Antiepileptic drugs (AEDs) are frequently prescribed in the elderly due to the high prevalence of AED-treatable neuropsychiatric disorders in this age group. There are several factors associated with AED therapy in the elderly that substantially increase the risk of clinically significant drug interactions. The elderly exhibit altered pharmacodynamics resulting in greater sensitivity to both pharmacological and toxicological drug effects. The use of polypharmacotherapy leaves the elderly patient at an increased risk for adverse events. There are no known drug interactions between anticoagulants/antiplatelets and the following AEDs: gabapentin (GBP), lamotrigine (LTG), levetiracetam (LEV), tiagabine (TGB), or zonisamide (ZNS). A number of AEDs either induce or inhibit drug metabolizing enzymes and, in turn, their metabolism is affected by many co-medications. Several of the newer AEDs do not appear to interact with other medications, while others are affected by enzyme induction of inhibition but do not appear to alter the disposition of co-medications.

Clinically important drug interactions occur essentially at two levels, at the pharmacokinetic level and at the pharmacodynamic level. This chapter describes the clinically significant interactions between antiepileptic drugs (AEDs) and non-AEDs. The interactions can be classified into three groups according to their risk of interaction with AEDs. Carbamazepine is a potent hepatic enzyme inducer and, as well as inducing its own metabolism via an action on CYP3A4, it also induces the metabolism of many other drugs that are CYP3A4 substrates. There are no clinical data to suggest ethosuximide induces or inhibits the metabolism of other non-AEDs. As a new AED, knowledge of the interaction profile of felbamate with non-AEDs is limited. Zonisamide undergoes extensive metabolism, via CYP3A4, and approximately 30% of zonisamide is excreted in urine as unchanged zonisamide. To date, there are no reports of zonisamide affecting the pharmacokinetics of non-AEDs.