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Could This Be The Big One!


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So far in trials (in spite of all the media hype), it has only modest effectiveness. However for someone with advanced PD, even a little is a lot. http://www.viartis.n...news/111218.htm [ Note: Of the PD sites I've read over the years, www.viartis.net is by far the most accurate, no-hype, not-after-donations place for info ]

"It seems to be having an overall beneficial effect in smoothing out people's days, probably allowing a slight dose reduction in medication and, in some patients, a better sleep pattern and a better quality of life for all" - so again it is helpful ... not a cure (they still must take Sinemet).

With the level of improvement being this modest, it would seem difficult to get medical professionals to do such an invasive procedure. And it would be impossible to order over the internet and self administer :P

It is important to clarify this statement: "Parkinson's disease occurs when the brain gradually stops producing the nerve-controlling chemical dopamine." Of itself it could mislead one in thinking the problem is merely production of dopamine. The problem is damaged dopaminergic synapsis - the neuron's 'communication ports' are partly burnt out. With PD, increasing dopamine helps the existing synapsis to make up the difference - with the potential risk of more burn out (the functioning parts have much more traffic and are more prone to future damage)

As for being the big one - dopamine functions are only part of the HPPD profile. While not to undermine the potential benefit of Sinemet (and readers know I greatly promote is benefit and that people should try it), there are people who do not get improvement from these meds. While not officially known for sure at this time, it has been reported that 30% of HPPDers get 70% improvement in symptoms. Clearly then more is needed.

It is reported that recreational drug use (such as LSD) alters gene expression. When this occurs the cells cannot operate fully normal. Using a virus to activate genes is an interesting approach that ProSavin uses. But on the surface it would seem more difficult to develop than using other means such as peptide therapies. Guess we will just have to see what they come up with.

In summary, the damage that has altered brain function is complex and multi-faceted. However, since 50% of HPPDers eventually recover - the brain can clearly heal and restore functions. Lifestyle is an important factor for that to occur. Possibly meds can assist recovery. Certainly meds can improve quality of life for those with symptoms that are disabling.

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I have a question visual.

With PD, increasing dopamine helps the existing synapsis to make up the difference - with the potential risk of more burn out (the functioning parts have much more traffic and are more prone to future damage)

wouldnt this happen to HPPDer too?

i mean would messing with brainchemestrys prevent the brain from healing on its own? or even could lead to more problems(like PD in the future)?

because it seems that messing with it (drugs) has lead to this condition.

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I have a question visual.

wouldnt this happen to HPPDer too?

i mean would messing with brainchemestrys prevent the brain from healing on its own? or even could lead to more problems(like PD in the future)?

because it seems that messing with it (drugs) has lead to this condition.

To put this in perspective, PD symptoms don't even begin to show until 75-80% of function is lost (that is huge). And this is considered early, mild PD. So at this point the existing connection are operating at about 5 times load (~500% capacity). That is like your V8 sports car having 6 dead pistons.

Now Parkinsonism is not typically progressive. And it seems with HPPD that once all the symptoms have settled in (usually a few months) there isn't progression for most people - often the opposite.

Another difference is that the problems with HPPD do not involve muscle control (such as tremors, tightness, spasms, coordination problems) though some members report these kinds of problems. The injury is in cognitive areas. People with PD do not notice cognitive problems until the disease is advanced (though it is detectable with certain neurocognitive tests).

It is logical to be concerned with taking any medication given that drugs cause HPPD. Again it comes down to amounts. While Sinemet can be a hallucinative, it is a poor way to get 'high' - it is too weak. Alcohol is probably better as far as that goes.

There has been much debate about neuroprotective effects of taking Sinemet with 2 camps of scientist busy throwing water balloons at each other (figuratively). The question is complicated by the universal view (both camps too) that it is inhuman to withhold it from people with the disease. But largely it seems accepted that the earlier a person with PD starts taking dopamine agonists (that is the less advanced the disease is) the slower it progresses. There are some on Sinemet for over 2 decades with no real progression of the disease. It makes sense - if 50% of function is lost the remaining connections are at 2 time normal load (~200%). Much less 'stress'. So research continues in how to diagnosis the problem before there are any symptoms.

Again with HPPD, it isn't progressive like PD - so there doesn't seem to be the hand-off-compensation of function that happens with motor control in the Basil Ganglia. The functional compensations seem to be cortical-loops (this happens with PD too) which don't involve much dopamine.

