Intracerebral hemorrhage (ICH) and epilepsy belong to the most common, serious neurological conditions in the world. Having an ICH is a known cause in the development of epilepsy, and epileptic activity in the acute phase post-ICH is likely to influence the outcome of ICH. In this project we use an experimental animal model for ICH to study the role of epileptic processes post-ICH. We will focus on the concept of the metabolic penumbra, which is defined as the zone around the bleeding, in which cells are still viable. We hypothesize that pathological epileptic processes contribute to increased secondary brain tissue damage and neuroinflammation, and worsen the outcome post-ICH. Unraveling these processes would form the basis to develop neuroprotective measures for prevention and/or treatment of secondary brain damage in ICH-patients. In a first stage, the metabolic penumbra following ICH will be defined and the occurrence of epileptic discharges within the metabolic penumbra will be studied. In the second stage, the effect of epileptic discharges on the metabolic penumbra and how this affects secondary brain damage and outcome will be studied. In the third stage, the effect of an increase or decrease in the occurrence of epileptic discharges on the penumbra is examined, and in the last stage a specific anti-epileptic compound is used to evaluate its possible neuroprotective effect.