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-1 beta (IL-1 beta) and Tumour
Necrosis Factor alpha (
TNF-alpha) 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-1 beta and
TNF-alpha 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.