Vocal Cord Palsy (Vocal Fold Paralysis)

Anatomy and Nerve Supply

• Recurrent laryngeal nerve (RLN): Supplies all intrinsic laryngeal muscles except cricothyroid. The left RLN has a longer course, descending into the thorax and looping under the aortic arch before ascending in the tracheo-oesophageal groove - making it more vulnerable to injury.
• Superior laryngeal nerve (internal and external branches): The external branch supplies the cricothyroid; the internal branch is sensory to the supraglottis. High vagal injury affecting both nerves is more functionally devastating than isolated RLN injury.

Causes

Unilateral VCP

• Thyroidectomy (most common in ENT practice); risk factors include Graves' disease, post-operative haematoma, revision surgery
• Oesophagectomy, tracheal resection, thymectomy, mediastinal procedures
• Cervical spine surgery
• Carotid endarterectomy

• Lung carcinoma (esp. left hilar/apical), thyroid cancer, oesophageal carcinoma, lymphoma, mediastinal tumours

• Aortic aneurysm (left RLN)
• Patent ductus arteriosus surgery
• Cardiac valve surgery
• Enlarged left atrium - Ortner syndrome (cardiovocal syndrome)

• Cerebrovascular accident (usually with other deficits)
• Wallenberg syndrome (lateral medullary infarct): vocal fold palsy + dysphagia + vertigo + ataxia + Horner syndrome + hemifacial sensory deficit
• Arnold-Chiari malformation
• Multiple sclerosis, Parkinson's disease, motor neurone disease, myasthenia gravis, Guillain-Barré syndrome

• Inflammatory: sarcoidosis, Lyme disease, syphilis, collagen vascular disease
• Organophosphate exposure, neurotoxic chemotherapy (vincristine, cisplatin)
• Congenital VCP: presents with hoarse cry + feeding/aspiration difficulties in infants

Clinical Features

Unilateral VCP

• Dysphonia: breathy, weak voice; vocal fatigue, diplophonia (double voice), decreased projection
• Aspiration: occasionally, especially liquids; worse with high vagal lesions affecting laryngeal sensation
• Wet voice quality: pooled secretions indicate laryngeal penetration - a warning sign
• Exertional breathlessness: from air escape during phonation and loss of the Valsalva mechanism
• Occasionally asymptomatic (found incidentally)

Bilateral VCP

• Medialized cords: Normal or near-normal voice, but stridor and dyspnoea (the key danger)
• Lateralized cords: Weak voice, possible dysphagia, but better airway
• Acute bilateral VCP (e.g., post-thyroidectomy) can cause life-threatening airway obstruction
• Chronic/progressive cases (e.g., neurological disease) may be better tolerated as patients compensate
• Inspiratory stridor is characteristic: negative pressure on inspiration pulls denervated folds together

Pathophysiology

Diagnosis

1. Flexible nasolaryngoscopy/laryngoscopy: Gold standard; directly visualizes cord mobility. Palpate the vocal process to assess for mechanical fixation (cricoarytenoid joint fixation, posterior glottic scar - must be distinguished from true neurogenic palsy).
2. Laryngeal EMG (LEMG): Evaluates nerve integrity; absence of activity or synkinetic patterns predict poor recovery. Guides prognosis before committing to permanent surgery.
3. Imaging:
   • CT neck and thorax (from skull base to thoracic inlet/aortic arch) to identify compressive/infiltrative lesions
   • MRI brain if central/neurological cause suspected
   • Chest X-ray for lung malignancy
4. Flow-volume loop: Bilateral VCP shows variable extra-thoracic obstruction pattern (passive adduction on inspiration, abduction on expiration).
5. Address underlying cause: full history including surgical history, chest symptoms, neurological review, smoking history.

