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Why do we have DP/DR?


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Hi everyone,

 

I've been thinking about this particular symptom and the reasons why us HPPDers have it, has there ever been any research in to why we should have DP/DR? This is an inescapable symptom for me and is by far the worst.

 

I do know that DP/DR type symptoms are usually a co-morbid symptom with anxiety, however I barely suffer with any anxiety yet am still dissociated constantly, it never changes or fluctuates, it is always the same. 

 

One theory I came up with was that at the start of the onset of HPPD, most of us had extreme anxiety and since there was no escape to the 'threat' (our vision) the only thing our brains could do was dissociate us to escape from it, like a defence mechanism. I guess you can't escape from your senses and extreme anxiety from something you can't escape from is much different to worrying about a final exam or financial troubles etc.

 

Unless something has actually changed in our neurochemistry and this symptom is a result of that? As Psychedelics agonise 5HT receptors which in turn overload NMDA receptors to provide their effects I believe (Correct me if I'm wrong), and NMDA receptors are the main receptors targeted from dissociatives such as Ketamine etc, perhaps this is why, as our NMDA receptors are still overloaded and as a result, we have dissociation? 

 

Perhaps an NMDA receptor agonist would provide relief from this symptom? Although I can't think of any.

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Actually Ketamine is a NMDA antagonist, meaning it blocks its function basically.
However it can't be ruled out that some glutamatergic storm took place, or that there has been a long-term alteration in glutamatergic transmission.

But I like your defense-mechanism theory as to why there's dissociation!
Following your neurochemical theory though; if there's still NMDA overload taking place, then an agonist would only worsen symptoms.
Glutamate is seen as the basic excitatory neurotransmitter, and seeing as there's believed to be pre-epileptic/convulsant/hyperexcitability involved in HPPD, I doubt there's a thereapeutic potential in NMDA agonists.

From what I've learned, it's best to focus not on a single neurotransmitter, but more on regional excitability and focal therapy (like tDCS: regional excitability changes.. I've had marginal succes with that, particularly for the DP/DR symptoms).

Indeed I believe DP/DR is closely related to anxiety as well, and there might be some dysfunction of the fear response. Personally I notice that after a period of anxiety, my DP/DR gets worse. When there's little anxiety, it doesn't get much better though, it just plateaus I suppose.
If you don't have anxiety, my guess is that raising excitability in your frontal regions (especially ventromedial PFC) would be beneficial.

Sam, I'm not in any position to make recommendations, but you might want to consider tDCS if you're not planning on medication. It's a non-invasive (and of its class, the least invasive) form of brain stimulation. Again, my experiences were.. how to say.. profound but very transient. Like I flashed back to reality for a few minutes, and then it was gone. But I must note that the device I used was homemade, moreover was the positioning done by myself (could've been that it wasn't directly over the correct region). I'm very eager to see HD-tDCS come to the market soon, as it provided for much better "aiming" and less (almost no) effects in the surrounding (non-targetted) regions.

Some believe HPPD is a form of Toxic Encephalitis or (glutamatergic/NMDA) excitotoxicity. Mitochondrial supporting supplements I suppose would help in this regard, limiting excitotoxicity to possibly reversing it (don't quote me on that, but I'm sure it won't hurt).

Anyway, I'd stay away from the NMDA agonists if I were you. Have a glance over at Research Articles for some other theories, and I believe recently I posted something about the neurobiological associations with DP/DR.

All the best,
Odisa.

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Actually Ketamine is a NMDA antagonist, meaning it blocks its function basically.

However it can't be ruled out that some glutamatergic storm took place, or that there has been a long-term alteration in glutamatergic transmission.

But I like your defense-mechanism theory as to why there's dissociation!

Following your neurochemical theory though; if there's still NMDA overload taking place, then an agonist would only worsen symptoms.

