JC101 (ENT) - Facial nerve palsy and salivary gland diseases Flashcards
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Three anatomical divisions and branches of the facial nerve
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Effectors innervated by the facial nerve
From intra-temporal facial nerve:
- Lacrimal gland, nasal and palatine mucosal gland
- Stapedius muscle (together with V3)
- Anterior 2/3 of tongue:
o Sensation: lingual nerve (V3)
o Taste, secretomotor: chorda tympani
- Submandibular ganglion: submandibular gland, sublingual gland
From post-temporal facial nerve: after stylomastoid foramen and through posteromedial parotid gland:
1) Temporal/ frontal - Frontalis
2) Zygomatic - orbicularis oculi muscle
3) Buccal - Buccinators
4) Marginal mandibular - depressor anguli oris, the depressor labii inferioris, the inferior fibers of the orbicularis oris and the mentalis muscles (2-4)
5) Cervical - Platysma
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5 possible locations of facial nerve palsy
Intracerebral:
- Supranuclear/ UMN lesion
- Facial nucleus, pons/ LMN lesion
Temporal bone:
- Temporal bone fracture
- Internal acoustic meatus/ cerebellopontine angle
Middle ear lesions - beyond geniculate ganglion
Post-temporal bone/ beyond stylomastoid foramen:
- Facial trauma
- Malignant parotid gland tumor
- Metastatic intracarotid LN
Lesion on nerve itself
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Intracerebral lesions that cause facial nerve palsy
Sequelae
- Supranuclear (lesion proximal to facial nucleus):
- UMN lesion
- Commonest cause = CVA
- Frontalis muscle spared (bilateral innervation) - Lesion in the facial nucleus, pons (rare):
- LMN lesion (sometimes UMN depending on how much of the facial nucleus is involved)
- E.g. CVA, tumour, demyelinating disease
- All effectors affected: Lacrimation, ipsilateral taste, facial movement
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Temporal bone lesions that cause facial nerve palsy
Sequelae
- Tumour in internal acoustic meatus/ cerebellopontine angle: Acoustic neuroma, Meningioma
- Facial nerve accommodates slow growing tumors, rarely palsy - Temporal bone fracture
Sequelae: Between geniculate ganglion and stylomastoid foramen:
Taste and lacrimation abnormal
Stapedial reflex affected = hyperacusis present
Facial movement affected
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Middle ear lesions that cause facial nerve palsy
Sequelae
- Acute otitis media
- Chronic suppurative otitis media – cholesteatoma
- Bell’s palsy: nerve swollen in the bony facial canal and neuropraxia
- Herpes zoster oticus: Ramsay Hunt Syndrome
- Tumour in middle ear (rare) – glomus, carcinoma
Sequelae: Between geniculate ganglion and stylomastoid foramen:
Taste and lacrimation abnormal
Stapedial reflex affected = hyperacusis present
Facial movement affected
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Lesions distal to stylomastoid foramen that cause facial nerve palsy
Sequelae
- Facial trauma to lateral side of face
- Neuropraxia or whole nerve cut
- Single or multiple branches affected - Malignant parotid tumor
- Slow growing tumors allow nerve accommodation with no palsy - Metastatic intraparotid LN (rare, e.g. skin cancer met.)
