Complete interruption of the intracranial portion of one vagus nerve results in a characteristic pattern of paralysis. The soft palate droops on the ipsilateral side and does not rise in phonation. The uvula often, but not always, deviates to the normal side on phonation. There is loss of the gag reflex on the affected side and of the curtain movement of the lateral wall of the pharynx, whereby the faucial pillars move medially as the palate rises in saying “ah.” The voice is hoarse, often nasal, and the vocal cord on the affected side lies immobile in a “cadaveric” position, that is, midway between abduction and adduction. With partial lesions, movements of abduction are affected more than those of adduction (Semon’s law). There may be a loss of sensation at the external auditory meatus and back of the pinna. Usually no change in visceral function can be demonstrated with a unilateral lesion except by special autonomic testing. If the pharyngeal branches of both vagi are affected, as in diphtheria, the voice has a nasal quality, and regurgitation of liquids through the nose occurs during the act of swallowing.
Diseases Affecting the Vagus
Complete bilateral paralysis is said to be incompatible with life, and this is probably true if the nuclei are entirely destroyed in the medulla by poliomyelitis or some other disease. However, in the cervical region, both vagi were blocked with procaine in the treatment of intractable asthma in past days without mishap. Of interest in this regard, Johnson and Stern reported a case of bilateral vocal cord paralysis in association with familial hypertrophic polyneuropathy, and Plott relates three brothers with congenital laryngeal abductor paralysis caused by bilateral dysgenesis of the nucleus ambiguus. Bannister and Oppenheimer have called attention to defects of phonation and laryngeal stridor as early features of autonomic failure in multiple system atrophy (see Chap. 38). We have seen several such patients in whom stridor was a prominent feature of the illness, persisting in one patient for almost a year before other features of the degenerative disease became evident.
The vagus nerve may be implicated within the meninges by infectious, neoplastic, and inflammatory processes, within the medulla by vascular lesions (e.g., the lateral medullary syndrome of Wallenberg, as described in
Chap. 33), and by motor neuron disease. Herpes zoster may attack this nerve, either alone or together with the ninth nerve as part of a jugular foramen syndrome. The vagus is often affected along with the glossopharyngeal nerve in spontaneous dissection of the carotid artery at the base of the skull. The nerves may be damaged in the course of thyroid surgery and may be involved in cases of advanced alcoholic or diabetic neuropathy. Finally, the vagus can be compressed by lesions of the jugular foramen as part of a multiple cranial nerve syndrome as summarized in
Table 44-1; metastatic tumors such as from the prostate or breast and jugular vein thrombosis are typical causes.