Posted by SLS on September 23, 2009, at 7:03:15
In reply to Re: depression + executive function, posted by linkadge on September 23, 2009, at 6:53:41
Hi.
I like Linkadge's explanations.
Here are a few of mine that doesn't take all of his into consideration:
> i was just curious whether it's productive to consider executive function issues apart from depression in terms of etiology
Probably not. Much of the hypofunction you allude to is reversed upon recovery from depression. That is, of course, unless there is comorbid ADD. To add a stimulant might help if the response to antidepressants is incomplete.
As seen through a PET Scan, most of my cerebral cortex, including prefrontal areas, were hypofunctioning during depression. This is corroborated by the observation of cognitive deficits and slow-thinking with me. I do not have ADD. As I have recovered from depression in the past. During times of remission, all of my cognitive powers seem to return along with an improvement in memory.
> most of my issues look like the negative symptoms of schizophreniaYes. This is what is often seen in bipolar depression. What you experience is sometimes described as the "deficit syndrome". Although more often used to characterize schizophrenia, this term has been used from time to time with depression.
> i was wondering if it's pointless to think of this as a 'low dopamine' depression?
Yes and no. It is too simplistic an idea if one sets out to try dopaminergic drugs exclusively. With depression (especially bipolar depression), deficits in the function of dopaminergic pathways may be the final step in a series of biological anomolies. As an example, SSRIs, drugs without direct dopaminergic effects, are capable of precipitating mania, presumed to be a hyperdopaminergic state.
> if it's just a shade of depression that can be caused by anything, or if there's some path i should be taking? i guess i'm just wondering if Parnate is the right way to go, or if i should be looking at something more receptor specific like the atypical AP's.
Parnate is a good choice of drug simply because it works. This is an empirical observation that is independent of whatever theories we would like to apply to its effectiveness. Parnate is one of the more effective treatments for bipolar depression. Interestingly, the application of high-dose Parnate (120mg and above) downregulates serotonin 5-HT2a receptors. This might be be a reaction to the accumulation of 5-HT in the synaptic cleft, but that doesn't explain why such is not seen as readily at lower dosages. Parnate almost certainly does things other than inhibit the MAO enzume.
> my EF issues
What are EF issues?
> seem to get more severe with time, and make it hard to stick with a treatment, since i can't really 'plan' or commit to a decision. there were some days on Memantine where i felt completely normal - calm and able to make decisions that 'felt right', but it wasn't very consistent in effect.
Have you tried Lamictal? It also works to reduce glutamate activity.
> i often feel like if my executive + social function improved, my depression would lift,
It has been my observation that executive + social function improve only upon the recovery from depression, and not before. It also seems be proportional to the degree of antidepressant response. With more severe depressions, I don't think it is likely that one can budge the biology very much by working on the psychology. This has been my experience, anyway.
> but again is that just a chicken/egg thing?
Off topic: The egg has my vote. I think the egg came first, as it is from the genetic mutations in germ cells that new phenotypes are expressed.
- Scott
poster:SLS
thread:918139
URL: http://www.dr-bob.org/babble/20090921/msgs/918143.html