Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability in cochlear and vertebro-basilar arteries: A potential cause of inner ear dysfunction in headache

Trigeminal neurogenic inflammation is one explanation for the development o f vascular migraine. The triggers for this inflammation and pain are not we ll understood, but are probably vasoactive components acting on the blood v essel wall. Migraine-related inner ear symptoms like phonophobia. tinnitus, fluctuation in hearing perception and increased noise sensitivity provide indirect evidence that cochlear blood vessels are also affected by basilar artery migraine. The purpose of this investigation was to determine if a fu nctional connection exists between the cochlea and the basilar artery. Neur onally mediated permeability changes in the cochlea and basilar artery were measured by colloidal silver and Evans Blue extravasation, following ortho dromic and antidromic stimulation of the trigeminal ganglion innervating th e cochlea. Capsaicin and electrical stimulation induced both dose- and time -dependent plasma extravasation of colloidal silver and Evans Blue from the basilar artery and anterior inferior cerebellar artery. Both orthodromic a nd antidromic activation of trigeminal sensory fibers also induced cochlear vascular permeability changes and significant quantitative differences bet ween the treated and control groups in spectrophotometric assays. These results characterize a vasoactive connection between the cochlea and vertebro-basilar system through the trigeminal sensory neurons. We propose that vertigo, tinnitus and hearing deficits associated with basilar migrain e could arise by excitation of the trigeminal nerve fibers in the cochlea, resulting in local plasma extravasation. In addition, cochlear "dysfunction " may also trigger basilar and cluster headache by afferent input to the tr igeminal system. (C) 2001 IBRO. Published by Elsevier Science Ltd. All righ ts reserved.