Sequelae:
- Only affects facial movement
- Normal stapedial reflex
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Lesions originating from facial nerve itself which cause palsy
Sequelae
- Surgical injury (common), e.g. traction during operation
- Facial nerve schwannoma/ neurofibroma (mimics malignant
cancer in middle ear) - CNS demyelinating disease (rare): affects whole facial nerve, usually accompanied by other cranial nerve palsy or other neurological signs
Sequelae:
Either segmental or all effectors affected
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Grading system for facial nerve palsy
House and Brackmann facial paralysis grading system
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Clinical P/E assessment of facial nerve palsy
Usually test motor function only
- Test** all 5 branches** in a systematic manner, rate severity with House and Brackmann facial paralysis grading system
- Examine other cranial nerves
- Examine the external ear and middle ear (vesicles, AOM, cholesteatoma)
- Palpate the** parotids and the neck**
- Test for cerebellar signs (e.g. large cerebellopontine angle tumor compressing on cerebellum)
First-line investigations for facial nerve palsy
Intracranial lesion (e.g. cerebellopontine angle tumor) = MRI brain
Middle ear pathology (e.g. cholesteatoma in mastoid) = MRI/CT temporal bone
Temporal bone trauma (fracture) = CT temporal bone
Suspect parotid lesion (e.g. mass palpated) = MRI/CT parotid + USG FNA (histology to confirm malignancy)
Electrophysiological testing: Electromyography and Electroneurography
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Electrophysiological testing for facial nerve
- Indication
- Functions
- Types
Indication:
To assess the need for operative decompression + anastomosis, e.g.:
Bell’s: don’t do
Trauma: do
Cancer case: don’t do as nerve will be sacrificed anyway
Functions:
To** differentiate neuropraxia (stretched and recover by itself) from more severe nerve injury **
To assess prognosis
Types:
- Electromyography (EMG)
- Electroneurography (ENoG)
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Electromyography (EMG) and Electroneurography (ENoG) for facial nerve palsy
Compare their application, procedure (simplified), Interpretation of results
EMG:
- Check recovery
- Insert electrode into muscle and record resting/ voluntary contraction
- Assess muscle activity, no comparison with normal side
ENoG:
- Diagnostic of damage
- Stimulate nerve at stylomastoid foramen, record summation potential in nasal alar/ nasolabial fold/ orbicularis oculi
- Compare 2 sides as a percentage of response:
If 90% degeneration (e.g. good side 10, bad side 1) = surgical decompression
If <90% degeneration = give steroids, spontaneous recovery
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Disadvantages of ENoG over EMG for facial nerve Electrophysiological testing
Discomfort
Cost
Test-retest variability (where you put the electrode affects the
reading)
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Bell’s palsy
- Pathogenesis
- Management, treatment options
commonest cause of facial nerve palsy
Pathogenesis:
- idiopathic facial nerve palsy caused by** herpes reactivation at geniculate nucleus causing neuritis**
- Nerve is swollen in the facial nerve canal (no space to expand), causing neuropraxia
Management:
- Diagnosis by exclusion after r/o causes
- Steroids, antivirals, eye protection, physiotherapy
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Detail treatment options for Bell’s palsy
Steroid: Prednisolone 1mg/kg/day in divided dose for 7-14 days
- Reduce nerve swelling
Antiviral: **Acyclovir or famciclovir **for 5 days
- Give early, before vesicles
Eye protection, eye drops, no contact lenses
- Prevent exposure keratitis
Facial nerve physiotherapy
- Maintain muscle tone, prevent disuse atrophy
No improvement after 6 weeks: Imaging brain and parotid for ddx
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General treatment options for facial nerve palsy
- Find underlying cause and treat
- **Surgical decompression **
- Nerve suture
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Surgery for facial reanimation: for corneal protection or mouth drooping
5.** Treat as Bell’s palsy after Dx of exclusion**
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Surgical decompression of facial nerve
Indications
Traumatic cause with immediate complete palsy
Middle ear infection or mass: surgical reduction e.g.mastoidectomy for cholesteatoma
Iatrogenic injury to middle ear/ parotids
Electrophysiology testing with ENoG <10% compared to normal
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Nerve suture for facial nerve
Indications
Types of suturing
Indications:
- Parotid cancer needing primary resection
- Traumatic damage to nerve segment
Types:
