Iritani H, Nishimura Y, Minatogawa T
Department of Otolaryngology, Hyogo College of Medicine, Nishinomiya Japan.
Acta Otolaryngol. 1991;111(5):934-42. doi: 10.3109/00016489109138433.
The establishment of an animal model for facial nerve paralysis is assuming increasing importance in clinical medicine and also in basic facial nerve research. We previously reported an animal model for ischemic facial nerve paralysis using selective vascular embolization through the internal maxillary and posterior auricular arteries in cats using Avitene which contains bovine microfibril collagen. In this paper, we determined the exact site of the lesion in established facial paralysis. A descending signal produced by direct stimulation to the contralateral motor cortex was able to elicit firing of the motor nucleus of the facial nerve, the extra-temporal portion of the peripheral nerve, and the orbicularis oris muscle. After achieving complete facial nerve paralysis, this descending signal was completely abolished within the temporal bone area, whereas peripheral facial nerve stimulation elicited a normal evoked electromyogram of the orbicularis oris muscle. The present results suggest that the site of the lesion of ischemic facial nerve paralysis produced by embolization in an animal model is within the temporal portion of the seventh nerve, and this animal model may lead to the advancement of future facial nerve research which cannot be conducted in humans.
面神经麻痹动物模型的建立在临床医学以及面神经基础研究中日益重要。我们之前报道了一种通过使用含牛微纤维胶原的阿维丁经猫的上颌内动脉和耳后动脉进行选择性血管栓塞建立的缺血性面神经麻痹动物模型。在本文中，我们确定了已建立的面神经麻痹病变的确切部位。对侧运动皮层直接刺激产生的下行信号能够引发面神经运动核、周围神经颞外部分以及口轮匝肌的放电。在实现完全性面神经麻痹后，该下行信号在颞骨区域内完全消失，而周围面神经刺激则引发口轮匝肌正常的诱发肌电图。目前的结果表明，在动物模型中通过栓塞产生的缺血性面神经麻痹的病变部位在第七神经的颞部，并且这种动物模型可能会推动未来无法在人类中进行的面神经研究的进展。
