Tldr, info on managing chronic dissociation/dpdr and ptsd pathophysiology is more or less useless or lacking significance/what to do about findings. Any input?
Alright can someone who isn't retarded clarify some things. In the context of ptsd itself but also emotional numbing/dissociation which of the below are true and the most heavily involved? Literature is usually just rambling with little useful data besides "x might be correlated with y based on skin conductance study" or generally shit everyone knows. This is for independent research reasons and I'd ask reddit but they just give useless replies for the sake of typing.
>General over activation of the PFC as a whole/under activation. Ie would it be therapeutically significant to reduce or increase activity as a whole
>Regarding the above (activity not the PFC specifically) , which regions are the most implicated and again, under or over activated? Off the top of my head I'm referring to the ACC, VLPFC, VMPFC, DLPFC (doubt), HPA axis, OFC, temporal lobe and TPJ. Similarly what options (again we need to know activity) do we have to directly affect these non pharmacologically? rTMS, dTMS/Theta burst, ECT and neurofeedback are all I can think of. Also again which should be prioritized.
>Regarding the above regions AGAIN in the context of neurochemistry, what sorts of targets are we looking at for general usefulness? In this case I'll give my inferences for agonism and antagonism via "am" and "ant" respectively, "?" is not sure of significance. 5ht1a (am), 5ht2a/c (ant). Not sure how useful these are: 5ht1e/d/f(?). a1 (ant/?), a2 (ant), b1 (ant), b2 (ant/2?). D1 (am/?), D2 (am/?, ant can eat a dick). AMPA (ant/?), NMDA (ant (I have reasons)), related a2d subunits/VDCCs etc(ant). mACHr (do we even intentionally touch this for psychiatry), nAChr (depends?). GABAa (am (not acutely post ptsd)). GABAb idk. Forgot if it was PAMs that do this.
Cunt 1/2
