Proinflammatory pathways in cervicogenic headache

P. Martelletti

Department of Clinical Medicine, University “La Sapienza”, Rome, Italy

ABSTRACT
Cervicogenic headache (CEH) is a relatively common form of headache arising from the neck structures. The pathophysiology probably results from various local pain-producing factors such as intervertebral dysfunction, with a no less important role played by the frequent coexistence of a history of head traumas. This report represents a series of pathophysiological studies in CEH patients and the results achieved by pharmacological treatment of the disease.
Interleukin-1b (IL-1b) and Tumour Necrosis Factor a (TNF-a) exert their multifunctional biological effects by promoting and increasing the molecular events of cellular inflammation. We found that the cytokine pattern of CEH patients is - similar to cluster headache - biased towards an inflammatory status. Higher levels of both IL-1b and TNF-a were detected in the sera of CEH patients than the levels in patients with migraine without aura and in healthy subjects. There were also differences between the spontaneous and mechanically worsened pain phases of CEH.
Nitric oxide (NO) synthase is also activated in cervicogenic headache. No change in NO metabolites levels has been observed after NO donor administration. This behaviour is clearly different from that observed in migraine and tension headache patients.
We conclude that the high degree of cytokine and NO production in CH may depend on the differing pathophysiological mechanisms at work in CEH than in other forms of headache.

Key words
Cervicogenic headache, cervical spine, inflammation, cytokines, nitric oxide, acetylsalicylic acid, cyclooxygenase.


Please address correspondence and reprint requests to: Paolo Martelletti, MD, Dipartimento di Medicina Clinica, Universitą degli Studi di Roma “La Sapienza”, Policlinico Umberto I, Viale del Policlinico, 155, 00161 Rome, Italy.
E-mail: martelletti@uniroma1.it

Clin Exp Rheumatol 2000: 18 (Suppl. 19): S33-S38.
© Copyright Clinical and Experimental Rheumatology 2000.