Antiepileptic Drugs

Anticonvulsants have a depressant action on acetylcholine release at the neuromuscular junction.^{[530] [531] [532] [533]} Patients receiving chronic anticonvulsant therapy demonstrated resistance to nondepolarizing muscle blockers (except mivacurium^[534] and probably atracurium as well^{[533] [535]} ), as evidenced by accelerated recovery from neuromuscular blockade and the need for increased doses to achieve a complete neuromuscular block.^{[536] [537] [538]} Vecuronium clearance is increased twofold in patients receiving chronic carbamazepine therapy. ^[539] Others, however, have attributed this resistance to increased binding (decreased free fraction) of the neuromuscular blockers to α₁ -acid glycoproteins or upregulation of neuromuscular acetylcholine receptors, or a combination of both mechanisms.^[540] The latter could also explain the hypersensitivity seen with succinylcholine.^[541] The slight prolongation of succinylcholine action in patients taking anticonvulsants has few clinical implications. On the other hand, the potential hyperkalemic response to succinylcholine in the presence of receptor upregulation is of concern.