Vocal cord paralysis: anatomy, imaging and pathology

The vocal cords are located in a subsite of the larynx, called the glottis. The glottis includes the true vocal cords, the anterior commissure and the posterior commissure. From medial to lateral the vocal cords consist of the mucosal surface, the vocal ligaments and the intrinsic laryngeal muscles (vocalis muscle and thyroarytenoid muscle). The anterior commissure is the midline area where the cords meet anteriorly and where they are attached to the thyroid cartilage. The posterior commissure is the mucosal surface anterior to the cricoid cartilage in between the arytenoid cartilages. Posteriorly, the vocal cords are attached to the arytenoid cartilages and laterally to the inside surface of the thyroid lamina. The medial margins are free to permit the opening and closing of the airway. During quiet respiration the cords are in a relaxed, abducted state (Fig. 1a). Breath-holding brings the cords together in an adducted midline position (Fig. 1b). Directly cranial to the vocal cords, the slit-like opening of the laryngeal ventricles separates the true vocal cords inferiorly from the false vocal cords superiorly (Fig. 1c). The movement of the vocal cords is controlled by the intrinsic laryngeal muscles. All intrinsic laryngeal muscles except the cricothyroid muscle are innervated by the recurrent laryngeal nerves, which are branches of the vagal nerves.

The vagal nerve (cranial nerve X) exits bilaterally from the medulla oblongata just lateral to the oliva through the olivary sulcus. There are three nuclei within the medulla that receive and transmit information from and to the vagal nerve. The nucleus ambiguus gives rise to motor fibres to the larynx and is located just dorsally to the inferior olive, lateral and ventral to the lower part of the fourth ventricle (Fig. 2). After exiting the medulla, the vagal nerve courses through the pre-medullary cisterns (Fig. 2) towards the pars vascularis of the jugular foramen (Fig. 3b). The nerve exits the skull through the pars vascularis of the jugular foramen and then runs within the carotid sheath together with the internal carotid artery, which lies medially to the nerve, and the jugular vein, which lies laterally (Fig. 3a and c). Upon entering the upper mediastinum the right vagal nerve crosses the right subclavian artery ventrally and then courses medially and dorsally toward the right side of the trachea. Just caudally to the right subclavian artery, the right recurrent laryngeal nerve branches from the vagal nerve (Fig. 3a and e). The right recurrent laryngeal nerve then runs dorsally to the right subclavian artery in a cranial and medial direction to reach the larynx via the right trachea-oesophageal (TE) groove (Fig. 3d). The left vagal nerve lies ventrally to the left subclavian artery upon entering the upper mediastinum (Fig. 3a and d). It remains on top of the subclavian artery and runs over the aortic arch on the left side (Fig. 3a). The left recurrent laryngeal nerve branches from the vagal nerve just below the ligamentum arteriosum at the level of the aorto-pulmonary (AP) window and moves dorsally under the aortic arch in the direction of the left TE groove (Fig. 3a and e). From there, like the recurrent laryngeal nerve on the right, it moves upward to the larynx. Both recurrent laryngeal nerves enter the larynx through the inferior constrictor muscles at the level of the cricothyroid joint. Since the left recurrent laryngeal nerve is longer than the right nerve (12 cm versus 6 cm), left VCP is more commonly encountered [7].

The most specific findings of unilateral VCP are [15, 16]: (1) widening of the laryngeal ventricle (Fig. 4a), (2) medial deviation and thickening of the aryepiglottic fold (Fig. 4b), and (3) dilatation of the piriform sinus (Fig. 4c). The widening of the laryngeal ventricle is the passive result of atrophy of the ipsilateral cord. The changes in the aryepiglottic fold and the piriform sinus are a result of paralysis of the posterior cricoarytenoid muscle. This muscle is the only muscle that abducts the vocal cords. Atrophy of this muscle and the inability to abduct the cord results in anteromedial rotation of the arytenoid, medial deviation of the aryepiglottic fold, and (passive) dilatation of the piriform sinus. In addition to these imaging findings, several other less specific supportive signs have been described in the literature [17]. On coronal reformats, the atrophied cord can have a pointed appearance due to reduced bulk (Fig. 5a). On axial images, the subglottic area on the affected side can appear full due to sagging of the paralysed cord (Fig. 5b). Also the paralysed cord often has a paramedian position due to the inability to abduct (Fig. 5c). Findings that can help to localise the level of vagal nerve impairment are involvement of other cranial nerves. For example, pathology at the level of the jugular foramen will frequently result in involvement of the glossopharyngeal nerve (IX), accessory nerve (XI), and hypoglossal nerve (XII), leading to atrophy of the pharyngeal constrictor muscles (IX), sternocleidomastoid and trapezius muscles (XI), and tongue muscles (XII) respectively.

Misdiagnosis of VCP may result in unnecessary additional evaluation or inappropriate management and delay. To avoid misdiagnosis, the radiologist must be aware of several mimics of VCP. First of all, the axial CT reformats have to be angulated parallel to the true vocal cords with both crycoarytenoid joints within the same plane. Tilted axial reformats may lead to subglottic air projecting anterior to the angulated normal vocal cord. This imaging appearance may mimic a widened laryngeal ventricle and thereby VCP (Fig. 6a). Second, malignant infiltration of the vocal cord can result in immobilisation or thickening, mimicking a paramedian position of the cord (Fig. 6b). However, this may only be relevant in incidental detection of a unilaterally abnormal vocal cord. When patients present with symptoms of VCP, laryngoscopy is usually performed prior to CT imaging. During laryngoscopy, focal lesions of the vocal cord can be easily differentiated from VCP. Third, traumatic injury to the arytenoid cartilage with medial dislocation may mimic VCP [18]. 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 paralysis 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 [19]. In addition, intubation can result in fibrosis of the vocal cord, which can also mimic VCP. A confusing imaging finding, which the radiologist should be aware of, can be seen on ¹⁸F-fluorodeoxyglucose positron emission tomography (FDG-PET) exams of patients with VCP. In such cases, the PET may show increased metabolism in the unaffected vocal cord due to compensatory hypertrophy (Fig. 7b). This finding mimics malignancy on the unaffected side [20]. Usually, correlation of the PET findings with the co-registered CT images will show signs of VCP on the non-metabolic side. Another confusing finding is bilateral VCP. The typical imaging characteristics of unilateral VCP can in these cases occur on both sides, making them more difficult to identify (Fig. 8).

Figures 9, 10, 11, 12, 13, 14 15 and 16 show illustrative cases from daily practice with various benign and malignant causes of VCP.