GC217 Facial Nerve Palsy And Salivary Gland Diseases
Facial nerve palsy is the loss of voluntary facial muscle movement due to dysfunction of cranial nerve VII, and salivary gland diseases encompass inflammatory, obstructive, and neoplastic conditions affecting the parotid, submandibular, and sublingual glands, often clinically linked because parotid pathology can compromise the facial nerve.
Facial Nerve Palsy and Salivary Gland Diseases
This GC 217 lecture by Dr. Stephanie Wong (HKU ENT) covers two major topics in a single deck: facial nerve paralysis and salivary gland diseases. These are classic ENT surgical topics that are heavily examined in both MCQ and SAQ formats. The lecture systematically walks through anatomy → causes → clinical assessment → investigations → treatment for both topics, and ends with parotidectomy complications.
Big ideas:
- The facial nerve has an extraordinarily long and complex course — understanding the anatomy is the key to localizing the lesion and predicting associated features.
- Salivary gland pathology spans infections, stones, and tumours — the "80/20 rules" for parotid tumours and sialolithiasis are classic exam facts.
- Parotidectomy is fundamentally a facial nerve dissection — its complications (especially Frey's syndrome) are high-yield.
How it fits into exams: Past papers have directly tested UMN vs LMN facial palsy, parotid tumour diagnosis, sialolithiasis radiology, and the anatomical branches of the facial nerve. This lecture integrates with GC 214 (ear diseases), GC 087 (hemiplegia/stroke), GC 192 (plastic/reconstructive surgery for facial reanimation), and neurology topics (CN VII examination).
Part 1: Facial Nerve Paralysis
1.1 Anatomy of the Facial Nerve (CN VII)
The facial nerve has a very complex course with an intimate relationship to the middle ear and parotid gland. It travels in a bony canal for a long distance. It divides into 3 parts: pre-temporal bone, intra-temporal bone, and post-temporal bone. [1]
Why this matters: The facial nerve is unique among cranial nerves because it runs through a rigid bony canal (the fallopian canal) for ~30 mm. Any swelling within this canal (e.g., Bell's palsy, herpes zoster) causes compression because there is no room to expand — this is the principle behind neuropraxia in the facial canal.
| Segment | Key landmarks | What travels with it |
|---|---|---|
| Pre-temporal bone (intracranial) | Motor cortex → pons → cerebellopontine angle (CPA) → internal acoustic meatus (IAM) | Nervus intermedius (sensory + parasympathetic) |
| Intra-temporal bone | IAM → geniculate ganglion → tympanic segment → mastoid segment | Greater superficial petrosal nerve (lacrimation), nerve to stapedius (stapedial reflex), chorda tympani (taste anterior 2/3 tongue + submandibular/sublingual secretion) |
| Post-temporal bone | Exits stylomastoid foramen → enters parotid gland → 5 terminal branches | Pure motor |
Post-temporal bone: Emerges from the stylomastoid foramen, pierces the parotid, gives 5 terminal branches: Frontal, Zygomatic, Buccal, Marginal mandibular, Cervical. [1]
Mnemonic: Terminal Branches
To Zanzibar By Motor Car = Temporal (Frontal), Zygomatic, Buccal, Marginal mandibular, Cervical. The lecture uses "Frontal" and "Temporal" interchangeably for the first branch.
Pes anserinus ("duck's foot"): The main trunk divides within the parotid into two main divisions — temporozygomatic and cervicofacial — before giving the 5 terminal branches. This is why the facial nerve divides the parotid into superficial and deep lobes (an anatomical relationship critical for parotidectomy). [1]
Arises from anterior border of parotid, 1.5 cm inferior to zygomatic arch and parallel to it, pierces buccinator next to the 2nd upper molar, 4–6 cm in length, 5 mm in diameter. [1]
1.2 Causes of Facial Nerve Palsy — Along Its Course
The lecture systematically organizes causes by anatomical location. This is exactly how exam questions are structured.
Supranuclear (UMN lesion): frontalis muscle spared. Commonest cause — CVA. [1]
Why frontalis is spared in UMN lesions: The upper face (frontalis, orbicularis oculi to some extent) receives bilateral cortical innervation — both left and right motor cortex send fibres to BOTH facial nuclei for the upper face. A unilateral cortical lesion therefore still allows the contralateral intact cortex to drive upper facial muscles. The lower face only gets contralateral cortical input, so it is weak.
