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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.

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An experimental model that reliably and easily produces acute ischemic facial nerve paralysis would be useful for the controlled study of treatment and to improve our understanding of the pathophysiology and treatment of facial nerve palsy. Most documented models that simulate clinical facial nerve palsy cause direct damage to the nerve. We describe an experimental model for ischemic facial nerve paralysis in the cat that employs arterial block of the internal and external maxillary and posterior auricular arteries using embolizing material (Avitene). All animals develop stable acute ischemic facial nerve palsy lasting for approximately 2 months. Electromyographic study of this model revealed that the site of the lesion resulting from selective embolization may be within the temporal bone. This model has the advantages of simplicity of technique, cost-effective use of cats, and reproducibility of facial nerve palsy.

The surgical management of congenital aural atresia is a challenging, complex procedure, and the risks are great. The otologic surgeon is responsible for keeping a patent external auditory canal and for achieving satisfactory hearing. The present report studied hearing changes that occurred after tympanoplasty and the long-term results of tympanoplasty in 12 cases of congenital aural atresia or stenosis. Patients were followed for more than 2 years after surgery. In four ears, an allograft of the tympanic membrane with an attached malleus was used, with a good graft take and hearing results. An autograft of temporal fascia was used in eight ears. Hearing acuity decreased in six of the eight ears and was maintained in two ears. Three primary surgery patients required revision surgery for postoperative restenosis of the external auditory canal. Some comments have been made with regard to this problem. Emphasis is also placed on the selection of patients for surgery using a thorough audiologic and roentgenologic evaluation.