ENT JC101: Facial Nerve Palsy And Salivary Gland Diseases Flashcards
Revision: CN7 anatomy
- Complex course
- Intimate relationship to middle ear + parotid gland
- Travel in a bony canal for a long distance
3 parts (Temporal bone as landmark):
1. Pre-temporal part
- just before Internal acoustic meatus / Geniculate ganglion
- 1st branch: ***Greater petrosal nerve
- Intra-temporal part
- Geniculate ganglion —> Stylomastoid foramen
- 2nd branch: ***Chorda tympani - Post-temporal part
- Exit Stylomastoid foramen —> pierce Parotid gland
- 5 terminal branches (Pes anserinus: 鴨腳) (or Upper / Lower trunk):
—> Temporal (Frontalis)
—> Zygomatic (Orbicularis oculi)
—> Buccal (upper / lower trunk) (Buccinator)
—> Marginal mandibular (Levator anguli oris)
—> Cervical (Platysma)
Causes of CN7 palsy
Intracerebral / Pre-temporal:
1. Supranuclear
- UMN lesion
- Frontalis muscle spared (∵ bilateral innervation)
- Cause: CVA (commonest)
- Lesion in Facial nucleus (rare)
- Lesion in ***Pons
- LMN (can be UMN depend on how much nucleus is involved)
- Cause: CVA, tumour, demyelinating disease
Intra-temporal / Temporal bone:
1. Tumour in Internal acoustic meatus / Cerebellopontine angle
- Acoustic neuroma
- Meningioma
—> usually slow growing, not cause palsy until tumour very big
—> usually cerebellar signs first
- Temporal bone fracture (common in head injury)
Middle ear (Facial nerve canal: normally a bony canal, 10% population do not have bone —> Facial nerve dehiscence —> CN7 only covered by mucosa in middle ear):
1. Acute otitis media
2. Chronic otitis media (Cholesteatoma: pressure effect / inflammation)
3. Bell’s palsy (CN7 neuritis, nerve swollen in rigid canal —> neuropraxia)
4. Herpes zoster oticus (Ramsay Hunt syndrome) vs Herpes zoster ophthalmicus (involve trigeminal ganglion: Hutchinson’s sign)
5. Tumour in middle ear (Glomus, carcinoma)
Post-temporal (beyond Stylomastoid foramen):
1. Facial trauma (blunt / penetrating) (may only affect a single branch)
2. Tumour in parotid gland (Malignant, benign will NOT cause palsy ∵ slow-growing)
3. Metastatic intraparotid LN (rare, very common in Australia ∵ skin cancer)
Other causes:
1. Facial nerve schwannoma / neurofibroma (tumour in CN7 itself)
2. Surgical injury (common)
3. CNS demyelinating disease (rare, usually accompanied by other CN palsy / neurological signs)
Location of lesion
- UMN lesion
- ***Frontalis spared - Proximal to Geniculate ganglion
- ***↓ in Lacrimation + Ipsilateral taste - Between Geniculate ganglion and Stylomastoid foramen
- Lacrimation + Taste normal
- ***Hyperacusis present (∵ Stapedial reflex affected) - Beyond Stylomastoid foramen
- Lacrimation + Taste normal
- Stapedial reflex normal
- ***Only facial movements affected
P/E of CN7
- Usually test motor function only
- Test all 5 branches systemically
- Examine other CN (∵ mostly polyneuropathies)
- Examine external + ***middle ear (exclude Otitis media, Zoster, Cholesteatoma etc.)