Lesion in the facial nucleus (pons): tumour, demyelinating disease. [1]
A nuclear (pontine) lesion behaves like a LMN palsy because the cell bodies themselves are destroyed. Importantly, adjacent structures in the pons (CN VI nucleus, corticospinal tract) may also be involved → look for ipsilateral CN VI palsy + contralateral hemiplegia (Millard-Gubler syndrome). [3]
Tumour in IAM/CPA: acoustic neuroma, meningioma. Also temporal bone fracture and facial nerve schwannoma. [1]
- Acoustic neuroma (vestibular schwannoma) is the most common CPA tumour. It typically presents with unilateral sensorineural hearing loss and tinnitus before facial weakness develops (CN VIII is affected first because the tumour arises from the vestibular division of VIII).
- Temporal bone fractures: transverse fractures (perpendicular to petrous bone) are more likely to injure the facial nerve than longitudinal fractures, though longitudinal fractures are more common overall.
Acute otitis media, chronic otitis media — cholesteatoma, Herpes zoster oticus — Ramsay Hunt Syndrome, middle ear tumours (glomus, carcinoma), Bell's palsy — nerve swollen in the facial canal. [1]
Ramsay Hunt Syndrome — High Yield
Herpes zoster oticus (Ramsay Hunt Syndrome) is caused by VZV reactivation in the geniculate ganglion. Classic triad: ipsilateral facial nerve palsy + vesicular eruption in the ear (pinna/EAC/tympanic membrane) + otalgia. The lecture specifically warns that vesicles in herpes may not show up in the first 2 days — so antiviral should be started empirically if clinical suspicion is high. [1]
- Cholesteatoma: A destructive keratinized squamous epithelium in the middle ear that can erode the bony canal of the facial nerve, causing gradual onset facial palsy. This is a surgical emergency requiring mastoid surgery. [1]
Facial trauma (blunt or penetrating) — may only affect a single branch. Malignant tumour in parotid gland. Metastatic intraparotid lymph node. Surgical injury — common. [1]
Key clinical point: A parotid mass + facial nerve palsy = malignant until proven otherwise. Benign parotid tumours (e.g., pleomorphic adenoma) virtually never cause facial palsy because they push the nerve aside rather than invading it.
UMN — Frontalis spared (bilateral innervation). [1] Proximal to geniculate ganglion — decreased lacrimation and affects ipsilateral taste sensation. [1] Between geniculate ganglion and stylomastoid foramen — taste and lacrimation normal, hyperacusis present, stapedial reflex affected. [1] Beyond stylomastoid foramen — only facial movements affected, normal stapedial reflex. [1]
| Lesion Site | Lacrimation | Taste (ant 2/3) | Stapedial Reflex | Hyperacusis | Motor |
|---|---|---|---|---|---|
| UMN (cortex/subcortex) | Normal | Normal | Normal | No | Lower face contralateral |
| Proximal to geniculate ganglion (CPA/IAM) | ↓ (greater superficial petrosal nerve involved) | ↓ | Abnormal | Yes | Whole ipsilateral face |
| Between geniculate ganglion & stylomastoid foramen (tympanic/mastoid segment) | Normal (greater petrosal already branched off) | ↓ (chorda tympani involved) | Abnormal | Yes (stapedius nerve involved) | Whole ipsilateral face |
| Distal to chorda tympani but proximal to stylomastoid | Normal | Normal | Abnormal | Yes | Whole ipsilateral face |
| Beyond stylomastoid foramen | Normal | Normal | Normal | No | Whole ipsilateral face (or single branch only) |
Why this matters clinically: If a patient has facial palsy + hyperacusis + loss of taste → the lesion is in the facial canal (likely Bell's palsy or Ramsay Hunt). If only motor deficit with no other features → think post-stylomastoid (parotid tumour, trauma).
