Evaluation of anticonvulsant action of cerebro-selective calcium channel blocker nimodipine an experimental study

Calcium (Ca++) a divalent cation, required to perform numerous physiological function within the body like cardiac and smooth muscle contraction. Increased excitatory and reduced inhibitory neurotransmission is responsible for excessive neuronal activity in epilepsy. Some of the CCBs induce reduction in current through Ca2+ channels and thus reducing the pacemaker current that underlies the thalamic rhythm in spikes and waves seen in generalized seizures. The dose of nimodipine was given at doses of 30 and 60 mg QID. This dose was given PO for the improvement of neurological outcome and is chaemic deficit in SAH patients. Either of the dose of nimodipine (30 and 60 mg QID) was not effective in maximum electroshock induced convulsions in experimental rats. When this dose was combined with standard anticonvulsant phenytoin at sub therapeutic dose in reducing tonic HLE was also not found statistically significant in our study.