Cotcha....what do you think about FBC's theory on the face tingling:
"The HPPD is caused by serotonin up-regulation in the visual cortex. This happens to maintain bloodflow to this region. When serotonin levels drop, certain parts of the brain experience a drop in bloodflow."
This is my first time hearing about this theory of his but there are a few problems with what he's saying
Just as a primer, some 5-HT2A receptor upregulation (about 20% in chronic abusers) has been spotted in some prior MDMA abusers. This is the receptor that is chiefly responsible for psychedelic visuals - basically all psychedelics work via 5-HT2A. Anyways, the problems are thusly
1. If 5-HT2A upregulation in the cortex is causing HPPD symptoms, then a 5-HT2A inverse agonist (a blocker like pimavanserin, risperidone, mirtazapine) should be curative of symptoms. From what I've read, this doesn't seem to be the case. Pimavanserin would be the best test for this theory so I'll leave that as a caveat.
Pimavanserin is used to treat visual hallucinations in Parkinson's disease that are due to 5-HT2A supersensitivity, however Parkinson's disease patients usually have pretty darn marked hallucinations, not just visual disturbances.
2. The relationship between serotonin and cerebral blood flow is complex. 5-HT2A/5-HT2B and other receptors like 5-HT1B/5-HT1D located on arteries mediate vasoconstriction, so in that instance a drop in serotonin could actually cause vasodilation. There are meds like sumatriptan that work for migraine by constricting the arteries - its an activator of 5-HT1B/5-HT1D receptors. So in that sense, blood flow may not necessarily drop when serotonin drops. Some studies of meds that work on serotonin seem to support the idea that the relationship between serotonin and blood flow is very region dependent.
To complicate matters, there is a relationship between neural activity, cerebral blood flow and changes in the microvasculature structure such so that an increase in brain activity is followed by an increase in blood flow to that region.
Since 5-HT2A is the principle excitatory serotonin receptor throughout the brain, increased activity of 5-HT2A on neurons might be expected to
increase bloodflow, and as an aside the thalamic visual processor called the LGN and the visual cortex have actually shown to have
increased blood flow and excitability in MDMA abusers during some tasks (MDMA abusers who are not necessarily representative of the HPPD symptom people, but these people should have serotonin upregulation in visual cortex yet they also have increased blood flow there during some tasks)
As a caveat, 5-HT2A isn't the only receptor at play here, and studying the brain on psilocybin (magic mushrooms) with blood oxygen related techniques is a bit difficult specifically because psilocybin can cause a decoupling of the link between neural activity and cerebral blood flow. There is some question of whether the observed blood flow changes track very closely with the neural activity that we actually care about.
"This is why you are having sensations on your face. Different parts of the brain are connected directly to the nerves on the face/head. That's why elderly people with strokes sometimes have facial paralysis. What you are feeling is decreases/increases in blood flow to specific regions of your brain."
I would care to differentiate between sensory nerves and motor neurons here, and also stroke is a shitty example. Facial
paralysis from stroke is most likely coming from issues with the brain but facial
palsy can often come from issues with cranial nerves in the periphery.
By and large neuropathic symptoms of the cranial nerves seem to come from the periphery. As an example, I had pins and needles over one side of my head that were relieved by manual release of the back of my head/neck (where these relevant cranial nerves are). We also have occipital neuralgia, a condition with visual symptoms involving the cranial nerves in the back of the head in which people can have various head symptoms that are relived by lidocaine injection into said cranial nerves.
One thing that you'll notice is that the community is all over the place on HPPD theories. We have Henry Abraham who had proposed at one time that HPPD symptoms were due to a loss of 5-HT receptors, now we have FBC suggesting its due to
too many serotonin receptors.
This kind of a sign that its all conjecture, when people are proposing completely opposite theories. I'm happy to throw in my shitty conjecture as well, but there is at least precedent for cranial nerves causing visual symptoms among other symptoms like the head tingling and pressure
keep going guys I'll check back in six months!