Facial Nerve Palsy

Facial nerve palsy is dysfunction of cranial nerve VII resulting in partial or complete weakness of the muscles of facial expression on the affected side.

Exam domain	One-glance essentials
Definition / diagnosis	Weakness from dysfunction of cranial nerve VII ^[1] Distinguish central facial weakness from peripheral palsy affecting the forehead ^[1]
Epidemiology / risks	Bell palsy is common; diabetes, pregnancy and viral reactivation increase risk ^[1] Trauma, otitis, parotid tumour and Ramsay Hunt are secondary causes ^[1]
Core mechanism	Peripheral nerve inflammation within the facial canal causes conduction block ^[1] Lesion level determines taste, lacrimation and hyperacusis findings ^[1]
Clinical picture	Unilateral facial droop, incomplete eye closure and reduced forehead movement ^[1] Vesicles/otalgia, hearing symptoms or other deficits suggest a secondary cause ^[1]
Investigations	Diagnosis of Bell palsy is clinical after full cranial/ear examination ^[2] Image or test when onset is gradual, recurrent, bilateral or accompanied by red flags ^[2]
Management	Protect the cornea immediately with lubrication and closure measures ^[3] Give early corticosteroid for Bell palsy; add antivirals for Ramsay Hunt ^[3]
Complications	Exposure keratitis, synkinesis and contracture ^[4] Missed stroke or tumour causes preventable morbidity ^[4]
Prevention / follow-up	Vaccinate against varicella-zoster where indicated and control diabetes ^[3] Eye-care education prevents corneal injury ^[3]
Exam traps	*Forehead sparing suggests a central lesion but is not infallible* ^[2] Facial palsy plus vesicular otalgia is Ramsay Hunt until assessed ^[3]

References

^[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p1–p9, p17, p19, p81)

^[2] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p9, p10, p11, p14, p16, p17, p18, p19, p20, p47, p81)

^[3] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p14, p16, p17, p18, p19, p20, p21, p24, p62, p69, p79)

^[4] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p7, p16, p17, p19, p21, p62, p69, p79, p80)

Facial nerve palsy (FNP) — also called "facial paralysis" — is weakness or complete paralysis of the muscles innervated by cranial nerve VII (CN VII, the facial nerve). The name itself is descriptive: "facial" = face, "nerve" = CN VII, "palsy" = weakness/paralysis. It can be upper motor neuron (UMN) or lower motor neuron (LMN) in origin, and the distinction between the two is one of the most important clinical exercises in neurology and ENT ^[1]^[2].

About half of all cases of facial palsy are diagnosed as Bell's palsy — an acute, idiopathic, peripheral (LMN) facial nerve palsy ^[2]. The other half are secondary to identifiable causes (tumour, infection, trauma, etc.), so the clinical priority is always to rule out a sinister cause before labelling someone as Bell's palsy.

Parameter	Detail
Overall incidence	~20–30 per 100,000 per year (most studies)
Bell's palsy incidence	~15–30 per 100,000 per year — the single commonest cause of facial palsy ^[1]
Age	Can occur at any age; peak 15–45 years
Sex	Slight female predominance; increased risk in pregnancy (especially third trimester, thought related to fluid retention compressing the nerve in its bony canal)
Laterality	Unilateral in the vast majority; bilateral facial palsy is uncommon and should immediately prompt consideration of Guillain-Barré syndrome, sarcoidosis, Lyme disease, or bilateral skull-base pathology ^[2]
Recurrence (Bell's)	~7–12% lifetime recurrence
Prognosis (Bell's)	> 90% good recovery ^[1]

Risk Factors

Diabetes mellitus — thought to predispose to microvascular ischaemia of the vasa nervorum
Pregnancy — especially third trimester/immediate postpartum (fluid retention → nerve oedema within the rigid bony facial canal)
Hypertension — microvascular disease
Upper respiratory tract infection — may trigger viral reactivation (HSV-1)
Immunosuppression — increased risk of herpes zoster reactivation (Ramsay Hunt syndrome)
Family history — occasional familial Bell's palsy (? anatomically narrower facial canal)

3. Anatomy and Function of CN VII

Understanding the anatomy is the key to localising the lesion and predicting clinical features. The facial nerve has one of the most complex courses of any cranial nerve.

