• Muscle tension dysphonia — excessive tension in perilaryngeal muscles without structural lesion. Often seen in high-demand voice users who develop maladaptive patterns.

• Functional voice disorder (the slide uses “conversion disorder”) — voice loss or alteration arising from disordered voice function after appropriate assessment. Preserved cough or laughing voice may be a clue, but is not diagnostic and should never replace laryngeal examination.

Key history points: Smoking, Occupation/voice demand, Details of hoarseness, and Red flag symptoms for malignancy. ^[1]

Additional history to consider (from integration with supporting material):

• GERD / laryngopharyngeal reflux — a common contributor to chronic laryngitis and Reinke's oedema ^[6]
• Alcohol — synergistic risk with smoking for laryngeal SCC ^[4]
• Previous neck surgery (thyroidectomy, anterior cervical spine surgery) — iatrogenic RLN injury
• Previous intubation — can cause cord palsy or granuloma
• History of head & neck radiotherapy — can cause chronic laryngeal changes

Examination of a patient with hoarseness: (1) Cervical lymphadenopathy, (2) Inspection of the larynx. ^[1]

Cervical lymphadenopathy — palpate all levels systematically. Enlarged, hard, fixed nodes suggest metastatic disease.

Laryngeal inspection methods (from simple to complex):

Stroboscopy samples successive vibratory cycles to create an apparent slow-motion view; it is not a true high-speed recording. Interpret symmetry, periodicity, amplitude, closure and mucosal wave. ^[1]

Orientation pearl: identify the epiglottis/supraglottis, the pale true vocal folds and the dark glottic airway first. Then compare laterality, surface, colour, bulk and mobility; a still image cannot assess vibration or movement.

Classically affects singers and teachers and is related to phonotrauma. The slide's classic pattern is bilateral, symmetric lesions at the junction of the anterior and middle thirds of the vocal folds. ^[1]

Pathophysiology from first principles:

• Repeated vocal trauma → localized oedema at the point of maximal collision between the vocal folds → fibrosis → nodules
• The junction of the anterior 1/3 and middle 1/3 is where the amplitude of vibration is greatest, hence this is where nodules form
• They are usually bilateral and opposing, but “always symmetrical” is an exam simplification; asymmetric nodules and a nodule with a contralateral reactive lesion occur

Clinical features:

• Husky voice and easy fatigue due to air leak — the nodules prevent complete glottic closure, so air leaks through, making the voice breathy and requiring more effort ^[1]

Management:

• Speech/voice therapy and vocal hygiene are first-line and often improve or resolve phonotraumatic nodules ^[1]
• Surgery is rarely needed; nodules often regress with proper voice use
• Vocal hygiene = adequate hydration, voice rest, avoiding shouting/whispering, treating reflux

Unilateral vocal cord lesion. Caused by acute vocal trauma → bleeding from mucosal vessel → organized haematoma → polyp. ^[1]

Pathophysiology:

• Acute phonotrauma with haemorrhage is the slide's model, but polyps can also reflect repeated phonotrauma and are not all organised haematomas
• They are typically unilateral; the opposite fold may show a reactive contact lesion

Clinical features:

• Husky voice and easy fatigue due to air leak — same mechanism as nodules (incomplete glottic closure) ^[1]

What the laryngoscopy views show: a unilateral reddish/lobulated or pale smooth polyp projecting from one cord into the glottic aperture — air leak = husky voice; management is microlaryngoscopy + excision, not “voice rest forever.” ^[1]

Management:

• Microlaryngoscopy + excision is the lecture's management. In practice, address phonotrauma and use voice therapy as appropriate; observation or therapy may be reasonable for selected small/recent lesions, while persistent or suspicious lesions require operative assessment. ^[1]

Fluid collection in Reinke's space (superficial lamina propria). Causes: smoking, laryngeal reflux, hypothyroidism. ^[1]

Pathophysiology:

• Reinke's space is the superficial layer of the lamina propria — a potential space between the epithelium and the vocal ligament
• Chronic irritation (smoke, acid reflux) → increased vascular permeability → fluid accumulation in this space
• The fluid makes the vocal folds heavy, bulky, and floppy

Clinical features:

• Effortful, low-pitched, and rough voice — the heavy, oedematous folds vibrate at a lower frequency, hence low pitch ^[1]
• Classic patient: middle-aged female smoker with a deep, gravelly voice

Management:

• Correct underlying causes (quit smoking!!) — most important step ^[1]
• Surgery is considered for persistent, functionally important or obstructive disease, using a mucosa-preserving microflap technique where possible; indiscriminate stripping risks scarring and poor voice ^[1]
• Treat reflux if contributing

Associated with HPV subtypes 6 and 11. Transmission: in-utero transfer, birth tract contact, oral sex. Affects both adults and children. ^[1]

Pathophysiology:

• HPV 6 and 11 are low-risk HPV types (same subtypes causing genital warts)
• The virus infects the basal layer of the laryngeal epithelium → papillomatous growth
• Juvenile-onset disease is associated with perinatal HPV exposure, while adult-onset acquisition/reactivation is less certain; the slide lists birth-tract contact, possible in-utero transfer and oral sexual exposure

Presentation:

• Hoarseness
• Airway obstruction — can be life-threatening, especially in children where the airway is narrower
• Malignant transformation (→ SCC) — rare but possible, especially with HPV 11 ^[1]

Management:

