reply to Question for psychosage, posted by linkadge on July 12, 2004, at 17:34:57
> Was it you who was on a trial of trileptal ?? How is that going. I have my reserves about anticonvulsants but I really want to know what others thing. Havn't heard from you in a while.
>
>
> Linkadgelinkadge, psychosage, please pardon the intrusion...i took trileptal not long ago, when the latest dx was bipolar II (we have since reverted to depression, anxiety, and putative adhd: what's next?). my regimen was 300 mg bid, on top of 30 mg dexedrine in divided doses (15/15), 10 mg diazepam bid, and 10 mg ambien hs. this was quite satisfactory for me as my mood was more of a problem than my depression and anxiety: although i am not a fan of the growing grey area around bipolar disorder, i think that at the time i was best characterized as mixed hypomanic, dysphoric, and anxious - not panicky. my girlfriend at the time - and several good friends and colleagues - noticed a profound difference, as did i. i even backed off on the valium, and rarely took more than 20 mg of dexedrine. about 6 months into this course, i developed what is best described as a pesky case of eczema. i was living in a part of the u.s. where humidity is low (which i was not used to), and there was considerable stress at work. numerous visits to the dermatologist at the local medical school were fruitless. i switched to topamax, 100 mg bid, and kept the rest of the meds mentioned above. things went downhill in a hurry, and i lost some pounds i didn't need to lose. but the main thing was, trileptal worked for me (in conjunction with the other meds) over the course of time it was needed. in retrospect, i should have been more objective about my (at the time) dermatological condition that i attributed to trileptal: these things do not appear - as a rule - 6 months after instigation, rather 6 days or a few weeks. again, please forgive my intrusion on your (directed) post, but i did want to relay that my trial with trileptal, although brief, made me even-keeled (although the other meds were a bit excessive, but when the only variable that changed was topamax for trileptal and my condition worsened, i think it's safe to say that the trileptal was indeed working in its own right). besides, it's a safe drug, is metabolized by a different pathway than tegretol, and does not require liver function monitoring. again, apologies for my jabber, but i figured perhaps this might be of use......all the best, chemist
Posted by linkadge on July 12, 2004, at 19:55:49
In reply to Re: Question for psychosage » linkadge, posted by chemist on July 12, 2004, at 19:15:05
If you don't mind me asking, what is your current diagnosis and what are you taking ?
You seem to know about medications and their actions. What is your take on the kindling hypothesis of certain mood disorders?
Thanks,
linkadge
Posted by chemist on July 12, 2004, at 20:31:45
In reply to question for chemist, posted by linkadge on July 12, 2004, at 19:55:49
> If you don't mind me asking, what is your current diagnosis and what are you taking ?
>
> You seem to know about medications and their actions. What is your take on the kindling hypothesis of certain mood disorders?
>
> Thanks,
>
> linkadgehello linkadge....my current diagnosis is interesting. my therapist, psychiatrist, and myself are all on the same page that placing a label on my condition is, for me, not of much use. so we address the issues and actual biochemical problems. the diagnosis is best described as mild to moderate depression - never vegetative or suicidal - coupled with heightened arousal that could by hypomania (i do silly things, but not too silly or self-destructive) or anxiety, the latter of which has been a problem for as long as i can remember. there are some indicators of adhd, but truth be told, i feel that adhd is this week's trendy diagnosis, and even when the chips are down, i remain productive and meet dealines, etc. i am not discounting it, if only for the reason that dexedrine helps me focus and does not make me bounce off the walls. my current regimen is: luvox 100 mg bid; xanax, 2 mg bid; and dexedrine, sometimes none, at most 15 or maybe 20 mg in divided doses. ususally, 5 or 10 mg in the a.m. i've been through a lot over the years, particularly this last one, and am doing just fine (that's the opinion of my therapist, psychiatrist, and others: i would like to be a little more comfortable, but ask for may, settle for june....). as for the kindling hypothesis, i am a believer. first and foremost, sensitization does occur with repeated stimuli, and the only leap one has to make is that at some point the stimuli are no longer required for the responses: they happen in a predictable way. i trust goodwin and jamison's text on manic depression inherently, and while there holes in the theory, i myself can look back over the course of my life and trace how certain events might have led to the ups and downs i have. whether or not i am bipolar or not, i do find the kindling model valid (and not just for bipolar)......all the best, chemist
Posted by psychosage on July 13, 2004, at 5:34:31
In reply to Re: question for chemist » linkadge, posted by chemist on July 12, 2004, at 20:31:45
I have been on trileptal for a year now, and I was up to 1200mg/day {600mg bid}, and now I take 600mg a day because of an interction with trileptal. Trileptal is supposed to decrease levels of provigil, but what ended up happening was I experienced side effects of trileptal {typical ones that aren't particularly intolerable} as if I were starting with it from scratch or increasing the dosage. Therefore, the provigil was making the trileptal more potent, so i felt severely drunk after my morning dose.
