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1 Department of Radiology, Tri-Service General Hospital, National Defense
Medical Center, Taipei, Taiwan.
2 Department of Radiology, Box 1234, The Mount Sinai Hospital and School of
Medicine, One Gustave Levy Pl., New York, NY 10029.
Received May 16, 2002;
accepted after revision August 29, 2002.
Address correspondence to P. M. Som.
Abstract
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MATERIALS AND METHODS. We retrospectively identified 40 patients who had clinically diagnosed vocal cord paralysis and had undergone CT. Eight imaging signs of vocal cord paralysis were assessed, and an imaging distinction between a central or peripheral vagal neuropathy was made by evaluating asymmetric dilatation of the oropharynx with thinning of the constrictor muscles. In two patients, we studied the use of reformatted coronal images from a multidetector CT scanner.
RESULTS. For unilateral vocal cord paralysis, the most sensitive imaging findings were ipsilateral pyriform sinus dilatation, medial positioning and thickening of the ipsilateral aryepiglottic fold, and ipsilateral laryngeal ventricle dilatation. In two patients, coronal reformatted images aided the diagnosis by better showing flattening of the subglottic arch. Imaging findings allowed localization of a central vagal neuropathy in four patients.
CONCLUSION. Three reliable imaging findings associated with vocal cord paralysis were identified on routine axial CT studies: ipsilateral pyriform sinus dilatation, medial positioning and thickening of the ipsilateral aryepiglottic fold, and ipsilateral laryngeal ventricle dilatation. Coronal reformatted images of the larynx may be helpful, but they are not necessary in 95% of patients. Ipsilateral pharyngeal constrictor muscle atrophy is a helpful imaging finding to localize a more central vagal neuropathy. Our findings can aid radiologists in identifying peripheral and central vagal neuropathy in patients who present for CT of the neck who have a normal voice and are without a history suggestive of a vagal problem.
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The imaging identification of a lesion either along the course of the recurrent laryngeal nerves or the main vagus nerve may allow the initiation of specific treatment. However, once the nerve is compromised in these patients, function rarely returns. If no causative lesion is identified on imaging, either an idiopathic or toxic cause is diagnosed. If a toxic cause is identified, treatment may be directed to a causative disease; however, complete return of nerve function is rare. Thus, the primary reason to image these patients is that failure to identify a causative lesion on imaging allows the clinician to follow a course of conservative management with more confidence.
At least 10 findings associated with a recurrent laryngeal nerve paralysis have been previously noted on coronal contrast-enhanced laryngographic studies [2]. No statistical analysis of the cases that formed these findings in Landman's work is available. The same findings have not been systematically studied on routine axial imaging studies of the neck to assess which ones are the most reliable in predicting the presence of vocal cord paralysis. Complicating the use of these findings is the observation that axial CT scans often are not properly aligned in the plane of the true vocal cords; as a result, partial visualization of portions of the ventricles, true vocal cords, and the subglottic larynx may be encountered on specific images. Although such misalignment of the scans may make application of the signs of a vocal cord paralysis difficult, we asked which, if any, of these findings could nonetheless be used with confidence.
The purpose of our study was to assess for the first time on routine axial CT scans of the neck the relative accuracy of eight of the 10 findings noted by Landman [2] to be associated with a recurrent laryngeal nerve paralysis. In addition, the finding of a dilated oropharynx with thinning of the pharyngeal constrictor muscle was assessed as a sign of a central vagal neuropathy.
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Eight imaging findings associated with a vocal cord paralysis were evaluated, and each case was reviewed by two neuroradiologists and one head and neck radiologist to evaluate whether each sign was present, the side of vocal cord paralysis as assessed on the images, and whether there was imaging evidence of a central vagal neuropathy or only a peripheral neuropathy. Identification of a mass that might account for the paralysis was also noted. Any differences in assessment were resolved by consensus among the three radiologists. For the radiologic assessment, all radiologists were unaware of the clinical findings; only after the imaging diagnosis was made was the imaging assessment compared with the clinical evaluation.
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Four (10%) of the 40 patients had pharyngeal plexus neuropathy and 36 patients (90%) had recurrent laryngeal nerve (peripheral) neuropathy. A lesion was identified along the course of the recurrent laryngeal nerve in five patients (12.5%): one aneurysm (arotic arch), two thyroid masses (right recurrent nerve), one pyriform sinus carcinoma (left recurrent nerve), and one apical lung tumor (left recurrent nerve). A mass was also seen in relation to the vagus nerve in one tumor of the skull base (schwannoma of the right vagus). Thus, in 34 (85%) of our patients, no lesions were identified along the course of the vagus nerve or the recurrent laryngeal nerve. On the basis of clinical assessment and imaging, the neuropathy in these 34 patients was diagnosed as being idiopathic. None of these patients had a complete recovery of nerve function.