Usually test motor function only. Test all 5 branches in a systematic manner. Examine other CNs. Examine the external ear and middle ear. Palpate the parotids and the neck. [1]
Testing the 5 branches [1][3]:
- Temporal/Frontal: "Look up / raise your eyebrows" — tests frontalis
- Zygomatic: "Close your eyes tightly" — tests orbicularis oculi (try to open them)
- Buccal: "Puff out your cheeks" — tests buccinator
- Marginal mandibular: "Show your teeth / smile" — tests depressor anguli oris
- Cervical: "Clench your neck muscles" — tests platysma
House-Brackmann Grading System [1]:
Grading of facial paralysis severity [1]
| Grade | Description | Gross | At rest | Motion |
|---|---|---|---|---|
| I | Normal | Normal | Normal symmetry | Normal |
| II | Mild dysfunction | Slight weakness on close inspection | Normal symmetry | Forehead: moderate-good; Eye: complete closure with effort; Mouth: slight asymmetry |
| III | Moderate dysfunction | Obvious but not disfiguring | Normal symmetry | Forehead: slight-moderate; Eye: complete closure with effort; Mouth: slightly weak with max effort |
| IV | Moderately severe | Obvious weakness/disfiguring | Normal symmetry | Forehead: none; Eye: incomplete closure; Mouth: asymmetric with max effort |
| V | Severe | Only barely perceptible motion | Asymmetry | Forehead: none; Eye: incomplete closure; Mouth: slight movement |
| VI | Total paralysis | No movement | — | No movement |
Depends on clinical findings [1]:
| Clinical suspicion | Investigation |
|---|---|
| Intracranial lesion | MRI brain |
| Middle ear pathology | MRI/CT temporal bone |
| Temporal bone trauma | CT temporal bone |
| Parotid lesion | MRI/CT parotid + USG + FNA |
Electrophysiological Testing
For differentiating neuropraxia vs more severe nerve injury. For assessment of need for operative decompression. For assessment of prognosis. [1]
EMG (Electromyography):
Determines activity of the muscle itself. Needle electrode inserted into the muscle; recordings made during rest and voluntary contraction. Does not require comparison with normal side. [1]
- At rest: fibrillation potentials indicate denervation (appear ~14–21 days after injury)
- During voluntary contraction: motor unit potentials indicate intact innervation; polyphasic potentials suggest reinnervation
ENoG (Electroneurography):
Thought to be the most accurate electrodiagnostic test. Stimulate the facial nerve at the stylomastoid foramen; summation potential recorded in the nasal alar. Peak-to-peak amplitude is proportional to number of intact axons. The two sides are compared as a percentage. [1]
ENoG Critical Thresholds — Exam Favourite
≥90% degeneration → surgical decompression should be performed. < 90% degeneration within 3 weeks → predicts 80–100% spontaneous recovery. Disadvantages: discomfort, cost, test-retest variability. [1]
Why ENoG is useful: It compares the number of functioning axons on the affected side vs the normal side. If > 90% of fibres have degenerated, the remaining 10% cannot sustain adequate recovery, and surgical decompression is warranted. If < 90% have degenerated within 3 weeks, the nerve will likely recover on its own (neuropraxia predominates over axonotmesis/neurotmesis).
Idiopathic facial nerve palsy. Commonest cause of facial nerve palsy. ? Herpes reactivation neuritis. Nerve swollen in the facial nerve canal causing neuropraxia. > 90% good recovery. [1]
Pathophysiology: The leading theory is that HSV-1 reactivation in the geniculate ganglion causes inflammation and oedema of the nerve. Because the nerve runs through the rigid fallopian canal, swelling causes compression → conduction block (neuropraxia). This is why steroids (anti-inflammatory) are the mainstay treatment.
Diagnosis by exclusion. Physical exam to rule out other causes like CVA, parotid tumour, middle ear infection etc. [1]
Red Flag: No Improvement After 6 Weeks
Consider imaging if no improvement or deterioration after 6 weeks — this is a critical safety-net statement. If Bell's palsy doesn't improve, you must reconsider the diagnosis (possible parotid malignancy, CPA tumour, or other sinister cause). [1]
Management of Bell's Palsy:
Reduce swelling with steroids — prednisolone 1mg/kg/day in daily dose for 5 days then taper if no contraindications. [1] Antiviral — acyclovir or famciclovir for 5 days. Vesicles in herpes may not show up in first 2 days. [1] Eye protection and eye drops. [1] Facial nerve physiotherapy — maintain muscle tone and hasten recovery. [1] May progress in the first 3 weeks — warn patient. [1]
| Component | Details | Rationale |
|---|---|---|
| Steroids | Prednisolone 1 mg/kg/day × 5 days then taper | Reduce nerve oedema within the bony canal |
| Antivirals | Acyclovir 400mg 5×/day or Famciclovir × 5 days | Target possible HSV/VZV reactivation; start early even if no vesicles |
| Eye care | Lubricating drops (day), ointment/tape (night) | Prevent exposure keratopathy — the eye cannot close → corneal drying → ulceration |
| Physiotherapy | Facial exercises | Maintain muscle tone; prevent contracture |
| Counselling | May worsen in first 3 weeks; seek review if no improvement by 6 weeks | Patient reassurance + safety-netting |
Why eye protection is critical: With orbicularis oculi paralysis, the eye cannot blink or close fully (lagophthalmos). Bell's phenomenon (eye rolls upward when attempting to close) exposes the cornea to drying. Corneal ulceration can lead to permanent visual loss — this is an easily preventable complication.
