Though I have done a considerable amount of research into this myself I would be interested if anyone with a medical/pharmacology background or personal experience would care to weigh in.
To begin with this was an incidence last December of new on-set seizures with no known cause, consisting of 5 grand-mal seizures occuring over a period of 10 days. The individual did not respond to 400mg phenytoin, but 600mg was effective. Since then phenytoin was switched to Keppra (levitiracetam). The individual is their mid-twenties, relatively healthy, and has no prior history of seizures.
This individual had been using a small regimen of CEs (piracetam, aniracetam, huperzine A, centrophenoxine, ALC) for over a year before this occurance but has since discontinued all of them. The specific CEs that they are interested in using are as follows; piracetam (this is of course a very similar compound to levetiracetam), hydergine, and possibly deprenyl). They are interested in gathering as much info as possible and so any useful insight would be appreciated.
Aniracetam reverses the effects of some anticonvulsant medications, though it does not produce convulsions on it's own -
Aniracetam reverses the anticonvulsant action of NBQX and GYKI 52466 in DBA/2 mice.
Chapman AG, al-Zubaidy Z, Meldrum BS.
Department of Neurology, Institute of Psychiatry, Denmark Hill, London, UK.
Aniracetam (1-p-anisoyl-2-pyrrolidinone) selectively reverses the anticonvulsant activities of the non-NMDA receptor antagonists, GYKI 52466 (1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3- benzodiazepine.HCl) and, to a lesser extent, NBQX (2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)quinoxaline), without affecting the anticonvulsant activity of the competitive NMDA receptor antagonist, D(-)-CPPene, in DBA/2 mice. Pretreatment with aniracetam (50 nmol i.c.v., 15 min before drugs) increases the ED50 values (mumol/kg i.p., 15 min) for GYKI 52466-induced protection against sound-induced clonic seizures in DBA/2 mice 7 fold, from 20.1 (11.9-33.9) to 142 (91.7-219), and for NBQX-induced protection 2 fold, from 39.7 (33.8-46.7) to 85.6 (63.9-115), respectively. Aniracetam on its own (12.5-100 nmol i.c.v.) has no convulsant activity, but reverses the anticonvulsant effect of GYKI 52466 (60 mumol/kg i.p., 15 min) in a dose-dependent manner.
I would rule out Piracetam, as it generally tends to enhance anticonvulsant activity, though having no such independent action.
Vinpocetine and Hydergine, as vasodialators, could aggravate previously existing conditions involving brain blood flow, such as cerebral artheriovenous malformation - one known cause for grand-mal seizures.
Huperzine A increases postsynaptic levels of acetylcholine, which may in turn increase the electrical "firing rate" of neurons, and possibly cause excesive stimulation beyond threshold levels in the CNS.
There have been few studies done on different combinations of nootropics, and thus the net biochemical effect thereof remains highly speculative. The best thing to do at this point, for the subject, would be to abstain from such substances and follow the physician's advice and guidance. It also serves as a reminder that many so-called nootropic drugs have potent effects on the nervous system, and that they are not something to be played around with frivilously.
