Hello,
please take a minute to contemplate my theory of tDCS. I see some of you here are quite knowledgable in the field.
it's been a while since I posted here. I've posted about HPPD before, yet this time I've put a good amount of effort into studying it's neuropathogenesis and related mechanisms, before posting anything. The following is merely a quick summarization of the more conclusive research I have conducted.
- If one were to have disinhibition of the visual apparatus1
- caused by MDMA2
2Note: LSD also modulates 5-HT2A receptors among others.3 - would cathodal stimulation of the occipital lobe4 5
- cause inhibition of the visual apparatus?
- And would anodal stimulation of the prefrontal cortex6 7
- enhance Prepulse Inhibition8
- inherently inhibiting sensory input/occipital disinhibition.9
- Thus, aside from cognitive enhancement, relieving one of visual perception distortions via this dual action inhibition?10 11
11Higher Phosphene Threshold = less phosphenes (flashes of light, common in HPPD)
I speculate the theory above is correct and will relieve me of my perception disorder, and hopefully others as well. Moreover, the information and referances provided above are only a fraction of what I have discovered to support this theory. Also, this is only one of many methods to alter this mechanism. Other, less developed theories, include calcium modulation (crucial I believe), NMDA modulation (agonism I believe raised PPI, but I haven't looked into it), glutaminergic modulation, obviously 5HT2A/2C plays a role (antagonism or inverse agonism would seem to ameliorate symptoms, see above. I have more studies regarding its relationship to HPPD pathogenesis, and are planned for future reviewing), DA modulation is already implemented but D2 specifically seems to be involved in various ways, and one of my most recent discoveries has been the possible involvement of the S100 proteïn and it's anti-bodies, and Calmodulum (see, calcium again, it's all interrelated).
Clonazepam seems to be a popular treatment for HPPD, but I rather not touch the stuff with a 20ft barge pole.
In the meanwhile I've been trying to get a prescription for Levetiracetam, but even that shows to be a mission by itself.
This is why I have ordered Tenoten (S100 anti-bodies), but that will take a couple of weeks.
The alternative is to wait another 6 months (I suspect) to get written down on the waiting list to see a neurologist, to wait another couple of months to get a qEEG, etc. etc. and by the time I'm 40 then maybe, just maybe, I'll find someone who's willing to help.
This is why tomorrow I am contacting a private institution specialized in helping cases subject to tedious incompetence, to have a qEEG and start tDCS. Albeit not knowing whether it will help or not, it seems like it at the very least wouldn't make things worse.
Lastly, I have already contacted on of the few experts in HPPD. Impatience got the best of me, this is why I posted here.
If you need further clarification, please ask.
Many thanks in advance.