Indications: traumatic cause, middle ear infection, iatrogenic injury (middle ear or parotid surgery). Bell's palsy — no proven benefits. Earlier the better. ENoG < 10% [i.e., ≥90% degeneration] as indication for decompression. Imaging for site of decompression. [1]
Important nuance: Surgical decompression for Bell's palsy remains controversial. The lecture states no proven benefits — this is the exam-safe answer. [1]
When the nerve is transected or a segment is resected (e.g., in parotid cancer surgery), reconstruction options include:
Primary anastomosis — only if tension-free. [1] Sural nerve or great auricular nerve grafting — for primary resection in parotid cancer or traumatic segment loss. [1] Facial-hypoglossal anastomosis — if grafting not feasible. [1] Cross facial nerve grafting — anastomosis of normal contralateral buccal branch to defective side. [1]
Surgery for Facial Reanimation:
| Procedure | Purpose | Details |
|---|---|---|
| Tarsorrhaphy | Corneal protection | Partial eyelid closure; poor cosmetic outcome [1] |
| Gold weight/Platinum chain implant | Dynamic eyelid closure | Implanted in upper eyelid; gravity-assisted closure [1] |
| Fascial sling | Aesthetic correction | Static sling to correct drooping mouth angle [1] |
| Muscle sling (temporalis) | Dynamic reanimation | Temporalis to angle of mouth; voluntary movement possible [1] |
| Free gracilis muscle flap | Dynamic reanimation | With neurovascular pedicle; cross-facial nerve graft provides motor input [1] |
Part 2: Salivary Gland Diseases
2.1 Anatomy of the Salivary Glands
Major salivary glands: 2 parotid, 2 submandibular, 2 sublingual. Minor salivary glands: hundreds — oral cavity, tongue base, larynx, nasopharynx. [1]
Boundaries — Superior: zygomatic arch; Posterior: EAC. 80% overlies masseter & mandible, 20% retromandibular. Posterior attaches to SCM and EAC. [1]
Superficial & deep lobe — divided by facial nerve. Imaginary lines on imaging: line from mandible to mastoid, medial to retromandibular vein. [1]
Key relationships:
- The facial nerve runs through the parotid, dividing it into superficial (lateral) and deep (medial) lobes
- Retromandibular vein is a radiological landmark for the division
- The external carotid artery also runs through the parotid
Stensen's Duct: arises from anterior border, 1.5 cm inferior to zygomatic arch (parallel), pierces buccinator next to 2nd upper molar, 4–6 cm length, 5 mm diameter. [1]
In the submandibular triangle. Gland wraps around the mylohyoid. Marginal mandibular branch of facial nerve is at risk. Capsule from superficial layer of deep cervical fascia. [1]
Wharton's duct: exits medial surface, between mylohyoid & hyoglossus, 5 cm in length. Lingual nerve and hypoglossal nerve are close relations. [1]
Why submandibular stones are so common: Wharton's duct is long (5 cm), runs upward against gravity, and has a narrow orifice. Submandibular saliva is more mucinous and alkaline than parotid saliva → more prone to calcium phosphate precipitation.
Between mandible & genioglossus. Lateral to submandibular duct. No capsule. Sialogram not possible (because there is no single duct to cannulate — it drains through multiple small ducts). [1]
600–1,000 glands. Simple ducts. Located in buccal, labial, palatal, lingual mucosa; also NP, larynx, hypopharynx. Tumour sites: palate, upper lip, buccal. [1]
Two common scenarios: (1) painless swelling, (2) pain (acute or intermittent). Rarer presentations: facial nerve palsy, metastatic LNs. [1]
Differentiate infection from neoplasm: Pain after a meal? Acute onset? Swelling persistent or intermittent? Symptoms of acute infection (fever, tenderness, pus)? [1]
Clinical pearl: Intermittent swelling that worsens with eating → sialolithiasis (stone causes obstruction → gland swells during salivation → resolves when saliva drains around the stone). Persistent, progressive swelling → neoplasm.
