INTRODUCTION: Epidemiologic data shows an association of various diseases and conditions in the trigeminal innervation area with an increased incidence of primary headaches (migraine, tension type and cluster headache). Rat experimental models of temporomandibular joint, facial muscle and facial subcutaneous tissue inflammation, as well as of neuropathic pain stemming from trigeminal nerve branches, showed that certain painful conditions in craniofacial region are accompanied by neurogenic dura mater inflammation and that this phenomenon is specific for the cranial dura, i.e. it is not observed in the spinal dura. ----- OBJECTIVES: Herein it was examined if nasal cavity and paranasal sinus inflammation is associated with neurogenic dural inflammation, since many inflammatory (allergic rhinitis, chronic sinusitis) or anatomical (septal spur, intranasal contact points) disorders are associated with higher primary headache incidence. ----- MATERIALS AND METHODS: Nasal cavity and paranasal sinus inflammation was induced by intranasal formalin (2.5%) or capsaicin (0.1%) injection. Nasal mucosa and dural inflammation was quantified by spectrophotometric measurement of extravasated Evans blue and plasma protein complex. Pain was measured by rat grimace scale during 40 minutes after induction of inflammation. Activation of spinal caudal trigeminal nucleus (Sp5C) was measured by counting immunohistochemically c-Fos (+) neurons. ----- RESULTS: Capsaicin and formalin administered in rat nasal cavity cause more intense Evans blue extravasation, i.e. inflammation in the nasal mucosa and dura compared to saline (p < 0.05). There is a correlation between inflammation intensity of the nasal mucosa and dura (R2 = 0,2712; p = 0.0155). Activation of c-Fos (+) neuron sin Sp5C and facial pain expression were higher in group administered formalin compared to saline (p < 0.01 and p < 0.05 respectively). ----- CONCLUSION: The results show that nasal cavity inflammation can induce dural inflammation, and suggest that dural inflammation could be one of the pathogenetic mechanisms of primary headaches associated with conditions of the nasal cavity and paranasal sinuses.