- Primary anastomosis (tension free)
- Facial hypoglossal anastomosis(tongue moves with face afterwards) with graft 3. Cross facial nerve graft (anastomosis of normal contralateral buccal branch to defective side)
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Free gracilis muscle flap transfer with neurovascular pedicle (long-term palsy)
a) Adductor artery and vein anastomosed to facial artery and vein
b) Anterior obturator nerve anastomosed to buccal nerve
Graft material: sural nerve (skin of sole, lateral border of foot)/ great auricular nerve
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Facial reanimation surgery for facial nerve palsy
2 functions
Types of surgeries
Corneal protection against exposure keratosis
a) Tarsorrhaphy (surgical procedure to partially close the eyelid): poor cosmesis
b) Gold weight implant to eyelid
Correct mouth angle drooping
a) Fascial sling: fascia lata suture with zygoma (Static, does not move with contralateral side)
b) Muscle sling: Temporalis muscle, Free gracilis muscle grafts
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List all salivary glands*
6 major salivary glands
2 parotid glands
2 submandiubular glands
2 sublingual glands
minor salivary glands
o Labial, buccal, lingual (tongue base), palatal
o Nasopharynx, larynx, hypopharynx
o Trachea
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Define the boundaries of the parotid, submandibular and sublingual glands
Parotid:
o Superior: zygomatic arch
o Posterior: attaches on external auditory canal and sternocleidomastoid muscle
Submandibular glands:
At the ‘submaxilla’, in the submandibular triangle
Gland wraps around mylohyoid
Sublingual:
Between mandible & genioglossus
Lies below and lateral to the termination of submandibular duct
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Parotid gland
3 methods to divide into superficial and deep lobe
Divided by facial nerve into superficial & deep lobe
Nerve not shown on imaging, need imaginary line:
o Line drawn from mandible to mastoid
Retromandibular vein = deep to facial nerve
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Submandibular gland
Anatomical structures that cross the gland
Gland wraps around mylohyoid, which divides the gland into superficial and deep lobes
Relationship with 3 nerves and facial artery:
o Crossed by marginal mandibular branch of facial nerve
o Lingual nerve and hypoglossal nerve are in between superficial and deep lobe
o Facial artery grooves the gland before turning around inferior border of mandible
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Parotid gland duct
- Name
- Size
- Course
- Opening
Stensen’s duct:
Arises from anterior border
Parallel to zygomatic arch, 1.5cm inferior
Pierces buccinator at 2nd molar (opening)
4-6 cm in length
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Submandibular gland duct
- Name
- Size
- Course
- Opening
Wharton’s duct:
5 cm in length
Exits medial surface
Between mylohyoid & hyoglossus
- Lingual nerve (begins lateral to submandibular duct, courses anteromedially by
looping beneath the duct; on hyoglossus) - Hypoglossal nerve (lies deep to submandibular gland; runs superficial to hyoglossus, deep to digastric)
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Submandibular gland ducts
- Opening
~15 ducts (no true duct):
Half open into submandibular duct
Half open directly on sublingual fold and papilla
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Compare the presentation of inflammatory vs neoplastic salivary gland disease
- swelling
- pain
- facial nerve palsy
- LN
- Signs of infection
Intermittent painless swelling or acute/ intermittent pain after meal + signs of acute infection (fever, tenderness, pus) = Inflammatory
Persistently growing, painless mass + Facial nerve palsy + LN = Neoplastic
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Outline P/E for salivary gland lesions
I. Inspection for both sides:
- Symmetrical swellings (Sjogren)
Scar (parotidectomy)
Look from the front: facial nerve palsy (cancer may affect certain branch)
- Intraoral inspection:
Parotid duct opening, submandibular duct opening: pus?
Floor of mouth swelling
Tumour
Displacement of tonsil (e.g. by deep lobe parotid tumor)
II. Palpation: low sensitivity
Confirm lesion not arising from the skin (e.g. sebaceous cyst)
Palpate the ducts: For stones and Express pus
III. Other examinations:
Complete H&N ENT examination
Facial nerve examination
Palpate neck lymph nodes
Endoscopy of the upper aerodigestive tract
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Conditions that mimic parotid gland swelling
How to rule out
Masseter hypertrophy
Neck lymph nodes
Lipoma
Vascular malformations
R/o with ultrasound
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Conditions that mimic submandibular gland swelling
How to rule out?
