Dysphonia and vocal fold lesions

Definition and Overview

• Hoarseness describes an altered vocal quality perceived by the patient or observer; it is a symptom.
• Dysphonia is the clinical diagnosis of impaired voice, encompassing changes in pitch, loudness, quality (timbre) or the effort required to produce voice, to the extent that communication is reduced or voice-related quality of life is impaired.
• The distinction matters: the clinician must move from the patient's symptom of hoarseness to a structured diagnostic formulation.
• Dysphonia is common in the general population and affects professional voice users (singers, teachers, clergy, barristers) disproportionately, with significant occupational consequences.
• The OHNS trainee must be able to: take a structured history, perform a complete head and neck and laryngeal examination, interpret flexible and rigid endoscopy, interpret stroboscopic findings, and formulate a differential diagnosis and management plan.

Anatomy Relevant to Dysphonia

Laryngeal Framework

• The larynx occupies the C4-C6 level and is composed of the thyroid, cricoid, arytenoid, epiglottic and corniculate cartilages.
• The vocal fold (true vocal cord) has a layered microstructure: epithelium, superficial lamina propria (Reinke's space), intermediate and deep lamina propria, and the vocalis (thyroarytenoid) muscle. This layered architecture is critical to the mucosal wave.
• The glottis is the space between the true vocal folds.
• The supraglottis (epiglottis, aryepiglottic folds, false cords, upper ventricle) and subglottis are relevant to lesion localisation and cancer staging.

Nerve Supply: Structures at Risk

• Unilateral RLN injury: paramedian cord, breathy-hoarse voice, weak cough; cricothyroid still adducts contralateral cord slightly.
• Unilateral RLN + EBSLN injury: cord assumes intermediate (lateral) position, more severe hoarseness, complete inability to cough effectively.
• Bilateral RLN injury: risk of airway compromise; voice may paradoxically be preserved due to median/paramedian positioning of both cords.

Pathophysiology of Voice Production

$$F_0 = \frac{1}{2L}\sqrt{\frac{T}{\rho}}$$

Where $F_0$ = fundamental frequency, $L$ = vocal fold length, $T$ = tension, $\rho$ = tissue density.

• Normal $F_0$: ~128 Hz (men, middle C one octave below); ~256 Hz (women, middle C).
• Voice is produced by the Bernoulli-driven oscillation of the vocal fold cover over the stiffer body; the mucosal wave propagates from inferior to superior along the cover.
• Dysphonia results from any disruption to this oscillation: mass lesions (nodules, polyps, cysts), stiffness (scarring, malignancy, oedema), neurogenic dysfunction (paresis, paralysis, spasmodic dysphonia), or functional/behavioural aetiology.
• Loudness is determined by subglottal pressure and vocal fold contact force.
• Quality (timbre) depends on synchronicity of vibration and the completeness of glottic closure.

History: Structured Approach

Character of the Dysphonia

• Onset: acute (infection, haemorrhage, trauma, intubation injury) versus gradual (malignancy, benign lesion progression, neurological).
• Duration: hoarseness persisting beyond 3 weeks in a patient with risk factors warrants urgent laryngoscopy; beyond 3 months warrants laryngoscopy regardless of risk.
• Time of day: morning hoarseness is characteristic of laryngopharyngeal reflux (LPR); evening hoarseness suggests vocal fatigue/abuse.
• Character: breathy (incomplete glottic closure, unilateral paralysis, atrophy); rough/harsh (mass lesion, oedema); strained (muscle tension dysphonia, adductor spasmodic dysphonia); diplophonia (asymmetric mass or paralysis); voice breaks; tremor.

Contributing and Risk Factors

• Vocal behaviours: abuse, misuse, professional demands (singers, teachers).
• Irritants: tobacco, alcohol, inhaled corticosteroids, airborne irritants.
• Reflux: LPR - key modifiable contributor.
• Systemic: hypothyroidism (laryngeal myxedema), rheumatoid arthritis (cricoarytenoid joint), sarcoidosis, amyloidosis.
• Neurological: Parkinson's disease, multiple sclerosis, cerebral palsy, stroke, myasthenia gravis, essential tremor.
• Surgical history: thyroidectomy, cardiothoracic surgery (left RLN at risk via aortopulmonary window), anterior cervical spine surgery, oesophagectomy, skull base surgery.
• Neck and chest: history of apical lung tumour (Pancoast), mediastinal adenopathy, aortic aneurysm.
• Paediatric: birth trauma, congenital lesions, neonatal intubation.

