Posted by SLS on April 15, 2002, at 20:53:24
In reply to Re: high-dose Lamictal: why not?, posted by Mondeo on April 14, 2002, at 23:26:36
Hi Mondeo.
> My opinion as a BP2 sufferer since 1972 !(normally and as usually,I haven't been aware of this dx for so many years and as always,resuming myself thenjust to different AD'S,the best PARTIAL results being obtained then,with Celexa )
I have been suffering from a treatment-resistant bipolar depression for many years. Like so many other people on this board, I have tried most of the available medications along with ECT. I have not yet tried Celexa. I am curious to know how you would characterize your partial response to it. Also, would you be kind enough to list the drugs that have benefited you in the past. For me, MAOIs and tricyclics have been helpful, along with Lamictal. Drugs that have made me worse include Wellbutrin, Vivactil (protriptyline), and reboxetine.
> so MY opinion is that Mood Stabilizers are indeed important or even obligatory(not only for BP1,BP2 etc.,but also for UP's)
That's an interesting idea. I don't think I have seen any studies designed specifically to systematically test the use of lithium and mood-stabilizing anticonvulsants in unipolar depression.
I tend to treat Lamictal as a drug that possesses two separate and distinct therapeutic properties. It might be that its mood-stabilizing and antidepressant effects are in dependant of each other and attributable to separate physiological activities. If this is true, I don't think Lamictal can be considered as an example to support an argument to be made for the utility of mood-stabilizing drugs in general to treat unipolar depression.
Supportive of my treatment of Lamictal as a drug possessing dual thymic properties are the observations that it:
1. inhibits voltage-dependent sodium channels and stabilizes neuronal membranes - a property it shares with the mood-stabilizing anticonvulsants like Depakote and Tegretol. This is most likely the mechanism by which it acts as an anticonvulsant and mood-stabilizer.
2. decreases the concentration of extracellular glutamate in the hippocampus by the inhibition of its release, leading to a reduction in the stimulation of the NMDA receptors found there. The reduction of NMDA receptor stimulation has been observed to increase the levels of dopamine and neuronal activity in areas of the limbic system - brain regions known to be involved in motivational drive and reward. Lamotrigine seems to characterized as a potent inhibitor of glutamate release relative to the other AEDs. I am guessing that it is this property that is responsible for the antidepressant effects lamotrigine demonstrates for both bipolar and unipolar depressions.
- Scott
poster:SLS
thread:100086
URL: http://www.dr-bob.org/babble/20020408/msgs/103183.html