Clinical History

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The primary clinical symptom of cranial nerve IX dysfunction is dysphagia or choking, and the most readily identified sign of vagal nerve damage is hoarseness. The clinical histories of patients with symptoms referable to the glossopharyngeal and vagus nerves necessarily reflect the location of the nerve dysfunction and the process producing it. Dependent upon these two factors the temporal appearance of symptoms may vary widely, ranging, for example, from the acute onset of hoarseness and dysphagia due to brain stem infarction involving the vagus nerve nuclei to the insidious appearance of hoarseness without dysphagia produced by the encroachment of a pulmonary neoplasm upon the intrathoracic recurrent laryngeal branch of the vagus nerve.

Intraparenchymal brain lesions of the medulla at the level of the glossopharyngeal and vagus nerves typically affect the nuclei of both, and possibly also of the eighth cranial nerve, resulting in symptoms of vertigo, hoarseness of speech, and dysphagia. Because cranial nerves IX, X, and XI pass together through the jugular foramen at the base of the skull, a lesion at this location can cause added neck muscle weakness. y Rarely, throat pain occurs, specifically in the syndrome of idiopathic glossopharyngeal neuralgia, in which fleeting pain at the base of the tongue is sometimes triggered by chewing or swallowing. An intramedullary lesion of the vagal motor nucleus producing vocal cord weakness and hoarseness of speech likely also affects adjacent structures, such as the spinal tract and nucleus of cranial nerve V, the spinothalamic tract, and cerebellar fibers. Hence, associated symptoms include a crossed sensory disturbance (ipsilateral face and contralateral limbs) and ataxia. An ipsilateral Horner's syndrome may be present from involvement of descending sympathetic fibers, although the patient is unlikely to describe accompanying symptoms, because an intracranial but extramedullary lesion of the vagus nerve involves also the ninth and eleventh cranial nerves. The presence or absence of dysphagia, with hoarseness of speech, is an important clue to the localization of the lesion of the vagus nerve. Hoarse speech without dysphagia occurs when the lesion site of the vagus nerve is below the upper cervical levels where the pharyngeal branches exit. This lesion most commonly occurs at the level of the recurrent laryngeal nerve branch. Possible mechanisms include an expanding aneurysm at the aortic arch, mediastinal adenopathy, and pulmonary neoplasms. y ,

Head, neck, or oral trauma, and surgery of these structures may result in damage of the ninth and tenth cranial nerves. Head injury with basilar skull fracture may compromise both nerves at the jugular foramen.y Vocal cord paralysis is a recognized complication of neck surgery, including thyroidectomy and carotid endarterectomy.y , M Both procedures may injure laryngeal branches of the vagus nerve by manipulation or transection. The recurrent laryngeal nerve is injured by thyroidectomy at a rate of approximately 7 percent, producing ipsilateral paralysis of all the laryngeal muscles except for the cricothyroid. This injury may result in breathiness of speech and aspiration. y

Underlying medical conditions or their treatment may cause injury to the glossopharyngeal and vagus nerves. Patients with neoplasms that involve the head or neck, either primary tumors or metastases, may experience impaired swallowing as a consequence of nerve compression at the jugular foramen or other sites. y Infectious or inflammatory processes involving the central nervous system (CNS) at the level of the brain stem can produce cranial neuropathies. Although the ninth and tenth cranial nerves may be involved, they generally do not produce prominent symptoms or signs. Neurological manifestations of sarcoidosis typically involve cranial nerves, particularly the facial nerve, yet involvement of cranial nerves IX and X can occur in conjunction with facial weakness, and their function should be assessed.^ The ninth and tenth nerves may also be damaged as a consequence of diabetes, syphilis, or alcoholism. [iii , y

Patients may have respiratory complaints, because abnormalities of ventilatory drive by hypoxic stimulation can occur with involvement of carotid body chemoreceptor afferent fibers from the glossopharyngeal nerve. y Patients may also have symptoms of lightheadedness and orthostatic dizziness from involvement of baroreceptor afferent fibers from the carotid sinus.U The Guillain-Barre(c) syndrome may have associated autonomic dysfunction resulting from demyelination of glossopharyngeal afferents from the carotid sinus and vagal fibers, producing instability of blood pressure and heart rhythm, and bowel motility disturbance such as ileus. y , [ie| A history of all medications and toxin exposures is important, because cranial nerve neuropathy due to exposure to known neurotoxins may involve the glossopharyngeal and vagus nerves. Patients undergoing cancer treatment with the chemotherapeutic agent vincristine may rapidly develop jaw pain due to peripheral injury of the glossopharyngeal nerve. ^

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