Alarm ("Red Flag") Features Requiring Urgent Assessment

• Tobacco and/or alcohol use with hoarseness of any duration.
• Progressive hoarseness with dysphagia, odynophagia, referred otalgia.
• Concomitant neck mass.
• Haemoptysis.
• Worsening airway compromise or stridor.
• Unexplained weight loss.
• Immunocompromise (recurrent respiratory papillomatosis, fungal laryngitis).
• Hoarseness following endotracheal intubation or neck/chest surgery.

Clinical Examination

General and Head and Neck

• Assess respiratory rate; note stridor (inspiratory: supraglottic/glottic; biphasic: subglottic/tracheal).
• Perceptual voice assessment: note roughness, breathiness, strain, asthenia, pitch, loudness (GRBAS or CAPE-V scales).
• Palpate neck: thyroid size, nodularity, tenderness; cervical lymphadenopathy (levels I-VI); laryngeal framework integrity, crepitus, tenderness.
• Complete cranial nerve examination: CN IX-XII involvement suggests skull base or parapharyngeal pathology.

Indirect Mirror Laryngoscopy

• Angled laryngeal mirror, warmed, placed in the oropharynx; patient phonates /ee/.
• Assesses: vocal fold appearance (colour, mass, erythema, oedema), cord mobility, arytenoid movement, pooling of secretions in pyriform sinuses (suggesting pharyngeal dysmotility or hypopharyngeal obstruction).
• Limitation: patient cooperation, gag reflex, tongue size; static snapshot, limited posterior commissure view.

Laryngeal Visualisation Techniques

Flexible Nasolaryngoscopy (FNL)

• Passed through the nasal cavity to the nasopharynx and positioned above the larynx.
• Allows dynamic assessment during connected speech, singing, cough, sniff and swallow.
• Evaluates: supraglottic hyperfunctional posturing, vocal fold mobility, arytenoid movement, pooling, and posterior glottis.
• Superior to mirror for patients with hyperactive gag, and for posterior commissure and arytenoid assessment.
• Coupled with a camera system enables video recording for documentation, comparison and medicolegal purposes.
• Limitation: image quality and magnification inferior to rigid telescope for subtle mucosal detail.

Rigid 70° Laryngeal Telescope (Transoral)

• Passed over the tongue with patient's tongue held forward.
• Provides high-resolution magnified static views of glottic and supraglottic structures.
• Preferred for detailed mucosal assessment, lesion characterisation and stroboscopy.
• Cannot assess dynamic voicing function across connected speech.

Choice of Endoscope

Stroboscopy: Principles and Interpretation

Physical Principles

• Normal vocal fold oscillation at 100-300 Hz exceeds the capacity of the human eye (flicker fusion ~5 Hz) to resolve individual cycles.
• Stroboscopy uses a flashing light source at a frequency slightly offset from the detected fundamental frequency of phonation ($\Delta F$, typically 1-2 Hz lower).
• The resulting apparent slow-motion image (the stroboscopic effect) represents a composite reconstructed pseudo-cycle, not a real single cycle.
• A microphone detects $F_0$; the strobe triggers at $F_0 - \Delta F$, sampling different points of successive vibratory cycles to create the illusion of slow motion.
• Important limitation: the reconstructed cycle assumes a periodic (regular) signal; during aperiodic or severely dysphonic phonation, stroboscopy produces unreliable or uninterpretable images. High-speed digital laryngoscopy (HSDL) is preferred in this setting.