Generally, I think it's a solid drug, but I have not been on any other anticonvulsant. The only other antimanics I have taken are antipsychotics. I loathe them, and I don't take them because they are debilitating.
I have posted often about Trileptal, so if you can search you will find I say them same things many others say. The side effect profile is better than other anticonvulsants, and I agree based on what real-time people have told me about lithium {not an anticonvulsant but antimanic}, depakote, topamax, and lamictal.
I asked about Lamictal, and if you can escape the rash it is pretty comparable to trileptal in terms of effect and low side effects.
Depakote can really knock you out I hear.
My impression is that trileptal at the optimal dose can clear your head up, but I am starting to think I need to dose three times a day or increase again because the "vibrations" in my head {drawn out cinematic-type memories, intense emotions {elation/fear/anxiety, inner tension} that draw me to distraction still exist.
I recall you mentioning anticonvulsants as dumb-down drugs, and in a sense they are. However, I have tried to stop seeing psych meds dualistically as activators/sedators, stimulators/tranquilizers or uppers/downers. You always have to makes some compromises, so you may trade in some vivacity in order to avoid the roller coaster bipolar ride. Those grand emotions and thoughts of genius aren't so valuable when you come down and realize how much time you waste in unproductive swings that always leave you craving more.
I am still on Trileptal, and I will stick on it for a while. If I feel I need a switch I would go to Lamictal before anything else.
The only concern about Trileptal is that it does affect other psych meds that are involved with the same liver enzyme as well as the fact you should have blood work done every 6 month or so to check on your sodium levels to make sure they are not too low. Enjoy your salty snacks!
I have not been on much since I have been back and forth from relatives and spending time outside a lot.
Good luck, Linkadge!
Posted by linkadge on July 13, 2004, at 9:04:33
In reply to hey linkdage, psychosage here, posted by psychosage on July 13, 2004, at 5:34:31
The only problem I have with trileptal is that it and tegretol don't seem to have the neuroprotective, and neurorestorative effects of lithium and depakote.
Both lithium and depakote increase BDNF, BCL-2. Lithium also increases NGF. Lihtium users show a robust increase in total grey matter after one month of use. Both lithium and depakote cause a marked increase in cell proliferation and axional growth. Lithium also causes shrunken brain cells to return to normal size.
I've started taking trileptal. It does something, but I don't really feel that it is improving my situation. Yes lithium and depakote had more side effects, but at the end of the day I actually felt as if my situation was improving.Trileptal does not increase any of these growth factors, one study even showed it decreased hippocampal BDNF. At the end of the day I feel like I have not improved at all. To be honest, it feels like valium. It's a real downer.
Linkadge
Posted by SLS on July 13, 2004, at 9:06:40
In reply to Re: question for chemist » linkadge, posted by chemist on July 12, 2004, at 20:31:45
Hi Chemist.
> as for the kindling hypothesis, i am a believer.
I like the kindling hypothesis for mania. Intuitively, it makes sense. To experience mania or watch someone else in a manic state, it is easy to imagine an electrical storm of overly excitable neurons occurring in the brain. In depression, however, with the global reduction of activity throughout most of the cerebral cortex and certain areas of the limbic system, it is a bit harder to conceptualize. However, there are some circuits in the brain that are overactive in depression. Perhaps therein lies the substrate for a kindling model of depression, although one could make a case that these overactive regions are the result of depression rather than its cause. Being depressed is extraordinarily stressful, and places great demands on the individual to maintain psychosocial function. It would not be surprising if those circuits in the amygdala and thalamus involved in the stress response to these demands, including the production of fear and anxiety, were to be working overtime. They might not necessarily be areas subject to kindling.
I think it is more complicated than simply a series of repeated exposures to stimuli. There is most probably a convergence of biological events superimposed upon genetic and epigenetic vulnerabilities that leads to a dysregulation of circuits within the system. It might be necessary, for example, for the hippocampus to be bathed in cortisol chronically as the result of a defect in a feedback loop failing to shut down the normal reaction to stress. I guess one can argue that this is the result of kindling in areas afferent to neuroendocrine links to the adrenal glands, but it could also be due to an exhaustion of the cellular machinery necessary to regulate gene transcription. There are some who suggest that people who develop depression are born with enlarged amygdalas. There are some people with bipolar disorder for whom there doesn't seem to be any precipitating environmental factors. I don't know how such things are determined, though.
I don't know. Sometimes I just don't give a damn.
- Scott
Posted by chemist on July 13, 2004, at 9:36:32
In reply to Re: question for chemist, posted by SLS on July 13, 2004, at 9:06:40
> Hi Chemist.
>
> > as for the kindling hypothesis, i am a believer.