Enlarged submandibular lymph node
Oral cavity mass with direct extension to submandibular space
Rule out:
Intraoral examination (tongue cancer extending to floor of mouth)
Bimanual palpation of submandibular gland (may find stone)
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First-line investigations for salivary gland diseases
- Ultrasound
- Plane X-ray - submandibular stones ONLY (radio-opaque)
- Sialogram- sialolithiasis only, therapeutics
- MRI - tumor, extent of invasion
- FNA - benign vs malignant lesions
- Biopsy: Trucut, incisional and excisional
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Ultrasound for salivary gland diseases
- Functions
Confirm origin of mass, location of tumor
Enlarged neck lymph nodes
Stones
Tumor vs. inflammation
Malignant vs. benign (not always accurate)
Dilated ducts
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Sialogram for salivary gland diseases
- Functions
- Limitations
Cannulate the duct, inject contrast into the duct for filling defect
Only for stones/ chronic sialolithiasis
Therapeutic (may flush out stones or debris)
Limitations:
Cannulation of the duct may be difficult
superseded by USG/ sialoendoscopy
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MRI for salivary gland disease
- Function
- Limitation
Best soft tissue differentiation, e.g.:
Submandibular vs. parapharyngeal space
Deep vs. superficial lobe
Assess tumor, accurate delineation of extent of invasion
Differentiate other pathologies, e.g. facial nerve schwannoma
Limitation:**
Cannot image the facial nerve*/ lingual nerve (e.g. cannot tell nerve invasion)
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CT/ CT sialogram for salivary gland disease
Functions
Limitations
Delineate deep lobe vs. superficial lobe tumor
Differentiate salivary gland swelling vs. other pathologies (good for inflammatory disease)
Can show enlarged lymph nodes
Not done anymore (parotid prefer MRI)
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FNA for salivary gland diseases
Functions
Limitations
80% accurate in differentiating benign vs. malignant lesions
Better prepares the patient (e.g. malignant > prepare for neck dissection)
Limitations:
- 20% inaccurate in differentiating benign vs. malignant lesions, used as a guideline only
- Cannot differentiate different pathologies (type of parotid cancer, cell of origin)
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Biopsies for salivary gland diseases
- Types of biopsy
- Limitations
Trucut
Incisional - minor salivary glands only (risk of tumor spillage for parotid)
Excisional - parotidectomy, submandibulectomy
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Ddx inflammatory causes of parotid gland enlargement
Most common:
-Acute parotitis
-Viral infections
-Chronic sialadenitis: stones, Sjogren’s syndrome
- Alcoholism, Bulimia, Starvation
Others:
Sarcoidosis (Heerfordt syndrome)
Benign lymphoepithelial lesions (associated with immunosuppression)
Cysts (congenital vs. acquired)
Diabetes mellitus
Drugs, e.g. phenytoin
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Causes of bilateral parotid enlargement
Pseudo-parotidemegaly, e.g. bruxism (grind/gnash/clench teeth),
masseter hypertrophy
Bulimia nervosa (binge eating followed by purging)
Alcoholic cirrhosis
Diabetes mellitus
Drugs, e.g. phenytoin
Viral infection (e.g. mumps)
Sjogren’s Syndrome
Warthin tumor
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Patient presents with acute onset of tender parotid swelling and spits out pus intermittently. Pt has mobility issues and seldomly drinks water.
Most likely Dx
Acute parotitis
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Pt presents with high fever, bilateral parotid swelling and pain, testicular discomfort
Most likely Dx
Viral infection of parotid e.g. Mumps
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Pt presents with mild parotid pain that’s worse after meal, and intermittent swelling over the parotid glands
Most likely Dx
Chronic sialadenitis e.g. stone obstruction, stasis and infection
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Pt presents with dry eyes, large, tender enlargement of the parotid glands and submandibular glands
Gland enlargement fluctuates and is diffuse
Constitutional symptoms: fatigue, low-grade fever
Most likely Dx
Sjogren’s syndrome
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Acute parotitis
Pathogenesis
Clinical features
Tx
Cause: Staphylococcus aureus infection **
- Dehydrated, infirmed elderly (no proper intake, stroke) decrease salivar flow, blocked duct
-poor oral hygiene **
Clinical features:
Tender parotid swelling
Pus from duct opening
Tx:
Rehydration (drip to establish salivary flow)
IV antibiotics (vancomycin)
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Viral infection of parotid and submandibular glands
- Causative pathogens
- Clinical presentation
- Diagnosis
Pathogen:
Mumps (commonest), but now vaccinated
