wooshka

Fuck me, 25-i is a weapon of a drug.

Must be a way to heal, I'm from Brisbane, you from around there?

And the results are still the same from the inception of this thread? Not a whole lot of change? 

Not to be ignorant or arrogant, how do we know that the substance you obtained is in fact Coluracetam, and if so, in it's more pure form? Like you said, it was different coloured, and also had a noticeable smell? When it's *supposed* to be White, and odorless? 

Do you think Migraines have any correlation in regards to the genetic predisposition of HPPD?

Interesting post, vennit. Glad to see that it's working for you.

Any luck so far in retrieving coluracetam? ODISA?

Holy shit. This looks so promising. Thank you david. Thank you onedayillsailagain.

As you all know, there hasn't always been a certain link between HPPD and the genetic predisposition it may impose. 

I have some interesting facts to share with you, as you know, I have HPPD, but.. so does my brother. 

Another interesting fact is that my mother has suffered from Migraines basically since I can remember, now if this isn't something to do with genetics involving Migraines and or a predisposition, it's one hell of a coincidence. 

Please share your thoughts and I'll try and answer any question you have. 

I don't see many Patterns, normally a honeycomb pattern when I close my eyes, but more or less a swirling drooping form on blank walls and surfaces etc.

I'm fairly sure this has been stated here before, but I'd like for it to be pinned or somewhat more recognized. 

http://www.facesofhppd.com/

Hey guys, I'm fairly active on this site even if I don't post much, I'm always browsing and always willing to have a conversation with you.
If you guys want to have a discussion about anything, if you're feeling like shit on a particular day or just need some reassurance or company that someone is going through this also, you can MSG me here, and I will reply mostly daily, or:

www.facebook.com/rawrdy

Hit me up for a chat if you need too. 
Hope this helps some of you.

-wooshy

What type of MG would you guys reccomend? and what dosage? I'm interested in trying this aswell as other multivitamins~ 

Hi bpl, how are you feeling as of late mate? 

Sorry to hear that you've had an unpleasant experience, this is what kinda pushes my away from taking substances as I don't want to indefinitely increase the severity of my symptoms. 

I agree with cali, how is it now Chris? And what changed when you started taking it?

Thank you for the reply Blunder, I'm just curious as to why it would seem that they're just progressing on their own, but I do understand what you mean in regards to the noticing of symptoms depending on your environmental factors. I'm not even into my first year with this stuff yet, so I'm feeling quite alot of zemblanity as to whats next. I will try magnesium as it has seemed to given most people a positive outcome. Thanks again. 

Hi MBAWTH, I see you're from Australia, where abouts if you don't mind me asking?

What symptoms have you noticed that have decreased may I ask? 

Sorry to hear man. Atleast you still have the job!

Any specific types man? And 3 cups of green, and 3 cups of white? or green & white tea. 6 cups of tea a day is fucked LOL

I can't believe how arrogant this post is, it makes me annoyed that you still want to keep continuing use whereas people here have only done these drugs once and developed full blown HPPD. And yet you want to gamble the circumstances. I agree with jay, it's a definitely not. It's really not worth it. Wake up.

"Atypical antipsychotic drugs (AAPDs) have been suggested to be more effective in improving cognitive impairment in schizophrenia than typical APDs, a conclusion supported by differences in receptor affinities and neurotransmitter efflux in the cortex and the hippocampus. More potent serotonin (5-HT)2A than dopamine (DA) D2 receptors antagonism, and direct or indirect 5-HT1A agonism, characterize almost all AAPDs. Blonanserin, an AAPD, has slightly greater affinity for D2 than 5-HT2A receptors. Using microdialysis and UPLC-MS/MS, we compared the abilities of the typical APD, haloperidol, three AAPDs, blonanserin, lurasidone, and olanzapine, and a selective 5-HT1A partial agonist, tandospirone, and all, except haloperidol, were found to ameliorate the cognitive deficits produced by the N-methyl-d-aspartate antagonist, phencyclidine, altering the efflux of neurotransmitters and metabolites in the rat cortex and nucleus accumbens. Blonanserin, lurasidone, olanzapine and tandospirone, but not haloperidol, increased the efflux of cortical DA and its metabolites, HVA and DOPAC. Olanzapine and lurasidone increased the efflux of acetylcholine; lurasidone increased glutamate as well. None of the compounds significantly altered the efflux of 5-HT or its metabolite, 5-HIAA, or GABA, serine, and glycine. The ability to increase cortical DA efflux was the only shared effect of the compounds which ameliorates the deficit in cognition in rodents following phencyclidine."

"Atypical antipsychotic drugs (AAPDs) have been suggested to be more effective in improving cognitive impairment in schizophrenia than typical APDs, a conclusion supported by differences in receptor affinities and neurotransmitter efflux in the cortex and the hippocampus. More potent serotonin (5-HT)2A than dopamine (DA) D2 receptors antagonism, and direct or indirect 5-HT1A agonism, characterize almost all AAPDs. Blonanserin, an AAPD, has slightly greater affinity for D2 than 5-HT2A receptors. Using microdialysis and UPLC-MS/MS, we compared the abilities of the typical APD, haloperidol, three AAPDs, blonanserin, lurasidone, and olanzapine, and a selective 5-HT1A partial agonist, tandospirone, and all, except haloperidol, were found to ameliorate the cognitive deficits produced by the N-methyl-d-aspartate antagonist, phencyclidine, altering the efflux of neurotransmitters and metabolites in the rat cortex and nucleus accumbens. Blonanserin, lurasidone, olanzapine and tandospirone, but not haloperidol, increased the efflux of cortical DA and its metabolites, HVA and DOPAC. Olanzapine and lurasidone increased the efflux of acetylcholine; lurasidone increased glutamate as well. None of the compounds significantly altered the efflux of 5-HT or its metabolite, 5-HIAA, or GABA, serine, and glycine. The ability to increase cortical DA efflux was the only shared effect of the compounds which ameliorates the deficit in cognition in rodents following phencyclidine."

Would these purpose any benefit to us? I've ever seen anyone on the forum discuss them before. Maybe some of you more well experienced users will have something to say in regards to this. 

Syntheso has just discovered something intriguing in his most recent thread, give it a look!