Application of the denervation in the cervical sympathetic nervous system for the treatment of facial palsy

颞骨面神经微循环障碍在贝尔麻痹的发病机制中起重要作用。然而，循环功能损害的发生机制尚不清楚。头颈部交感神经系统的活动被认为是面神经微循环系统变化的重要因素。我们证实，电刺激颈交感干和低通气引起的高碳酸血症减少了面神经组织的血流量。此外，颈部交感干的化学阻塞改善了颈总动脉和面神经组织的血流量。在本项目中，我们研究了电刺激和化学阻断颈交感干对面神经微循环的影响。电刺激颈胸神经节后，颈总动脉和面神经组织的血流量均明显减少。向该神经节注射甲哌卡因后，颈总动脉血流量和面神经组织血流量立即恢复到基线值。由此可见，颈交感神经系统的高张力损害了面神经的微循环，即使在交感神经活动的刺激条件下，该神经系统的去神经支配也能改善面神经的循环。基于这些发现，临床化学阻断颈交感干可能是治疗头颈部交感神经亢进所致贝尔麻痹的一种非常有效的方法。我们还研究了高碳酸血症和颈交感干化学阻塞对面神经微循环的影响。颈总动脉血流无明显变化，但高碳酸血症时面神经组织血流明显减少。在神经节注射甲哌卡因后，颈总动脉血流量明显增加，但面神经组织血流量持续减少。随着通气恢复正常，颈总动脉和面神经组织的血流量均恢复到基线值。高动脉CO_2张力通过刺激下丘脑和肾上腺素能介导引起交感神经系统活动水平的升高。我们的研究结果表明，高碳酸血症会刺激交感神经系统，损害面神经的微循环。此外，当交感神经系统的活动受到集中刺激时，颈交感神经系统的去神经支配并不能改善面神经的微循环。前列腺素E1 （PGE1）的药物治疗应用可增加颈总动脉的血流量。我们还检测了PGE1对面神经组织血流量的影响。应用PGE1后，颈总动脉的血流量增加并维持，但面神经组织的血流量仅在短时间内略有增加。需要大剂量静脉注射PGE1来暂时增加面部组织的血流量。少

Microcirculatory disorders of the facial nerves in the temporal bone play an important role in the pathogenesis of Bell's palsy. However, the mechanism of onset of circulatory impairment is still unknown. The activity of the sympathetic nervous system in the head and neck is presumed to be an important factor in the changes of the microcirculatory system in the facial nerves. We confirmed that that electrical stimulation given to the cervical sympathetic trunks and hypercapnia induced by hypoventilation decreased the blood flow in facial nerve tissues. In addition, chemical blockage of the cervical sympathetic trunks improved the blood flow in both the common carotid artery and the facial nerve tissues. In this project, we investigated the combined effects of electrical stimulation and chemical blockage of cervical sympathetic trunks on microcirculation in the facial nerve. With the electrical stimulation of cervicothoracic ganglion, the blood flow in both the common carotid artery and … More facial nerve tissue decreased significantly. Both the common carotid arterial blood flow and facial nervous tissue blood flow returned to the baseline value immediately following the injection of mepivacaine to that ganglion. From these result, the hypertonicity of cervical sympathetic nervous system impairs the microcirculation of the facial nerve, and the denervation of such nervous system improves the circulation even if under the stimulus condition of sympathetic activity. On the basis of these findings, clinical chemical blockage of cervical sympathetic trunks could be extremely effective treatment method for Bell's palsy that might be under the sympathetic hyperactivity in head and neck. We also investigated the combined effects of hypercapnia and chemical blockage of cervical sympathetic trunks on microcirculation in the facial nerves. The blood flow in the common carotid artery did not change significantly, but remarkable decrease was observed in the tissue blood flow of facial nerve with hypercapnia. And immediately following the injection of mepivacaine to the ganglion, the common carotid arterial blood flow showed a significant increase, but the facial nerve tissue blood flow continued to decrease. With the return of ventilation to the normal condition, the blood flow in both the common carotid arterial and facial nerve tissues returned to the baseline values. High arterial CO_2 tension induced elevation of the activity level of the sympathetic nervous system through the stimulation of the hypothalamus and an adrenergic mediation. Our findings indicate that the hypercapnia, which stimulates the sympathetic nervous system, impairs the microcirculation of the facial nerve. In addition, the denervation of the cervical sympathetic nervous system does not improve the microcirculation of facial nerves when the activity of the sympathetic nervous system is centrally stimulated. The pharmacotherapeutic application of prostaglandin E1 (PGE1) can be used to increase blood flow volume in the common carotid artery. We also examined the effects of PGE1 on the blood flow volume in facial nervous tissue. The blood flow volume of the common carotid artery was increased and sustained by the application of PGE1, but The blood flow volume in the facial nervous tissue increased slightly for a short time only. A large intravenous dosage of PGE1 was required to temporarily increase the blood flow volume in facial tissue. Less