- Palpate ***parotids + neck (for any lesions)
House and Brackmann facial paralysis grading system:
- Grade degree of CN7 palsy
- Grade 1-6 (6 most severe)
Investigations for CN7 palsy
Depends on clinical findings
- Bell’s palsy (commonest) —> Diagnosis of exclusion
- mostly clinical diagnosis + recover on its own
- MRI brain
- for suspected intracranial lesion / parotid lesion - MRI / CT temporal bone
- if middle ear pathology suspected - CT temporal bone
- if suspect temporal bone trauma (e.g. temporal bone fracture, Cholesteatoma)
—> can look at bony canal whether damaged - MRI / CT parotid + USG FNAC
- if parotid lesion suspected - Electrophysiological testing
- to differentiate neuropraxia (just stretched, will recover) vs more severe nerve injury (e.g. axonotmesis, neurotmesis)
- to assess need for operative decompression / anastomosis
- to assess prognosis - Electromyography (EMG)
- determines activity of muscle itself
- NOT require comparison with normal side
- not very useful, only used to predict recovery -
**Electroneurography (ENoG)
- most accurate of electrodiagnostic tests
- maximum stimulus to CN7 at Stylomastoid foramen (↑ stimulation until response cannot go bigger)
—> **summation potential recorded in nasal alar
—> **peak to peak amplitude is proportional to no. of intact axons
—> 2 sides are compared as % of response
- **90% degeneration (i.e. damage is more than neuropraxia) —> Surgical decompression should be done
- ***<90% degeneration within 3 weeks —> predict 80-100% spontaneous recovery
- disadvantage: discomfort, cost, test-retest variability
Treatment of CN7 palsy
- Identify cause
- cancer: remove cancer
- Bell’s palsy: steroid - Removal of causative agent
- e.g. mastoid surgery to remove Cholesteatoma - Consider nerve exploration + surgical decompression in ***traumatic cause with immediate complete palsy
- if delayed palsy after injury —> more likely due to swelling of nerve rather than transection —> observe - Other surgical options
- **Facial nerve grafting
- **Surgery for facial animation
—> Tarsorrhaphy
—> Gold weight implant to eyelid
—> Facial sling
—> Muscle sling
Bell’s palsy
- Idiopathic CN7 palsy
- Commonest cause of CN7 palsy
- Now identified as ***Herpes reactivation neuritis (Herpes virus reactivating at Geniculate ganglion —> neuritis)
- Nerve swollen in rigid facial canal —> Neuropraxia
- > 90% good recovery
Management:
- Diagnosis by **exclusion
- P/E to rule out other causes e.g. CVA, Parotid tumour, Middle ear infection etc.
- May progress in first 3 weeks —> warn patient (∵ degeneration comes first in 1-2 weeks before recovery)
- Consider imaging if no improvement / deterioration after **6 weeks
—> if imaging on 1st day
—> will show up very swollen CN7, contrast enhancing
—> can be mistaken as tumour
Treatment:
1. ***Steroid (Prednisolone)
- to reduce swelling
- 1 mg/kg/day in divided dose for 7-14 days if no CI
- Antiviral (Aciclovir / Famciclovir for 5 days)
- vesicles in herpes (Ramsay Hunt syndrome) may not show up in first 2 days of palsy
- only useful when given early - Eye protection / Eye drops
- prevent exposure keratitis - CN7 physiotherapy
- maintain muscle tone + hasten recovery
- prevent disuse atrophy - Consider other causes if no improvement after 6 weeks
Surgical decompression of nerve
Indications:
1. Traumatic cause
2. Middle ear infection
3. Iatrogenic injury (middle ear / parotid surgery)
- Earlier the better (within 2 weeks)
- Electrical testing as indication for decompression: ***ENoG of affected side <10% of normal side
- Imaging for site of decompression
- Bell’s palsy: No proven benefit
Facial nerve grafting
- Primary anastomosis (將斷開兩邊駁埋)
- only if tension free -
**Sural nerve / **Great auricular nerve grafting
- after primary resection of CN7 in parotid cancer
- damage of a segment of nerve in traumatic cases - ***Facial-Hypoglossal anastomosis
- if grafting not feasible
- train patient to move tongue in order to move face - ***Cross (Contralateral) facial nerve grafting
- anastomosis of normal contralateral buccal branch to the defective side
- also avoid disuse atrophy - Neurovascular free-muscle transfer
- free ***gracilis muscle flap together with neurovascular bundle
- put it on face