Coxsackie virus
CMV
Influenza
S/S:
High fever
Usuallybilateral parotid and submandibular enlargement
Mumps also affects other exocrine glands: pancreas, testes
Diagnosis:
Clinica picture (high fever + symmetrical swelling)
Serology
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Chronic sialadenitis
- 2 main causes
- General clinical features
- Diagnosis
- General Tx
Main causes: Stones, Sjogren’s disease
S/S:
Mild pain, worsens after meal
Recurrent parotid/ submandibular swelling after meal
Dx:
Clinical
Sialogram/ USG
Tx:
- Hydration, sialogogues e.g. cevimeline, massage, heat
- Antibiotics during acute attacks
- Excision of the gland
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Sialolithiasis
Which gland most affected
Clinical presentation
Complications
Diagnosis
Tx
Gland:
80% submandibular gland (more mucous, higher Ca content), 20% parotid
S/S:
Recurrent swelling
Pain worse with eating
Complications:
Sialadenitis
Ductal ectasia
Benign Stricture
CT: submandibular stones only (radio- opaque), parotid gland stones are radiolucent
Tx:
- Hydration, Sialagogues (cevimeline), conservative for spontaneous passage
- Remove stone: Transoral excision, Sialoendoscopy
- Gland excision: recurrent stones, multiple stones, proximal stones (inaccessible)
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Sjogren’s syndrome
- Demographics
- Pathogenesis
- Differentiate primary vs secondary cause
- Demographics : F>M, usually 3rd & 4th decade
- Pathogenesis: autoimmune disease: lymphocyte- mediated destruction of exocrine glands, e.g. salivary, lacrimal
- Differentiate primary vs secondary cause
Primary - no a/w other autoimmune diseases
Secondary - a/w autoimmune diseases e.g. SLE
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Sjogren’s syndrome
Clinical presentation
Diagnostic tests
S/S:
- Eyes: Keratoconjunctivitis sicca (dry eyes), injected cornea, conjunctivitis
- Xerostomia (dry mouth)
- Diffuse, tender, fluctuating enlargement of parotid and submandibular glands
- Constitutional: fatigue, low-grade fever
Dx tests:
- Blood test:
High ESR, CRP
Serology (similar to SLE): ANA, Rheumatoid factor, Anti-Ro/ SS-A, Anti-LA/SS-B antibodies
- Biopsy of sub-labial minor salivary glands: gland destruction with lymphocytes infiltration
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Sjogren’s syndrome
Treatment options
No cure, only supportive Tx
Artificial saliva, adequate hydration
Eye drops, glasses
pilocarpine for tear and saliva production
Lubricants and moisturizers
Monitor for lymphoma in submandibular and parotid gland (44-fold increased risk):
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Compare the distribution of cancer in major salivary gland + proportion of benign vs malignant
Distribution (the smaller the salivary gland, the less chance of a tumor, but the higher chance of a malignant tumor):
Parotid: 80% overall; 80% benign, 80% pleomorphic adenoma
Submandibular: 15% overall; 50% benign
Sublingual/minor: 5% overall; 40% benign
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List benign tumors of the major salivary glands
Benign:
Pleomorphic adenoma
-Warthin’s tumor/ Papillary cystadenoma lymphomatosum
-Oncocytoma
-Monomorphic adenoma
-Basal cell adenoma
- Myoepithelioma
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List malignant tumors of the major salivary glands
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Squamous cell carcinoma
Lymphoepithelial- like carcinoma (LELC)
Acinic cell carcinoma
Carcinoma ex- pleomorphic adenomav(from Mucoepidermoid carcinoma
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Pleomorphic adenoma
- Demographics
- S/S
- Which glands most affected
- Biological behavior
- Tx
- Demographics: middle aged women
- S/S:
Slow-growing, painless mass, massive
Mostly occurs in superficial lobe at the tail of parotid glands
Also occurs in submandibular and minor salivary glands
Rarely in sublingual gland - Biological behavior
Benign with 10% malignant potential (carcinoma ex- pleomorphic adenoma) - Tx
Complete surgical excision: - Parotidectomy with facial nerve preservation
- Submandibular gland excision
- Wide local excision of minor salivary glands
Radiotherapy: Prevent recurrence/ Tumor spillage/ Recurrent tumor
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Warthin’s tumor/ papillary cystadenoma lymphomatosum
- Demographics
- S/S
- Which gland most affected
- Biological behavior
- Demographics: Old male, smokers
- S/S:
Slow-growing, painless, Cystic mass, soft - Which gland most affected:
Parotid glands, rarely bilateral, Multifocal - Biological behavior
Benign, no malignant potential
Arise from intraparotid LN
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Parotidectomy
- Extent of excision
- Approach technique
Excision of tumour with a cuff of normal parotid tissue, with facial nerve dissection
Excisional biopsy of parotid tumour
Modified Blair’s incision, aka lazy S incision: scar from preauricular area, string around ear lobe,
