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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 2 of 2. This is the beginning of the thread.
Posted by AVR on September 4, 2001, at 13:08:56
Is there a possible way of finding which of the mood related chemicals in the brain you have an imbalance of ? I have dysthymia. It is genetic because a lot of my family had what I'm going through. They just never got help for it. I took paxil which seemed to help my dysthymia for 6 months and after that it still helped but it made me hypomanic.Paxil helped my other problems (touretts(tics), panic and anxiety attacks) but it didn't help my adhd. It made my adhd worse. I failed grade 11 two years in a row because of paxil. I don't know why I kept taking it for two years. I am thinking wellbutrin now but what if my illnesses are not dopeamine and neurpinephrine related but only serotonin? I know tourretts and adhd can be caused by too much dopeamine , wellbutrin is supposed to help this?/? Is tryin different meds the trial and error procedure the only way to go?
Posted by SalArmy4me on September 4, 2001, at 16:16:04
In reply to genetic disorders, posted by AVR on September 4, 2001, at 13:08:56
Trial and error is the only way to go. Drugs that work on just norepinephrine seem to work as well as those which work on dopamine or serotonin:
Frazer, Alan PhD. Pharmacology of Antidepressants. Journal of Clinical Psychopharmacology. 17(2S) Supplement:2S-18S, April 1997.
"The advent of the newer ADs clarifies some issues and raises other ones about mechanism(s) of action of antidepressants. The acute pharmacologic actions of TCAs and MAOIs formed the basis for the 30-year-old monoamine hypotheses of depression, [3-6] postulating a functional deficiency of noradrenergic or serotonergic transmission at key sites in brain. These hypotheses followed the discovery that antidepressants either blocked the reuptake of norepinephrine (NE) selectively, NE and 5-HT nonselectively, or blocked MAO. Because none of the TCAs selectively blocked the uptake of serotonin in vivo, it was difficult to ascertain what effect, if any, serotonin uptake inhibition contributed to antidepressant activity. Several theories were proposed in which different behavioral effects of antidepressants were attributed to these actions on noradrenergic and/or serotonergic neurons. It was speculated, for example, that noradrenergic neurons might be more involved in the ability of antidepressants to increase psychomotor activity or drive, whereas serotonergic neurons were more important for their ability to brighten mood. [7] The development of the SSRIs coupled with the known selectivity of the secondary amine TCAs for norepinephrine uptake demonstrated that drugs with selective effects on either NE or serotonin can ameliorate the components of the syndrome of depression. Further, there seems little evidence to distinguish between the efficacy of these two types of antidepressants or to differentiate among the patients that they help. Whether the initial pattern of behavioral improvement elicited by these two different classes of ADs is similar or different needs to be addressed given that maximal improvement with drugs such as paroxetine or desipramine seems to be equivalent. Finally, it is of interest that drugs that block the uptake of NE or serotonin selectively produce therapeutic effects equivalent to drugs that block the uptake of both monoamines. At present, what we can state with confidence is that most depressives will respond to a drug that blocks the uptake of either NE or serotonin or to one that blocks the uptake of both of these monoamines..."
This is the end of the thread.
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