The dendritic arbor is the site of complex interactions between synaptic excitation and intrinsic excitability. It has become apparent recently, that the dendritic arbor cannot be viewed as a passive antenna that simply receives and relays synaptic input to the cell body. Instead, dendrites express an abundance of voltage-gated channels that are capable of initiating regenerative spikes and actively regulate the local dendritic resting membrane potential. Active properties can be expressed as back-propagating action potentials along the main apical trunk and as localized spikes confined to individual terminal dendritic segments. The notion of the dendritic arbor as a highly active structure has profound implications for the generation of epilepsy. This chapter will focus on recent data on perturbations to dendritic intrinsic excitability associated with epileptic conditions. An attempt will be made to understand how hyperexcitability may be the result of maladaptive homeostatic mechanism. Topics to be addressed relevant to the functional reorganization of dendrites include activity-dependent down regulation of IA (Kv4.2), epilepsy induced down regulation of Ih (HCN1 and HCN2), and deafferentation induced down regulation of SK-type potassium channels. Other topics to be addressed include the concept of electrical compartmentalization within the dendritic arbor and the recruitment of NMDA receptors as part of intrinsic excitability. A clearer understanding of dendritic mechanisms of neuronal hyperexcitability may offer novel insights for therapeutic interventions.