Effects of noninvasive facial nerve stimulation in the dog middle cerebral artery occlusion model of ischemic stroke.

BACKGROUND AND PURPOSE: Facial nerve stimulation has been proposed as a new treatment of ischemic stroke because autonomic components of the nerve dilate cerebral arteries and increase cerebral blood flow when activated. A noninvasive facial nerve stimulator device based on pulsed magnetic stimulation was tested in a dog middle cerebral artery occlusion model. METHODS: We used an ischemic stroke dog model involving injection of autologous blood clot into the internal carotid artery that reliably embolizes to the middle cerebral artery. Thirty minutes after middle cerebral artery occlusion, the geniculate ganglion region of the facial nerve was stimulated for 5 minutes. Brain perfusion was measured using gadolinium-enhanced contrast MRI, and ATP and total phosphate levels were measured using 31P spectroscopy. Separately, a dog model of brain hemorrhage involving puncture of the intracranial internal carotid artery served as an initial examination of facial nerve stimulation safety. RESULTS: Facial nerve stimulation caused a significant improvement in perfusion in the hemisphere affected by ischemic stroke and a reduction in ischemic core volume in comparison to sham stimulation control. The ATP/total phosphate ratio showed a large decrease poststroke in the control group versus a normal level in the stimulation group. The same stimulation administered to dogs with brain hemorrhage did not cause hematoma enlargement. CONCLUSIONS: These results support the development and evaluation of a noninvasive facial nerve stimulator device as a treatment of ischemic stroke.

Effect of pulsed magnetic stimulation of the facial nerve on cerebral blood flow.

In these experiments we define an effective means of pulsed magnetic stimulation of the facial nerve for the purpose of increasing cerebral blood flow (CBF). In normal anesthetized dog and sheep, a focal magnetic field was directed toward the facial nerve within the temporal bone by placing a 6.5 cm figure-8 stimulation coil over the ear. In an initial set of experiments, CBF was measured by laser Doppler flowmetry and the cerebral vasculature was visualized by angiography. The effect of facial nerve stimulation was found to be dependent on stimulation power, frequency, and the precise positioning of the stimulation coil. Furthermore, an increase in CBF was not observed after direct electrical stimulation in the middle ear space, indicating that non-specific stimulation of the tympanic plexus, an intervening neural structure with vasoactive effects, was not responsible for the increase in CBF after pulsed magnetic stimulation. Subsequent experiments using perfusion MRI demonstrated reproducible increases in CBF throughout the forebrain that manifested bilaterally, albeit with an ipsilateral predominance. These experiments support the development of a non-invasive pulsed magnetic facial nerve stimulator that will increase CBF as a treatment of ischemic stroke.