NEUROPHYSIOLOGY OF TRIGEMINAL NEURALGIA

三叉神经痛是一种严重的，复发性（发作性，但否则慢性）面部疼痛综合征，影响主要是老年患者。三叉神经痛的疼痛是独特的，其阵发性，痛苦的强度，割伤的质量，并局限于三叉神经系统。对于这种疾病，有各种各样的药物和手术治疗方法，但没有一种是一致和永久有效的。看来，三叉神经痛的长期治疗的实质性改善可能会受到这种疾病的神经基础缺乏基本了解的阻碍。过去曾有人提出涉及外周神经系统异常感觉输入和/或中枢神经系统突触处理改变的理论，但迄今为止还没有直接的实验证据支持它们。在缺乏足够的动物模型的三叉神经痛，理论的成因进行了测试，在有症状的人类患者。 本研究的目的是应用一种新的显微神经电图记录技术，直接研究三叉神经痛患者三叉神经节神经元的神经生理学特征。该技术，我们已经开发，允许术中微电极记录在三叉神经节之前，患者接受经皮神经节松解术治疗疼痛。该研究将检测触发区的轻微机械刺激是否引起三叉神经初级传入神经元的异常（自我维持）动作电位放电。轴突的电刺激将用于检测三叉神经节神经元的根或胞体中的自动节律活动。最后，将尝试识别可能发生在三叉神经节的动作电位放电！离子神经元同时患者三叉神经痛的经验。预计术中记录将首次提供三叉神经痛与外周神经系统异常感觉输入相关的直接证据。 合唱团在神经或神经节的冲动交通在疼痛发作的观察应大大阐明三叉神经痛的神经机制，允许在实验动物中的综合征建模，并指导研究更好的医疗和手术治疗疼痛发作在这种和其他神经性疼痛疾病。

Trigeminal neuralgia is a severe, recurrent (episodic, but otherwise chronic) facial pain syndrome which affects chiefly older patients. The pain of trigeminal neuralgia is unique in its paroxysmal nature, excruciating intensity, lancinating quality, and confinement to the trigeminal nervous system. Various medical and surgical treatments are available for this disorder, but none is uniformly and permanently effective. It appears that a substantial improvement in the long-term treatment of trigeminal neuralgia may be hindered by the lack of basic understanding of the neurological basis of this disorder. Theories involving abnormal sensory input from the peripheral nervous system and/or alteration of synaptic processing in the central nervous system have been invoked in the past, but thus far there is no direct experimental evidence to support them. In the absence of an adequate animal model of trigeminal neuralgia, theories of genesis have to be tested in symptomatic human patients. The goal of this research proposal is to apply a novel micro-neurographic recording technique to study directly the neurophysiological characteristics of trigeminal ganglion neurons in patients with trigeminal neuralgia. The technique, which we have developed, allows intra-operative microelectrode recordings in the trigeminal ganglion before the patients undergo percutaneous gangliolysis for treatment of the pain. The proposed study will examine if light mechanical stimulation of the trigger zone elicits abnormal (self-sustained) action potential discharge in trigeminal primary afferent neurons. Electrical stimulation of the axons will be used to detect auto-rhythmic activity in the roots or somata of trigeminal ganglion neurons. Finally, an attempt will be made to identify action potential discharges which may occur in trigeminal gang!ion neurons concurrent with patient's experience of trigeminal neuralgic pain. It is anticipated that intra-operative recordings will provide, for the first time, direct evidence that trigeminal neuralgia is associated with abnormal sensory input from the peripheral nervous system. Choral made observations of impulse traffic in the nerve or ganglion during paroxysms of pain should greatly illuminate the neural mechanism of trigeminal neuralgia, allow for modelling of the syndrome in experimental animals, and direct research toward better medical and surgical treatment of pain paroxysms in this and other neuropathic pain disorders.