Using the V8 engine example again, you would probably notice 1 dead piston ... certainly 2 dead pistons. With 4 dead pistons it would handle like a Yugo. The motor functions in the Basil Ganglia are automatic (unconscious) but our visual problems involve our active attention and perception (our consciousness). It is hard to ignore our symptoms - you have to train yourself or distract yourself to ignore them. Now if a finger is a little twitchy, that is hard to notice (unless it is your trigger finger, but most of us don't carry side arms like in old Westerns)

The information about 'ambient visual processing' verses 'focal visual processing' does not show any plasticity involved - just the problems of the focal system being overloaded. And there is no report of burning out neurons - just frustrating problems. [Note: ambient visual processing involves the mid-brain - the major dopamine area]

I know of very few that have even tried Sinemet, let alone being on it for a time. It has been 3 1/2 years for me. Merkin just started around last September. More feedback for others would help. So time may tell.

Because some visual problems began correcting immediately upon taking the med and remain improved even when skipping the med for weeks - there does not seem to be synaptic burnout by increasing dopamine. (BTW, the half-life of levodopa is around 45 minutes) Why there is actual healing remains unknown ... at least with any certainty.

With PD there is 0% improvement over time - there is no such thing as remission (though not all is black). With HPPD there is 50% improvement over time. If burnout is involved, the rate of healing exceeds the rate of deterioration.

I would advise anyone with HPPD to start with healthy living (food, sleep, exercise, friends, no drugs) and get anxiety under control. Only after 6-12 months have gone by would you consider medications. Or if you are actually disabled by it. Note: it usually takes years even to get a HPPD diagnosis, let alone meds for it. I have not heard of anyone being hurt by not taking medication right away for HPPD - so you have time. [Please correct me if this is not so]

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thanks for your reply!

yeah this sound plausible....

But what do you think why do some people say their symptoms mostly the afterimages do not settle down and gradually get worse?

Do you think they dont have "classic" HPPD? or does HPPD normally doesnt get worse after it has developed completly, and (in germany you would say) "exceptions confirm the norm"?

A lot of my symptoms started 3 years after my last acid trip i only smoked a lot of weed at this time, but had a stressfull time, antibiotics, weed, alcohol...but i had also symptoms after my first psychodelic trips, you could find the whole story under the introduction area.

Maybe gene silences caused my brain to regrow neurons in a wrong way?

Could this mean a lot of people which had used hallucinogens in the past could trigger HPPD later in life with some bad environmental factors?!

Is it possible (only my theory), that HPPD is a form of acquired Migraine?

Serotonin is one of the brain's main neurotransmitters—chemicals that act as signals for neurons. According to the serotonin theory, disruptions in the brain's normal chemistry cause migraine headaches.

Lab studies of people undergoing migraines document variations in serotonin levels during an attack. Serotonin levels initially increase, which constricts the blood vessels and reduces blood flow in the brain enough to cause an aura. Serotonin levels in the brain then decrease as the supply of this neurotransmitter is used up, causing dilation—and migraine pain.

One particular structure in the brain stem (the most primitive part of the brain, located just above the spinal cord) is very sensitive to brain serotonin levels. It's called the ‘dorsal raphe nucleus,' and many of its neurons both secrete serotonin and intertwine with cerebral blood vessels, allowing the serotonin to directly affect the vessels. Part of the serotonin theory of migraines is that the dorsal raphe nucleus may function as a ‘migraine generator,' triggering the constriction and dilation of blood vessels.

i read that some drugs (Cannabis; mushrooms; LSD) could hold back migraines, maybe a brain which isnt predefined for migraines could trigger a form migraines which wasnt there before?

maybe some HPPDer additional get migraine attacks which cause the symptoms to get worse?

Some people with persisten migraine aura report success with drugs like Flunarizine(Sibelium) could this help people which doesnt have relief from taking Sinemet?

i found this in a study which shows that cannabis could trigger HPPD like visuals:

Two key players in the processing of light information in the retina are photoreceptors, which catch light and turn it into a signal that can be interpreted by other cells, and bipolar cells, which are next in line in the flow of information,” said Straiker. “Communication between the cells requires the release of a neurotransmitter called glutamate, triggered by calcium currents passing through a specific calcium channel. Cannabinoids are known to inhibit calcium channels. If you shut down the channel, you shut down the release of glutamate, and profoundly alter the cell's ability to signal.