Parameters Assessed on Stroboscopy

Clinical Value of Stroboscopy

• Distinguishes surface (cover) lesions from deep/submucosal lesions: a cyst deep to the epithelium produces a fixed segment of absent mucosal wave adjacent to a normally vibrating fold, whereas a nodule causes a symmetric stiffening at the point of contact.
• Identifies subclinical vocal fold paresis: subtle asymmetry of amplitude, phase or mucosal wave not apparent on white-light endoscopy.
• Guides surgical decision-making: a lesion with intact mucosal wave is more likely to be confined to the superficial lamina propria and amenable to microlaryngoscopy with vocal fold preservation; absent wave suggests deeper infiltration.
• Monitors disease course and treatment response (interval examination): baseline stroboscopy in professional voice users while voice is healthy provides comparison during dysphonic episodes.
• Medicolegal documentation: recorded stroboscopic examinations constitute a timestamped visual record.

Narrow-Band Imaging (NBI)

• Optical filter technique using specific wavelengths (415 nm blue; 540 nm green) absorbed by haemoglobin to enhance visualisation of mucosal vasculature.
• Abnormal vascular patterns (intrapapillary capillary loops, irregular vessels) are associated with dysplasia and malignancy.
• Complementary to stroboscopy; does not replace it.

Differential Diagnosis of Dysphonia

Investigation

First-Line

• Flexible nasolaryngoscopy: mandatory for all patients with dysphonia exceeding 3 weeks (risk factors present) or 3 months (all patients).
• Rigid stroboscopy: for professional voice users, persistent dysphonia, lesion characterisation, and preoperative planning.
• Perceptual voice analysis: GRBAS scale (Grade, Roughness, Breathiness, Asthenia, Strain) or CAPE-V (Consensus Auditory-Perceptual Evaluation of Voice).
• Patient-reported outcomes: Voice Handicap Index (VHI); VHI-10 for screening.
• Acoustic analysis: jitter (frequency perturbation), shimmer (amplitude perturbation), harmonic-to-noise ratio (HNR); performed via computerised voice laboratory.

Second-Line / Directed

• CT neck and chest: first investigation for suspected malignancy, vocal fold paralysis (trace RLN course from skull base to aortopulmonary window); mediastinal pathology.
• MRI larynx: cartilage invasion assessment in laryngeal SCC; perineural spread.
• Laryngeal EMG (LEMG): differentiates neurogenic from mechanical vocal fold immobility (cricoarytenoid joint fixation vs. RLN paralysis); guides prognosis of RLN injury and timing of intervention.
• Direct microlaryngoscopy under GA: diagnostic and therapeutic; allows palpation of arytenoids (exclude fixation), biopsy, and microsurgical intervention.
• Autoimmune / endocrine screen: TFTs, ANA, ANCA, RF; as directed by history.
• Oesophagoscopy / pH impedance monitoring: if LPR suspected and not responding to empirical therapy.

Thyroid Surgery Voice Assessment (AAO-HNS Position)

Pre- and postoperative assessment for thyroid and parathyroid surgery must include:

1. Patient-reported voice outcome (validated questionnaire, e.g. VHI).
2. Auditory-perceptual assessment (e.g. GRBAS, CAPE-V).
3. Audio recording of patient voice.
4. Direct visualisation of vocal fold mobility (flexible nasolaryngoscopy).

Management Principles

General Framework

1. Address modifiable contributors first: voice rest (relative), vocal hygiene, treat LPR (PPI ± alginate), cease smoking, reduce alcohol, treat hypothyroidism.
2. Voice therapy: cornerstone for functional dysphonia, muscle tension dysphonia, and nodules; also adjunctive after surgery.
3. Medical: antimicrobial (bacterial/fungal laryngitis); systemic immunosuppression (autoimmune/granulomatous); botulinum toxin (spasmodic dysphonia, essential tremor).
4. Surgical: microlaryngoscopy for persistent benign lesions, papillomatosis debulking, biopsies, arytenoid procedures, laryngeal framework surgery.
5. Oncological MDT: for malignancy - see laryngeal SCC notes.

Specific Conditions

Vocal fold nodules: bilateral, symmetric, at the free edge at the junction of the anterior and middle thirds; arise from phonotrauma; management is voice therapy first; microlaryngoscopy if persistent after adequate therapy trial.

Vocal fold polyps: usually unilateral, haemorrhagic or oedematous; may arise from a single phonotrauma event; microlaryngoscopy with cold-instrument or KTP laser excision; superficial lamina propria preservation essential.