- reanatomose artery + vein
- reanatomose nerve to contralateral buccal nerve
- only for chronic facial palsy where nerve is not salvageable
Surgery for facial animation
- Tarsorrhaphy
- partial closure of eyelid
- for corneal protection
- but poor cosmetic outcome - Gold weight implant to eyelid
- gold: inert + heavy - Facial sling
- static sling to correct drooping of angle of mouth
- aesthetic correct - Muscle sling
- suture **temporalis muscle to angle of mouth, can have voluntary movement
- free **gracilis muscle graft with neurovascular bundle
Revision: Salivary gland anatomy
Major salivary glands:
- Parotid x2
- Submandibular x2
- Sublingual x2
Minor salivary glands:
- Hundreds
- Oral cavity, Tongue base, Larynx, Trachea, NP
i.e. Cancer can occur anywhere along upper aerodigestive tract
Revision: Parotid gland anatomy
Boundary:
- Superior boundary: Zygomatic arch
- Posterior boundary: EAC
- can extend anterior / inferiorly (esp. in elderly) but never posteriorly / superiorly
- Tail of Parotid: Posteriorly can attach on SCM (can extend posteriorly to cover nearly whole SCM)
Location:
- 80% overlies Masseter + Mandible
- 20% Retromandibular
- Posterior attaches on SCM + EAC
Parts:
- Superficial + Deep lobe
—> divided by CN7 (NO true capsule as landmark)
—> only an imaginary line
—> CT: drawn from Mandible to Mastoid
—> MRI: deep lobe: medial to Retromandibular vein
**Stensen’s duct (Parotid duct):
- arise from anterior border
- **1.5cm inferior to zygomatic arch, parallel
- opening: pierces Buccinator at ***2nd upper molar
- length: 4-6 cm
- diameter: 5 mm
Revision: Submandibular gland anatomy
- “Submaxilla”
- Submandibular triangle
- Has a true capsule: from superficial layer of Deep cervical fascia
- Gland wraps around ***Mylohyoid (FOM) —> a real physical boundary
- 3 nerves close in proximity
—> **Marginal mandibular nerve (CN7)
—> between superficial + deep lobe: **Lingual nerve + ***Hypoglossal nerve (inferior + deep to Hyoglossus muscle)
**Wharton’s duct:
- exits medial surface (just lateral to frenulum) at FOM
- **between Mylohyoid + Hyoglossus
- length: 5 cm
- wraps around Lingual nerve
Revision: Sublingual gland
- Between Mandible + Genioglossus
- Lateral to submandibular duct
- No capsule —> Sialogram not possible
- No true duct (multiple ducts)
Revision: Minor salivary glands
- 600-1000
- Simple ducts
- Buccal, Labial, Palatal, Lingual
- NP, Larynx, Hypopharynx
- Tumour sites: Palate, Upper lip, Cheek
History taking of Salivary gland diseases
2 common scenarios (Inflammation / Neoplastic):
1. Pain (acute / intermittent)
2. Painless swelling
Differentiate between inflammation / neoplastic:
1. Pain (after a meal?)
2. Swelling (persistent / progressive / intermittent?)
3. Presence of symptoms of ***acute infection (fever, tenderness, pus)
Rarer presentations:
- CN7 palsy
- Metastatic LNs
***P/E of Salivary gland diseases
- Confirm genuine Parotid swelling —> P/E + USG
- Masseter hypertrophy
- Neck LN
- Lipoma, Vascular malformations - Confirm genuine Submandibular gland swelling —> P/E + USG
- Enlarged submandibular LN (**very hard to differentiate)
- Oral cavity mass (e.g. tongue cancer) with direct extension to submandibular space: **Intraoral examination
- Stones: Bimanual palpation (sometimes can feel stone within submandibular duct)
Inspection:
1. Both sides
2. Scar
3. CN7 (esp. sometimes subtle palsy in parotid cancer)
4. **Symmetrical swellings (e.g. can be **Sjögren’s syndrome)
5. Intraoral
- **Duct openings: Parotid duct, Submandibular duct, Pus
- **FOM swelling
- Tumour in FOM / Oral cavity —> Deviation of tonsils
Palpation:
1. Confirm lesion not arising from skin (e.g. sebaceous cyst)
2. Difficult to differentiate submandibular LN / gland —> USG
3. Difficult to ascertain mass is a parotid tumour —> USG
4. Palpate ducts
- Stones
- Express pus
Other examinations:
1. Complete HN ENT examination
2. **CN7 examination
3. Palpation of neck **LN
4. Endoscopy of upper ***aerodigestive tract
Investigations of Salivary gland diseases
-
**USG (1st line)
- confirm **origin of mass
- detect enlarged neck LN / stones / dilated ducts - Plain X-ray (obsolete)
- ***90% parotid stones radiolucent
- 90% submandibular stones radio-opaque
- still can miss small stones -
