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Vocal cord palsy
etiology, evaluation & management
Dr Sandeep
Vocal fold paralysis
Inability of one or both folds to move because
of the lack of innervation to particular intrinsic
laryngeal muscles
 central
Neurapraxia  Full recovery
Axonotmesis  Recovery ensues
Neurotemesis  Reinnervation may be inappropriate,
inadequate, or nonexistent
Although spontaneous dysfunctional reinnervation
does not restore motion, it may yield a better voice than
complete denervation because it maintains vocal fold
bulk & tonus
Interference with voice production.
Interference with the protection of the
tracheobronchial tree & respiration
In recurrent laryngeal nerve paralysis, the vocal
folds may assume a number of positions
Six positions have been described.
Median, Paramedian, Cadaveric (intermediate),
Gentle/ Slight abduction & Full abduction
Semons law (1881)
Semon & Rosenbach
In all progressive lesions involving the
recurrent laryngeal nerve, the abductors
paralyze first followed by the adductors.
When recovery takes place the first muscle
group to recover will be the adductors
Differential Innervation theory
The recurrent laryngeal nerve often
branches outside the larynx.
Injury to individual branches could cause
paralysis of specific groups of muscles
accounting for the varying positions
assumed by the paralysed cord
Interarytenoid muscle theory
Disturbance of autonomic supply
Changes in cricoayrtenoid joint & paralysed
Wagner & Grossman theory (1897)
In complete paralysis of recurrent laryngeal nerve
the cord lies in the paramedian position because
the intact cricothyroid muscle adducts the
cord. (Because the superior laryngeal nerve is
If the superior laryngeal nerve is also paralysed the
cord will assume an intermediate position because
of the loss of adductive force.
Adductor Paralysis
Bilateral Adductor palsy
Folds are usually in a paramedian position
 Patient is aphonic
Unilateral Adductor palsy
Involved fold is in paramedian position; complete
glottal closure is not possible
 Air is wasted during phonation
 Breathy, hoarse vocal quality
Unilateral adductor palsy Mx
Mx. is directed at increasing the
the “sharpness” of glottal attack possibly
with effort closure
sometimes will give the patient, a stronger, better
Electrotherapy to stimulate the fold
Bilateral Adductor Paralysis Mx
Voice therapy is rarely effective
Surgical repositioning
Spontaneous recovery period: approximately 6-9
months; varies in individual cases
Abductor Paralysis
Paralyzed fold lying
near the midline
Some cases may abduct laterally to the intermediate position,
but never full abduction as in deep inhalation
Pt complains more about SOB than dysphonia
Primary symptom: usually impaired respiration with
little/ no voice change
Bilateral Abductor Paralysis
Both folds are relatively
fixed in an adducted
midline position
Immediate intervention is required to preserve the
Initially requires tracheostomy
A second procedure to reposition the folds
Voice therapy may be prescribed
Rec Laryngeal nerve palsy
> airway compromise
> change in voice
> no airway obstr
> no aspiration
Recurrent laryngeal nerve paralysis
Mechanisms of nerve damage
Vascular insults
Infections - Viral, Bacterial
Neurotoxic drugs
Trauma – Iatrogenic & Non- iatrogenic
Slow-growing tumors
 Thyroid
 Paragangliomas
 Neurilemmomas
 Skull base meningiomas
Risk of injury increased in surgery of the neck,
mediastinum, & skull base
Mechs. of damage
 Thermal damage
 Stretch
 Cutting
 Compression
 Vascular compromise
Recurrent laryngeal nerve paralysis :
Left RLN more frequently
involved than right RLN
 Longer course 
additional vulnerability
 Especially within the
lung cancer, esophageal
cancer, aortic aneurysm,
lymphoma, tuberculosis,
sarcoidosis, silicosis,
mediastinal metastasis
Recurrent laryngeal nerve paralysis
Surgical etiologies
Anterior approaches to the cervical spine
Carotid endarterectomy
Thyroid surgery (MOST COMMON)
Skull base surgery
 vagal paraganglioma, jugular paraganglioma
 neoplasms in the parapharyngeal space/ infratemporal
fossa/ upper neck
Thoracic surgery & thoracic disorders
 Ortner syndrome
 Sx-pneumoctemy, lobectomy, open heart Sx, Sx on
