颈性眩晕发病机制新进展

摘要：The pathogenesis of cervical vertigo is still not clear. Currently there are several hypotheses including proprioceptive cervical vertigo, vertebral artery compressive hypothesis, neurohumor factor hypothesis,cervical sympathetic nerve related vertigo and Migraine associated cervicogenic vertigo. These hypotheses tried to explain the pathogenesis of cervical vertigo from different perspectives, however, they all failed to reveal it completely. Neck proprioceptive cervical vertigo hypothesis indicated that abnormal afferent input to the vestibular nucleus from damaged joint receptors in the upper cervical region could alter the vestibular nuclei of the brainstem, resulting in cervical vertigo. Vertebral artery compressive hypothesis thought that compression of the vertebral artery might lead to vertebrobasilar insufficiency, initiate vestibular organ ischemia, thus result in vertigo. Some authors indicated that neurohumor factors played an important role in the pathogenesis of cervical vertigo. Cervical sympathetic nerve related vertigo hypothesis suggested that sympathetic plexus surrounding the vertebral arteries could be stimulated by cervical degenerative disease. And this stimulation could contribute to the reflexive vasoconstriction of the vertebrobasilar system, thus accounting for the cervical vertigo. Migraine associated cervicogenic vertigo hypothesis postulated that there were relations between migraine and cervicogenic vertigo. The reciprocal connections between the vestibular nuclei and the trigeminal nucleus caudalis can provide a mechanism in which the vestibular signals would influence the vascular trigeminal paths, widely related to the processing of the vestibular and trigeminal information during the migraine attacks.