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fold and supraglottic contraction, pushing rotation of the

petiole toward the weakened side, and asymmetric fatigability

on repetitive movement. Findings associated with compensa-

tory hyperfunction may also be present, including contralat-

eral supraglottic contraction, and benign vocal fold lesions

such as nodules, polyps, or pseudocysts.

4

On stroboscopy,

asymmetry of mucosal wave motion may be the only mani-

festation. The diagnostic accuracy of these signs is controver-

sial, but when they are identified on nasoendoscopy, along

with a suggestive history, a diagnosis of paresis is made.

Idiopathic paresis is diagnosed when no cause is found

on thorough history and examination. In our clinic, paresis

with a history of preceding upper respiratory infection is

defined as idiopathic, as there is no definitive test to con-

firm causality.

Laryngeal electromyography (LEMG) is used as a diagnos-

tic and prognostic tool in cases of vocal fold paralysis. There

is no consensus on the use of LEMG in the context of vocal

fold hypomobility. When performed correctly, LEMG can con-

firm the presence and laterality of a neuropathy and identify

neuromuscular junction abnormalities and myopathies, as well

as ongoing degeneration or regeneration. Some advocates pro-

pose that it be employed systematically in paresis,

3

while

others use it in situations where the results would alter patient

management.

5

Certainly, it does not obviate the role of ima-

ging studies in the evaluation of vocal fold paresis.

The rationale of imaging in paresis is twofold: First, par-

esis may be an early sentinel of an underlying pathology

that, where identified, would require further investigation

and management in its own right, particularly neoplasia.

Second, finding an underlying pathologic process may guide

management of the paresis itself. The role of computed

tomography (CT) in the evaluation of vocal fold paralysis is

well established, given a high overall diagnostic yield (35%

to 62%)

6,7

and a high proportion of neoplastic causes (13%

to 33%).

8-11

However, its role in the evaluation of paresis is

not clearly established, and current practice seems to be

extrapolated from the paralysis literature. A single previous

study assessed the diagnostic yield of CT in the investiga-

tion of paresis.

12

In our institution, CT is performed when

there is a clinical diagnosis of paresis but the cause remains

‘‘idiopathic’’ after thorough history and examination—that

is, no clear history of preceding nerve injury or other com-

pressive or infiltrative lesion and no evidence of a cause on

otolaryngologic, neurologic, and chest examination and

video endoscopy. Patients may also refuse or strongly desire

a CT study.

Our study objectives are twofold: first, to establish a

diagnostic yield in performing CT in patients with idio-

pathic vocal fold paresis; second, to establish a percentage

yield of incidental lesions requiring further management in

this cohort of patients. This has important clinical, cost, and

medicolegal implications.

Method

This study was approved by the Massachusetts Eye and Ear

Infirmary Institutional Review Board. With a precision-based

sample size calculation based on an expected diagnostic yield

of approximately 2.0%,

12

an acceptable precision of 1.99%,

and a confidence level of 95%, an estimated 191 patients

were required. The practice records from January 2004 to

January 2014 of 2 senior laryngologists from a single tertiary

practice were reviewed. All adult patients were identified

who had a clinical diagnosis of idiopathic unilateral vocal

fold paresis (IUVFP) and underwent contrast-enhanced CT

from skull base to mediastinum. Patients were excluded if

they had bilateral vocal fold hypomobility due to the

decreased reliability of clinical assessment and the higher

likelihood of a central etiology.

13

Patients were also excluded

if there was a history of a neurologic diagnosis, such as lar-

yngeal dystonia or tremor, myoclonus, parkinsonism, stroke,

or other central neurologic process.

In each case, a diagnosis of paresis was made by a senior

laryngologist, using the above-described symptoms and

signs. CT images and reports were reviewed. In each case,

any etiology for paresis and any incidental finding were

recorded. An etiology for paresis was defined as any lesion

along the expected extracranial course of the ipsilateral

superior or recurrent laryngeal nerve or vagus, which could

be causing pathologic compression, invasion, stretch, or

inflammation. An incidental lesion was defined as any clini-

cally silent lesion, not associated with the diagnosis of par-

esis, but that could lead to further diagnostic or therapeutic

intervention.

Longitudinal review of files was also undertaken to iden-

tify evolution of findings or interval evidence of an etiology

for the diagnosed paresis. Due to the evolution in endo-

scopic diagnostic criteria for paresis over the 10 years of the

study, a sensitivity analysis was performed comparing the

mean diagnostic yield of the first 5 years with that of the

second 5 years. The null hypothesis of no difference

between the means was tested with an unpaired 2-sample

t

test. Excel 2010 and Stata 10.0 were used for data storage

and statistical analysis.

Results

Patients (n = 237) with unilateral paresis were identified

over the period January 2004 to January 2014. Of these, 174

(73%) underwent contrast-enhanced CT scans of skull base

to mediastinum and were included in the study. The other

63 (27%) did not undergo CT due to either a clear etiology

of their paresis or patient refusal. There was no systematic

difference in the demographic characteristics of the CT and

non-CT workup patient populations. In the CT workup

group of patients, the mean age at diagnosis was 54.5 years

(range, 21 to 82). There were a greater proportion of

women (56%), while laterality of paresis was evenly distrib-

uted, with 51% of lesions being left sided (

Table 1

).

The most common patient symptom was hoarseness.

Symptoms of glottic inefficiency were also common, such

as vocal fatigue, increased phonatory effort, and decreased

projection (

Table 2

). Patients less commonly complained of

loss of range, cough, laryngospasm, globus/dysphagia, and

pain.

Paddle et al

12