More than 50% of the childhood epilepsies are focal. Family and developmental history, seizure semiology, electroencephalography (EEG, awake and asleep), magnetic resonance imaging (MRI) and neurological examination enable a first assignment regarding the etiology (structural vs. MRI-negative epilepsy) and if possible the classification of an epilepsy syndrome, e. g. various self-limiting focal epilepsies in childhood. As a rule, the latter are treated differently and typically with a shorter duration of medication. Sulthiame is the established therapy for Rolandic epilepsy and for children with benign (familial or sporadic) epilepsy in infancy and Panayiotopoulos syndrome oxcarbazepine is the first-line treatment. In general, the antiepileptic drug therapy of structural and MRI-negative focal epilepsy do not differ. Antiepileptic drugs of first choice are lamotrigine, levetiracetam, oxcarbazepine/eslicarbazepine acetate, and lacosamide. Treatment differs, for example, in children with tuberous sclerosis for whom vigabatrine plays a role in infancy and everolimus in the case of pharmacoresistance. The continuation of antiepileptic treatment is usually recommended in seizure-free patients with structural focal epilepsy. If there is a strong wish to stop treatment, the attempt should be made before adulthood, comparable to the recommendation in MRI-negative, non-syndromic focal epilepsy after 3–5 years of seizure freedom. Epilepsy surgery is by far the most effective treatment for suitable candidates with pharmacoresistant focal epilepsy rendering approximately 60% of the children seizure-free. Ketogenic diets and vagus nerve stimulation are further nonmedicinal alterative treatment options.