In all papers published up to now it is stated or surmised that in cervicogenic headache, described by Sjaastad and collaborators (Cephalalgia, 3(4): [240][241][242][243][244][245][246][247][248][249][250][251][252][253][254][255][256] 1983), the painful stimulus is carried mainly or exclusively by the greateroccipital nerve. As a contribution to the study in this modality of headache, the authors made 16 dissection in eight cadavers looking for the anatomical relations of the lesser occipital nerve. T h e results showed that the head and face pain originating from the ventral ramus of the second cervical nerve (C,) can be explained in three different ways: 1) through anatomical regional peculiarities which make it vulnerable to mechanisms of compression and stretching; 2) through the relationship between Cz ventral ramus, the superior cervical ganglion, and the ophthalmic branch of the trigeminal nerve; 3) through clinical evidence related to painful sensibility.T h e authors emphasize the possible role of the lesser occipital nerve on the genesis of cervicogenic headache. It is expected that the conclusions reached will be of help to clinical studies of headache. 0 1994 WiIey-Liss, Inc.Address reprint requests to Edgard Raffaelli Jr., M.D., PhD., Av. Euskbio Matoso, 366, CEP 05423-000, S5o Paulo -SP, Brazil.
The aim of this study was to investigate the possible interactions between the nociceptive system, the sympathetic system and the inflammatory process. Thus, the superior cervical ganglion of rats was submitted to chronic inflammation and Fos expression was used as a marker for neuronal activity throughout central neurons following painful peripheral stimulation. The painful stimulus consisted of subcutaneously injected formalin applied to the supra-ocular region. Fos-positive neurons were identified by conventional immunohistochemical techniques, and analyzed from the obex through the cervical levels of the spinal cord. In the caudal sub-nucleus of the spinal trigeminal nuclear complex, the number of Fos-positive neurons was much higher in rats with inflammation of the superior cervical ganglion than in control rats, either sham-operated or with saline applied to the ganglion. There was a highly significant difference in the density of Fos-positive neurons between the inflamed and control groups. No significant difference was found between control groups. These results suggest that the inflammation of the superior cervical ganglion generated an increased responsiveness to painful stimuli, which may have been due to a diminished sympathetic influence upon the sensory peripheral innervation.
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