A fact of some importance is that the left recurrent laryngeal nerve, because of its long course under the aortic arch, can become damaged as a result of lesions in the thorax. There is no dysphagia with lesions at this point in the nerve because the branches to the pharynx (but not to the larynx) have already been given off. For this reason, an aneurysm of the aortic arch, an enlarged left atrium, mediastinal lymph nodes from bronchial carcinoma, and a mediastinal or superior sulcus lung tumor are more frequent causes of an isolated (left) vocal cord palsy than are intracranial diseases. It is estimated that in one-quarter to one-third of all cases of paralysis of the recurrent laryngeal nerve no cause can be established, that is, they are idiopathic. The highest incidence is in the third decade, and males are more susceptible than females. Of the 21 cases reported by Blau and Kapadia, 5 recovered completely and 5 partially within a few months; no other disease appeared in the 8-year period that followed. Berry and Blair described palsies of the superior and recurrent laryngeal nerves, occurring as part of isolated vagal neuropathies. A few were bilateral and, again, the majority of the cases were idiopathic and had much the same prognosis as isolated palsies of the recurrent laryngeal nerve.
Laryngeal neuralgia is a rare entity in which paroxysms of pain are localized over the upper portion of the thyroid cartilage or hyoid bone on one or both sides. The pain may be evoked by coughing, yawning, talking, or sneezing. In the case reported by Brownstone and coworkers, the symptoms were relieved by carbamazepine.
Neurologic Diagnosis of Vocal Cord Paralysis
Clues from the history and examination can help determine the site of the lesion producing vocal cord palsy. If intramedullary, there are usually ipsilateral cerebellar signs, loss of pain and temperature sensation over the ipsilateral face and contralateral arm and leg, and an ipsilateral Bernard-Horner syndrome (see Table 33-3). If the lesion is extramedullary but intracranial, the glossopharyngeal and spinal accessory nerves are frequently involved as well (jugular foramen syndrome; see Table 44-1).
If extracranial in the posterior lateral condylar or retroparotid space, there may be a combination of ninth, tenth, eleventh, and twelfth cranial nerve palsies and a Horner syndrome. Combinations of these lower cranial nerve palsies, which have a variety of eponymic designations (see Table 44-1) are caused by various tumors, both primary and metastatic, or by chronic inflammations or granulomas involving lymph nodes at the base of the skull. If there is no palatal weakness and no pharyngeal or palatal sensory loss, the lesion is below the origin of the pharyngeal branches, which leaves the vagus nerve high in the cervical region. The usual site of disease is then the mediastinum.
The Eleventh, or Spinal Accessory, Nerve