Glutamate is seen as the basic excitatory neurotransmitter, and seeing as there's believed to be pre-epileptic/convulsant/hyperexcitability involved in HPPD, I doubt there's a thereapeutic potential in NMDA agonists.

From what I've learned, it's best to focus not on a single neurotransmitter, but more on regional excitability and focal therapy (like tDCS: regional excitability changes.. I've had marginal succes with that, particularly for the DP/DR symptoms).

Indeed I believe DP/DR is closely related to anxiety as well, and there might be some dysfunction of the fear response. Personally I notice that after a period of anxiety, my DP/DR gets worse. When there's little anxiety, it doesn't get much better though, it just plateaus I suppose.

If you don't have anxiety, my guess is that raising excitability in your frontal regions (especially ventromedial PFC) would be beneficial.

Sam, I'm not in any position to make recommendations, but you might want to consider tDCS if you're not planning on medication. It's a non-invasive (and of its class, the least invasive) form of brain stimulation. Again, my experiences were.. how to say.. profound but very transient. Like I flashed back to reality for a few minutes, and then it was gone. But I must note that the device I used was homemade, moreover was the positioning done by myself (could've been that it wasn't directly over the correct region). I'm very eager to see HD-tDCS come to the market soon, as it provided for much better "aiming" and less (almost no) effects in the surrounding (non-targetted) regions.

Some believe HPPD is a form of Toxic Encephalitis or (glutamatergic/NMDA) excitotoxicity. Mitochondrial supporting supplements I suppose would help in this regard, limiting excitotoxicity to possibly reversing it (don't quote me on that, but I'm sure it won't hurt).

Anyway, I'd stay away from the NMDA agonists if I were you. Have a glance over at Research Articles for some other theories, and I believe recently I posted something about the neurobiological associations with DP/DR.

All the best,

Odisa.

 

Interesting information, thank you for that. 

 

By tDCS I assume you mean Transcranial direct-current stimulation right? I'm not too familiar with that but your results do sound interesting!

 

Indeed there does seem to be dysfunction in the fear response, as my startle response has definitely declined significantly post-hppd. With DP/DR it is all emotional response that is declined or 'numbed' and not just fear though I suppose.

 

Perhaps due to the cerebral dis-inhibition and hyperexcitability in the brain, somewhere in the brain the hyper excitability has been 'mistaken' for strong anxiety and as a result, dissociation has happened? Just a wild theory.

 

I do think our DP/DR is slightly different to that of full blown depersonalization disorder or dissociation from PTSD for instance. For example, if I hear something funny enough, I can still cry with laughter, or I can still appreciate music, or a beautiful scenery in nature etc. It's just the emotional response that is missing. Maybe this is some dysfunction in some part of the brain that deals with emotional response to external stimuli (Possibly the Amygdala?) or perhaps it could even be a dopamine issue / something wrong in the rewards system, who knows. 

 

I suppose in DP/DR there seems to be a blockade or disruption of communication between the areas of the brain that deal with emotions/emotional responses and the areas that deal with our experience of reality/consciousness. However I do know Science is far from understanding the Neurochemical/Psychological mechanism behind consciousness. 

 

What makes me think it's more than just an excitatory issue is the fact that sedatives such as benzodiazepines do absolutely nothing for my DP/DR, 

 

Thanks for your post!

Sam.

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I read a study on what's wrong in the when you have HPPD. I'll search for it and link it here when I find it.

But to put it simple: the "channel" opened the psychedelic drug is not properly closed. There is some kind of overactivation of the 5HT2a serotonin receptor still left, which in turn shuts off GABA-B inhibition. There are a lot more pyramidical cells involved also, the brain is like a clockwork were one cog malfunctioning may effect the whole system. I'm no neurologist..

Anyways the effects of this "channel" being opened are visual symptoms such as wiggling of peripheral lines, sharpened colors, trails, loss of texture resolution "i.e cartooning", and choppy visual framerate. But there's also a general change in consciousness which is could be described as a "dream-like state" Sound familiar? DP/DR! 