With regard to the specific imaging findings of a vocal cord paralysis in the 40 patients, ipsilateral medial positioning and thickening of the aryepiglottic fold were seen in 31 patients (77.5%); ipsilateral pyriform sinus dilatation, in 31 patients (77.5%); ipsilateral laryngeal ventricle dilatation, in 31 patients (77.5%); anteromedial positioning of the ipsilateral arytenoid cartilage, in 20 patients (50%); fullness of the ipsilateral true vocal cord, in 18 patients (45%); ipsilateral subglottic fullness, in nine patients (22.5%); and ipsilateral vallecular dilatation, in seven patients (17.5%) (Figs. 1A, 1B, 1C, 2A, 2B, 2C, 2D, 3A, 3B, 3C, 3D, 4A, 4B). Dilatation of the ipsilateral pharyngeal wall was seen in four patients (10%). Flattening of the subglottic arch was identified in the two patients with unilateral paralysis for whom we had coronal reformatted multidetector images (Fig. 3A, 3B, 3C, 3D).
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Of these imaging findings, the finding was on the contralateral side in two (6.4%) of 31 patients with pyriform sinus dilatation, in one (5%) of 20 patients with arytenoid displacement, and in one (12.5%) of eight patients with subglottic fullness. In the four patients with bilateral vocal cord paralysis, laryngeal ventricle dilatation was absent on one side in two patients, pyriform sinus dilatation was absent on one side in one patient, and vallecular dilatation was absent on one side in one patient.
For the 31 patients with unilateral vocal cord paralysis, three findings (ipsilateral pyriform sinus dilatation, medial positioning and thickening of the ipsilateral aryepiglottic fold, and ipsilateral laryngeal ventricle dilatation) were seen in 77.5% of patients. When two of these three findings were in agreement, all patients were correctly diagnosed as to the side affected. Fullness of the affected vocal cord was seen in only 45% of the patients in our study. However, this concordance of findings did not hold up for the four patients with bilateral vocal cord paralysis; in two of these patients, a unilateral paralysis was diagnosed on imaging.
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Lesions affecting the brainstem, skull base, and carotid sheath have been associated with vagal neuropathy, whereas specific lesions affecting the recurrent laryngeal nerves include thyroid and cervical esophageal tumors. Only rarely has benign thyroid disease been cited. Overall, approximately 4% of patients with a unilateral vocal cord paralysis have thyroid disease, but only 0.7% of patients with benign thyroid disease have a recurrent laryngeal nerve paralysis [1, 3]. On the left side, aortic aneurysm, cardiomegaly, and upper lobe tumors have been implicated as potential causes, whereas on the right side, supraclavicular tumors and aneurysm of the subclavian artery may be the cause. Recurrent laryngeal paralysis may also result from trauma or prior surgery [1, 3].
Clinically, localizing the affected side of the larynx is relatively straightforward: the true vocal cord can be seen either to be immobile or to have sluggish mobility. However, imaging of some patients with a unilateral recurrent nerve paralysis may have few, if any, sectional imaging findings; 35% of these patients may be asymptomatic and may have a normal voice [3]. In our series, all of the patients had hoarseness. If the history provided to the radiologist at the time of the imaging study includes the suspected cause and the side affected by the vocal cord paralysis, specific focus can be made during the imaging study to evaluate the localized area of neurologic damage or, in the proper clinical setting, the presence of recurrent disease.
Unfortunately, a specific history is often not available at the time of imaging assessment, and only a history of hoarseness or vocal cord paralysis is provided. In addition, because some patients with a vocal cord paralysis may have a normal voice, the imaging identification of such a paralysis may be an incidental and new finding for the clinician. The usefulness of this study is that radiologists now have imaging findings to help them reliably suggest the presence of a vocal cord paralysis on routine CT of the neck in patients who present without a history suggestive of a paralyzed vocal cord. Such a finding can then alert the clinician to further evaluate the patient.
A causative lesion was not seen on the imaging study in 85% of our patients. The differential diagnosis and potential treatment differ for patients with a central vagal neuropathy and those with a specific recurrent laryngeal nerve problem. For this reason, an imaging distinction at the time of the study could help the radiologist further focus the study. One distinguishing feature of a central vagal problem (seen in four patients in our series) is the paralysis or paresis of the ispilateral pharyngeal constrictor muscles that occurs when the pharyngeal plexus is affected.
The pharyngeal plexus is formed from branches of the cranial nerves IX, X, XI and rami from the sympathetic trunk. The vagal branches arise from the nodose ganglion situated just below the skull base and enter the pharyngeal muscles along the upper border of the middle constrictor (just caudal relative to the level of the hard palate), sending branches to the superior and inferior constrictors. The inferior constrictor is also supplied from branches of the superior and recurrent laryngeal nerves [4]. A lesion affecting the pharyngeal plexus will cause paresis or paralysis of the ipsilateral constrictor muscles, which eventually become thinner as they atrophy. This finding is especially noted when the thickness of these muscles is compared with the normal thickness of the contralateral pharyngeal constrictor muscles.