>
> I like the kindling hypothesis for mania. Intuitively, it makes sense. To experience mania or watch someone else in a manic state, it is easy to imagine an electrical storm of overly excitable neurons occurring in the brain. In depression, however, with the global reduction of activity throughout most of the cerebral cortex and certain areas of the limbic system, it is a bit harder to conceptualize. However, there are some circuits in the brain that are overactive in depression. Perhaps therein lies the substrate for a kindling model of depression, although one could make a case that these overactive regions are the result of depression rather than its cause. Being depressed is extraordinarily stressful, and places great demands on the individual to maintain psychosocial function. It would not be surprising if those circuits in the amygdala and thalamus involved in the stress response to these demands, including the production of fear and anxiety, were to be working overtime. They might not necessarily be areas subject to kindling.
>
> I think it is more complicated than simply a series of repeated exposures to stimuli. There is most probably a convergence of biological events superimposed upon genetic and epigenetic vulnerabilities that leads to a dysregulation of circuits within the system. It might be necessary, for example, for the hippocampus to be bathed in cortisol chronically as the result of a defect in a feedback loop failing to shut down the normal reaction to stress. I guess one can argue that this is the result of kindling in areas afferent to neuroendocrine links to the adrenal glands, but it could also be due to an exhaustion of the cellular machinery necessary to regulate gene transcription. There are some who suggest that people who develop depression are born with enlarged amygdalas. There are some people with bipolar disorder for whom there doesn't seem to be any precipitating environmental factors. I don't know how such things are determined, though.
>
> I don't know. Sometimes I just don't give a damn.
>
>
> - Scotthi scott.....i must say i omitted the side of the kindling hypothesis you mention, as do goodwin and jamison, who point out the same things you do. in citing kraepelin (1921), g&J give more than a nod to it: ``We must regard all alleged injuries as possibly sparks for the discharge of individual attacks, but that the real cause of the malady must be sought in permanent internal changes, which at least very often, perhaps always, are innate... Unfortunately, the powerlessness of our efforts to cure must only too often convince us that the attacks of manic-depressive insanity may be to an astonishing degree independent of external influences (pp. 180-181)'' g&j follow this quote with their observation that ``However, the independence from external influences appears to develop over time...It was, in fact, Kraepelin who first noted that precipitating events play an important role in the onset of the first few episodes, but then, as the illness unfolds, the process driving the onset of new episodes seems to become more autonomous, with stressful events contributing little or nothing.'' and so on...perhaps my (revised) position can best be summed up in another gem from g&j: ``Early precipitating events, rather than merely influencing the timing of an episode, may actually activate the preexisting vulnerability, thereby making the individual more vulnerable to the next episode.'' anyhow, like you, sometime i don't care why, but more ``how can we address this?''.....anyhow, thanks for the food for thought, i do enjoy your posts. all the best to you, chemist
Posted by SLS on July 13, 2004, at 16:56:43
In reply to question for chemist, posted by linkadge on July 12, 2004, at 19:55:49
Hi Linkadge.
Speaking of hypotheses, at this point in your studies, do you believe that it is actually neurogenesis that produces the antidepressant response as early as the second week of treatment, without which no improvement is otherwise experienced?
- Scott
Posted by linkadge on July 13, 2004, at 18:36:00
In reply to Re: question for linkadge » linkadge, posted by SLS on July 13, 2004, at 16:56:43
I think a mood disorder is composed of two things.
First, there is the abnormal circutry and cellular structure that caused the HPA axis disregulation,
and then there is the HPA axis disregulation that caused the amormal circutry and cellular structure.
I think that some of the newer mood stabalizers are doing nothing more than short circuiting the limbic system. Good mood stabalizers (so far the only time tested ones) like lithium and valproate acutally repair some of the dammage.
Stopping the cyle is not necessarily sufficiant to ameliorate/reverse the underlying disease.
lithium has an antisuicide effect that is not shared by the other mood stabalizers.
Linkadge
Posted by rod on July 14, 2004, at 5:57:50
In reply to Re: question for linkadge, posted by linkadge on July 13, 2004, at 18:36:00
> I think that some of the newer mood stabalizers are doing nothing more than short circuiting the limbic system.
hmm, maybe this is a stupid question and you have explained this before, then sorry for asking again, but I just dont understand what you mean.
So how and why do they "short circuit" the limbic system?thank you
Roland
Posted by linkadge on July 14, 2004, at 8:20:03
In reply to Re: question for linkadge » linkadge, posted by rod on July 14, 2004, at 5:57:50
I think that the right medication helps you to see your problems in a different light. They help the depression, without taking away your joy.
Anticonvulsants, sedatives, alchohol etc, can help certain forms depression, but they simply dampen down all nerve activity. They may quench crippling emotional pain, but they can also rub out joy, motivation, excitement etc, ie. they're short curcuting emotion. They're what we've got right now however.
Some of the newer treatments on the horizon purportedly target the source of the problem better.
Linkadge
This is the end of the thread.
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