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Bit of an idea for possible CURE. Has some weight to it.


Fawkinchit

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Guess it is how you define Visual Snow

Blue field entoptic phenomenon: "the dots keep darting around" ... "The dots are white blood cells moving in the capilaries in front of the retina of the eye" ... "The dots won't appear at the very center of the visual field" Note: If you see it in the center of your vision, it isn't BFEP. http://en.wikipedia....ptic_phenomenon

orgon.gif

Floaters "are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent" http://en.wikipedia.org/wiki/Floater

Floaters.png

Scintillating scotomais "the most common visual aura preceding migraine and was first described by 19th century physician Hubert Airy (1838–1903). It is often confused with ocular migraine which originates in the eyeball or socket." http://en.wikipedia....llating_scotoma

Scintillating_scotoma.gif

Visual Snow "is a transitory or persisting visual symptom where people see snow or television-like static in parts or the whole of their visual fields, especially against dark backgrounds. It is much like camera noise in low light conditions." http://en.wikipedia....iki/Visual_snow

visual-snow-simulation.gif

It isn't so easy to distinguish some of these. However, I've never experienced BFEP since symptoms have always been in entire visual field. There is one (in this "snow" category) where it looks like smoke but in traveling patterns (some others have described) which doesn't fit any of these ... perhaps close to CEV definitions.

Getting accurate pictures is not so easy. Googling give images that are clearly misapplied. BFEP and Floaters are NOT visual snow.

Wish List to Administrators (and willing assistants): Make a standard list (with illustrations when applicable) of All HPPD symptoms, including comorbids stuff like anxiety, brain fog, tinnitus, body-pains, etc. Then pin it. Then make some kind of poll/survey that people can use like a medical interview. It should also be possible to take at yearly intervals to track progress of symptoms and/or recovery.

This would facilitate collecting detailed information which then could be applied to research including medical responses, psychological adaptation, etc. I realize that probably additional programming would be needed to fully implement ... but the categorizing of symptoms (definition of project) can start now.

Frankly, I don't see how we can make progress on HPPD without establishing this goundwork. If I read correctly, there is already work on way to get the DSM definition of HPPD "corrected". I realize that there has been poor participation in the simple existing polls, but perhaps there would be more enthusiasm to participate in a full scale "interview". This has got to be more productive than posting scattered articles about brain functions, research, and the like. Continuity is even more important than reductionism. And how can you "cure" a problem without accurately defining it?

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I definitely see the BFEP kind of movement in the center of my vision.... So it is either something that is very, very similar, or wiki is wrong..

It is that exact movement, just more particles and flashes faster. If I look at something non defined.... It looks more like normal VS, but if I concentrate on it (blue sky)... it is just like BEFP.

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Yea, Wiki is full of crap. However since BFEP is from white blood cells flowing in the capillaries, note the vascular structure around our center vision:

Snodfovea.jpgFoveal-Avascular-Zone.jpg

So perhaps we can give Wiki an "A" or "B"?

As a side point, the human retina is "inverted". This means that the blood vessels are in front of the photoreceptors (in between the light and the receptors) so that light has to travel through the blood vessels.

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BFEP: I don't have it as bad anymore; but when i was kinda normal i had it thick, Thick, like 2,000 surface-floating bugs in a dance. [esp. when i looked at the sky].

...Oh and yea...It was in my entire field of vision ....

and it seemed almost mainly in the center area.

[the very center area maybe so small that it is virtually un-perceivable].

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If I cover one eye... I see a very, very small "shadow" in the center that perhaps isn't as active as the areas around it.

With both eyes open, this area reduces to nothing, as the centers of vision of each eye overlap.

What I don't get though is the flashing seems to be sync'd with my CEVs.... Surely CEVs in a pitch black room can't be BFEP related?

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the very center area maybe so small that it is virtually un-perceivable

Yes and No. Since the center is where nearly all of your visual attention is, then it is significant even if relatively small. Ask a person with macular degeneration (which only affects this area) if this is un-perceivable.

What I don't get though is the flashing seems to be sync'd with my CEVs.... Surely CEVs in a pitch black room can't be BFEP related?

CEVs have to be the brain given the complex shapes and movement. However, non-HPPD people can generate mild CEVs by gently pressing and messaging their eyes. This would suggest that the mechanical stimulation increases (generates) signals from the retina that the brain tries to contruct into something real ... so you get CEVs. This would also match what were are told about HPPD, namely 'cerebral disinhibition' (over active cortex).

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Yea, my only grandparent has macular degeneration and my father has a partial vitreous detachment.

And i've had scintillating scotomais.

Not fun stuff boys and girls.

What's the cause our problem?: interference and signal anomalies.

Maybe it's time to change the spark plugs. <shakes head>

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8:00 AM November 27th, 2012

Acadia Pharmaceuticals announces the results of the Phase III trials for a possible-new class of antipsychotics for use with Parkinson's Psychosis.

These are the 5ht2a inverse agonists. The drug is Pimavanserin. If found effective, it could end up being used for a whole group of psychiatric disorders possibly.

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  • 3 weeks later...

Please explain what you are posting.

I am still strongly leaning towards specifically located cellular over stimulation and apoptosis. Mg actually posted that hallucinogens may be active by increase glutamate in specific sites in the brain, this leads to furthre proof that this is the possible case, as excessive glutamate release cause neuronal death/apoptosis.

It seems to be very clear.
 

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Yes, absolutely, it would be the limiting factor in healing here.

Another thing to add is that we've discussed that healing/recovery is a pseudo recovery, even though so claim healed, the effects and damage is still there its just under threshold, basically we heal like scar tissue heals a cut in the skin.

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