The vagus is the longest cranial nerve, and has the most extensive distribution, with a wide range of functions (sensory, special sensory, motor and parasympathetic). Its nuclei are situated within the medulla oblongata (specifically, the nucleus ambiguus contains the cell bodies of neurons that innervate the muscles of the larynx). The nerve exits the medulla between the olivary sulcus and the inferior cerebellar peduncle, it has a cisternal course through the lateral cerebellomedullary cistern and then emerges from the skull base through the pars vascularis of the jugular foramen (Fig. 1). Below the skull base is not possible to directly visualize the vagus nerves at CT in their descending course at the neck, but their anatomical location within the carotid sheath can be identified. On the right side, the vagus nerve descends with the carotid sheath into the upper mediastinum; the right recurrent laryngeal nerve (RLN) branches from the main vagus nerve anterior to the subclavian artery and courses posteriorly under the artery at the level of the brachiocephalic bifurcation. It has a short mediastinal course, coursing obliquely toward the right tracheoesophageal groove over the surface of the apical parietal pleura. On the left side, the vagus nerve also descends with the carotid sheath into the mediastinum before descending anterolateral to the thoracic aorta; the left RLN separates from the main vagus nerve at the level of the aortic arch, then courses posteromedially beneath it, and thus passes through the aortopulmonary window posterior to the ligamentum arteriosum. It then ascends vertically through the superior mediastinum to reach the tracheoesophageal groove. Both RLN ascend in the tracheoesophageal grooves and then pierce the inferior pharyngeal constrictor muscle at the level of the cricothyroid joint to enter the larynx. The left nerve is longer than the right due to its mediastinal origin (12 versus 6 cm), making it more vulnerable to injury. In the Fig. 2 are presented the expected anatomic sites of the vagus nerves in the neck and mediastinum at CT, also the RLN origins and courses.

Vocal cord paralysis (VCP) may be produced by a wide spectrum of causes affecting the vagus and RLN, from the brainstem to the inferior margin of the nerve. Neoplastic and traumatic pathology (especially post-surgical injury) account for around two thirds of the VCP cases. Fig. 3 presents the distribution of VCP causes in the biggest reported case series. Sixteen percent of cases are defined as “idiopathic”; it means a VCP without a demonstrable cause after a complete clinical evaluation, cross-sectional neck and mediastinum imaging study (CT and/or MRI) and laryngoscopic examination.

The glottis is the middle part of the larynx; the area where the vocal cords are located. For its appropriate evaluation with CT an axial oblique reformation is required. This reformation must be done parallel to the axis of the true vocal cords, at the level of the vocal cords (level of the cricoarytenoid joints). The strict axial plane is not the best way to evaluate the glottis, because subglottic air interposes anterior to the angulated normal vocal cords. This imaging appearance may mimic a widened laryngeal ventricle and thereby VCP. Fig. 4 explains the difference between the axial strict plane and the axial oblique plane, and illustrates the normal glottic anatomy in CT.

There have been reported several signs of VCP in CT (Fig. 5). The most sensitive of these signs are: 1) dilation of the ipsilateral pyriform sinus; 2) medial deviation and thickening of the ipsilateral aryepiglottic fold; 3) enlargement of the ipsilateral laryngeal ventricle (Fig. 6). Each of these 3 signs is present in about 80% of patients with VCP. When 2 of these signs occur simultaneously, it is possible to diagnose a cord palsy with about 100% specificity.

In unilateral VCP the combination of medialization of the posterior vocal cord margin and air distending the ipsilateral laryngeal ventricle due to thyroarytenoid muscle atrophy result in the residual airway having a shape similar to a ship’s sail, a finding commonly referred to as the “sail sign”. The strict axial images (ie, images not reformatted parallel to the axis of the true vocal cords) also show subglottic air anteriorly, contralateral to a dilated laryngeal ventricle on the side of the VCP. This results in the airway having a mushroom-like appearance, with the “stem” of the mushroom between the posterior vocal cord margins and the “head” tilted toward the side of the VCP. Some authors propose that this “mushroom sign” be taken as supportive evidence of unilateral VCP on strict axial CT images. Both signs (“sail sign” and “mushroom sign”) are shown on Fig. 7.

Important simulators of cord palsy are glottic carcinomas (Fig. 8), where the neoplastic lesion results in immobilization or thickening of the involved vocal cord, mimicking a paramedian position of the cord. Traumatic injury to the arytenoid cartilage with medial dislocation may also mimic VCP; this dislocation can be either the result of direct blunt trauma to the larynx or intubation. Especially after intubation the differentiation between traumatic dislocation and paralysis can be difficult since intubation can cause both. VCP can be the result of compression of the anterior motor branch of the recurrent laryngeal nerve between the inflated cuff of the endotracheal tube, the lateral projection of the abducted arytenoid, and the thyroid cartilage. Another confusing imaging finding, which the radiologist should be aware of, can be seen on FDG-PET exams of patients with VCP. In such cases, the PET may show increased metabolism in the unaffected vocal cord due to compensatory muscle hypertrophy (Fig. 9). This finding may mimic malignancy on the unaffected side. Usually, correlation of the PET findings with the coregistered CT images will show signs of VCP on the non-metabolic side.

Contrast-enhanced CT is the preferred imaging study for investigating the cause of a VCP (with extension from the midbrain up to the aortic arch, and oblique axial reformation at the level of the true vocal cords). When a central cause is suspected (e.g. bilateral VCP, acute onset of symptoms, multiple cranial nerve involvement, high vagal paralysis signs) an MRI of the posterior fossa and skull base is suggested. VCP in children should be investigated with MRI, because its absence of ionizing radiation. Fig. 10 presents the suggested imaging studies for the aetiologic investigation of VCP.

Fig. 11 , Fig. 12 , Fig. 13 , Fig. 14 , Fig. 15 and Fig. 16 present different cases of VCP, with varied etiologies.