Physical Examination:
Is it really a parotid swelling? DDx: masseter hypertrophy, neck LN, lipoma, vascular malformation. [1] Is it really a submandibular swelling? DDx: submandibular LN, oral cavity mass extending into submandibular space — do intraoral examination. [1]
Inspection:
Inspect both sides. Don't miss a scar. Look for facial nerve palsy. Symmetrical swellings. [1] Intraoral: parotid duct opening, submandibular duct opening, floor of mouth swelling, tumour, pus from duct openings. [1]
Palpation:
Confirm lesion not arising from skin. Cannot easily differentiate submandibular LN from gland tumour. Palpate the ducts — for stones, express pus. [1]
Other examinations:
Complete H&N ENT examination. Facial nerve examination. Palpation of neck lymph nodes. Endoscopy of upper aerodigestive tract. [1]
Bimanual palpation technique [4]:
- Parotid: clench teeth to tighten masseter; feel behind masseter and in front of ear; palpate parotid duct intraorally opposite upper 2nd molar
- Submandibular: one gloved finger on floor of mouth beside tongue, other hand behind body of mandible
| Investigation | Key points from lecture |
|---|---|
| Ultrasound (first line) | Confirm origin of mass, enlarged neck LN, stones, dilated ducts [1] |
| Plain X-ray | 90% parotid stones radiolucent; 90% submandibular stones radio-opaque. Still can miss small stones. [1] |
| Sialogram | Useful for chronic sialolithiasis. Superseded by USG/sialoendoscopy. May flush out stones (therapeutic). [1] |
| CT scan / CT sialogram | Delineate deep vs superficial lobe tumour. Differentiate salivary swelling vs other pathologies. Enlarged LN. [1] |
| MRI | Best soft tissue differentiation. Still cannot image the facial nerve or lingual nerve. [1] |
| FNA | May not be totally accurate — 80% accuracy in differentiating benign vs malignant. Difficult in differentiating different pathologies. [1] |
| Biopsy | Trucut. Incisional biopsy — tumour spillage risk, only for minor salivary glands. Excisional biopsy = parotidectomy or submandibulectomy. [1] |
The 90% Radiology Rule — Classic Exam Fact
90% of parotid stones are radiolucent (not visible on plain X-ray). 90% of submandibular stones are radio-opaque (visible on plain X-ray). This is because submandibular stones are predominantly calcium phosphate, while parotid stones are more mucinous/organic. [1]
For malignant salivary gland tumour workup [1]:
USG (tumour vs inflammation, location, cervical LN), CT (bony invasion, cervical LN), MRI (accurate delineation, may see nerve invasion), PET-CT (distant metastasis workup). [1]
2.4 Salivary Gland Infections
Dehydrated infirm elderly. Tender swelling. Pus from duct opening. Staphylococcus aureus. Treatment: rehydration + IV antibiotics. [1]
Why dehydrated elderly? Dehydration → reduced salivary flow → stasis → bacterial colonization (retrograde via duct). Staph. aureus is the commonest organism. Classic clinical scenario: post-operative elderly patient who is NPO and dehydrated.
Commonest — mumps. Also Coxsackie, CMV, Influenza. Diagnosis by clinical and serology. [1]
- Mumps: bilateral parotid swelling, fever, tender. Now less common due to MMR vaccination.
Commonest caused by stones. Destruction of gland tissue after acute infection. Blockage of saliva drainage. Mild pain, worsened after meal. Recurrent parotid or submandibular swelling after meal. Can be caused by autoimmune disease — Sjögren syndrome. [1]
Investigations: USG/sialogram to rule out stones/masses; rule out Sjögren syndrome (anti-Ro, anti-La, Schirmer test, lip biopsy). [1][5]
Treatment:
Hydration. Sialogogues, massage, heat, antibiotics during acute attacks. Remove stones (exploration of submandibular duct or sialoendoscopy). Excision of the gland if refractory. [1]
80% submandibular gland, 20% parotid. Only 1 stone in 3/4 cases. 90% of submandibular stones radio-opaque; 90% of parotid stones radiolucent. [1] Presentation: recurrent swelling, pain worse with eating. [1] Complications: sialadenitis, ductal ectasia, and stricture. [1]
Treatment ladder:
Conservative — small stones may pass spontaneously. Transoral removal/excision. Sialoendoscopy and removal. Excision of gland — for proximal stone inaccessible by scope/transoral excision, recurrent stones, or multiple stones. [1]
Pseudoparotidomegaly (e.g., masseter hypertrophy). Bulimia nervosa. Alcoholic cirrhosis. DM. Hypothyroidism. Drugs (e.g., phenytoin). [1]
Why these conditions?
- Bulimia: recurrent vomiting → chronic parotid stimulation → hypertrophy (also seen in binge eating)
- Alcoholic cirrhosis: fatty infiltration of parotid; the enlarged parotid is a useful clinical sign in GI examination [4]
- DM/Hypothyroidism: fatty infiltration and sialosis
- Phenytoin: drug-induced glandular hypertrophy
2.7 Salivary Gland Neoplasms
Diverse histopathology. Relatively uncommon — 2% of head and neck neoplasms. [1]
Parotid: 80% of all salivary tumours; 80% benign; 80% are pleomorphic adenoma. Submandibular: 15% overall; 50% benign. Sublingual/Minor: 5% overall; 40% benign. [1]
The Smaller the Gland, the Higher the Malignancy Rate
This is a classic principle: parotid tumours are mostly benign (80%), but sublingual/minor salivary gland tumours are more likely malignant (60%). So a hard palate mass from a minor salivary gland should raise more suspicion for malignancy than a parotid lump.
