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.