Management

Unilateral VCP

• Many cases show spontaneous recovery or natural compensation within 6-12 months
• Voice therapy as first-line: strengthening techniques, pushes/pulls to improve adduction
• Temporary injection augmentation while awaiting recovery

• Temporary materials (while awaiting recovery): Carboxymethylcellulose (2-3 months), hyaluronic acid (2-4 months), micronized cadaveric dermis (2-6 months)
• Longer-lasting: Calcium hydroxyapatite (Radiesse Voice; ~18 months) - requires deep injection
• Permanent: Autologous fat (unpredictable absorption; 30-50% absorbed early)
• Teflon: historical only - no longer used due to granuloma formation

• Permanent medialization via external approach; Gore-Tex or silastic implant placed through a window in the thyroid cartilage
• Done under local anaesthesia + light sedation to allow real-time voice monitoring
• Implant placed in the inferior half of the thyroid cartilage (vocal folds are deep to the inferior half)
• Complications: airway oedema, implant extrusion, poor voice if implant too high/anterior
• Not adequate alone if there is a large posterior glottic gap (lateralized arytenoid)

• Mimics the lateral cricoarytenoid muscle action
• Indicated when there is a large posterior glottic gap with lateralized vocal process
• Muscular process of arytenoid exposed, suture passed to rotate it medially
• Often combined with Type I thyroplasty (Zeitels technique)

• Restores muscle bulk and tone rather than functional motion
• Improves voice long-term; takes months to show effect

Bilateral VCP

1. Tracheotomy: Gold standard; speech possible with Passy-Muir valve or digital occlusion
2. Endoscopic arytenoidectomy (medial or total): Enlarges the glottis; preserves membranous cord for phonation
3. Transverse cordotomy (posterior cordotomy): Incision across the vocal fold at the vocal process to widen the airway; can be extended as needed
4. Suture lateralization: Lateralizes one cord if no joint fixation present
5. Arytenoid abduction (external approach)
6. Laryngeal pacing: Experimental implantable stimulator to restore abductor function

Vocal Fold Paresis (Incomplete Palsy)

Prognosis

• Spontaneous recovery most likely within 6-12 months of onset
• LEMG findings guide prognosis: absent or synkinetic activity = poor recovery
• Idiopathic cases have a better prognosis than neoplastic causes
• Congenital unilateral VCP often improves as the child develops compensatory mechanisms

Features of RLN and SLN Palsy

Anatomy First - What Each Nerve Does

RLN Palsy

Unilateral RLN Palsy

• Hoarseness - breathy, weak, flaccid dysphonia
• Reduced loudness, short phrases due to excessive air escape
• Diplophonia (two simultaneous pitch levels from unequal vibration of the two cords)
• Mild inspiratory stridor during contextual speech
• "Paralytic falsetto": if SLN is intact, the patient may compensate by raising pitch via cricothyroid - generates a higher-pitched, strained voice quality

• Paralysed cord lies near the midline (paramedian position) at rest
• Normal cord crosses the midline to meet the paralysed cord during phonation - glottic gap remains
• Spindle-shaped gap if the membranous cord is predominant; V-shaped (posterior) gap if the vocal process is lateralized
• Increasing tension on the paralysed cord when the patient raises pitch suggests the SLN/cricothyroid is intact (Figure 78.1 below)
• Prolapsed arytenoid: the arytenoid on the paralysed side may fall forward into the laryngeal introitus - sign of profound denervation and muscular support loss
• Supraglottic hyperfunction: ventricular fold adduction as compensation for glottic insufficiency

• Occasional aspiration, mainly liquids
• Dysphagia worse if it is a "high vagal" lesion (SLN also involved) due to added ipsilateral laryngeal anaesthesia, pharyngeal constrictor weakness, and cricopharyngeal hyperfunction

With progressive/peripheral RLN injury, adductor muscles are affected first, then abductors last. So in early/partial palsy the cord may still adduct but cannot abduct (abductor paralysis). In complete palsy, all muscles are paralysed and the cord lies paramedian.

• Paramedian in most cases (partial tone from intact cricothyroid + muscle atrophy over time)
• More lateral (cadaveric position) with high vagal lesions (complete tone loss)

Bilateral RLN Palsy

• Inspiratory stridor - negative inspiratory pressure sucks denervated cords medially
• Progressive dyspnoea and exercise intolerance
• In acute bilateral palsy (e.g., post-thyroidectomy extubation): life-threatening respiratory distress - emergency
• In chronic (e.g., progressive neurological disease): patients may compensate as paralysis develops slowly

• Bilateral abductor paralysis = cords approximated in midline
• Severe airway limitation, often requiring tracheostomy
• Can occur in spinocerebellar ataxia type I (associated with nocturnal stridor and mild dysphagia)

SLN Palsy

External Branch SLN (EBSLN) Palsy - Motor

• Lengthens and tenses the vocal folds
• Is responsible for increasing pitch and projecting the voice
• Maintains longitudinal tension of the cord

