http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1978.tb31530.x/abstract
This abstract suggests that the serotonergic neurotoxic damage (measured by 5-hydroxyindoleacetic acid depletion post use) produced in response to 4-haloamphetamines is irreversible, or if recovery occurs, it will be only partial.
http://www.sciencedirect.com/science/article/pii/0028390875900994 This abstract states that depletion of serotonin levels and 5HIAA levels in response to 4-fluoroamphetamine lasts mere 4-6 hours, whereas 4-bromo, and para-chloroamphetamine lasts many months at the very least, and that in the case of administration of the haloamphetamines (well para-chloro and bromo, no mention is made of 4-iodoamphetamine, but it is known to be extremely neurotoxic, and the pharmacology in this case is likely not to be any different) the damage is irreversible by administration of a serotonin reuptake inhibitor such as an SSRI or tricyclic antidepressant after a certain period, but within 24-48 hours, it can be prevented.
While this is an untested idea, it may be adviseable to take an SSRI, a day after this, if somebody has been naiive or stupid enough to try this damn idiotic cathinone product...taking it along with the drug is likely to produce a hideously painful, or potentially fatal case of serotonin syndrome, but after the drug has gone...I don't imagine it doing so.
This is conjecture, and until some other well educated people chime in on this respecting likely half life and weather after a day (the longer the period before this may be done, the more potential for irreversible damage I would be very confident in saying) the drug may still be active, or the hugely elevated 5HT levels would still be present, or weather serotonin levels by this time may already start getting hammered on.
5HT syndrome is and awful, awful, nasty thing to experience...I know from hearing it first hand from somebody who it happened to. The woman I love, it happened to her, she takes an SSRI daily, and suffers from migraines sometimes, sometimes very severe ones, and took sumatriptan without problems for a long period of time, until suddenly she had a reaction and it caused serotonin syndrome.
She collapsed, in horrendous pain, stuck on the floor, thinking she was going to die that day, overheated, muscles stiff to the point of being unable to move to seek help, she would have done then, which says something, she normally won't see a doctor, or take medication of any sort, as she doesn't want to have to depend on anything, ever, for any reason, although if its something so critical her life is at risk, she will do so if it gets to the point her life is actually under threat though
(she hates having to take any sort of meds and being tied to doing so, to the point where she even avoids taking corticosteroids above the absolute, maybe way too low, minimum she can get away with without being close to adrenal insufficiency even more severe than she already has), but when this happened, she couldn't even get to the phone to get help. I would in a heartbeat have traded places, and had that been me, rather than her, but of course, that isn't possible.
She is one hell of a tough cookie, determined to the max to do things in life as she wants them done, to live life the way she wants to live her life, and have the things she needs, and have them her way. But would have gone to hospital if she could, and feared for her life. She is NOT a person who sways from her chosen path, or bends her will, or scares easily, yet in this case, like I say, thought her time had come.
Bear that in mind, when considering the possibility of serotonin syndrome, and the use of a serotonin reuptake inhibiting drug to retard the development of severe, possible permanent neurotoxic damage, with accompanying pronounced deficits in memory and cognitive function, before the safety of this may be discussed and established either way.
This suggestion may be useless, given the fact that anybody reading this thread, who has not yet taken 'brephedrone' yet has some in their possession or is about to purchase some or receive a free sample of some sort, is most unlikely, unless they are exceptionally fucking stupid, to take any.
Serotonin syndrome is likely mediated by overstimulation of the 5HT2a subtype (primary target of serotonergic psychedelics that produces psychdelia in response to taking them), so taking a serotonin antagonist, especially one targeting 5H22a specifically, such as pizotifen, an antimigraine drug currently in clinical use as a preventative, and I believe as an anxiolytic, also a 5HT2c antagonist.
Nefazadone and trazadone are also potent 5HT2a antagonists, and antagonists at 5HT2a, although in the case of trazadone at least, it is a partial 5HT1a antagonist, although not particularly efficacious, greater so than buspirone/buspar. The caveat here is that whilst they are, they release 3-chlorophenylpiperazine (yes the same stuff thats been sold as a shite MDxx alternative at times) which is a 5HT agonist, as a metabolite which may complicate things, probably wouldn't overpower the effect as an antagonist, given its use as such in clinical practise as an antidepressant.
I am going to suggest aggressive action against the potential neurotoxicity here, and say get to hospital, and tell them the above, and suggest that a dose of a combination of pizotifen and an SSRI be given, they will have the capability to treat serotonin syndrome if it occurs due to the the SSRI, dantrolene is usually given, for emergency treatment of serotonin syndrome, but this should not be attempted at home. Unlike the use of pizotifen, which has no such SSRI or serotonergic agonist activity, I believe that safe if its available.
But get to hospital and suggest they give pizotifen and an SSRI as soon as possible, why to do so, and to watch for serotonin syndrome, under close observation, or try, if pizotifen is not available by any means, trazadone or nefazadone, and do so very carefully, keeping under observation.
I would act fast, and without reserve, I say hospital, going there without hesitation and suggesting such potentially risky treatment as a possible treatment (but NOT doing it at home, in case of the occurence of serotonin syndrome with the antidepressants mentioned, if the chlorophenylpiperazine metabolite is sufficient to cause it potentially, although given the time elapse and the fact that its a mere metabolite, slowly released, of a potent 5HT2a and 5HT2c antagonist, it is unlikely)
I say hospital, because of the fact that damage from this drug, is both very likely indeed, to follow the pattern of the para-haloamphetamines and to be permanent quite possibly, and at the least, almost certain to last from 4-6 months to a year if it is not permanent.
Bring the drug remainder with you, and print the links off.
This article states that lengthening the sidechain coming off the phenyl ring to a phenisobutylamine abolishes the neurotoxic activity (at least, the pronounced and prolonged depletion of 5HTIAA and profound serotonin depletion) and shortening it to an alphamethylbenzylamine also prevents it being a neurotoxin like the 4-chloroamphetamine parent is. I hope that the increased bulk of the sidechain, I.e the beta-carbonyl group, and differences between the pharmacology of the cathinones vs amphetamines stop this being a vicious, longterm-damaging or permanently damaging potent neurotoxin, but that is whilst perhaps possible, unknown and absolutely by no means either certain, or known to be likely.
Perhaps if so, it will save some people some really nasty consequences of taking this shite, but quite likely it will not.
Although I have heard that para-chloroamphetamine was used as an antidepressant at one point, without causing this longterm memory and cognitive destruction, humans are not rats, and its quite possible that 4-Cl-amphetamine and the other haloamphetamines other than 4-fluoro may not do this instantly, after a single dose, as it seems to in the rat or mouse model. Also bear in mind that not all studies were done via normal injection or by forced oral gavage (I.E forcing it into the stomach with a tube...sick..sick shit...), but to lesion selectively, areas of the brain intended as a target via injection directly into the brain.
But I am fairly sure some such studies have been done by forced oral administration, or intraperitoneal injection into the body cavity (disgusting and abhorrently cruel...but common as a method of administration to a lab animal) and produced such profound neurotoxic insult.
All my suggestions and info given, now I say again-do NOT FUCKING TAKE THIS DRUG! FLUSH THE FUCKING STUFF AND HAVE NOTHING ELSE TO DO WITH IT! don't give it away like you might with something you just weren't satisfied with, don't sell it, save to somebody truly deserving of suffering, get the hell rid of it!