Maybe there are a few mechanism which causes people to have visuals like that?!

Sorry for this paragraph of questions^^

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There are lots of promising treatments on the horizon. I believe there will soon be a cure, or at least very effective treatments, i.e. increasing dopamine without long term side effects (involuntary movements). MDMA can actually stop these side effects for some. But of course, that's not a practical treatment! Especially for someone with HPPD.

But as Visual says, HPPD is very different from Parkinson's. For some, for example, Klonopin takes away all symptoms. The same will obviously not work for someone with Parkinson's. There are lots of disorders which in part involve dopamine.

To confuse matters even more, for two thirds (Dr. Abraham trial), increasing dopamine has no effect. Although those that took part in the trial only took dopamine boosting meds for one day if I am correct. Maybe if they had a longer trial, e.g. one week, effects would be seen.

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Wow, lots of questions … and most are impossible to know at this time.

Do you think they dont have "classic" HPPD? or does HPPD normally doesnt get worse after it has developed completly, and (in germany you would say) "exceptions confirm the norm"?

HPPD is a complex, multi-faceted disorder. Visual processing is staged throughout the brain. HPPD is a disruption in normal processing which cause persistent weird vision. There isn’t one place or one neurotransmitter shortage causing all this. Because it is complex, each individual has their own ‘version’ of HPPD. It isn’t like a broken arm (simple or complex fracture).

"Classic" should be subdivided into several categories.

The progression for several weeks (or sometimes continuous) could by many reasons. Some ideas:

Plasticity during ‘tripping’ has built alternate pathways/balances of functioning. The brain now has more that one way of ‘seeing’ so it must settle in, which would take time.

Gene silencing would disable important enzymes, peptides, proteins, and whatnots. This causes the cell to be unable to work properly (but is not fatal). So chemical responses are altered, hence firing rates and responses alter, hence altered vision.

Excitotoxicity while ‘tripping’. Synaptic damage reduces neuronal communication. If communication is severely restricted, then synapses are absorbed. Worst case scenario is neuron death.

Whatever is happening at the microscopic level, "Progression" – either better or worse – is the net balance of what is going on. Aging is downhill. Healing is uphill. The more pathways were altered, the harder to ‘get back’ to the way things are. If there are areas ‘choked’ by lack of a neurotransmitter, healing is hampered.

But what do you think why do some people say their symptoms mostly the afterimages do not settle down and gradually get worse?

IMO, negative afterimages are dopaminergic neuron problem. Directly connected to each photoreceptor in the retina is a D2 synapse. These involve spot adjusting contrast and other fine tuning. There are also D1 synapses in the eye. It is well known that photoreceptors need to ‘recharge’, hence a small amount of negative afterimaging is completely normal. But if either the metabolism is reduced or the sensitivity to the signal too heightened, the persistence is extended.

IMO, positive afterimages indicate a failure in ultra-short-term-memory systems. And in how vision is integrated.

All this comes down to understanding: What is visual perception? (a long long topic)

A lot of my symptoms started 3 years after my last acid trip i only smoked a lot of weed at this time, but had a stressfull time, antibiotics, weed, alcohol...but i had also symptoms after my first psychodelic trips, you could find the whole story under the introduction area.

Since some people get HPPD just from weed, if you want to get better, stop the weed. Weed affects dopamine (http://jpet.aspetjournals.org/content/292/3/952.full) and other neurotransmitters. By continuing to smoke it, you are teaching the brain to operate that way.

Maybe gene silences caused my brain to re-grow neurons in a wrong way?

If a cell cannot fully function in the way it communicates with others, then this would alter how they grow.

Could this mean a lot of people which had used hallucinogens in the past could trigger HPPD later in life with some bad environmental factors?!

If drug use has altered brain functioning – especially if it has weakened gene expression and/or ‘burnt’ synapses – a person will be more susceptible to environmental stressors.

Is it possible (only my theory), that HPPD is a form of acquired Migraine?

IMO, Migraine is an overused term. Traditionally migraine is understood to involve blood circulation. Persistent migraine is a bit of bull-shit. They need to use a different term for non-circulation-related visual problems. Perhaps this, like much of neurology, has developed by physicians struggling for answers. Or because people accept the term ‘migraine’ without freaking out (tell them ‘brain disorder’ and watch them shrivel up and freak out).

