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KEYWORDS
Vocal fold paresis Vocal fold paralysis Vocal fatigue Glottic incompetence
Sensory neuropathy Laryngeal electromyography
KEY POINTS
Clinical suspicion for paresis should be raised in patients with voice changes, vocal
fatigue, difficulty projecting, or pain with voice use.
Signs of paresis noted on light laryngoscopy include motion abnormalities, bowing
atrophy, level difference, and length asymmetries.
Videostroboscopic signs of paresis include asymmetric mucosal wave, tension asymme-
tries, phase abnormalities, and evidence of glottic insufficiency.
Laryngeal electromyography is used as a confirmatory examination after having clinical
suspicion for paresis.
Voice therapy, injection augmentation, and medialization thyroplasty may decrease the
glottic incompetence associated with vocal fold paresis and improve symptoms.
Vocal fold paresis is the partial impairment of vocal fold motor function that is caused
by nerve or neuromuscular abnormality.1 This partial damage changes glottic closure
and efficiency, which contributes to voice impairment. Paresis can be considered
separate from vocal fold paralysis, with a distinct set of complaints and findings on ex-
amination. The diagnosis of vocal fold paresis has been noted in approximately one-
sixth, or 15% of new voice patients presenting to the laryngologist.2 In many cases the
symptoms are rather vague and may be attributed to a laundry list of potential etiol-
ogies. One study found that paresis was one of the most commonly missed diagnoses
in patients with voice symptoms attributed to laryngopharyngeal reflux.3 Even the clin-
ical signs leading to suspicion for vocal fold paresis may be varied and subtle, causing
doubt in their clinical relevance and often leading to underdiagnosis of this problem.
SLN RLN
Fig. 1. Afferent and efferent contributions to the SLN and the RLN. Figure displays where
alterations in any portions of the afferent or efferent pathways of the SLN and RLN may
lead to abnormal motion or sensation causing symptoms and signs of paresis. Sensory inputs
have been placed on one side of the larynx and motor has been placed on the other for ease
of description but operate ipsilaterally.
Vocal Fold Paresis 639
Box 1
Possible causes of vocal fold paresis
Box 2
Possible symptoms of vocal fold paresis
Fig. 2. Light laryngoscopy displaying static signs of paresis: vocal process asymmetry and
vocal fold bowing. The vocal process on the right is posterior to that on the left and the
right vocal fold shows bowing, both indicative of right vocal fold paresis.
Vocal Fold Paresis 641
Fig. 3. Light laryngoscopy showing dynamic signs of paresis: vocal fold level difference. The
vocal fold on the right is approximating under the left, showing possible vocal fold paresis.
Table 1
Possible signs of vocal fold paresis
Static Dynamic
Arytenoid prolapse or asymmetry Asymmetric mucosal wave
Asymmetry of the vocal process Asymmetry of the vocal process
Bowing of the vocal folda Axis deviation
False fold hypertrophy Decreased vocal fold motion
Height differencea Differential AB-duction
Laxity of the vocal fold Differential AD-duction
Length asymmetrya Dysdiadochokinesis
Piriform sinus widening False fold hypertrophy
Shortening of the vocal fold Height differencea
a
Thinning (atrophy) of the vocal fold Phase lag/shift
Ventricular widening Supraglottic hyperfunction
Signs of paresis may be considered as either static (noted while the vocal fold is at rest) or dynamic
(noted while the vocal fold is in motion). At times asymmetries may change or be more apparent
during alternating breathing and speaking. Some signs may be noted both during static and
dynamic tasks and are listed in both columns.
a
Indicates the most reliable signs found on laryngoscopy across different levels of experience as
determined in Isseroff et al.9
Data from Isseroff TF, Parasher AK, Richards A, et al. Interrater reliability in analysis of laryngo-
scopic features for unilateral vocal fold paresis. J Voice 2016;30(6):736–40.
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Interestingly, these are all measures easily notable on light laryngoscopy; some of the
key stroboscopic findings were noted by the more senior reviewers but were not used
by the less experienced viewers. This implies that the general otolaryngologist will be
able to use tools they likely already have in their office to reliably predict vocal fold
paresis, and may need to refer to the laryngologist for confirmation and management,
not for diagnosis.