Most common of all salivary gland neoplasms. 80% of parotid tumours, 50% of submandibular, 45% of minor salivary gland, 6% of sublingual. 4th–6th decades. F:M = 2:1. [1]
Slow-growing, painless mass. Parotid: 90% in superficial lobe, most in tail of gland. Minor salivary gland: lateral palate, submucosal mass. [1]
Malignant degeneration: 10–15% risk in 10 years. [1]
Why We Don't Simply Observe Pleomorphic Adenoma
Malignant degeneration risk of 10–15% over 10 years is the key reason for surgical excision. The longer a pleomorphic adenoma is left untreated, the higher the risk of transformation into carcinoma ex-pleomorphic adenoma — a very aggressive cancer. [1]
Treatment:
Complete surgical excision: parotidectomy with facial nerve preservation, submandibular gland excision, or wide local excision of minor salivary gland. Avoid enucleation and tumour spillage. Consider radiotherapy for recurrent tumour or spillage. [1]
Why not simple enucleation? Pleomorphic adenomas have pseudopods (irregular extensions) that extend beyond the visible capsule. Simple enucleation leaves behind microscopic tumour → high recurrence rate (up to 45%). Formal parotidectomy with a cuff of normal tissue minimizes recurrence to < 5%.
6–10% of parotid neoplasms. Older males 60–70 y.o. Smokers. Multifocal, 10% bilateral. Slow-growing, painless mass. Usually in tail of parotid. Soft cystic mass. [1]
Key exam discriminator: Warthin's is the only common bilateral parotid tumour. If a question describes a bilateral parotid mass in an elderly male smoker → Warthin's.
Most common salivary gland malignancy. 5–9% of salivary neoplasms. Parotid 45–70% of cases. 3rd–8th decades, peak 5th decade. F > M. [1]
Low-grade: slow growing, painless. High-grade: rapidly enlarging, ± pain. Minor salivary gland tumours may be mistaken as benign. Ulcerates in later stages. [1]
Treatment:
Influenced by site, stage, grade. Localized: excision of gland. Neck node metastasis: neck dissection. RT for high-grade, close margin, extraglandular spread. [1]
Overall 2nd most common malignancy. Most common in submandibular, sublingual and minor salivary glands. M = F. 5th decade. [1]
Presentation: asymptomatic enlarging mass. Pain, paraesthesia, facial weakness/paralysis. [1]
Adenoid Cystic Carcinoma — Perineural Invasion
Tendency for perineural invasion — this is the hallmark feature of adenoid cystic carcinoma. It tracks along nerve sheaths, can extend far beyond the visible tumour, and is the reason for:
- Pain/paraesthesia as presenting symptoms
- Possible facial nerve sacrifice during surgery
- High local recurrence (40%) even after apparent complete excision
- Indolent course: 5-year survival 75%, but 20-year survival only 13% [1]
Treatment: complete local excision ± facial nerve sacrifice + postoperative XRT. Distant metastasis common: lung. [1]
2nd most common parotid and pediatric malignancy. 5th decade. F > M. Bilateral 3%. Solitary, slow-growing, painless mass. Prognosis good: 5-year 82%, 10-year 68%, 25-year 50%. [1]
Malignant degeneration of pleomorphic adenoma. 6th–8th decades. Risk: 1.5% in first 5 years; 9.5% after 15 years. [1]
Presentation: longstanding painless mass that undergoes sudden enlargement. [1]
Exam pearl: Any patient with a long-standing parotid mass that suddenly grows rapidly → suspect carcinoma ex-pleomorphic adenoma. Treatment is radical excision + neck dissection + postop RT. Prognosis usually poor. [1]
Rare (1.6%). 7th–8th decades. M:F = 2:1. MUST RULE OUT: high-grade mucoepidermoid carcinoma, metastatic SCC to intraglandular lymph nodes (usually from scalp SCC), direct extension of skin SCC. [1]
Histology exactly like NPC. EBV-related (EBER+ve). May present as metastatic LN with unknown primary. Surgery + postop RT. Prognosis better than SCC and adenocarcinoma. [1]
HK context: This is important in Hong Kong because of the high prevalence of EBV-associated malignancies. The histological similarity to NPC means the pathologist must confirm the primary site.
| Tumour | Most common site | Key features | Malignancy? |
|---|---|---|---|
| Pleomorphic adenoma | Parotid (80%) | Slow, painless, tail of parotid, F > M | Benign; 10-15% malignant degeneration at 10y |
| Warthin's tumour | Parotid (tail) | Elderly male smoker, bilateral 10%, cystic | Benign |
| Mucoepidermoid CA | Parotid (45-70%) | Most common salivary malignancy, F > M | Malignant; low vs high grade |
| Adenoid cystic CA | Submandibular/minor | Perineural invasion, indolent but lethal | Malignant; lung mets common |
| Acinic cell CA | Parotid | 2nd most common parotid malignancy, good prognosis | Malignant (low grade) |
| CA ex-pleomorphic | Any (from prior PA) | Sudden enlargement of longstanding mass | Highly malignant |
| SCC | Parotid | Rule out metastatic SCC first | Malignant |
| Lymphoepithelial CA | Parotid | EBV+, like NPC histology | Malignant; better prognosis |
An exercise of facial nerve dissection. Excision of tumour with a cuff of normal parotid tissue. Excisional biopsy of parotid tumour = parotidectomy. Modified Blair's incision. [1]
Modified Blair's incision: Pre-auricular, curves under the earlobe, and extends into the neck along the anterior border of SCM — provides excellent access while hiding the scar.