thoracic oesophagus & trachea
 Mediastinoscopy
Incidence of iatrogeic palsy
 Permanent paralysis - 0.5% to 2.4%
 Temporary paralysis - 2.6% to 5.9%
Thyroid surgery/ pathology
 Carcinoma (Most common)
 Chronic lymphocytic thyroiditis
 Reidel thyroiditis
 Thyroid abscess
Increased risk
 Nerve not identified [3-4 times greater risk]
 Anything that increases local scar formation
(thyroiditis, previous surgery, radiation)
 Concomitant neck surgery
 Mediastinal dissection [ especially on the left side]
Neoplastic etiologies
Nonlaryngeal tumors
17% to 32%
> Thyroid
> Nasopharyngeal cancer treated with radiation
> Lung, esophgeal, mediastinal lesions
Neurogenic tumors
 vagal neurilemmomas
 vagal paraganglioma
Furukawa et al's study of 69 tumors causing paralysis
A statistical study of clinical cases of malignant tumors first
manifested by vocal cord paralysis. (1990)
(41%) - thyroid
(30%) - lung
(20%) - esophageal
(4%) - mediastinal lesions
Endotracheal intubation
7.1% to 11% of RLN paralysis
Anterior branch of the RLN can be compressed between
the lateralized arytenoid cartilage, thyroid cartilage, &
inflated cuff of ET tube
In prolonged intubation posterior commissure stenosis
Recover spontaneously within 6 months
Marie et al
The viral hypothesis. A case report. Eur Arch Otorhinolaryngol
RLN paralyzed after intubation could be secondary to viral
infections triggered after local trauma, such as herpes zoster
Idiopathic etiology
Viral etiologies
 HSV,
VZV, EBV, Influenza virus, CMV,
HIV, West nile virus
 Neural edema, loss of myelin, & axonal
disruption- from either direct viral injury or
the immunologic response
 RLN paralysis ascribed to HSV - frequently
 Influenza - related RLN paralysis may recover
Drug-induced etiologies
 Lead, arsenic & alcohol
 Injections of local anesthetics
 Cisplatin, Vinca alkaloids
 affect axoplasmic flow Neuronal loss
 Organo phosphorous poisoning
Miscellaneous etiologies
Radioactive iodine ablation after thyroid cancer Sx
Vagal nerve stimulation for seizure control
Jugular vein thrombosis
Central venous access procedures
Clinical Evaluation
 Chief symptoms
 Onset
 Progression
 H/o intubation, surgery
 Tobacco use/ smoking
 In children- H/o birth trauma, CNS abnormality, intubations, or Sx
Physical examination
 Listening to the voice and airway
 vocal capability battery
 Speaking voice
 Projected voice
 Vocal range
 Maximum phonation time
Head and neck examination
Cranial nerves examination
Auscultation of neck for bruit
Endoscopic evaluation
laryngeal gargle
superior laryngeal nerve block
Nebulized lidocaine
“verbal anesthesia”
Soft palate
Pharynx & hypopharynx
Laryngeal examination
During quiet breathing, the vocal folds are
evaluated for
 1. Rest position
 2. Position & direction of the vocal
processes in relation to each other
 3. Symmetry of vocal fold contour
4. Evidence of tissue
loss (arytenoid)/
synechia in the
posterior glottis
5. Scarring along the crico arytenoid joint
6. Subglottic & tracheal granulation,
scarring, or stenosis
During phonation,
7. Mobility of the membranous part of the vocal folds
as compared with the body & apex of the
8. Glottic closure
9. Level of the match between vocal processes
10. Flaccidity of vocal fold structures
11. Lesions in the trachea or mainstem bronchi
Lab Studies
 Serum
K+ , Ca , glucose level
 Tuberculosis
skin test
 RF/ ANA test
 Anti neutrophil cytoplasmic antibody
(ANCA) test
 Venereal disease research laboratory (VDRL)
 Determination of Lyme disease titer
 Uric acid levels
Imaging Studies
No identifiable cause & involvement limited to the
vocal fold CECT skull base to upper thorax
 Involvement of other branches of vagus
[ palatal/ pharyngeal palsy]
Gadolinium enhanced MRI of skull base &
neck, HRCT skull base
Other Tests
X-ray STN- “dilated ventricle sign”
Pulmonary function tests
Neurologic tests
Diagnostic Procedures
Fiberoptic laryngoscopy
 Mainstay of clinical assessment.
 Stroboscopic videolaryngoscopy > vocal fold motion
abnormalities when asymmetric mucosal wave patterns are
 Malingering or other psychogenic disorders may be identified
by asking the patient to sniff or whistle
Direct laryngoscopy
 Examination of the posterior glottis & palpation of the
arytenoid cartilages.
