Posted by SLS on July 29, 2014, at 11:24:55
In reply to Re: ongoing akathisia, posted by g_g_g_unit on July 29, 2014, at 8:58:24
> > Although there are many possible hypotheses for the pathophysiology of acute akathisia, all are insufficient and incompletely satisfactory, but it is unlikely that a single neurotransmitter hypothesis will explain all the complex features of the disorder, and the interaction of several neurotransmitters is undoubted involved.
> >
> > Research seems to indicate that akathisia likely arises from complex interactions of the dopamine/norepinephrine systems in the subcortical area of the brain and possibly spinal cord. Historically, the most attractive hypothesis explaining akathisia the so-called Dopamine hypothesis predicts that akathisia will result from blocking dopamine receptors on nerves in the mesocortical and mesolimbic regions (areas of the brain involved in regulation of motivation, attention and reward).
> >
> > I would focus on drugs that agonize dopamine. Requip, Mirapex and Cogentin are all options.
> >
> > Eric
>
> NMDA antagonists also supposedly help. I've been having quite a noticeable improvement since starting Magnesium Threonate a few days ago. Once I get to a doctor, I'll discuss the other options.
If you find other treatments inadequate, you could explore using 5-HT2 receptor antagonists like cyproheptadine or low-dose mirtazapine, perhaps in combination with propranalol.
- Scott
>
Some see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1068586
URL: http://www.dr-bob.org/babble/20140717/msgs/1068937.html