Neurophysiology of Ischemic Facial Nerve Paralysis in an Animal Model

Abstract

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.

Thiol/disulphide homeostasis in Bell's palsy as a novel pathogenetic marker

“…The most likely cause of Bell's palsy is oedema of the facial nerve induced by the herpes virus and varicella zoster virus . Other suggested causes include ischaemia, autoimmune inflammatory disorders and heredity . Although the aetiology of Bells palsy is not clear, the facial weakness is thought to result from facial nerve inflammation and oedema.…”

“…Later a secondary ischaemic theory is an inflammatory, viral or immunologic oedema causing disturbances of the microcirculation, leading to loss of nerve conductivity. Both concepts suggest that these processes lead to anoxia followed by compensatory dilation of the vessels and transudation …”

Impaired Ranvier Node Sodium‐Potassium Adenosine Triphosphatase May Induce Facial Palsy

“…An experimental animal model of ischemic facial palsy was first reported by McGovern et al 9,10 Ischemic facial palsy was induced by the injection of a vasoconstrictor into the facial canal. Iritani et al 11 and Kumoi et al 12 created a new ischemic animal model by the selective embolization of the middle meningeal artery in adult cats. Since this model was atraumatic and reproducible, it was widely applied to basic facial research.…”

“…Table I summarizes the results obtained from normal untreated animals, 15,16 animals in which facial palsy was experimentally induced, 11,12 and animals after reserpinization. In a previous study, Na‐K ATPase activity in normal guinea pigs 15 and cats 16 was found to be localized to the entire axolemma and to the Schmidt‐Lanterman incisures and terminal loops of Schwann cells.…”

“…Using the cat model 11,12 described above, Kanoh et al 19 reported that 4 hours after the experimental induction of facial palsy, degeneration of axon cylinders and Schmidt‐Lanterman incisures was observed and that K‐NPPase reaction product was no longer observed along the entire axolemma of the axon cylinder or at the incisures of Schmidt‐Lanterman.…”