 Cricoarytenoid (CA) joint ankylosis or IA scars that limit
arytenoid motion (with the patient under GA)
 The subglottis, trachea > subglottic stenosis, subtle infiltrative
Electromyography (EMG)
Faaborg-Andersen and Buchtal in the late 1950s
Studying electrical activity in muscle
Two active [+ & -] & one ground electrode
Monopolar Or concentric electrodes
At minimum, cricothyroid (CT) & thyroarytenoid
(TA) muscles to investigate SLN & RLN integrity on
each side are tested
 No anaesthesia / LA rather than GA
 The glottic compromise in BVFI  EMG hazardous
 wait until after tracheostomy
 EMG provides information on
Differentiating between fixation & paralysis
 Prognosis of return of function
 Site of neurologic lesion
 Determining the presence of neuromuscular disorders or
peripheral neuropathy
Immediately after a nerve injury
Complete injury  electrical silence at rest as
well as with efforts at movement.
Incomplete injury > symptomatic vocal fold paresis
 incomplete interference pattern at maximal effort
Over time, in denervated ms EMG shows
 Fibrillation
potentials or positive sharp waves
 Prolonged insertional activity
In renervation > polyphasic & prolonged MUAPs as
early as 2 months
If no reinnervation,  spontaneous activity persists until
the muscle atrophies
recording from the thyroarytenoid muscle of a patient with longstanding vocal fold paralysis and shows activation when the patient is
asked to sniff (black arrows)
Indicators of good chance of recovery of vocal
fold motion
preservation of normal MUAP waveforms
 activation of ms during an appropriate voluntary task
 recruitment
 absence of electrical silence or spontaneous activity
 absence of aberrant MUAP morphology
 absence of patterns of activation during inappropriate
 As soon as 2 days after injury to aid in differential diagnosis
 As a prognostic tool,
 a baseline EMG > at least 30 days after injury
 a second one > 60 days after injury
 > 6 months, used only to differentiate between fixation and
paralysis and not to assess neural regeneration
The superior laryngeal nerve dysfunction
Bilateral  cannot elevate pitch
Unilateral  hoarse voice,
lacking pitch variation, with
adequate loudness
Glottic closure - complete/
Arnold [Laryngoscope 1961]: voice
findings in SLN dysfunction
 vocal “weakness” [in terms of
resonance, projection, fatigue]
 shortened phonation time
 lowered pitch
 reduction of vocal range
 monotony of voice
Arnold [Laryngoscope 71 ;1961] Laryngeal signs of
SLN palsy which are evident only on phonation:
 Torsion
of the glottis with a shift of the
posterior commissure to the affected side
 Shortened vocal fold
 Height mismatch between the vocal folds,
with the affected side below the intact one
 Lack of mucosal blanching on the affected
side because of a lack of tension
 Asymmetric mucosal wave vibration
 Greater/ diminished excursion of the wave
 Phase asymmetry
Adour et al Otolaryngol Head Neck Surg
(1980)] sensory manifestations in SLN palsy
 Globus sensation
 Cough
 Pain
EMG in the diagnosis of SLN dysfunction
Definitive diagnosis
 decrease in electrical activity on voluntary
cricothyroid muscle activation
 signs of frank denervation (spontaneous
fibrillations or positive sharp waves)
SLN is at risk in
 Neck dissection
 Cricopharyngeal myotomy
 Anterior approaches to the cervical spine
 Carotid endarterectomy
 Supraglottic laryngectomy
Antivirals & corticosteroids in idiopathic cases
Voice therapy
Surgical medialization
Anastomosis of a transected or dysfunctional SLN
Superior & Recurrent laryngeal
nerve injury
High vagal lesions(Posterior fossa, jugular
foramen, parapharyngeal lesions)
Brain stem & medullary lesions
Thyroid surgery
Vocal folds are in intermediate position
Breathy voice
There is also a tendency to aspirate.