**Sialogram
- injection of dye into duct
- useful for **chronic sialolithiasis
- superseded by USG / ***Sialoendoscopy
- cannulation of duct may be difficult
- may be therapeutic: may flush out stones / debris - CT scan / CT sialogram (obsolete)
- poor soft tissue differentiation
- delineate deep lobe vs superficial lobe tumour
- differentiate salivary gland swelling vs other pathologies
- also can show enlarged LN - ***MRI
- best soft tissue differentiation —> e.g. lesion extension to other space
- multiple planes of imaging
- still cannot see CN7 / Lingual nerve - ***FNA
- may not be totally accurate in differentiating benign + malignant lesions (80%)
- difficult in differentiating different pathologies (i.e. exact histology of tumour) -
**Biopsy
- Trucut: may not have enough tissue
- Incisional: **not recommended, **tumour spillage, for minor salivary glands only
- **Excisional: Parotidectomy, Submandibulectomy
Conclusion: FNAC first —> then Excisional biopsy (other biopsy not recommended)
Infection of Salivary glands
- Acute parotitis
- bacterial infection of gland: **Staphylococcus aureus
- **dehydrated infirmed elderly —> reduced salivary flow —> blocked duct + poor oral hygiene —> infection
- tender + swelling + pus from duct opening
- treatment: rehydration (reestablish salivary flow) + IV antibiotics - Viral infection
- Mumps (commonest) (affect all **exocrine glands: pancreas, submandibular, parotid, testes)
- Coxsackie virus
- CMV
- Influenza
- high fever + **symmetrical swelling on both sides
- diagnosis by **clinical + **serology - Chronic sialoadenitis
- chronic inflammation of gland
- caused by **stones (commonest) / **recurrent infection
- can be caused by **autoimmune diseases (e.g. Sjögren’s syndrome)
- **destruction of gland tissue —> blockage of saliva —> stasis + repeated infection
- mild pain, worsen after meal
- recurrent swelling (parotid / submandibular) after meal
- investigations:
—> Clinical
—> Blood test to rule out Sjögren’s syndrome
—> Sialogram to rule out stones
—> USG for status of gland (destroyed or not)
Treatment of Sialoadenitis
Conservative:
1. Hydration
2. Sialogogues, Massage, Heat
3. Antibiotics during acute attacks
Definitive:
4. Remove stones
- exploration of submandibular duct
- Sialoendoscopy (superceded Sialogram)
- Excision of gland
Sialolithiasis
- 80% ***submandibular, 20% parotid
- only 1 stone in 75% cases
- 90% parotid stones radiolucent, 90% submandibular stones radio-opaque (∵ more mucous, higher Ca content)
Presentation:
- **Recurrent swelling
- **Pain worse with eating
Complications:
1. Sialoadenitis
2. Ductal ectasia
3. Stricture
Treatment:
1. **Conservative: small stones pass by themselves (hydration, pro-secretory food e.g. sour food)
2. Transoral removal / excision
3. **Sialoendoscopy + removal
4. ***Excision of gland
- Proximal stone (inaccessible by scope / transoral excision)
- Recurrent stones
- Multiple stones
Sjögren’s syndrome
- Autoimmune disease attacking exocrine gland
- ***Lymphocyte mediated destruction of salivary + lacrimal gland
- Parotid gland: largest HN exocrine gland (usually swollen)
Presentation:
- F>M
- usually in 3rd/4th decade
- **Keratoconjunctivitis sicca (dry eyes)
- **Xerostomia (dry mouth)
- Diffuse, tender enlargement of parotid + submandibular glands (with fluctuations)
- Injected cornea, conjunctivitis
- Features of other associated autoimmune diseases e.g. Fatigue, Low grade fever
Types:
1. Primary Sjögren’s syndrome
- not associated with other autoimmune diseases
- Secondary Sjögren’s syndrome
- associated with other autoimmune diseases e.g. RA, SLE
Serology (~ pattern to **SLE):
1. ANA (50-80%)
2. RF (75%)
3. **Anti-Ro/SSA Ab (up to 90%)
4. ***Anti-La/SSB Ab (up to 90%)
Diagnosis:
1. ↑ ESR, CRP (during acute phase)
2. Anti-Ro/SSA Ab + Anti-La/SSB Ab
3. Biopsy of sub-labial minor salivary glands (diagnostic)
- gland destruction with lymphocyte infiltration
Treatment:
- Rheumatologist: Steroid, Treat underlying causes
- Artificial saliva, adequate hydration
- Eye drops (for dry eyes)
- Monitor for **Lymphoma (44x ↑ risk) in parotid / submandibular gland (∵ chronic lymphocytic inflammation)
—> **non-symmetrical parotid / submandibular swelling warrants FNAC / biopsy!!!
