shaolinbomber

Careful with Suboxone both for it's strength and it's addiction potential.

Be sure to let us know how Flunarizine is if you decide to try it.

So Visual you're saying that Tasmar can be taken safely for longer periods of time while being monitored by a doctor and having regular testing/check-ups done?

Soccer... . . . . .

I know how you feel. HPPd ruined what "was" my life in an instant. Deep depression set in for me as well when it all started but instead of killing myself I turned to pain pills to numb it and then eventually Heroin. now I can confidently say that I am moving on with my life and am recovering from the addiction so it's not the end of the world even though it feels like it.

It's cause the people who really have HPPD know that it never really goes away. Atleast at this stage of it for me with over 3 years into it I can't see the visuals just going away on their own.

Nah bro. Tussionex is liquid hydrocodone with an anti-cholinergic like promethazine. It's a narcotic cough syrup. Trust me I know all too well (unfortunately). http://www.tussionex.com/

I psyched myself into believing that Sinemet actually was doing anything positive for me. After I read what the other drug was in this thread it got me very curious with wondering if it's the key to allowing other meds to do their job in the brain. I got absolutely nothing from Sinemet by itself and nothing from Keppra by itself. My next bet was to try Flunarizine but now I really want to see if this COMT inhibitor would do anything for me.

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Careful with opiates man. I progressed from pain pills to heroin rather quickly. (under 18 months infact.) I know those opiates produce a very comfortable high that makes the HPPD and DP/DR fade and it is fantastic but it leads down another ugly road.

This is the theory that made the most sense to me back when I was reading up on all of this non-stop. It's either this theory or cell-death that could explain why some people get HPPD and it never goes away. I just think cell death has so many other implications that comes with it that it's hard for me to believe that we've lost so many neurons that our vision has become fucked up. Cell death certainly does make sense for us past drug users but it doesn't make sense when hearing about people only taking SSRI's or anti-biotics and developing VS or other visuals. I stay optimisstic that something will come along in the medical community that will help us.

I thought about giving Flunarizine a try but am hesitant because I don't want to be let down yet again. I was waiting to see if more people were going to report back to the site about it first.

I hit 3 years this past March. It's kinda depressing looking back at the last 3 years or so and wishing you could turn back time before this ever happened to you and wondering if it will ever be like that again.

Only opiates drastically decrease visuals for me but they are not a viable option due to their addictive nature. Best bet is to try and cope with the condition without any chemicals.

Interesting results. Do you mind keeping your progress updated on the site?

Keppra didn't effect me at all.

Opiates have a considerable effect on the dopamine system but I have yet to see any permanent healing from using them A LOT. I do feel a thousand times better when they are active in my brain though.

It's crazy that so many other members here get negative effects from opiates but I felyet im very catious with my use. I bet it has domrthing fo

http://brain.oxfordj...awr157.full.pdf Here's another good article I found about the newer types of diagnostic tools they are using in neurology to identify the problems with disorders involving persisting visual disturbances. Also notice that on all of the readings from the mEEG done on all of the test groups who complained of visual disturbances, the Persistent Visual Aura crowd (I believe HPPDers can be summed in with this group) had the highest readings of cortical excitability. " The present finding of persistent hyperexcitability across ictal-interictal phases suggests that sustained cortical spreading depression reverberations might be the culprit in persistent visual aura. We hereby provide two possible reasons why a vicious cycle of sustained cortical spreading depression is formed in persistent visual aura. First, persistent potentiation in persistent visual aura may lead to enduring and excessive neuronal stress, and the accumulation of metabolites such as lactate and protons that may induce repetitive cortical spreading depression (Scheller et al., 1992). Given the protective nature of habituation, persistent potentiation leads to brain sensory overload, depletes the cortical energy reserve and finally leads to neuronal stress and a biochemical shift that triggers cortical spreading depression (Coppola et al., 2009; Rankin et al., 2009). On the other hand, the excitatory waves piloting each cortical spreading depression propagation and the detrimental effects of repetitive cortical spreading depression upon intracortical inhibition (Kruger et al., 1996) may upregulate cerebral excitability and eventually increase vulnerability to cortical spreading depression (Holland et al., 2010). The association between cortical spreading depression and hyperexcitability here is further supported by a clinical observation that 45% of patients with persistent visual aura had worsening headache during aura persistence (Wang et al., 2008). Despite PET evidence of sustained metabolic activation in the medial occipital cortex with persistent visual aura, there was no corresponding metabolic change during a typical migraine aura (Andersson et al., 1997). Therefore, single cortical spreading depression propagation per se (hence migraine aura) cannot explain the persistent potentiation in persistent visual aura. The culprit should be, again, the complex interaction between cortical spreading depression reverberations and central excitability. The entanglement between central excitability and cortical spreading depression reverberations may further explain the lack of correlation between magnetoencephalography and most clinical measures." CONCLUSION "Persistent visual aura is characterized by persistent hyperexcitability of the visual cortex without interictal-ictal variation, compatible with the excitatory effect of sustained reverberations of cortical spreading depression. Our magnetoencephalography data on the excitability changes in the visual cortex differentiates persistent visual aura from other migraine disorders (migraine with aura, migraine without aura and chronic migraine). Therefore, while belonging to the migraine spectrum, persistent visual aura may be considered a distinct disorder."

http://sibelium.com.cn/sibelium/WX/fulltext_WX_9/06.pdf I came across this article on the Sibelium Website and they talk a lot about Visual Snow and all of the other common visual disturbances associated with HPPD. It is rather informative about how they are classifying these problems in the nuerological community now and they think that the problems could be associated with low magnesium levels in the occipital cortex which might explain why Sibelium is seeing success when applied to patients with these visual phenomena problems seeing as how Sebelium works by blocking calcium gated ion channels and magnesium works by the same method.

http://sibelium.com.cn/sibelium/WX/fulltext_WX_9/06.pdf I came across this article on the Sibelium Website and they talk a lot about Visual Snow and all of the other common visual disturbances associated with HPPD. It is rather informative about how they are classifying these problems in the nuerological community now and they think that the problems could be associated with low magnesium levels in the occipital cortex which might explain why Sibelium is seeing success when applied to patients with these visual phenomena problems seeing as how Sebelium works by blocking calcium gated ion channels and magnesium works by the same method.

I have an appointment with my doc on Wednesday and im going to ask about this as well.

HPPD and the visuals must widely differ from person to person because I can't see how someone wouldn't get mental and phsyical relief from taking opiates. The more euphoric ones like Hydrocodone and Oxycodone totally eliminate DP/DR and extremely reduce my visuals. Jay- That regiment your dr. has you on looks suitable for your goal of avoiding any kind of dependance. Let me know how the Sub goes for reducing your DP/DR and visuals. It's helped me a lot although im prone to using opiates for those specific reasons so maybe it's a preferance type of thing. However it's definitely not a placebo effect as you can attest to. P.S. Also Jay, ask your doctor about Promethazine for the nausea if it continues or gets worse.