Abstract
The goal of this investigation was to test the hypothesis that tympanic membrane exposure to cold air is a cause of acute facial palsy. A series of acute invasive experiments and a series of chronic noninvasive experiments were conducted in both cats and dogs. In the acute studies, stimulation was applied intracranially to the facial nerve root through a stereotaxically placed microelectrode and recordings of compound action potentials obtained extracranially from the facial nerve. Nerve conduction was monitored continuously during the application of cold air to the tympanic membrane. Nerve conduction disturbances were observed in all animals tested (8), and reduction in compound action potential amplitude ranged from 33% to 96%. Histologic analysis of the infratemporal portion of the facial nerve was performed in the animal exhibiting the greatest block in conduction, representative of a near-total paralysis. Axon swelling, demyelinization, and degeneration (Bungner's bands) without inflammation were apparent along the entire tympanic membrane segment. Interstitial swelling of nerve endoneurium was also present at the second genu and vertical segment. In the chronic studies, animals were exposed to cold air and monitored daily for facial paralysis after recovery from anesthesia. None of the animals demonstrated any detectable behavioral facial paralysis.
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