Other non-neoplastic diseases
- Sarcoidosis (Heerfordt syndrome)
- Benign lymphoepithelial lesions
- associated with immunosuppression e.g. HIV, transplant patients - Cysts
- congenital / acquired
***Causes of Bilateral parotid enlargement
- ***Pseudoparotidmegaly
- e.g. bruxism (磨牙), masseter hypertrophy - Bulimia nervosa (binge eating then purging)
- repeated vomiting - ***Alcoholic cirrhosis
- DM
- Drugs e.g. phenytoin
- ***Sjögren’s syndrome
- ***Warthin’s tumour
Salivary gland neoplasms
- Diverse histopathology
- Relatively uncommon (2% of HN neoplasms)
Distribution:
- Parotid: 80% overall, 80% benign, 80% pleomorphic adenoma (記: 80 80 80)
- Submandibular: 15% overall, 50% benign
- Sublingual / Minor: 5% overall, 40% benign
(***記: smaller size of gland —> higher chance of malignancy)
Pleomorphic adenoma
Most common of all salivary gland neoplasms
- 80% parotid tumours
- 50% submandibular tumours
- 45% minor salivary gland tumours
- 6% sublingual tumours
Epidemiology:
- 4-6th decade
- F:M = 3-4:1
Presentation:
- **Slow-growing, painless mass
- Parotid: 90% superficial lobe, mostly in **tail of gland
- Minor salivary gland: lateral palatal / submucosal mass
- ***malignant transformation 10-15% risk in 10 years
Treatment:
1. Complete surgical excision
- Parotidectomy with CN7 preservation
- Submandibular gland excision
- Wide local excision of minor salivary gland
- Avoid enucleation + tumour spillage
—> high risk of seeding —> take it out ***without rupture capsule!!!
- RT
- consider for recurrent tumour / prevention of recurrence in case of spillage
Warthin’s tumour
Aka Papillary cystadenoma lymphomatosum
- tumour arise from ***intraparotid LN
- 6-10% parotid neoplasms
- older males 60-70
- smokers
Presentation:
- Slow-growing, painless mass
- **Soft cystic mass
- Multifocal, 10% bilateral, usually in **tail of parotid
- Not cause CN7 palsy / malignant transformation
Other benign tumours of Salivary glands
- Oncocytoma
- Monomorphic adenoma
- Basal cell adenoma
- Myoepithelioma
***Mucoepidermoid carcinoma
- most common salivary gland malignancy
- ***mucoepidermoid: mucus secreting component + squamous component
- 5-9% salivary neoplasms
- parotid 45-70% cases
- palate 18%
- peak in 5th decade (30-80)
- F>M
Presentation:
- Low-grade: Slow-growing, painless mass (~Pleomorphic adenoma)
- High-grade: Rapidly enlarging +/- Pain
- ***Minor salivary glands: may be mistaken for benign / inflammatory process (ulcerates in later stages)
Treatment:
- depend on Site, Stage, Grade
1. Localised to gland —> Excision
2. Neck node metastasis —> Neck dissection
3. RT for high grade tumour, close margin, extraglandular spread
Adenoid cystic carcinoma
2nd most common malignancy
- Most common in ***submandibular, sublingual, minor salivary glands
- M=F
- 5th decade
Presentation:
- Asymptomatic enlarging mass
- ***Propensity to invade nerve: Pain (great auricular nerve), Paresthesia, Facial weakness / paralysis, Tongue paralysis / numbness
Treatment:
1. Complete local excision
2. CN7 sacrifice? (∵ tendency for perineural invasion)
3. Post-op RT (for perineural invasion esp. to skull base)
Prognosis:
- ***Local recurrence: 42% (high ∵ spread far away along nerve)
- Distant metastasis common: Lung
- Indolent course: 75% 5-year survival, 13% 20-year survival (∵ slow-growing)
Acinic cell carcinoma
- 2nd most common parotid + ***paediatric malignancy
- rather low-grade tumour
- 5th decade
- F>M
- Bilateral parotid disease in 3%
Presentation:
- Solitary, slow-growing, often painless mass
- usually NO nerve palsy
Treatment:
1. Complete local excision
2. +/- Post-op RT
Prognosis (Good):
- 5-year survival: 82%
- 10-year survival: 68%
- 20-year survival: 50%