Treatment options
Adductor cord palsy
Voice therapy
Intracordal injection
Type-I thyroplasty
Arytenoid adduction
Abductor cord paralysis
Reinnervation techniques
Electrical pacing
Permanent procedures
Posterior cordectomy, transverse cordotomy
Suture lateralization
Medialization thyroplasty
1st described by Isshiki in 1974
Aspiration secondary to unilateral paralysis or atrophy of
the vocal folds
Open method: placement of a silastic subperichondrial
implant to medialize the vocal fold
 Endoscopic method: injection of varying substances to
stiffen and/ or medialize the vocal fold
(e.g. Telfon, Gelfoam)
If no aspiration is present and EMG is positively
prognostic  temporary injection augmentation of
the paretic vc
 If no reinnervation potentials on laryngeal EMG by
3 months early surgical medialization may be
considered even in patients without aspiration
Implant system
 Silastic
 Titanium implant system
 Gore-Tex implant system
 Hydroxyapatite implant system
Anterior laryngeal support 
implants placed adjacent to the
lateral aspect of the
thyroarytenoid muscle through
thyroplasty type windows
 A midfold glottal gap with good
apposition of the arytenoid
cartilage  unilateral or bilateral
thyroplasty implants
Medialization thyroplasty
The images below depict the medialization thyroplasty
procedure. The image on the left shows the placement of the
shim in the thyroid cartilage. The coronal image on the right
demonstrates how this shim, when correctly placed, an help
push a motion-impaired vocal fold medially.
Medialization Thyroplasty
Airway edema
Acute laryngeal bleeding
Injury to the pyriform sinus
Extrusion/ Displacement
Misplacement – most often superior
Under correction
Poor closure of posterior glottic gap
Injection laryngoplasty
Introduced in 1911 by Bruening [Injected
 Popularised by Arnold in 1962 [Teflon]
 GA/ LA
 Materials
Teflon paste
 Silicone paste
 Collagen
 Autologous fat
 Autologous fascia
 Hyaluron-based compounds
[Hylan B gel, Dextranomer hyaluronan]
Autologus fat advantages
 Abundant availability
 Easy to harvest & inject
 Well tolerated
 Viscoelastic property similar to VC mucosa
 Overinjection is recommended
Teflon paste [with glycerine] disadv
Improper placement
Granuloma formation
Poor long-term results
Difficult revision Sx
Bovine collagen
Stimulates native collagen production
Stimulates native collagenase  tissue
remodellingscar softening
Hypersensitivity reaction
Arytenoid Adduction
Isshiki, M. Tanabe and M. Sawada 1978
The muscle process is pulled by two 3-0 nylon
sutures in simulation of the functions of the
lateral cricoarytenoid muscle & the lateral
thyroarytenoid muscle
Posterior cordectomy
Kashima and Dennis -1989
Effective & Easily repeatable
 suspension laryngoscopy
 CO2 laser with attached microscope with a 400-mm lens
 Ventilation
 laser-resistant endotracheal (ET) tube positioned in the
IA region
 CO2 laser, continuous delivery at 2-5 W
 Incision in the posterior true vocal fold (TVF) at the vocal
process  wedge-shaped defect
 C-shape of membranous vocal ford removed just anterior
to vocal process
Tranverse cordotomy
Kashima HK 1991
Posterior portion of vocal cord released from
vocal process
Modified kashima procedure (segas etal,
Posterior cordectomy of true & false folds
Removal of some or all of the arytenoid cartilage.
Endoscopically by microsurgical or
laser technique
An external, lateral neck approach
(The Woodman procedure)
Lateral neck incision, exposure of the arytenoid
cartilage posteriorly with removal of the majority of
the cartilage, sparing the vocal process.
A suture is then placed into the remnant of vocal
process and fixed to the lateral thyroid ala.
Endoscopic limited or complete arytenoidectomy
Ossoff et al in 1984
 Expose the larynx with a suspension device
that provides a satisfactory view of the
posterior glottis. Use a microscope with a 400mm lens & a laser attachment.
 Vaporize the mucosa overlying the arytenoid
and corniculate cartilage.
 Vaporize the bulk of the arytenoid preserving
the vocal or muscular process.
Laryngofissure with arytenoidectomy
Expose the larynx with a previous tracheotomy by making a
curvilinear transverse neck incision through skin and
Create a midline thyrotomy through thyroid cartilage &
cricoid cartilage
Visualize the posterior larynx
Make a transverse incision through the mucosa to free the
arytenoids from the cricoid and muscles.
Hemostasis with bipolar cautery, & close the mucosa with a
chromic suture
Lateralization sutures around the TVF, exiting the thyroid
lamina and overlying skin
Close the thyrotomy in layers. Close the skin and place a
Suture lateralization (Ejnell procedure)
Lichtenberger needle
 Via the laryngoscope, introduce the
laryngeal needle holder.