• Very subtle clinically - often missed
• Slight hoarseness, reduced upper vocal range
• Loss of high notes; reduced voice projection
• Loss of ability to increase pitch voluntarily
• On laryngoscopy: oblique glottis - the anterior commissure rotates toward the paralysed side because the opposite cricothyroid pulls it across; asymmetric cord tension
• Cricothyroid muscle atrophy on the affected side

• Hoarseness, easy voice fatigue
• Significant loss of pitch control and voice projection
• Cannot reach high notes
• Airway is not jeopardized (no abductor/adductor function affected)
• Particularly disabling for singers and professional voice users

Internal Branch SLN (IBSLN) Palsy - Sensory

• Loss of laryngeal sensation above the vocal cords
• Impaired laryngeal protective reflexes
• Silent aspiration - fluid/food enters the airway without triggering cough/laryngospasm
• Penetration and aspiration of secretions without awareness
• Increased aspiration pneumonia risk

Combined SLN + RLN Palsy (High Vagal Lesion)

Summary Comparison Table

Positions of the Vocal Cord

The Classic Positions (Medial to Lateral)

MIDLINE ←————————————————————→ FULL ABDUCTION
  |        |           |         |          |
Median  Paramedian  Intermediate  Lateral  Full abduction
(closed) (nearly    (cadaveric)           (deep inspiration)
          closed)

Position in Different Nerve Lesions

1. RLN Palsy - Paramedian position

• RLN carries both abductor (PCA) and adductor fibres
• In RLN palsy: all intrinsic muscles paralysed except cricothyroid (SLN intact)
• The intact cricothyroid still acts on the cord, maintaining some tension and pulling it toward midline
• Result: cord rests just lateral to the midline (paramedian)
• Voice: hoarse but present; reasonable phonation because normal cord can cross to meet the paralysed one
• Semon's law: in progressive/incomplete RLN injury, abductor fibres (PCA) are affected before adductors - so early partial RLN palsy shows abductor paralysis with preserved adduction (cord can adduct but not abduct)

2. Vagal (High) Lesion - Intermediate / Cadaveric position

• Complete vagal lesion = RLN + SLN both paralysed
• Loss of all intrinsic laryngeal muscle tone, including cricothyroid
• No residual tension pulling the cord medially
• Cord lies midway between adduction and abduction - the "cadaveric position" - so called because it mimics the position seen at post-mortem
• This position causes severe glottic incompetence with a wide gap
• Voice: very breathy or aphonic; cough weak/absent
• Associated features: ipsilateral palatal paralysis, nasal voice ("nasal twang"), dysphagia, absent ipsilateral gag reflex

3. Normal Physiological Positions

Why Position Matters Clinically

Important Notes on Traditional Terminology (Modern Revision)

"The traditional terms for vocal fold position - intermediate, paramedian, and cadaveric - do not adequately characterize glottic configuration, and the distance of the vocal fold from the midline is not a reliable indicator of lesion site."

1. Completeness of nerve injury (complete vs. partial)
2. Degree of re-innervation and synkinesis over time
3. Muscle atrophy (partial medialization over months as muscle fibres are replaced by fibrofatty tissue)
4. Presence/absence of intact SLN/cricothyroid (pulls cord toward midline)

Gutman Sign (SLN Palsy)

• Normal: lateral pressure on thyroid cartilage → increased pitch; anterior pressure → decreased pitch
• SLN palsy: the reverse - anterior pressure increases pitch, lateral pressure decreases it

Positions of the Vocal Cord

Spectrum (Medial → Lateral)

MIDLINE ←─────────────────────────────→ FULL ABDUCTION
   │           │              │              │
Median    Paramedian    Intermediate      Lateral
(phonation) (RLN palsy)  (vagal palsy /   (deep breath)
                          cadaveric)

Positions in Nerve Lesions

Normal Physiological Positions

Key Points

• Paramedian = just off midline; voice hoarse but present; airway safe
• Cadaveric (intermediate) = midway; very breathy/aphonic; severe glottic gap
• Bilateral RLN palsy with both cords paramedian = airway compromised (stridor/dyspnoea) despite relatively preserved voice
• Semon's law: in progressive RLN injury, abductors fail before adductors (PCA fibres most vulnerable)
• Modern view (Cummings): cord position alone is not a reliable indicator of lesion site - EMG + laryngoscopy are needed for accurate localisation