DIAGNOSTIC TESTING
Computed Tomography
When vocal fold paralysis is noted, computed tomography (CT) is often recommended
if no iatrogenic cause is noted. This allows the skull base, neck, and chest to be
imaged in search for a potential cause for the nerve damage. It is important to recog-
nize that use of CT in cases of paresis has not been shown to be helpful.17 Badia and
colleagues17 retrospectively investigated 81 cases of unilateral vocal fold paresis and
ultimately found a 0% positive rate for identifying causative pathology using this test.
This is in contrast to a fair rate of return for use of CT for idiopathic paralysis, listed at
between 35% and 55%.18,19
Vocal Fold Paresis 643
Laryngeal Electromyography
Currently, LEMG is the test of choice for confirmation of vocal fold paresis. The use of
this tool for diagnosis of vocal fold paralysis has been more extensively studied, but a
few studies distinctly reporting on its utility for hypomobility have been published.20–23
Routine testing of bilateral TA and cricothyroid muscles, and selective testing of PCA
muscles is common when performing LEMG. Heman-Ackah and Barr23 compiled
data from patients with clinical evidence of paresis where electromyography (EMG)
had been performed.23 Activity parameters that were tested are listed in Box 3. Neurop-
athy was confirmed if decreased recruitment, increased motor unit action potential
(MUAP) amplitude, and/or polyphasic MUAPs were present. Eighty-six percent of pa-
tients suspected of having paresis on clinical examination had positive confirmation of
this by LEMG. More than half of the patients were found to have bilateral paresis based
on the strict criteria used in this study. It was noted that no specific pattern of muscle
activity found on examination could accurately predict the pattern of abnormality noted
on LEMG. Although the clinician could adequately predict that there was asymmetry
and likely paresis, the site and side was not always correlated by the EMG data. This
observation has been supported by other similar studies.24 Use of LEMG for confirma-
tion of vocal fold paresis has been criticized because of these factors. It is also criticized
because decreased MUAP recruitment, one of the most common abnormal findings to
diagnose paresis, also may be attributed to decreased patient effort, making it less spe-
cific. Many clinicians also feel that LEMG is still qualitative, so therefore cannot be used
for confirmation. Effort is being made to systematize LEMG so that its use may be more
wholeheartedly accepted to diagnose this condition.
There has been no study of the prevalence of asymptomatic vocal fold paresis in the
general population. An idea of how prevalent this is in an asymptomatic cohort would
offer better understanding of asymmetries in vocal fold mobility in general, as well as
allow for study of the differences between patients who show functional deficits and
those who do not. There are also no studies published specifically on the natural his-
tory or recovery after vocal fold partial paralysis. It is thought that most patients likely
resolve without treatment because their symptoms are mild or vague. Extrapolation
from recent studies on idiopathic vocal fold paralysis may offer some potential bench-
marks.25 This showed that 69% of symptomatic patients recovered function within
6 months of onset. Patients with vocal fold paresis often go undiagnosed for many
months and are more likely to be treated as primary muscle tension or reflux-related
dysphonia without significant improvement. It has previously been noted that
Box 3
Laryngeal electromyography (LEMG) parameters for vocal fold paresis*
Insertional activity
Motor unit action potential (MUAP) amplitude
MUAP duration
MUAP morphology
Recruitment pattern
Synkinetic activity
* As noted in Heman-Ackah and Barr.23
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Most of the voice symptoms present with vocal fold paresis are thought to occur due
to glottic incompetence. Because the tone or motion of the affected vocal fold is inad-
equate, this generates altered subglottic pressure, flow, and dyssynchronous mucosal
wave propagation that leads to poor projection of the voice or lack of stability over
time. Compensatory maneuvers of the unaffected vocal fold or other intrinsic muscles
of the larynx, as well abnormal recruitment of the extrinsic vocal fold muscles occurs
to improve the voice stability. This may lead to secondary MTD, the major symptoms
of which are vocal strain, worsening voice or fatigue over time, and potential pain with
voice use. Voice therapy is recommended for patients with these symptoms as first-
line therapy.26 Goals of this intervention are to dispel dysfunctional compensation in
favor of more functional techniques for improving subglottic pressure and flow char-
acteristics. Patients often respond favorably to these exercises and rebalancing of
the vocal system, despite the fact that therapy does not intrinsically change the dener-
vation that has occurred.