 Insert a curved needle while holding a 2-0
polypropylene suture in the distal end of
the curved shaft with the plunger within the
shaft retracted.
 Place the shaft into the supraglottic larynx
in the middle of the false vocal fold (FVF).
Direct the shaft laterally and engage the
plunger, directing the needle from the shaft
through the mucosa, cartilage, and neck
skin. At this point, retrieve the needle.
 Repeat the procedure in the subglottic
larynx by using the same suture.
Cricothyroid subluxation
Zietels etal (1999)
Lengthen a vocal cord which has become flaccid
secondary to paralysis & neurologic injury
Placing a suture around the inferior thyroid cornu &
the anterior cricoid
Tightening this suture pulls the thyroid forward relative
to the cricoid, lengthening the flaccid vocal cord
By simulating the action of the cricothyroid muscle,
cricothyroid subluxation allows patients with vocal cord
paralysis to enjoy more normal pitch variation than they
might otherwise experience
Skeletanization of inferior
cornu of thyroid cartilage
Cricoid cartilage freed
Cricothyroid joint is
2-0 prolene passed through
neck of infr cornu & then
passed underneath anterior
cricoid cartilage & then in
submucosal plane in anterior
A.Thakar, K.Sikka, R.Verma, C.Preetam
(eur arch otorhinolayngol)nov 2011
Physiological solution to the motor deficits that
result from high vagal paralysis
The procedure restores vocal fold tension,
vertical vocal fold position & partially restores
horizontal vocal fold position
Good swallowing & voice outcomes.
A 1-0 Prolene suture passed through
the thyroid lamina positioned about 8
mm paramedian and 6–8 mm above
its inferior margin; the needle was
passed from outside-in, brought out
through the cricothyroid space, & then
re-inserted inferiorly so as to encircle
the cricoid ring.
A similar suture was passed 5 mm
posterior to the first suture, & the two
sutures were then pulled and tied so as
to approximate the cricoid & thyroid
cartilages & to close the cricothyroid
Laryngeal Reinnervation
Intended to restore neural connections to the larynx
(RLN or its subdivisions/ SLN)
direct end-to-end anastomosis (neurorrhaphy)
direct implantation of a nerve ending into a muscle
nerve-muscle pedicle (NMP) technique
muscle-nerve-muscle (MNM) methods
Potential donor nerves
original RLN
ansa cervicalis
hypoglossal nerve
Contralateral RLN
Ipsilateral SLN
Under local or general anesthesia.
A lateral neck-crease incision is made
The ansa hypoglossi is identified as it lies on the jugular
vein. It is traced to it's point of entry into the anterior
belly of the omohyoid muscle.
A free block (approximately 2-3mm on a side) of
muscle from the omohyoid is excised, including the
point of entry of the nerve.
A window is created in the thyroid ala exposing the
thyroarytenoid muscle.
The nerve-muscle pedicle is then sutured to this
The incision is closed after placement of a penrose
 Normal or near-normal voice without synthetic materials
placed inside the laryngeal framework
 Does not alter the stiffness of the vocal folds
 Restoration of bulk to the thyroarytenoid (TA) muscle
 Improved vocal fold positioning
 Does not preclude static methods if it should fail
 Elimination of dysphonia because of synkinesis if present (by
sectioning the RLN)
Disadvantages/ limitations
 The need for an intact donor nerve
 The need for an identifiable distal stump of the RLN
 A delay of several months before reinnervation becomes
Electrical pacing
Laryngeal stimulators send a stimulus that can be administered as
a continuous current, an intermittent current, or a triggered
(preferably by respiratory effort) pacing current.
In patients with BVFP, laryngeal pacing involves the use
of an external apparatus that senses inspiration &
reanimates the paralyzed larynx of the patient.
Stimuli are delivered through a needle electrode to locate
& pace the abductor muscle & through an electrode
implanted in the PCA muscle or RLN branch that
extends to the PCA muscle.
imprecise & excessive electrical stimulation,
scar formation
bulky power sources, muscle fatigue with
continuous stimulation
difficulty in synchronizing the pacing with the
respiratory effort in a convenient way
Pediatric U/L vocal cord immobility
Congenital stridor
U/L or B/L vc immobility
Neonates - stridor/ feeding
Familial B/L VFI- [chr-6q16]
Rx <6mo  conservative/
 >6mo  conservative/
inj thyroplasty/
type-I thyroplasty
anomalies &
Sx of
Neoplasia of
Sx for
ageal atresia
Vagal nerve
Speech therapy