Neuroplasticity refers to functional and structural changes in brain regions in response to healthy and pathological activity. Neuroplasticity induced by epileptic activity can involve healthy brain regions into the epileptogenic network by perturbing their excitation/inhibition balance. In this article, we present a new neural mass model that accounts for neuroplasticity and that is used to investigate the possible mechanisms underlying the epileptogenic network expansion. We formulate physiological calciummediated synaptic plasticity and pathological structural plasticity in a multiple-timescale framework. The model highlights that synaptic plasticity at excitatory connections and structural changes in the inhibitory system can transform a healthy region into a secondary epileptic focus under recurrent seizures and interictal activity occurring in the primary focus. Our results suggest that the latent period of this transformation can provide a window of opportunity to preventthe expansion of epileptogenic networks, formation of an epileptic focus, or other comorbidities associated with epileptic activity.