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tDCS research: a potential treatment for a rare neurological disorder

tdcs hppd

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9 replies to this topic

#1 formergenius

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Posted 07 May 2013 - 02:38 AM


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)
Important: Pathogenesis of both HPPD and Schizophrenia seem to overlap, but marginally. DA hypothesis with SZP has been argumented, and the overlap with HPPD is derived from the fact 5HT2A/2C modulation seems to be a crucial component in the pathogenesis of both disorders. Evidence points out that antagonism/inverse agonism of 5HT2A Furthermore there is an overlap with PPI, in that both disorders are charactarized by low levels of PPI. DA involvement however seems contradicted between the pathogenesis of the two disorders. And no, I am not psychotic :-D

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.

#2 formergenius

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Posted 07 May 2013 - 10:44 AM

Hmm can't seem to edit the post. If left a sentence unfinished in the red typing there.
"agonism of 5HT2A ameliorates symptoms in both disorders".

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#3 medievil

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Posted 08 May 2013 - 11:57 PM

5HT2A is hypoactive in shizophrenia.

#4 formergenius

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Posted 09 May 2013 - 01:20 AM

Thanks, I'll re-evaluate that.

#5 formergenius

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Posted 09 May 2013 - 01:31 AM

Recent related research I have found is linked above.


Update:
"For example, prepulse inhibition (PPI) is a widely accepted animal model of schizophrenia. If PFC LTP-induction can reverse PPI abnormalities, neurotransmitters that play a role in animal PFC LTP may become promising targets for new psychopharmacological approaches."
-Oxford Handbook of Transcranial Stimulation


Update 2 (NTS: goldmine?): [PDF]Reducing Intracortical Inhibition in the Adult Visual Cortex Promotes Ocular Dominance Plasticity

Note: haven't read the study yet, could be unrelated(update 2)

Edited by formergenius, 09 May 2013 - 02:13 AM.


#6 formergenius

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Posted 09 May 2013 - 02:34 AM

5HT2A is hypoactive in shizophrenia.


Observe the following:
In' class='bbc_url' title='External link' rel='nofollow external'>http://www.ncbi.nlm.nih.gov/pubmed/8935804']In summary, these data indicate that serotonergic overactivation can disrupt auditory and visual sensorimotor gating as measured using sound and light prepulse inhibition in rats. These data support a potential role of excessive 5-HT activity as a contributing factor to disrupted sensory gating processes seen in schizophrenia and possibly other neuropsychiatric disorders.

→ source (external link)


Again, I have this written down for re-evaluation.

Edited by formergenius, 09 May 2013 - 02:35 AM.


#7 soulfiremage

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Posted 19 May 2013 - 02:21 PM

Did you ever apply the tdcs to your problem in the end?

#8 formergenius

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Posted 23 May 2013 - 11:12 PM

Hmm tried it twice with succes (in co-morbid symptoms), albeit transiently.
However I have the possible oppertunity to get a medication prescribed for my condition, which has shown to be quite effective.
I will let that take effect before continuing this research. Also I would really like to apply HD-tDCS to this theory, for its enhanced focality.
We'll see, digression for now :)

#9 Multicultural Harmony

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Posted 28 December 2013 - 12:14 AM

I am currently reading 5-HT2C Receptors in the Pathophysiology of CNS Disease by. Di Giovanni. It is dense and boring but full of crap I've picked from pubmed over time. One receptor with many tricks. I currently don't have the mental energy to divulge more.

It is a good place to start if you want to know all about this receptor.

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#10 formergenius

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Posted 28 December 2013 - 12:21 AM

Thanks for that Pitolisant. Been a while back since I explored this area.. dunno who bumped my thread :P
Co-incidentally I just shaved my head 2 days ago; figured I'd give tDCS another go whilst I wait for NSI-189.
If I see any improvements I'll be sure to post it.





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