"According to the serotonin theory, disruptions in the brain's normal chemistry cause migraine headaches." Oh? What is this serotonin theory? Seems there are ‘serotonin theories’ about everything. Of course theories are just ideas and now that these meds exist we can play with them to our hearts content.

The phrases "serotonin theory" and "serotonin hypothesis" are popular buzz words to use to prove how savvy and intelligent you are.

The Serotonin Hypothesis was published in 1969 – but the article was about how "in depression the activity of liver tryptophan-pyrrolase is stimulated by raised blood corticosteroids levels, and metabolism of tryptophan is shunted away from serotonin production, and towards kynurenine production.". Basically: Stress causes more kynureninic acid which causes inflammation which is hard on the body.

Researchers and pharmaceuticals jumped on the idea of increasing serotonin to treat depression and developed SSRIs. These have largely replaced tricyclic antidepressants. FYI: SSRIs are 8% more effective than a placebo while tricyclics are histamine based and 12% more effective than placebo (but have more immediate side effects). Talk therapy is more effective than either. Remember, science is driven by funding … $$$.

There are several meds prescribed for migraine that are serotonin based. Since serotonin is vasoconstrictive there is logic to this. But for brain injuries, this is potentially dangerous.

While there are some who feel benefits with SSRIs, these meds are less effective than other routes, far more destructive to the person than is commonly reported, and VERY profitable.

i read that some drugs (Cannabis; mushrooms; LSD) could hold back migraines, maybe a brain which isnt predefined for migraines could trigger a form migraines which wasnt there before?

maybe some HPPDer additional get migraine attacks which cause the symptoms to get worse?

Some people with persisten migraine aura report success with drugs like Flunarizine(Sibelium) could this help people which doesnt have relief from taking Sinemet?

Again, define ‘migraine’. How many HPPDer have had their visual distortions improved with an SSRI? No doubt anything is possible given each person is unique. If someone has benefited … great! … this post isn’t meant to slam them … it is about what is most probable.

"Cannabinoids are known to inhibit calcium channels"

Great quote. So weed must be good for high blood pressure treatment. But how does this explain persistent visual problems?

Maybe there are a few mechanism which causes people to have visuals like that?!

There must be several mechanisms involved. So there isn’t going to be a one-size-fits-all treatment.

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Wow thank you mate great post!!

Iam happy to cut out weed out of my life 6 month ago, my only drug is nicotine atm.

cant stop it yet because after ten years of excessive marijuana consumption i have to slowly give up smoking i think i will stop it in a few month too.

"Cannabinoids are known to inhibit calcium channels"

Great quote. So weed must be good for high blood pressure treatment. But how does this explain persistent visual problems?

funny because i allways thought weed gives you a high blood pressure

http://ucsdnews.ucsd...lth/potpnas.htm

here is the full article

Some of the reported effects of the use of marijuana and hashish include the perception of a snowy visual field, increased light intensity and altered vision. In fact, Straiker said his interest in seeking CB1 receptors in the retina was sparked in part by accounts of dramatic alterations in visual perception following marijuana use.

These findings suggest that at least some of the visual effects of marijuana and hashish use occur at the earliest stage of visual processing, as the calcium channels critical for the normal processing of visual information are inhibited.

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yes i believe that not only the brain plays a role in this whole HPPD thing...

i read that negative afterimages has their origin in the eye itself and you also mentioned it in your theory above

but how could it be possible that the photoreceptor cells "become tired" only after staring at something for a second

i think that this isnt a "filtering problem" of the brain the eyes have to play a role....

Also my ghosting seems to have its origin in my eye, after doing the pinhole test it is completly gone.

thats a sign of beeing a cornea problem...

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the one that is probably going to kick this and maybe a lot of others in the face much more effectively is a chem in the works call bl-1020 much, three years maybe, sorry if it brings anybody down, they're others way off the radar if I wanted to go listing but I never tried them, i'm good, so fuck it. there's more potent pirecatam type drugs too, in the same catergory as keppra btw although they're all unique, peace

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"Also my ghosting seems to have its origin in my eye, after doing the pinhole test it is completly gone.

thats a sign of beeing a cornea problem..."

Could be more specific? in two weeks im going to check my eyes, what is pinhole test? really you're ghostings are gone?

thanks for any answer dude.

