Introduction: Up to now, neurogenic inflammation of dura mater was associated to pathophysiology of migraine pain. The main finding of this doctoral thesis is that pain in the head and neck region elicits dural neurogenic inflammation as well. This phenomenon is caused by the neuropeptides release from the dural sensory neurons and could be prevented by triptans and/or botulinum toxin type A (BoNT/A). Material and methods: Male Wistar rats were used in all experiments. Neurogenic inflammation of cranial dura mater was measured (as plasma protein extravasation and proinflammatory cell infiltration) in models of acute and chronic inflammatory and neuropathic pain in the trigeminal innervation area, and neuropathic pain in the innervation area of major occipital and ischiadic nerve. Additionally, occurrence of neurogenic inflammation of spinal dura was measured in the models of neuropathic pain in the innervation area of ischiadic nerve. The effect of different analgesic drugs (triptans, morphine, local anesthetic) on allodynia and dural neurogenic inflammation was measured in the neuropathic pain model (constriction of the infraorbital nerve). Furthermore we investigated the effect of BoNT/A (s.c. in the whisker pad, 3.5 IJ/kg; i.a. in the temporomandibular joint, 5 IJ/kg; i.g. in the trigeminal ganglion, 2 IJ/kg) on allodynia and dural neurogenic inflammation in the models of acute and chronic inflammatory and neuropathic pain in the trigeminal innervation area. Additionally, we used colchicine (axonal transport inhibitor) to investigate the mechanism of the BoNT/A. Results: Neurogenic inflammation of cranial dura was elicited by inflammatory and neuropathic pain from trigeminal and occipital innervation area. However, neuropathic pain from the innervation area of ischiadic nerve did not result in neurogenic inflammation of cranial and spinal dura mater. Triptans (sumatriptan and zolmitriptan), morphine and local anesthetic decreased both allodynia and dural neurogenic inflammation in the model of trigeminal neuropathic pain. BoNT/A abolished allodynia and dural neurogenic inflammation in the models of acute and chronic inflammatory and neuropathic pain. The effect of BoNT/A was abolished by blocking the axonal transport through trigeminal ganglion. Conclusion: Results of this doctoral thesis indicates that different pain in trigeminal and also occipital area (head and neck region) results in neurogenic inflammation of cranial dura. Antinociceptive mechanism of action of several analgesic and anti-migraine drugs is associated with reduction of dural neurogenic inflammation.