• Microlaryngoscopy + Excision — the mainstay; typically requires multiple procedures because of recurrence ^[1]
• Prophylactic HPV vaccination is important for prevention; adjunctive vaccination after diagnosis may reduce recurrence in some studies but is not a substitute for surgery ^[1]
• Selected recurrent/aggressive cases may receive specialist adjuvant therapy such as intralesional bevacizumab; cidofovir is off-label and interferon is largely historical ^[1]

Leukoplakia = whitish plaque. Erythroplakia = reddish plaque. Both can be premalignant (dysplasia) or malignant (SCC). MUST BIOPSY!!! ^[1]

Why biopsy is mandatory:

• You cannot distinguish dysplasia from carcinoma-in-situ from invasive SCC by appearance alone
• Erythroplakia has a higher risk of malignancy than leukoplakia — the redness reflects increased vascularity and inflammation associated with neoplasia
• Investigation: Microlaryngoscopy + biopsy ^[1]

Risk factor: smoking. Commonest pathology: squamous cell carcinoma. Clinical features: hoarseness, airway obstruction, cervical lymph node metastasis. ^[1]

Key anatomical regions of the larynx (from supporting material ^[4]):

Why glottic cancer has the best prognosis:

1. Early symptom (hoarseness) → detected early
2. Poor lymphatic drainage → low risk of nodal spread
3. Therefore often curable with radiotherapy or limited surgery

Risk factors (from lecture + supporting material ^[4]):

• Smoking (single most important)
• Alcohol (synergistic with smoking)
• Occupational exposures and previous head-and-neck irradiation may contribute in selected patients

Do not treat laryngopharyngeal reflux as an established major carcinogen on the strength of association alone; smoking and alcohol are the dominant modifiable risks in this lecture.

The slide quotes an 8–10% synchronous-cancer risk, attributed to field change from carcinogen exposure. Treat this as a lecture-era estimate whose value varies by site, population and detection method. ^[1]

Field change (field cancerization) explained from first principles:

• The entire upper aerodigestive mucosa (mouth, pharynx, larynx, oesophagus, bronchi) is exposed to the same carcinogen (smoke + alcohol)
• Multiple foci of dysplasia/carcinoma can develop simultaneously
• Therefore, finding one cancer means you must look for others

The slide presents panendoscopy (bronchoscopy + oesophagoscopy) to detect synchronous lesions. Modern cross-sectional/PET imaging and office endoscopy have made examination under anaesthesia and additional endoscopy more selective; use it for tumour mapping, biopsy or when symptoms/site/imaging suggest another upper-aerodigestive lesion rather than as an automatic test for every patient.

Two methods shown: (1) local-anaesthetic flexible laryngoscopy with office biopsy in a suitable visible lesion and cooperative patient, or (2) general-anaesthetic direct microlaryngoscopy with biopsy when exposure, precision, airway control or tumour mapping requires it. ^[1]

The slide sequence is: flexible laryngoscopy, histological biopsy, panendoscopy, neck ultrasound ± FNA and contrast CT neck. ^[1]

Use the sequence as a framework rather than a rigid order. Airway safety comes first; imaging, biopsy route and any additional endoscopy are tailored by the head-and-neck multidisciplinary team.

Three main categories: (1) Neurogenic, (2) Cricoarytenoid joint, (3) Intrinsic muscle. ^[1]

Reading the Nerve-Course Diagram

The longer intrathoracic course of the left RLN explains its vulnerability to aortic/mediastinal disease and cardiothoracic surgery. Remember that the posterior cricoarytenoid is the only vocal-fold abductor; bilateral loss with folds near midline can therefore cause stridor.

The slide quotes malignancy 25%, iatrogenic 25% and idiopathic 20%. These are lecture-era proportions from an unspecified population, not timeless prevalence figures; the distribution varies by referral setting and surgical practice. ^[1]

Malignant causes (arise along the course of the vagus/RLN):

• Ca thyroid, oesophagus, lung, lymphoma, NPC, metastatic LNs ^[1]

Iatrogenic causes:

• Thyroid surgery, neck dissection, anterior spinal surgery, cardiothoracic surgery (more common on LEFT), intubation ^[1]

Injection laryngoplasty: material (e.g. fat, hyaluronic acid, calcium hydroxylapatite) injected into the paralysed cord to medialize it → improves glottic closure → better voice and less aspiration. ^[1]

Thyroplasty: a silastic implant is placed through a window in the thyroid cartilage to medialize the paralysed cord permanently. ^[1]

Reflux can contribute to laryngeal symptoms including hoarseness, throat discomfort and chronic cough ^[6], but these symptoms and nonspecific laryngeal redness are not diagnostic by themselves. Consider reflux in context, visualise persistent dysphonia and avoid reflexively prescribing prolonged PPI therapy without an appropriate indication/reassessment.

Post-thyroidectomy RLN injury is one of the most feared complications ^[5]:

• Unilateral RLN injury → vocal-fold immobility with hoarseness ± aspiration; confirm by laryngoscopy, assess recovery and use voice/swallow therapy or selected medialisation
• Bilateral RLN injury with folds near midline can cause stridor on extubation → urgent airway assessment and intubation/tracheostomy when required
• SLN injury → weak voice, cannot sing high pitch — important to warn professional singers pre-operatively

Left RLN palsy causing hoarseness can be a presenting feature of lung cancer (especially left hilar/mediastinal tumours compressing the nerve as it loops under the aortic arch) ^[5]. Also causes "bovine cough" (cough without explosive quality because cords can't adduct properly).

Advanced laryngeal cancer or bilateral cord palsy can cause upper airway obstruction requiring tracheostomy. This connects to GC 220 (Upper airway obstruction and tracheostomy).

Percentages are not universal and should not replace a side-specific search along the vagus/RLN course.