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pinhole test,

1 a test performed on a person who has diminished visual acuity to distinguish a refractive error from organic disease. A refractive error may be corrected with glasses, whereas organic disease may signal the development of preventable blindness. Several pinholes, 0.5 to 2 mm in diameter, are punched in a card. The patient selects one and looks through it with one eye at a time, without wearing corrective lenses. If visual acuity is improved, the defect is refractive; if not, it is organic. The pinhole effect results from blocking peripheral light waves, which are most distorted by refractive error.

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BL-1020

It is difficult to see how an antipsychotic could be useful for the majority with HPPD. While increasing GABA is a big plus, and decreasing serotonin might be useful, decreasing dopamine is probably the opposite of what is needed (at least for the 30-50% :lol: ).

Pinhole

The pinhole would reduce astigmatism - just as being outside on a bright day can. Perhaps with HPPD our brains are hypersensitive to lens irregularities that were just find prior to HPPD. As my ghosting changes sometimes (and usually at first glance it isn't even there) it would seem highly unlikely that the physical structure of our eye keeps shifting.

another interessting observation was a few years ago as i used to take a lot of drugs. the movement/melting thing allways disappeard while intoxicated with Amphetamine/Cocain.

could this be a sign of dopamine would help?

I would say yes - amphetamines, meth, and cocaine are the big dopamine kickers. I found that when discontinuing all meds simultaneously last summer, the movement thing was the absolute worse for a couple weeks corresponding with the dropping of the effects of Sinemet and Gabapentin. Curiously, Gabapentin has far more connection with my 'movement thing' than the Sinemet (but drop them both and Wow).

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BL-1020

It is difficult to see how an antipsychotic could be useful for the majority with HPPD. While increasing GABA is a big plus, and decreasing serotonin might be useful, decreasing dopamine is probably the opposite of what is needed (at least for the 30-50% :lol: ).

maybe in combination with a dopamine boosting drug?

but sounds like messing your head completly^^

Pinhole

The pinhole would reduce astigmatism - just as being outside on a bright day can. Perhaps with HPPD our brains are hypersensitive to lens irregularities that were just find prior to HPPD. As my ghosting changes sometimes (and usually at first glance it isn't even there) it would seem highly unlikely that the physical structure of our eye keeps shifting.

L

it would not only correct astigmatism, also dry eye and the eyelid pressure thing(Rolladenphänomen :))! and maybe floaters which causes refractive errors?!

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I tried the pinhole test before, and there was no ghosting. But that was inside when ghosting is less. I will test again outside when looking at the moon at night time – that will give the biggest indicator.

A theory of mine which I've mentioned before, and which is similar to what Visual says above, is that the eyes aren't perfect and everyone has a slight astigmatism. Normally a brain filters out information that it does not need. However, in our case, the filter is broken. It is known that the brain can filter out information. For example, children with sixth nerve palsy and thus double vision can filter out information from one eye so that the double vision does not show, until later on in life due to reduced plasticity that occurs with age. But this is just a theory from someone who doesn't know much!

Also, whilst that pinhole test may be indicative for standard disorders, HPPD is highly unusual so normal principles perhaps do not apply!

The leading expert, Dr. Abraham, views the disorder as one of the central nervous system, not the peripheral, although it affects the peripheral fields.

Additionally, ghosting has improved for some with certain medications. If the ghosting were due to the structure of the eye, this would not be possible.

So in conclusion, it is my opinion that ghosting is a disorder or the brain rather than the eyes.

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I tried the pinhole test before, and there was no ghosting. But that was inside when ghosting is less

Interesting ... this is oposite of what would be corrective for astigmatism. With a lens (camera or eye) smaller apertures use smaller portions of the lens thus depth of field increases and the quality of refraction is according to the smaller area of the lens. A pinhole is the ultimate perfect lens - no distortions for materials used (lens) but some refraction around perimeter (???)

Good old Wiki:

http://en.wikipedia.org/wiki/Aperture

http://en.wikipedia....iki/Astigmatism

http://en.wikipedia....stigmatism_(eye)

Astigmatism_text_blur.png

The sample image is different than what I see. Dots can be multiples and text is thin horizontally. Instead of just a blur it is more like multiple clear images like post #1 in http://hppdonline.co...ut-medications/

Another theory (Gawd I'm just full if crap these days) is that the muscles around the lens are not pulling evenly. This would be consistant with both dopamine problems and sympathetic/parasypathetic issues. And with variations at different times. If it was just a dopamine problem, then it should be affected by agonists and anti choleretics - but I don't notice change with either type of med ... so back to the drawing board...

disorder as one of the central nervous system, not the peripheral

Just for clarity, the retina and optic nerve are considered part of the CNS (although, does it really matter? :o )

Additionally, ghosting has improved for some with certain medications

Would you point to some of these ... what meds, etc.?