That's also why for us HPPD'ers we can never fully escape this nasty DP/DR state. It's always there - with or without anxiety. Of course anxiety increases the dissociation, but even when you're calm and tranquil, you're still dissociated!

I still have constant DP/DR 7 years after getting HPPD..

 

As Aldous Huxley said - "the doors of perception are not so much closed, as they are cracked open and left askew." 

 

There seems to be no real way to close them fully again, but anti-EP's such as Keppra and sadly benzodiazepines are at least a way to partly restrict the excess activity flowing through the cracked open "doors of perception" or "channel" if you will..

 

Sorry if my reply is a bit philosophical but I hope it at least partly answered the question "Why do we have DP/DR"..

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415, here are some hppders' who dont have dp dr, only visual symptoms. I think we can do some training into our brains to ignore the visual disturbances as a sign of danger. In fact, in vipassana meditation you can learn something like that.

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415, here are some hppders' who dont have dp dr, only visual symptoms. I think we can do some training into our brains to ignore the visual disturbances as a sign of danger. In fact, in vipassana meditation you can learn something like that.

 

Read a bit about this vipassana meditation, sounds interesting, though it could be a double edged sword and make you spin even more out of control. But it could also of course make the psyche more calm and accepting, but like with psychedelic drugs - if you use it, use with caution and with proper preparations. A meditative trance is actually a psychedelic state of conciousness, it does what LSD and the like does faster and more forceful, in a slower and more prepared state.

 

I have a chronic state of DP/DR, but years of mental training have taken the "charge of fear" away from the state. It no longer causes so much anxiety. I used another "use with caution" tool - CBT. Basically reprogramming the hippocampus (where the basal fears seems to be located).. 

I definately agree that the fear of the visuals needs to be removed, as it is possibly the largest step one needs to take begin some kind of healing..

In my case I found out that the DP/DR was not as connected to my anxiety as I had thought, it didn't disappear when most of my anxiety did.

I must have broke open my "doors of perception" a bit too much.. :wacko:

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  • 2 weeks later...

I realized I hadn't responded to this.

Sam93:
Yes I do mean transcranial direct-current stimulation. The lack of improvement from BZD's needn't necessarily indicate you do not have hyperexcitability issues, as BZD's are not focal to a specific area. Rather, they inhibit total brain excitability, and as such it could be that the inhibition of afferent areas (such as those involved in the top-down modulation) is cancelling out any improvements.
Inter-intracortical communication dysfunction is likely to be present indeed. Raising DA in the PFC has been shown to ameliorate HPPD symptoms. Alterations in the amygdala could have occurred from prolonged exposure to HPPD, I suppose.

415_STYLEE:
AFAIK, there's no evidence to indicate that 5HT2a receptor hyperagonism is still present in HPPD. I think the "dream-like state" you're referring to is Oneirophrenia?

 

 

 

As Aldous Huxley said - "the doors of perception are not so much closed, as they are cracked open and left askew." 

 

There seems to be no real way to close them fully again, but anti-EP's such as Keppra and sadly benzodiazepines are at least a way to partly restrict the excess activity flowing through the cracked open "doors of perception" or "channel" if you will..

 

Sorry if my reply is a bit philosophical but I hope it at least partly answered the question "Why do we have DP/DR"..


Indeed quite on the philosophical side, haha. It seems like you're saying that acquiring HPPD is like opening Pandora's box, never to be closed again! A bit grim mate ;) The only reason I can think of why "the doors of perception remain unhinged", would be the lack of research into HPPD! But that doesn't mean that it's not possible! Just that for the time being, we don't know how exactly. Damn I was gonna quote some awesome physicist, but I haven't really been listening to my brother (studies physics) with that much attention lately. Anyway, the only real way to know if it can be done, is after it has been done!


Sorry for the short replies, I'm tired.

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