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This master thesis investigates both retrospectively as prospectively the possible risk factors for the occurrence of epileptiform activity on an EEG after an out-of-hospital cardiac arrest and the possible association between this epileptiform activity, global hemodynamics and outcome after an out-of-hospital CA. Since there was only an association found between epileptiform activity and the presence of a shockable rhythm and BLS, this suggests that rather the pre-hospital no-flow time than the low-flow time is responsible for the occurrence of epileptiform activity after a cardiac arrest. Hemodynamic parameters such as mean arterial pressure, the time that a patient shows blood pressure values below 65 mmHg and above 85 mmHg seemed not be associated with the occurrence of epileptiform activity. We observed that the occurrence of (refractory) epileptiform activity is associated with significantly reduced survival and that this malign activity might worsen the brain damage. This latter finding is supported by the results of the analysis in which the evolution of the marker for neurological damage, Neuron Specific Enolase (NSE), is studied. These results show that patients who developed epileptiform activity on an EEG, have low values of NSE at baseline but that after 24 and 48 hours, the timeframe in which epileptiform activity occurs frequently, the NSE-values increase significantly. Besides the epileptiform activity, the presence of BLS, the presence of a shockable rhythm and a shorter period of time in which a patient showed blood pressure values below 65 mmHg, were also found to be independent predictors of survival.