I will test again outside when looking at the moon at night time

Yes, please let us know ... hopefully it isn't cloudy. Does the moon look like any of these - Post #3 in http://hppdonline.co...ut-medications/

When I look, the shadows(?) or blurring increases of a period of a few seconds

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Here is one example of improvement of symptoms with diazepam which I posted in the other thread: http://thosewithvisu...-s#.T5GNrtWJGYR

I'm sure I've read other accounts as well. But I have read so many threads that it becomes difficult to recall! I remember reading one account on the visual snow forum of double vision (don't know if they meant ghosting) and other symptoms going away after a few years. Whilst not related to medications, it may be of interest.

I will do some digging over the next few days and see what I can find. I will go through old threads and provide links that may be of interest for the benefit of members, in relation to ghosting and other symptoms. I have lots of threads saved which I need to go back to.

I will also start a poll to find out of anyone's ghosting has improved with Klonopin, which seems to be the best at improving symptoms (but people often don't give specifics).

Does the moon look like any of these?

It does not look exactly like any of them, but there is some relation to the third moon. Especially when I squint. For example I get them lines that comes down when I squint, and more moons appear. I get the same lines with other light sources when I squint, for example street lamps or car lights.

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A theory of mine which I've mentioned before, and which is similar to what Visual says above, is that the eyes aren't perfect and everyone has a slight astigmatism. Normally a brain filters out information that it does not need. However, in our case, the filter is broken. It is known that the brain can filter out information. For example, children with sixth nerve palsy and thus double vision can filter out information from one eye so that the double vision does not show, until later on in life due to reduced plasticity that occurs with age. But this is just a theory from someone who doesn't know much!

that is a possibility but i think a ophthalmologist is able to measure the slightest astigmatism today(as my did). soi believe that the reason should be more likely the Venetian Blind Phenomenon(https://www.thieme-c.../s-2008-1045693) or a dry eye(whichis one of the most diagnosis a ophthamologist expresses)

Here is one example of improvement of symptoms with diazepam which I posted in the other thread: http://thosewithvisu...-s#.T5GNrtWJGYR

i thin the reason could be that benzos has an effect on the pupils. they seem to constrict them. maybe the same effect a pinhole would do?!

http://www.ehow.com/...all-pupils.html

Edit: this wouldnt also explain the negative afterimages. it is not normal that the photoreceptor cells "become tired" after only a second this must have its origin in the eye itself

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When I had my eyes tested in September (before I had ghosting) the lady who tested my eyes wrote on the report 'minimal refractive error', suggesting there may have been a tiny but insignficant refractive error?

My eyes are not at all dry. But I did try eye drops for a couple of weeks just to see if anything would happen. It didn't.

I did not know benzodiazpines restrict pupils. If this is the case, then yes possibly the drug is not treating the ghosting through the brain but rather the eyes by way of pupil constriction, in the same way opiates treat ghosting by restricting pupils.

Whilst I have said I view ghosting as a problem of the brain, it is well known that it can be caused by problems with the eyes themselves. It's interesting that some other symptoms can be caused by problems with the eyes as well, such as starburts and halos. Those with laser eye surgery sometimes report ghosting, starbusts and halos.

-------

I will come back to the other link you provided. I need to read it properly and I am too tired right now!

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maybe some sort of eye drops which causes the pupil to constrict could clear this up

Parasympathomimetics. These drugs work by increasing the outflow of aqueous humor from the eye. They are frequently used to control IOP in narrow-angle glaucoma. These eye drops cause the pupil to constrict, which assists in opening the narrowed or blocked angle where drainage occurs. Common side effects experienced with these types of eye drops include brow ache, pupil constriction, burning, and reduced night vision. FDA-approved drugs in this class include pilocarpine, carbachol, echothiophate and demecarium.

but as HPPD is not a official diagnosis in germany and i dont wont to get my slight astigmatism operated i think my doc wont pescribe me this^^

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