The aim: Neurogenic inflammation may contribute to the (max 1400 znak6w) pathogenesis of migraine, but not episodic tension-type headache (ETTH). The aim of this research was to establish whether in children during migraine and ETTH the level of IL-1 beta, IL-6, TNF and soluble TNF receptor type I (sTNFRI) was changed, and whether the level of those cytokines in headache-free period differs between groups with headache and controls. Material: 89 children aged 6-17 years were included ( 16 with migraine with aura, 14 without aura, 31 with ETTH and 28 controls without headaches). Methods: In children with headaches, the blood was sampled in the first hour and in 3 and in 6 hour of the headache, 6 hours after pain termination, in the headachefree period, and in controls under the same conditions. Results: No differences in cytokine levels were detected during headache attack between groups with migraine and ETTH and during headache-free interval between groups of headache and controls. In 12/30 children with migraine the significant increase in IL-6 level was detected in the first hour of attack. The level of IL-1 beta was higher in migraine without aura during headache-free period and in the 1. hour of attack, TNF level was higher in this group 6 hours after pain termination, as compared with migraine with aura. There was significant increase in IL-6 level ; s in 61 children in 3 and 6 hour of headache. Conclusions: The significant mcrease m IL-6 level in several children with migraine in the first hour of the attack may suggest inflammatory pathogenesis of migraine. The significantly lower IL-1 beta and TNF levels in children with migraine with aura may reflect difference in the pathogenesis of both types of the migraine. The increase in IL-6 level in children with longer duration of headache may reflect a stress reaction.