The nasopharynx is supported, in part, by the pharyngobasilar fascia, a thick fascia that arises from the superior edge of this muscle and attaches to the base of the skull. It has been suggested that the purpose of this fascia is to maintain the configuration of the nasopharynx during breathing, thereby maximizing pressure equalization in the ear through the eustacian tube [5]. Whether this premise is true or not, this strong fascia tends to maintain the nasopharyngeal configuration during breathing so that asymmetry is usually not seen in cases of unilateral pharyngeal plexopathy. However, no such supporting fascia is present at the levels of the middle and inferior pharyngeal constrictor muscles, and a unilateral pharyngeal plexopathy leads not only to muscle wasting, but also to dilatation of the ipsilateral pharynx. This outcome is associated with loss of constrictor function, and it is also reflective of the fact that the primary cause of pharyngeal dilatation is increased intrapharyngeal pressure. Thus, the findings on imaging of an outward bowing of the oropharyngeal and hypopharyngeal contour in conjunction with thinning of the constrictor muscle are evidence of ipsilateral pharyngeal plexus damage (Fig. 4A, 4B). As such, these findings localize the abnormality to a level either just below the skull base or more cranially in the brainstem.
With regard to the larynx and the imaging identification of vocal cord paralysis, at least 10 findings have been associated with such paralysis as described by Landman [2]. These include incomplete abduction of both the true and false cords in quiet breathing, dilated ipsilateral laryngeal ventricle, a flattened ipsilateral subglottic arch, the interarytenoid notch displaced to the normal side during phonation, the paralyzed arytenoid cartilage anteriorly positioned and abutting or crossing the midline, thinner-than-normal edge of the paralyzed true cord, dilated ipsilateral pyriform sinus (associated with medial folding of the aryepiglottic fold), dilated ipsilateral vallecula, the paralyzed cord lower than the normal cord during inspiration but higher than the normal cord during phonation, and flattened ipsilateral lateral wall of the vestibule [2]. These observations were derived from frontal contrast laryngography and cine studies.
Routine neck CT is performed in the axial plane. Of the 10 findings associated with vocal cord paralysis [2], tilting of the interarytrenoid notch, a thin edge of the paralyzed cord, and the changing craniocaudal position of the paralyzed cord in phonation and inspiration were considered unlikely to be consistently identified on CT. On axial CT, the findings thought to be most consistently seen in a patient with vocal cord paralysis include thickening and medial positioning of the ipsilateral aryepiglottic fold, dilatation of the ipsilateral pyriform sinus, dilatation of the ipsilateral laryngeal ventricle, anterior and medial positioning of the ipsilateral arytenoid cartilage, fullness of the ipsilateral true vocal cord, ipsilateral subglottic fullness, dilatation of the ipsilasteral valleculla, and flattening of the ipsilateral subglottic arch. Of these eight findings, only three (medial positioning and thickening of the ipsilateral aryepiglottic fold, ipsilateral pyriform sinus dilatation, and ipsilateral laryngeal ventricle) were seen in more than 75% of the patients in our study. Two other findings (anteromedial positioning of the ipsilateral arytenoid cartilage and fullness of the ipsilateral true vocal cord) were seen in more than 45% of the patients.
With the advent of multidetector CT, high-resolution reformatted coronal images are now be routinely available. This capability has allowed more definitive analysis of the larynx for determining the presence of ipsilateral vocal cord paralysis. In particular, flattening of the subglottic arch is better and more consistently seen on reformatted coronal images than on axial images. However, such images were not necessary for diagnosis in 38 patients (95%); thus, we cannot suggest that reformatted images are routinely necessary.
Because the typical paralyzed vocal cord fails to completely abduct during quiet breathing, one might expect that the most common imaging finding would be asymmetry in the appearance of the true vocal cords. However, a fullness of the paralyzed vocal cord was seen in only 45% of our patients. The explanation of the relatively low frequency of this imaging finding may be the failure in many cases of technicians to precisely align the scanning plane with the true vocal cords. It appears that the routine nature of the neck CT study and the pressure placed on technicians to achieve rapid patient throughput may affect such precise plane alignment.
Although some of the imaging findings discussed in this study may be known to radiologists, a paucity of documentation of all these imaging signs—much less an assessment of their significance—is found in the literature. The purpose of our study was to determine what CT findings on axial studies of the neck best allowed the radiologist to diagnose the presence of a vocal cord paralysis. Our study suggests that the indirect findings of ipsilateral pyriform sinus dilatation, medial positioning and thickening of the ipsilateral aryepiglottic fold, and ipsilateral laryngeal ventricle dilatation are more reliable imaging criteria than the appearance of the true vocal cord itself for assessing unilateral vocal cord paralysis. In difficult cases, the use of coronal reformatted images of the larynx may further refine diagnosis by revealing ipsilateral flattening of the subglottic arch, but these reformatted images were used in only two patients. We cannot form a reliable conclusion regarding their use in all patients as part of the routine examination; such a statement requires further studies. Because a specific history is not always available at the time of imaging interpretation, the presence of the findings we have discussed may help the radiologist avoid missing the diagnosis of vocal cord paralysis, central vagal neuropathy, or both.
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  B. S. Kim, K. J. Ahn, Y. H. Park, and S. T. Hahn Usefulness of Laryngeal Phonation CT in the Diagnosis of Vocal Cord Paralysis Am. J. Roentgenol., May 1, 2008; 190(5): 1376 - 1379. [Abstract] [Full Text] [PDF]
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