Vagus Nerve Branches and Disorders


Below its inferior ganglion, the vagus nerve descends within a homolateral carotid sheath, shared with the internal jugular vein and carotid artery, to the thoracic inlet. The vagus nerve intercommunicates with filaments from the cervical sympathetic trunks or branches so that it is a mixed parasympathetic-sympathetic nerve from the neck downward. Within the neck, the vagus gives off the cardiac rami; these branches join the sympathetic fibers via the cardiac plexus of the heart.


VAGAL NERVE BRANCHES IN THE THORAX


The right vagus nerve enters the thorax behind the internal jugular vein and in front of the first part of the subclavian artery. Here it gives off the right recurrent laryngeal nerve, which hooks under the artery before ascending to the larynx. The recurrent laryngeal nerves divide into anterior and posterior rami and supply the larynx. The main nerve climbs posteromedially, behind the right brachiocephalic vein and the superior vena cava, and runs medial to the azygos vein to reach the root of the right lung, where it splits into smaller anterior and larger posterior branches, both of which contribute rami to the anterior and posterior pulmonary plexuses.


The left vagus nerve enters the thorax between the left common carotid and left subclavian arteries, behind the left brachiocephalic vein. It crosses the left side of the aortic arch, giving off the left recurrent laryngeal nerve; thereafter, as on the right side, it participates in the formation of the pulmonary and esophageal plexuses. The left recurrent laryngeal nerve passes underneath the aorta on the outer side of the ligamentum arteriosum and then ascends to the larynx. The left recurrent laryngeal nerve, with the right recurrent laryngeal nerve, innervates the laryngeal muscles (all except the cricothyroids, which are supplied by the external ramus of the superior laryngeal nerve).


The vagal pulmonary branches, along with filaments derived from the second to fifth or sixth thoracic sympathetic trunk ganglia, form anterior and posterior pulmonary plexuses. The pulmonary plexuses become dispersed around the vascular and bronchial structures, and some of their terminal filaments reach the peripheral portion of the lungs. Along the course of the larger bronchi, small ganglia provide relay stations for the preganglionic parasympathetic (vagal) fibers. The sympathetic fibers relay outside the organs, primarily in the sympathetic trunk ganglia. Sympathetic and parasympathetic pulmonary afferent fibers are also present.


The esophageal plexus forms below the lung roots as the vagus nerves break up into two to four parts and travel on the esophagus as it descends through the posterior mediastinum, then divide and reunite to form the esophageal plexus. Filaments from the thoracic parts of the sympathetic trunks and from the thoracic splanchnic nerves then join the esophageal plexus. Most of the branches of the right vagus incline posteriorly, while most of those from the left vagus incline anteriorly. Above the esophageal hiatus in the diaphragm, the meshes of the esophageal plexus become reconstituted into two or more vagal trunks, which travel by way of the esophageal diaphragm to innervate the abdominal viscera.


VAGAL NERVE DISORDERS


Bilateral supranuclear lesions may result in dysphagia, spastic dysarthria, emotional incontinence, pharyngeal and laryngeal incoordination, and altered sensation with an increased risk of aspiration. Unilateral supranuclear lesions rarely cause vagal dysfunction because the supranuclear control is bilateral. Dysphagia rarely occurs with unilateral precentral gyrus lesions.


Isolated proximal vagus nerve injuries are rare because lesions at or around the jugular foramen, such as those caused by trauma or tumors (glomus vagale paragangliomas), usually also injure the glossopharyngeal and accessory nerves. Unilateral vagus neuropathy may cause ipsilateral pharyngeal (e.g., dysphagia) and laryngeal (e.g., change in voice) weakness and impaired sensation with inadequate airway protection. Ipsilateral soft palate weakness may manifest as nasal regurgitation and nasal speech. Ipsilateral vocal cord paralysis may be the result of superior laryngeal nerve injury (cricothyroid muscle for vocal cord lengthening and laryngeal sensation) or more distal recurrent laryngeal neuropathy (cricoarytenoids and thyroarytenoid muscles for adduction, abduction, and shortening of vocal cords). Recurrent laryngeal nerve lesions affect all laryngeal muscles, with the exception of the cricothyroid, which is innervated by the superior laryngeal nerve. Superior laryngeal neuropathy leads to loss of high vocal pitches, a weak voice, and aspiration due to altered laryngeal sensation. The causes include thyroiditis, local neck infections, or surgery; however, a good proportion of cases are idiopathic. Recurrent laryngeal nerve lesions cause variable symptoms, from slight voice fatigue and breathiness to significantly altered speech, hoarseness, and ineffective cough. When unilateral, they typically cause transient hoarseness. Common causes include thyroid, neck, and lung tumors; thoracic surgery; and, rarely, thyroiditis. Diabetes, amyloidosis, and other acquired etiologies of polyneuropathy may cause vagal neuropathy, usually accompanied by symptoms and signs of more widespread sensorimotor polyneuropathy.


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Sep 2, 2016 | Posted by in NEUROLOGY | Comments Off on Vagus Nerve Branches and Disorders

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