I have to confess that I’m currently attending drug dinners. The reason? My wife (also a physician) happens to like the food.
Even more shameful than attending them is writing about them. Why posting about one now? Sometimes you can hear about interesting problems even in prosaic events.
In this particular case the speaker brought up the old but still important issue of neuroprotection in stroke. Apparently, Lamotrigine may reduce the extension of the infarct when given shortly after the beginning of the process. I was aware of the use of Phenytoin experimentally for the same purpose in the old times (decades ago), with ambiguous results. It was found later on that there were different stages after the initial ischemic process, with a different type of intervention being useful for each stage. Phenytoin showed some limited efficacy on one of the early stages; however, at the end, the area of infarct was about the same as in controls. After a rather cursory search posterior to the drug dinner, it appeared to me that the neuroprotective power of Lamotrigine on an ischemic setting was equally controversial. In general, antiepileptic drugs have been good candidates for neuroprotective agents. It could be speculated that, since the effect of some of them (in this case Lamotrigine) is on voltage gated channels, they may help by curbing the excitotoxicity vicious cycle (NMDA receptors, calcium influx, further excitation, all of this enhanced by open potassium channels in the astroglia, which conforms a ionic syncitium when the pH is low).
It is always a pleasant surprise when, in a typically non-scientific event such a as a drug dinner, the speaker brings up, even en passant, a scientific topic.