Complications of Parotidectomy:
Early:
Bleeding/haematoma. Facial nerve palsy — transient ~5%, permanent ~1%. Wound infection. Salivary fistula. [1]
Late:
Recurrence. Frey's syndrome (gustatory sweating). Hypertrophic scar/keloid. Sunken parotid area (cosmetic problem). [1]
Frey's Syndrome — High Yield Exam Topic
Frey's syndrome (gustatory sweating) occurs after parotidectomy due to aberrant regeneration of parasympathetic secretomotor fibres (originally innervating salivary gland tissue via auriculotemporal nerve) into the cut sympathetic fibres supplying sweat glands and subcutaneous blood vessels in the overlying skin. When eating stimulates salivation, the misdirected parasympathetic impulses instead cause sweating and flushing of the facial skin over the parotid bed. [1][2]
Clinical test: Starch-iodine test (Minor's test) — apply iodine to the skin, dust with starch, then stimulate salivation (e.g., lemon juice). Sweating turns the starch purple/black.
Treatment: Antiperspirant, botulinum toxin injection, interposition of fascia or fat graft at surgery (to prevent aberrant regeneration).
Common Traps and Discriminators:
| Trap | Correct reasoning |
|---|---|
| Confusing UMN vs LMN facial palsy | UMN = forehead sparing (bilateral cortical innervation); LMN = whole face affected. The frontalis is the key. |
| Assuming all parotid tumours need biopsy before surgery | Incisional biopsy of parotid tumour → tumour spillage → contraindicated. Excisional biopsy = parotidectomy. FNA is acceptable but only 80% accurate. |
| Missing that painless parotid mass + facial palsy = malignancy | Benign tumours don't invade the nerve. Facial nerve involvement = malignant. |
| Forgetting 90% rule reversal | Parotid stones: 90% radiolucent. Submandibular stones: 90% radio-opaque. Students often reverse these. |
| Not knowing that "most common salivary malignancy" = mucoepidermoid CA | Adenoid cystic is 2nd most common overall but most common in submandibular/minor glands. |
| Thinking Bell's palsy benefits from surgical decompression | The lecture explicitly says no proven benefits for Bell's palsy. |
| Forgetting to rule out alternative diagnoses for SCC in parotid | Must exclude metastatic SCC (scalp), direct extension of skin SCC, and high-grade mucoepidermoid carcinoma. |
Past Paper Questions
Stem: "A 60-year-old gentleman who is a chronic smoker came to your clinic with a 5 cm right neck mass which has been there for 2 months."
- Q11: "He also has progressive hoarseness." → Most likely site: Carcinoma of the glottis (B) (hoarseness = vocal cord involvement)
- Q12: "He also has facial asymmetry." → Most likely site: Parotid gland cancer (H) (facial nerve palsy from parotid malignancy)
Rationale: Facial asymmetry + neck mass in the context of a parotid malignancy arises because malignant parotid tumours can invade the facial nerve (within the gland) and metastasize to cervical lymph nodes.
Q11: "Progressive enlarging parotid mass for 5 years without other symptoms in a 60-year-old lady" → Answer: J. Pleomorphic adenoma
Rationale: Slow-growing (5 years), painless, parotid mass, elderly female — classic pleomorphic adenoma. The key discriminator is the absence of pain, facial nerve involvement, or rapid growth (which would suggest malignancy).
"A 48-year-old woman developed right-sided facial weakness for over 24 hours. Which of the following features would MOST LIKELY be compatible with a diagnosis of lower motor neuron facial palsy on the right side?"
- A. Weakness of jaw closure on the right side
- B. Weakness of jaw opening on the right side
- C. Weakness with right eye closure ✓
- D. Weakness with right eye opening
Rationale: LMN facial palsy = entire ipsilateral face affected, including orbicularis oculi (eye closure). Options A and B relate to CN V (trigeminal — muscles of mastication), not CN VII. Option D (eye opening) is levator palpebrae superioris (CN III). The key discriminator is that eye closure = CN VII (zygomatic branch), while eye opening = CN III.
