shaolinbomber

Gawd I know what that's like all too well.

I would just stick to klonopin if you definitely have to take it. Switching around to others is probably a bad idea, especially Xanax or Valium. Those 2 are by far the most addicting. Hell I think Valium feels more like an opiate than a benzo.

The 5ht2a sites on the inhibitory interneurons should trigger an inhibitory response down"stream" from them. This is part of Dr. Abrahams hypothesis. The 5ht2a receptors on inhibitory interneurons in probably the V1 circuit have been downregulated or altered so they no longer respond and the resulting inhibitory response ceases to exist thus resulting in altered perception like similar visual disturbances seen on hallucinogenic drugs.

I get slight breathing when i look at them. It used to be a lot worse though.

I've only read through one but it seems that some of the researchers here are saying the HPPD research is valuable to understanding problems arising from more widespread disease and mental illness like Alzheimers...So maybe we will see more research for HPPD taking off soon.

Recovery is a point of view imo. I've come to terms with the fact that I will never be able to forget what DP/DR feels like and with that realization comes the acceptance of never really ridding myself of it. "Recovery" from HPPD is more of an adaptation to whatever new functioning pathways the brain had to use in order to compensate for the chaotic environment that whichever drug caused during the high/experience, and with the brain's "rewiring" comes a definite change in feeling of your reality. This is where the DP/Dr comes in. Everything feels so different or "alien" and everything looks different (visuals) and most people can't accept this so we retract and thus the dissociation becomes a loop that plays over and over again until we can realize that this isn't gonna go anywhere anytime soon if ever.

I've been wanting to try an SSRI for a little bit now. I used to be dead-set against them but after thinkiing about what caused my HPPD (MDMA) and seeing as how MDMA primarily works on the serotonin system then maybe a powerful SSRI like prozac will help rewire something that got crossed.

Damn are you serious? I've never heard of that happening to anyone from just promethazine. Are you sure there wasn't some opiate narcotic mixed in there with it?

See if your doctor would be comfortable starting you out on a real low dose of Suboxone/buperinorphine or another opiate/opioid. The pupil constriction caused by these drugs lowers by visuals substantially but it might not be for everyone. Give it a shot and see how it goes.

It's definitely an alteration to the inhibitory interneurons in the visual cortex and probably elsewhere. The 5-ht2a receptors have been altered to the point where they dom't release GABA after the neuron reaches it's max excitatory point to stop the nerve signal so the excitatory currents stick around for much longer than they rightfully should. This is why afterimages linger for so long or why we all have tinnitus or why we see visual snow and etc. etc. etc. It's all evidence that the inhibition that should be occuring to calm the neuronal circuits isn't working like it used to anymore. My personal opinion is that gene therapy is the only type of medicine that is going to have a sure fire chance at making any REAL permanent improvement to people with the disorder.

I can attest to this. Lunesta totally wipes my memory clean whenever I use it for sleep. I wake up not remembering anything up to about 4 hours before I fall asleep.

This drug sounds like a pre-emptive med to prevent excitotoxicity from happening and is not able to reverse it. Is that correct or am I reading it wrong?

We definitely don't want this to be due to excitotoxicity because if that is what caused it then we're dealing with permanent loss of vital neurons in the visual cortex and this is in all likeliness a permanent state for most of us. These are things that we already know though...so?

I havn't been on Sinemet in about a year. I think my comment on my pupil size being smaller whist on it was wishful thinking. However I do want to try Sinemet again with Tolcapone and see if it goes a little better.

If your visuals are real bad like mine then you should see quite a bit of improvement due to the effect of opiates on the pupil. They constrict them a lot and make them pinned so a lot less light gets through. In normal people this would usually give them tunnel vision but for me it just makes my eye sight normal again.

Depending on what kind of surgery you're having you'll probably get some strong meds like oxycodone or 10mg hydrocodone or they might hook you up with morphine or hydromorphone if you're lucky. But ya i'm on Methadone Maintenance Treatment because opiates/oids help so much with my visuals and DP/DR. For me it decreases ghosting, trails, afterimages, light sensitivity, halos and starbursts.

I have a sympathetic doctor who I think would prescribe Tolcapone if we start out slow with it. I might try to get it and let you guys know how it goes.