Speech language pathologists are trained in multifactorial approaches to MTD and
are able to spend time assessing nonmedical factors that may also affect dysphonia.27
This may include psychological factors or stressors in the patient’s environment that
may be impeding optimal voice use. Vocal hygiene routines, if not already imple-
mented by the physician, are used to maximize hydration and lubrication, and
adjuncts like microphones, whistles, or other tools are recommended when appro-
priate. Manual decompression techniques like circumlaryngeal massage to relieve
muscle tightness are also used. These changes may assist in developing improved
voice use techniques and more functional voicing.
Voice therapy has been shown to help some of the dyspnea and urge to cough
symptoms that may accompany vocal fold paresis. Respiratory retraining may
decrease stridor noted from inappropriate vocal fold motion, and may improve
some dyspnea by retraining breathing and speaking coordination.
As previously mentioned, medical therapy may be indicated for some of the associ-
ated sensory or breathing abnormalities accompanying vocal fold paresis. Trials of
gabapentin and pregabalin have been published showing positive symptom control
of cough due to sensory neuropathy.28 These neuromodulators seem to have greater
effect in patients with chronic cough that also show laryngeal signs of paresis.29 The
effective dose varies and utility is often limited by side effects of fatigue, dizziness, and
nausea. A recent meta-analysis was able to show positive effects of gabapentin, bac-
lofen, and amitriptyline on neurogenic cough, but no single mechanism by which all 3
classes of drugs influence neuropathic symptoms was found.30 Amitriptyline has been
shown to be more effective than codeine cough suppressants for neuropathic cough
in a prospective randomized controlled study.31 This medication is often first-line
medical therapy for symptoms of neurogenic cough or urge to cough sensation.
One older study has been published on use of baclofen to increase cough threshold
Vocal Fold Paresis 645
with promising effects.32 It is important to remember these studies are publishing off-
label uses of medications in small numbers of subjects, so should not be taken as
standard of care.
Botulinum toxin A has been used to decrease stridor and dyspnea in conditions
such as paradoxic vocal fold motion, unilateral and bilateral vocal fold paralysis,
and focal dystonia.33 This has also been used with positive results in chronic cough.34
Treatment efficacy is likely due to weakening of the adductor ability of the TA muscle
that then leads to weaker cough and less airway obstruction during inspiration. This
treatment is used to prevent surgical intervention, such as cordotomy or tracheotomy,
in borderline cases of airway obstruction. Botulinum toxin A use in the larynx is also
off-label but is considered standard of care in cases of laryngeal dystonia. This treat-
ment is not considered gold standard for dyspnea or symptomatic synkinesis.
Injection Augmentation
Injection augmentation was popularized with the introduction of Teflon in the 1960s
and was used to close large vocal fold gaps from vocal fold paralysis.35 This proced-
ure was straightforward and could even be performed in the office setting once fiber-
optic technology became widely available.36 Teflon injection fell out of favor over time
due to inflammatory foreign body reaction that detrimentally affected the vibratory fea-
tures of the larynx and caused large granuloma formation that could obstruct the
airway. Other injectable materials are now available and are considered safe, so there
has been a significant resurgence in the popularity of this procedure. Box 4 includes
many of the available injectable materials commonly used at this time.
Box 4
Materials currently available for injection augmentation
Autologous fascia
Autologous fat
Bioplastique
Bovine-derived collagen
Calcium hydroxylapatite
Carboxymethylcellulose
Gel carrier
Gelfoam
Human-derived fibroblasts
Hyaluronic acid derivatives
Micronized AlloDerm
(Teflon)
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SUMMARY
Vocal fold paresis is abnormal neuromotor function that is diagnosed when patients
complain of vocal fatigue, difficulty projecting, pain with speaking, and hoarseness,
but have mobile vocal folds. Constellations of signs and symptoms have been
reviewed with the goal of familiarizing physicians on the nuances of diagnosis for
paresis. Associated respiratory and sensory deficits commonly noted have been
reviewed and should be documented and treated when appropriate. Current therapies
including voice therapy, surgical intervention for persistent glottic incompetence, and
adjuvant therapies for concurrent sensory neuropathy and synkinesis are described.
Most importantly, a high level of suspicion for potential paresis is recommended for
patients who have complaints suggestive of glottic incompetence regardless of overt
mobility of the vocal folds.
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