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Possibly new "evidence" in phatophysiology of HPPD.


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I have some news for you guys. Doctor Rafael Higashi in Rio De Janeiro, who is a neurologist, nutritionist and a specialist in TMS/tDCS that I have started consultations with. He seems to be a very decent person with a great approach towards his profession. After the first consultation I received a 25 pages long and in-depth form to fill out with many very detailed questions about my body and mental health. This is first time I came across such detailed examination. Every doctor that consider his job serious should be doing the same.
Doctor Rafael got me to do scintigraphy examination before proceeding with tDCS. It is similar to SPECT/PET, but from what he said - Scintigraphy only shows underactivity in the brain. I think he said SPECT - can show both over and underactivity.
I did the examination and this is what came up (in portuguese):
A analise das imagens tomograficas (cortes transversais, sagitais e coronais) e da reconstrucao tridimensional obtidas apos a administracao EV do radiotracador (99m Tc - ECD) evidencia areas de hipoperfusao na projecao do lobo front-paretial superior (bilateral) e fronto temporal (esquerdo, discreta), bem observado nos cortes tomograficos transversais nos 11 ao 13, coronais 16 ao 18 e sagitais 7 ao 10, bem como nas reconstrucoes tridimensionais.
Translation by google:
The analysis of CT images (cross sections, sagittal and coronal) and three-dimensional reconstruction obtained after the administration of EV radiotracer (99mTc - ECD) evidence of hypoperfusion areas in the projection of the upper front-paretial wolf (bilateral) and fronto temporal (left , discrete) and observed in cross-sectional tomographic cuts 11-13, coronal and sagittal 16-18 7-10 as well as in three-dimensional reconstructions.
Hypoperfusion for those who don't know is a decreased blood flow through an organ.
Since I showed him the studies about HPPD and VS and he assumes that I do have overactivity in the occipital area as shown in one of the studies, hence the visual hallucinations. 
Doctor Rafael explained to me one of the affected parts of the brain is responsible for language, but he indicated that its to do with the thoughts we hear/think to ourselves and the other area being responsible for planning (and so I guess critical thinking). I am not sure what fronto temporal stands for, but I will find out later (looks like wrong translation). 
I am going to be treated with tDCS - he said this could activate those areas. 

I asked him what he thinks about HPPD, why those areas have less activity, is it that some receptors became damaged? He answered that he doesn't think its a damage of receptors - if that was the case I would not be functioning properly (biologogically I guess). He added that it's more to do with insufficient production of neurotransmitters and that tDCS could increase it. 
He picked a protocol for me of tDCS. The anode (+) will be located at FZ point (between front and middle of the head) and the cathode somewhere at the back of the head. The anode will stimulate one part/increase the activity and the cathode will lessen the activity in occipital area.
Fingers crossed ! I am starting the treatment tomorrow. Will let you know of the progress.
A friend got a very bad reaction with one session of tDCS, his hppd worsened so that he felt like after taking ayahuasca (in terms of hppd symptoms) for day or two, but I think it went back to normal after few days. He discontinued the therapy. He had a different protocol though. It was for depression instead of for the parts affected by hppd specifically. 
I also asked the doctor to prescribe me Sinemet which I will make another post about, because I have some worries about it and how it can affect me. 
Regarding the evidences - I haven't heard about hypoperfusion in any person with HPPD. Is my case different or am I the first one to have this kind of examination done? I hope this will shine some light on our understanding of HPPD.
New things to wonder about.. why those parts of the brain undergo hypo/hyper perfusion and what mechanism could cause it? How could it be dealt with? I hope tDCS is some kind of answer to the last question. 
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