Yes, thanks for the report and update. I've tried the Sinemet approach and didn't get any benefit from it. I'm curious about tolcapone though and am wondering if I need both of those medicines for either of them to work. I see that if Sinemet is to have it's full on desired effect that some peole need the strong COMT inhibitor Tolcapone in order for the Dopamine to be synthesized and reach the brain.

http://en.wikipedia....tical_resonance Recurrent thalamo-cortical resonance "Recurrent thalamo-cortical resonance is an observed phenomenon of oscillatory neural activity between the thalamus and various cortical regions of the brain. It is proposed by Rodolfo Llinas and others as a theory for the integration of sensory information into the whole of perception in the brain.[1][2] Thalamocortical oscillation is proposed to be a mechanism of synchronization between different cortical regions of the brain, a process known as temporal binding.[3] This is possible through the existence of thalamocortical networks, groupings of thalamic and cortical cells that exhibit oscillatory properties." "The thalamus in this system acts as both the gate for sensory input to the cortex as well as the site for feedback from cortical pyramidal cells, implying a processing role in sensory perception in addition to its function in directing information flow." "Reticular neurons (RE), on the other hand, are highly interconnected and have their own intrinsic oscillatory properties. These neurons are capable of inhibiting thalamocortical activity via their direct connections to TCs. Corticothalamic neurons are the cortical neurons that TC neurons synapse on. These cells are glutaminergic excitatory cells that exhibit increasing activity as they become more depolarized. This activity is described as "bursting", firing in the gamma range at rates between 20 and 50 Hz." Now i'm wondering if these http://neuronbank.or...eticular_neuron could be part of the inhibitory interneuron theory presented by Dr. Abraham. This is relevant because that is (or atleast was) his primary theory in trying to explain what causes HPPD and the visuals. The theory says that these inhibitory interneurons had been changed somehow and were no longer functioning properly by inhibiting our vision and that is what is causing all of the visuals. These Thalamic reticular neurons would fit this description quite nicely for an inhibitory interneuron in the visual cortex. If I understand this theory correctly, then the thalamocortical feedback loop receives information from our sensory input of the eyes, yet perhaps in the case of an HPPDer the correct inhibitory responses to this sensory input is not functioning properly and we're left with too much sensory input resulting in afterimages, trails, floaters (when, in a young healthy human, there should be none or very little) and so on. "Thalamic cells synapse on apical dendrites of pyramidal cells in the cortex. These pyramidal cells reciprocally synapse back on thalamic neurons. Each loop is self-contained and modulated by sensory input. Inhibitory interneurons both in the cortex and the reticular nucleus of the thalamus regulate circuit activity." "The lateral geniculate nucleus, known as the major relay center from the sensory neurons in the eyes to the visual cortex, is found in the thalamus and has thalamocortical oscillatory properties,[7] forming a feedback loop between the thalamus and the visual cortex. Sensory input can be seen to modulate the oscillatory patterns of thalamocortical activity while awake. Visual perception is no exception, and stimulation from light sources can be seen to cause direct changes in the amplitude of the thalamocortical oscillations as measured by EEG." Then we have basically the proposed theory that I have stated yet put into a scientific model to be presentable to the scientific community. Thalamocortical dysrhythmia "Thalamocortical dysrhythmia (TCD) is a proposed explanation for certain cognitive disorders. It occurs upon the disruption of normal gamma-band electrical activity between the cortex and thalamic neurons during awakened, conscious states.[13] This disorder is associated with diseases and conditions such as neuropathic pain, tinnitus, and Parkinson’s disease[14] and is characterized by the presence of unusually low-frequency resonance in the thalamocortical system. TCD is associated with disruption of many brain functions including , and motor control and occurs when thalamocortical neurons become inappropriately hyperpolarized, allowing T-type calcium channels to activate and the oscillatory properties of the thalamocortical neurons to change.[13] A repeated burst of action potentials occurs at lower frequencies in the 4–10 Hz range. These bursts can be sustained by inhibition from the thalamic reticular nucleus and may cause an activation of cortical regions that are normally inhibited by gamma-band activity during resonance column formation. While the effect of the deviation from normal patterns of gamma oscillatory activity during conscious perception is not entirely settled, it is proposed that the phenomenon can be used to explain chronic pain in cases where there is no specific peripheral nerve damage." Here is the wiki link about it.:http://en.wikipedia.org/wiki/Thalamocortical_dysrhythmia

+1. I accredit it to the dissociation.

Ya...I would probably forget all about my HPPD while i'm walking away in handcuffs for exposing myself in public

Sounds like you have trouble binging on meds. I have/had the same problem. I'm glad you realize that it's not a good idea to do so as that type of thing can lead you down a dark road very quickly. Take it from me. I've been there and it's best to avoid it completely

I'm not sure if you were referring to Doxylamine with this but it's not a controlled substance in America.

Taking Klonopin every now and again is not going to make you dependent. In my opinion, jay's philosophy on this subject is correct. If you're having an extremely uncomfortable day and you just can't seem to get back to a stage of normality then a mg or 2 of kpin will do the trick quite nicely. That or an opiate but I dont advise doing that.

I came to this conclusion as well. I believe it might be because as you become more sleep deprived your brain continues to have reduced amounts of glutamate which is the primary excitatory neurotransmitter in the brain.