down to mastoid area, back to neck
Early complications of parotidectomy and submandibulectomy
Bleeding/ haematoma (bruise over the area
Nerve injury:
Parotidectomy: Facial nerve palsy
Submandibulectomy: Lingual nerve, Marginal mandibular nerve, Hypoglossal nerve
Wound infection/ abscess from mouth mucosa
Salivary fistula: commonly parotidectomy
Late complications of parotidectomy and submandibulectomy
Recurrence
Hypertrophic scar/keloid scar
Frey’s syndrome – gustatory sweating/ parotid area becomes red and swollen after eating
Sunken parotid area, cosmetic problem (asymmetrical face)
Submandibulectomy: Permanent nerve damage
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Pathogenesis of Frey’s syndrome
common in parotidectomy:
- when patient eats, parotid area will sweat because secretory parasympathetic nerve has no end organ
- nerve aberrantly innervates the skin and sweat gland
- causes sweat instead of salivary secretion
- parotid area becomes red and swollen after eating
Very rare in submandibulectomy as whole gland is excised including the capsule, and the nerve is ligated
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Pt presents with Long-standing, painless parotid mass with sudden enlargement
Most likely neoplastic ddx
Carcinoma ex- pleomorphic adenoma
High grade Mucoepidermoid carcinoma
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Pt presents with pain in parotid area, paraesthesia over tongue and some facial weakness
Most likely neoplastic Dx
Adenoid cystic carcinoma in Submandibular gland
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Pt presents with slow-growing, painless mass over parotid glands
Most likely neoplastic ddx
Low grade Mucoepidermoid carcinoma
Acinic cell carcinoma
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Mucoepidermoid carcinoma
- Demographic
- Most affected gland
- Presentation
- histology
- Tx
- Demographic: children, middle-aged women
- Most affected gland:Parotid gland(45-70%), 18% in palate
- Presentation:
Low-grade= slow-growing, painless mass
High-grade: rapidly enlarging +/- painful oral cavity ulcers - histology: Glandular, mucus-secreting and sequamous components
- Tx:
localized = gland excision
LN = neck dissection
High grade = radiotherapy
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Adenoid cystic carcinoma
- Demographic
- Most affected gland
- Presentation
- Tx
- Demographic: 5th decade, M=F
- Most affected gland: submandibular, sublingual and minor salivary glands (cf mucoepidermoid carcinoma at parotid)
- Presentation:
Asymptomatic enlarging mass
Invading nerves: - Pain in parotid area (greater auricular nerve)
- Paraesthesia, numbness of tongue (lingual nerve)
- Facial nerve palsy weakness/ paralysis
- Hypoglossal nerve paralysis
Distant metastasis to LUNGS - Tx:
Complete local excision
perineural invasion common - postoperative radiotherapy
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Acinic cell carcinoma
- Demographic
- Most affected gland
- Presentation
- Tx
- Demographic: pediatrics, 5th decade female predominant
- Most affected gland: unilateral parotid
- Presentation: Slow growing, often painless mass, no nerve palsy
- Tx
Complete local excision
+/- postoperative radiotherapy
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Carcinoma ex- pleomorphic adenoma
- Demographic
- Most affected gland
- Biological behavior
- Presentation
- Tx
- Demographic: old age, no sex predominant
- Most affected gland: Parotid
- Presentation
Longstanding painless mass that undergoes sudden enlargement - Biological behavior: Malignant degeneration of pleomorphic adenoma
Poorly circumscribed, invasive mass
Infiltrative, hemorrhagic, necrotic
25% with neck node involvement - Tx
Radical excision
Neck dissection (25% with lymph node involvement at presentation)
Postoperative radiotherapy
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Squamous cell carcinoma of salivary glands
- Demographic
- Origin of neoplastic cells
- Demographic: rare, 7th - 8th decade male
Neoplasm from:
- Direct extension of skin SCC (overlying parotid region; less common)
- Metastatic SCC to intraglandular lymph nodes, usually from scalp SCC (skin cancer)
- High-grade mucoepidermoid carcinoma
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Lymphoepithelial- like carcinoma (LELC)
Histology
Tx
Undifferentiated carcinoma:
Histology exactly like NPC
EBV-related (tumor cells = EBER-RNA +ve
Surgery + post-op radiotherapy to primary and neck
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Most common and 2nd most common salivary gland neoplasms
Most common pediatric salivary gland neoplasms
Most common parotid tumor to cause facial paralysis
Mucoepidermoid carcinoma = most common
Adenoid cystic carcinoma = 2nd most
Pediatrics:
Mucoepidermoid carcinoma
Acinic cell carcinoma
Facial paralysis
High grade Adenoid cystic carcinoma (at submandibular gland)