Reinke's oedema: diffuse bilateral gelatinous oedema of the superficial lamina propria; associated with long-term smoking and LPR; management includes cessation of smoking, voice therapy, then microlaryngoscopic decortication with preservation of the leading edge.

Vocal fold cysts: epidermoid or mucus retention; stroboscopy shows a fixed segment with absent mucosal wave on the affected fold and compensatory increased amplitude on the other; requires microlaryngoscopy; full excision necessary to prevent recurrence.

Contact granuloma / intubation granuloma: posterior glottis; associated with LPR, chronic throat clearing, prolonged intubation; first-line is PPI and voice therapy; surgical excision has high recurrence; consider botulinum toxin injection to reduce contact force.

Recurrent respiratory papillomatosis (RRP): HPV 6 and 11; can be juvenile-onset (aggressive) or adult-onset; treated by repeated microlaryngoscopic debulking (cold steel, microdebrider, pulsed KTP laser); adjuvant intralesional cidofovir or bevacizumab for aggressive disease; HPV vaccination.

Unilateral vocal fold paralysis: assess for reversibility (LEMG, cause, timeline); if glottic insufficiency is symptomatic, medialization laryngoplasty (type I thyroplasty, Isshiki) or injection augmentation (temporary: carboxymethylcellulose, Gelfoam; longer-lasting: calcium hydroxyapatite, fat, Radiesse); arytenoid adduction for posterior gap.

Spasmodic dysphonia: adductor type (most common): strained voice quality with voice breaks on voiced sounds; botulinum toxin injection into thyroarytenoid muscles is the mainstay; abductor type: breathy breaks, injection to posterior cricoarytenoid.

Muscle tension dysphonia: hypercontraction of supraglottic and extrinsic laryngeal musculature; often secondary to underlying organic pathology; exclude malignancy; management is laryngeal manipulation and voice therapy with speech-language pathologist.

Complications and Special Considerations

The Professional Voice User

• The stakes of misdiagnosis or poorly timed surgery are high: career-defining consequences.
• Baseline stroboscopic examination while the voice is healthy is best practice.
• Voice rest, optimised hydration, humidification and avoidance of phonotraumatic behaviour are core.
• Surgery should be performed by an experienced laryngologist; timing relative to performance schedules must be factored into consent.
• Post-surgical voice therapy is essential.

Laryngoscopy Indications: AAO-HNS Guideline Position

Laryngoscopy should be performed when:

• Hoarseness does not resolve after 3 months of conservative management; OR
• A serious underlying cause is suspected at any time point, including: tobacco or alcohol use, concomitant neck mass, haemoptysis, dysphagia, odynophagia, referred otalgia, compromised airway, neurological symptoms, unexplained weight loss, immunocompromise, possible foreign body aspiration, neonatal hoarseness, hoarseness following intubation or neck/chest surgery.

Pitfalls in Interpretation

• Stroboscopy is unreliable in severely aperiodic voice (near-total paralysis, severe oedema, malignancy); HSDL is preferred but less widely available.
• A normal-appearing larynx on white-light endoscopy does not exclude significant functional or early mucosal disease; stroboscopy adds sensitivity.
• Posterior glottic gap in women during quiet breathing is a normal variant; must not be over-interpreted as paresis without EMG confirmation.
• Arytenoid motion asymmetry may represent neurogenic paresis or cricoarytenoid joint fixation; LEMG and/or direct palpation under GA are needed to differentiate.

Perioperative and Consent Considerations

• Consent for diagnostic microlaryngoscopy: dental injury, laryngeal oedema, voice change, poor suspension laryngoscopy view, biopsy-related scarring, need for tracheostomy (rare).
• For injection augmentation: risk of airway compromise (over-injection), infection, suboptimal voice outcome, need for revision.
• For type I thyroplasty: risk of airway compromise, extrusion of implant, infection, subcutaneous haematoma, need for revision.
• Documentation of pre-existing voice quality and vocal fold findings prior to any head/neck or thoracic surgery with RLN risk forms part of standard surgical care and medicolegal best practice.
• Involve a speech-language pathologist in pre- and postoperative care for professional voice users and all surgical voice cases.