Carcinoma ex-pleomorphic adenoma
- Malignant transformation of Pleomorphic adenoma (1.5% first 5 years, 10% after 15 years)
- Rare cancer
- 6-8th decade
Presentation:
- **Longstanding painless mass (Pleomorphic adenoma) that undergoes **sudden enlargement (Carcinoma ex-pleomorphic adenoma)
- Benign tumour suddenly becomes very aggressive
Gross pathology:
- Poorly circumscribed
- Infiltrative, Very aggressive
- Haemorrhage + necrosis
Treatment:
1. Radical excision
2. Neck dissection (usually needed, 25% with LN involvement at presentation)
3. Post-op RT
Prognosis (not good):
- Dependent upon stage + histology
- ∵ complete excision usually not possible at presentation
Squamous cell carcinoma
- Rare (1.6% of all salivary gland neoplasms)
- 7-8th decade
- M:F = 2:1
Must rule out:
1. High-grade mucoepidermoid carcinoma (squamous differentiation, need to look for mucoid differentiation as well)
2. ***Metastatic SCC of skin cancer to intraglandular LN, usually from scalp SCC
3. Direct extension of skin SCC
Undifferentiated carcinoma / Lymphoepithelial carcinoma (LELC)
- Histopathology ***exactly like NPC
- ***EBV related (tumour cells EBER +ve)
Presentation:
- Metastatic LN, unknown primary
Treatment:
- Surgery + Post-op RT (to primary site + neck)
Prognosis:
- better than SCC, adenocarcinoma
Investigations of Parotid mass
- History
- tumour vs inflammation - P/E
- parotid / submandibular mass vs other structures -
**USG
- **tumour vs inflammation
- **stones
- location of tumour
- **lymphadenopathy
- malignant vs benign (not always accurate) - Sialogram
- only for stones / sialoadenitis, most replaced by USG
- may be therapeutic - CT scan
- good for inflammatory disease - MRI
- better for tumour, accurate delineation of extent of invasion
- still cannot see nerve invasion
- differentiate other pathologies e.g. CN7 schwannoma - FNAC
- not totally accurate
- guideline only, not for sole decision making
- prepare patient better (e.g. if positive FNAC —> neck dissection)
Parotidectomy
- Excision of CN7
- Excision of tumour with a cuff of normal parotid tissue
- Excisional biopsy of parotid tumour
Modified Blair’s incision (aka Lazy S incision)
Complications:
Early:
1. Bleeding / haematoma
2. **CN7 palsy
- transient ~5%, permanent ~1%
3. Wound infection
4. **Salivary fistula
Late:
1. Recurrence
2. Frey’s syndrome (Gustatory sweating) —> sweating of parotid area during eating (∵ parasympathetic nerve of parotid area cannot innervate parotid since gone —> grow into skin —> innervate sweat gland)
3. Hypertrophic scar / Keloid
4. Sunken parotid area, cosmetic problem
Submandibulectomy
Complications:
Early:
1. Bleeding / haematoma
2. Nerve injury
- **Marginal mandibular nerve
- **Lingual nerve
- ***Hypoglossal nerve
3. Salivary fistula (rare)
4. Wound infection / abscess
- accidental breach of FOM mucosa
Late:
1. Permanent nerve damage
2. Hypertrophic scar / keloid
3. Frey’s syndrome (very rare as whole gland is excised + nerve ligated)
4. Recurrence
***Summary of Salivary gland diseases
Infection:
1. Acute parotitis
2. Viral infection (e.g. Mumps, Coxsackie virus, CMV, Influenza)
3. Chronic sialoadenitis
4. Sialoadenitis
Stones:
1. Sialolithiasis
Autoimmune:
1. Sjögren’s syndrome (Primary / Secondary)
Other diseases:
1. Sarcoidosis (Heerfordt syndrome)
2. Benign lymphoepithelial lesions
3. Cysts (congenital / acquired)
***Neoplasms:
Benign:
1. Pleomorphic adenoma
2. Warthin’s tumour
3. Oncocytoma
4. Monomorphic adenoma
5. Basal cell adenoma
6. Myoepithelioma
Malignant:
1. Mucoepidermoid carcinoma
2. Adenoid cystic carcinoma
3. Acinic cell carcinoma
4. Carcinoma ex-pleomorphic adenoma
5. Squamous cell carcinoma
6. Undifferentiated carcinoma / Lymphoepithelial carcinoma (LELC)