"A 42-year-old secretary had a sudden onset of facial asymmetry with inability to close her right eye and deviation of her mouth to the left side upon speaking and smiling. One day later, she was not able to lift up her left arm or hold things in her left hand, unable to stand/walk because of left leg weakness, slurred speech, choked upon drinking water."
- (a) Neurological deficits: Right LMN facial nerve palsy (inability to close right eye = whole face), left hemiparesis, dysarthria, dysphagia
- (b) Lesion site: Right pons (ipsilateral LMN CN VII + contralateral hemiplegia = alternating hemiplegia pattern, e.g., Millard-Gubler or Foville syndrome)
- (c) Reflexes: Hyperreflexia on left side; left upgoing plantar (Babinski positive)
Rationale: This is a classic brainstem stroke question. The right LMN facial palsy (note: cannot close the eye = entire face affected, not UMN pattern) localizes to the right pons. The contralateral (left) hemiplegia is from corticospinal tract involvement at the pons before decussation. Dysarthria and dysphagia suggest additional bulbar involvement.
"Mr. Chow presented with weakness and numbness of right face as well as weakness and numbness of left arm and left leg... Where is the lesion MOST LIKELY located?" Answer: A. Brainstem
Rationale: Right facial weakness/numbness (ipsilateral CN V and VII) + contralateral limb weakness = crossed/alternating signs = brainstem lesion. This is the hallmark of brainstem pathology.
For "Autoimmune myasthenia gravis" → Answer: A. Facial asymmetry on smiling (fatigable weakness of facial muscles, including buccal/marginal mandibular branches)
Discriminator: MG causes fatigable weakness, often affecting facial muscles (myasthenic snarl). This is muscular-level pathology, not a CN VII nerve lesion per se, but presents with facial weakness.
High Yield Summary
Facial Nerve Palsy:
- UMN = frontalis spared (bilateral cortical innervation); LMN = whole face. CVA is commonest UMN cause.
- Localize by associated features: lacrimation, taste, stapedial reflex, hyperacusis.
- Bell's palsy: commonest overall cause, diagnosis of exclusion, >90% recovery, treat with prednisolone 1mg/kg × 5d + antiviral + eye care + physio. NO proven benefit from surgical decompression.
- Red flag: no improvement at 6 weeks → image to exclude sinister pathology.
- ENoG: ≥90% degeneration → consider surgical decompression (NOT for Bell's).
- Ramsay Hunt = VZV + facial palsy + ear vesicles (vesicles may lag by 2 days).
- Parotid mass + facial palsy = malignant until proven otherwise.
Salivary Gland Diseases:
- The 80/20 rules: 80% salivary tumours in parotid; 80% of parotid tumours benign; 80% of benign parotid tumours are pleomorphic adenoma.
- Smaller gland = higher malignancy rate.
- Sialolithiasis: 80% submandibular, 90% radio-opaque; parotid stones 90% radiolucent.
- Pleomorphic adenoma: excise (don't enucleate); 10–15% malignant degeneration risk at 10y.
- Mucoepidermoid CA = most common salivary malignancy; Adenoid cystic CA = perineural invasion, lung mets, indolent but lethal.
- Parotidectomy complications: facial nerve palsy (transient 5%, permanent 1%), Frey's syndrome (gustatory sweating from aberrant parasympathetic reinnervation of sweat glands).
Active Recall - Facial Nerve Palsy and Salivary Gland Diseases
[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf [2] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (ENT Diseases — Salivary gland tumour, p.235) [3] Senior notes: Ryan Ho Neurology.pdf (CN VII, pp.19–20) [4] Senior notes: Ryan Ho GI.pdf (Salivary glands examination, p.9) [5] Senior notes: Maksim Medicine Notes.pdf (Sjogren's syndrome, p.322) [6] Past papers: 2019 Fourth Summative MCQ.pdf (EMQ Q11–12, p.7) [7] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (EMQ Q11, p.37) [8] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Q39, p.15) [9] Past papers: 2025 Fourth Summative SAQ.pdf (Q1, p.3) [10] Past papers: 2024 Fourth Summative MCQ.pdf (Q9, p.4) [11] Past papers: 2022 Fourth Summative MCQ.pdf (EMQ Q5, p.35)
GC216 Dysphonia Laryngitis, Voice Abuse, Tumour And Laryngeal Cancer
Dysphonia is an alteration in voice quality resulting from conditions such as laryngitis, vocal misuse or overuse, benign laryngeal lesions, or laryngeal carcinoma that affect vocal fold structure or function.
GC218 I Have A Swelling In The Neck Neck Mass
A neck mass is an abnormal lump or swelling in the neck that may arise from enlarged lymph nodes, thyroid pathology, salivary gland disorders, congenital cysts, or neoplastic processes requiring systematic evaluation based on patient age, location, and duration.