Unilateral vocal cord paralysis: An unusual cause and rare imaging pattern seen on FDG PET/CT in a case of oropharyngeal cancer

Sir,

The intrinsic muscles of larynx are supplied by recurrent laryngeal nerve (RLN), and its involvement leads to vocal cord paralysis (VCP) on the side of affectation. The longer course of the left RLN makes it more susceptible to damage, especially in the mediastinum. We report an uncommon cause of VCP in the case of oropharyngeal cancer, due to involvement of the vagus nerve in the skull base. On¹⁸F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography (FDG PET/CT) it showed an unusual pattern of FDG uptake in the larynx. A 47-year-old gentleman, diagnosed with oropharyngeal cancer, underwent a whole body PET/CT study for staging. Maximum Intensity Projection (MIP) image showed two large foci of intense FDG uptake in left neck region [Figure 1a-arrows]. These corresponded to the primary mass involving the base of tongue, left vallecula and tonsilo-lingual sulcus [Figure 1b-arrow], and a large metastatic left cervical level II nodal mass [Figure 1c-dark arrow] on fused axial PET/CT images. Carotid sheath was uninvolved. Two discrete foci of uptake were seen on coronal and sagittal MIP images, one at the base of skull on left [Figure 2-arrow-head], and other, on the right side at the root of neck [Figure 2-arrow]. Axial CT and fused PET/CT images showed an enhancing FDG avid metastatic node immediately below the jugular foramina [Figure 3a and b-arrow]. The other low-grade focus was seen in the right postcricoid region [Figure 3d-arrow], with the left vocal cord in paramedian location [Figure 3c-arrow], suggestive of left Vocal Cord Paralysis (VCP). As no abnormal FDG uptake was seen in the mediastinum or rest of the neck, only possible cause of VCP was the metastatic node. Magnetic Resonance Imaging (MRI) of the head and neck region, which was done during staging workup, was reviewed for confirmation. Axial T2-weighted (T2W) image [Figure 4b-arrow] showed a hypo- to isointense soft tissue opacity at the posterolateral part of left jugular foramen, with post-contrast enhancement on axial T1W fat saturation sequence [Figure 4d-arrow]. It corresponded exactly with the site of FDG uptake on axial PET and PET/CT images [Figure 4a and c-arrows]. Unilateral VCP results from compression or damage to the RLN anywhere along its course.[1] The left RLN exits the vagus nerve at the level of aortic arch, descends into the aortopulmonary space, hooks around the ligamentum arteriosum, and ascends into the tracheo-esophageal groove, to innervate the intrinsic laryngeal muscles.[2] This long course makes it more prone to injury or compression. Although laryngeal trauma or local radical surgery is the most common and obvious cause, a variety of extralaryngeal lesions involving the RLN lead to VCP. Malignant neoplasms, especially from thyroid, esophagus, mediastinum and lung, have been reported as being the most common extralaryngeal causes of VCP, the most common of these being bronchogenic carcinoma.[3] However, we rarely find an instance of vagal involvement in the skull base leading to VCP, as in our case.[4] An enlarged node at the jugular foramen or a jugular schwannoma is the most likely cause, but not all lesions at this location lead to VCP.[5] Although the vagus nerve exits at jugular foramina, the origin of RLN occurs much distally, at the root of the neck on right and in the mediastinum on the left.[6] Thus not all, but only the lesions exactly involving the fibers of the exiting vagus, which branch into the RLN downstream, result in VCP.[6] Unilateral VCP is seen on FDG PET/CT as tracer uptake in a non-paralysed contralateral vocal cord, as a result of its compensatory activation due to lack of activity in the paralysed cord.[7] Very rarely, as in our case, uptake is not seen in the contralateral cord, but in the thyroarytenoid muscle, due to atrophy of this muscle on the affected side, which is also a result of RLN palsy. Both the cause, that is, the metastatic node and its effect, that is, VCP, although distant from each other, are exquisitely seen on PET/CT, as FDG localizes in metastatic cells and also in hyperactive muscles.[8] In addition, this case underlines the importance of knowing the entire anatomical course of not only the RLN, but also the vagus, from which it originates.

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Figure 1 MIP image (a) Two foci of FDG uptake in the neck region, one at the primary site, at the base of tongue and vallecula (a-thin arrow) and other in metastatic left cervical nodal mass (a-thick arrow), as seen on axial fused PET/CT images (b and c-arrows)

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Figure 2 Two other discrete foci of FDG uptake seen on coronal (a) and sagittal (b) PET images at the skull base (arrow-head) and in the neck (arrow)

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Figure 3 Axial CECT and fused PET/CT images showed FDG uptake in enhancing soft tissue mass in the region of left jugular foramina (a and b-arrow). Also seen is FDG uptake in the right post-cricoid region (d-arrow) with paramedially located left vocal cord (c-arrow), suggestive of left VCP

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Figure 4 Axial T2-weighted MRI image shows hypo- to isointense soft tissue opacity at the posterolateral part of left jugular foramen (b-arrow), with post-contrast enhancement on axial T1W fat-saturation sequence (d-arrow), which corresponded to FDG uptake on PET and PET/CT images (a and c-arrows)

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