1. health and fitness
2. disease

Using CT to Localize Side and
Level of Vocal Cord Paralysis
Shy-Chyi Chin 1
Simon Edelstein 2
Cheng-Yu Chen 1
Peter M. Som 2
OBJECTIVE. The purpose of our study was to assess the relative accuracy of imaging
findings related to peripheral recurrent nerve paralysis on axial CT studies of the neck. Also
assessed were imaging findings of a central vagal neuropathy.
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.
T
Received May 16, 2002; accepted after revision
August 29, 2002.
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. Address correspondence to P. M. Som.
AJR 2003;180:1165–1170
0361–803X/03/1804–1165
© American Roentgen Ray Society
AJR:180, April 2003
he causes of vocal cord paralysis
are varied, and nearly half of the
cases are reported as being either
toxic or idiopathic [1]. That is, in at least half of
all patients with vocal cord paralysis, sectional
imaging studies may fail to identify a lesion
along the course of either the vagus nerve or the
recurrent laryngeal nerves. In these patients, our
data indicate that the imaging differentiation of
a central vagal neuropathy from a purely recurrent laryngeal nerve (peripheral) neuropathy
may be possible by observing the effects of a
pharyngeal plexus neuropathy on the ipsilateral
pharyngeal constrictor muscles. Once the distinction is made, further workup may be specifically focused either just below the skull base or
at the posterior fossa.
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 as-
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Chin et al.
sess 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.
Materials and Methods
We retrospectively reviewed the records of 40
consecutive patients with clinically identified vocal cord paralysis who had undergone CT of the
neck in the previous 18 months. CT in these patients was performed either as contrast-enhanced
helical studies with 2.5-mm contiguous scans obtained with a pitch of 0.7, or as 3-mm contiguous
helical scans of the neck obtained on single-detector scanners. The CT scanners were HiSpeed and
LightSpeed Ultra units (General Electric Medical
Systems, Milwaukee, WI).
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 clini-
A
cal findings; only after the imaging diagnosis was
made was the imaging assessment compared with
the clinical evaluation.
Results
Of the 40 total patients, four patients (10%)
clinically had bilateral vocal cord paralysis, 15
patients (37.5%) had a right vocal cord paralysis, and 21 patients (52.5%) had a left vocal
cord paralysis. The clinical side of paralysis
was correctly diagnosed on imaging in all 36
patients with unilateral disease. In four of these
patients (10%), findings were mixed on the axial images as to the side affected. In all four of
these patients, the correct clinical side was diagnosed on the basis of the preponderance of
the imaging findings as to side. In two of these
equivocal examinations, coronal reformatted
images of the larynx revealed flattening of the
subglottic arch on the affected side, aiding the
diagnosis. Overall, of the four patients with
clinically bilateral paralysis, one was diag-
B
Fig. 1.—45-year-old woman with hoarseness and right recurrent laryngeal nerve paralysis who underwent axial contrast-enhanced CT.
A–C, Scans show dilatation of right vallecula (arrow, A) and dilatation of right pyriform sinus (A), dilatation of right pyriform sinus and thickening and medial positioning of right
aryepiglottic fold (B), and dilatation of right laryngeal ventricle (white arrow, C) and anterior positioning of right arytenoid cartilage (black arrow, C).
C
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CT of the Vocal Cords
nosed on imaging as having a right paralysis;
one, as having a left paralysis; and two, as
probably having bilateral paralysis.
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 la-
ryngeal 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. 1–4). 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. 3).
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.
A
B
C
D
Fig. 2.—54-year-old man with hoarseness and right vocal cord paralysis who underwent axial contrast-enhanced CT.
A–D, Scans show dilatation of right vallecula (A), dilatation of right pyriform sinus and thickening and medial positioning of right aryepiglottic fold (B), fullness of right true
vocal cord and slight anterior positioning of right arytenoid cartilage (C), and right subglottic fullness (D).
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Chin et al.
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.
Discussion
The recurrent laryngeal nerve may become paralyzed as a result of disease any-
where along its course from the brainstem to
the caudal margins of each recurrent nerve.
Because of its longer course and its extension into the mediastinum, the left side is
more often affected than the right side (52.5%
of the unilateral peripheral neuropathies in this
series). Peripheral vocal cord paralysis is more
common than a central cause, with only 10% of
cases being central in one large series [3] (10%
in our series). Overall, vocal cord paralysis has
been reported, among other causes, to be the result of a peripheral neuritis associated with alcoholism, viruses, acute bacterial infections,
and drug toxicities [1, 3]. Neuropathies associated with multiple sclerosis, polio, myasthenia
gravis, Parkinson’s disease, amyotrophic lateral
sclerosis, cerebrovascular diseases, and complications of acromegaly have also been implicated [1, 3].
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
A
B
C
D
Fig. 3.—33-year-old woman with weak voice and left vocal cord paralysis.
A–C, Axial contrast-enhanced CT scans show dilatation of right pyriform sinus (large arrow, A), thickening and medial positioning of left aryepiglottic fold (small arrow, A),
dilatation of left laryngeal ventricle (arrow, B), and fullness of right true vocal cord (arrow, C).
D, Coronal reformatted CT scan shows flattening of left subglottic arch (small arrow) and dilatation of left laryngeal ventricle (large arrow).
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CT of the Vocal Cords
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.
A
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.
4). 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-thannormal 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.
B
Fig. 4.—64-year-old man with hoarseness, left vocal cord paralysis, and left-sided palatal weakness who underwent axial contrast-enhanced CT.
A and B, Scans show dilated left oropharynx with thinning and atrophy of pharyngeal wall (arrow A) and dilatation of left pyriform sinus and thickening and medial positioning of left aryepiglottic fold (B).
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Chin et al.
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, highresolution 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
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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.
References
1. Thornell WC. Vocal cord paralysis. In: Paparella MM,
Shumrick DA, eds. Otolaryngology, vol. 3. Head and
neck. Philadelphia: Saunders, 1973:649–657
2. Landman GHM. Laryngography: cine laryngography. Baltimore: Williams & Wilkins, 1970:62–75
3. Levine HL, Tucker HM. Surgical management of
the paralyzed larynx. In: Baily BJ, Biller HF, eds.
Surgery of the larynx. Philadelphia: Saunders,
1985:117–134
4. Williams PL, Bannister LH, Berry MM. Gray’s
anatomy, 38th ed. Edinburgh: Churchill Livingstone, 1999:1251–1252, 1729–1733
5. Last RJ. Anatomy regional and applied, 6th ed.
Edinburgh: Churchill Livingstone, 1978:414–418
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