The facial nerve has a very complex course and an intimate relationship to the middle ear and parotid gland. It travels in a bony canal for a long distance. ^[1]

The nerve is a mixed nerve containing ^[2]:

Motor (branchial efferent) — muscles of facial expression, stapedius, stylohyoid, posterior belly of digastric
Sensory (special afferent) — taste from anterior 2/3 of tongue (via chorda tympani → lingual nerve)
Parasympathetic (general visceral efferent) — secretomotor to submandibular gland, sublingual gland (via chorda tympani → submandibular ganglion) and lacrimal gland + palatine glands (via greater petrosal nerve → pterygopalatine ganglion)
General somatic afferent — small cutaneous sensory area around the ear (Ramsay Hunt zone / Hitselberger sign area)

3.2 Course of CN VII — Divided into 3 parts [1]

The course is divided into: pre-temporal bone, intra-temporal bone, and post-temporal bone. ^[1]

Segment	Course
Brainstem	Motor nucleus lies in the caudal pons. Fibres loop around the abducens (CN VI) nucleus (the "internal genu") before exiting. This is why a pontine lesion can give combined CN VI + CN VII palsy (e.g. Millard-Gubler syndrome).
Cerebellopontine angle (CPA)	CN VII arises at the junction between pons and medulla oblongata → courses laterally through the CPA ^[2], in close company with CN VIII (vestibulocochlear) and the nervus intermedius (sensory + parasympathetic root of VII).
Internal acoustic meatus (IAM)	Enters the temporal bone via the IAM accompanied by CN VIII ^[2]. Here it lies in the anterosuperior compartment. This is the site compressed by acoustic neuromas (vestibular schwannomas) and meningiomas.

This is the longest bony canal that any nerve traverses in the body — about 30 mm — and is the segment most vulnerable to compression from oedema (Bell's palsy) or fracture.

Segment	Description	Key branches given off
Labyrinthine segment	From fundus of IAM to geniculate ganglion. Narrowest part of the facial canal (~0.68 mm). Most common site of compression in Bell's palsy.	—
Geniculate ganglion	Sharp bend (external genu) where the nerve turns posteriorly. Cell bodies for taste and somatic sensation.	Greater petrosal nerve → enters foramen lacerum → pterygopalatine ganglion → lacrimal gland, palatine glands ^[2]
Tympanic segment	Runs along the medial wall of the middle ear (above the oval window, below the lateral semicircular canal). Can be dehiscent in ~50% of individuals, making it vulnerable in middle ear surgery or infection.	—
Mastoid (vertical) segment	Descends in the posterior wall of the middle ear cavity toward the stylomastoid foramen.	Nerve to stapedius → stapedius muscle (dampens sound) ^[2]; Chorda tympani → crosses middle ear → exits through petrotympanic fissure → joins lingual nerve → taste anterior 2/3 tongue + secretomotor to submandibular & sublingual glands ^[2]

Clinical Pearl: Localisation by Branch

If the lesion is proximal to the geniculate ganglion → loss of lacrimation (greater petrosal nerve), taste, salivation, hyperacusis, AND motor function.

If the lesion is between the geniculate ganglion and the departure of the nerve to stapedius → taste loss, hyperacusis, motor weakness, BUT lacrimation preserved.

If the lesion is between the nerve to stapedius and chorda tympani → taste loss, motor weakness, BUT no hyperacusis, lacrimation normal.

If the lesion is beyond the stylomastoid foramen → only facial movements affected, normal stapedial reflex ^[1]. Taste and lacrimation are both normal.

The nerve emerges from the stylomastoid foramen ^[1]^[2] and gives:

Posterior auricular nerve — supplies occipitalis and posterior auricular muscle
Branches to stylohyoid and posterior belly of digastric

It then pierces the parotid gland ^[1] — does NOT innervate the parotid (that's CN IX via lesser petrosal nerve → otic ganglion → auriculotemporal nerve) — and divides into 5 terminal branches ^[1]:

Branch	Muscles supplied	Clinical test
Temporal (frontal)	Frontalis, upper orbicularis oculi, corrugator supercilii	"Raise your eyebrows"
Zygomatic	Lower orbicularis oculi	"Close your eyes tightly"
Buccal	Buccinator, zygomaticus major/minor, levator labii superioris, nasalis, orbicularis oris (upper)	"Puff out your cheeks", "Show your teeth"
Marginal mandibular	Depressor anguli oris, depressor labii inferioris, mentalis	"Show your bottom teeth"
Cervical	Platysma	"Tense your neck"

Mnemonic for the 5 branches: To Zanzibar By Motor Car (Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical) — tracing from superior to inferior.

High Yield

The marginal mandibular branch is the most surgically important branch because (a) it runs superficially near the angle of the mandible and is at risk during neck dissection, submandibular gland excision, or parotidectomy; and (b) it has the fewest anastomoses with other branches, so damage is least likely to recover.

4. Aetiology

The approach to aetiology is anatomical — trace the course of CN VII from the brain to the face and list causes at each level. This is exactly how the lecture organises it ^[1].

4.1 Classification by Location

Cause	Notes
CVA (stroke)	Commonest cause of UMN facial palsy ^[1]. Upper face (frontalis) is spared because the upper facial nucleus receives bilateral cortical input.
Tumour	Cerebral metastases, glioma, etc.
Demyelinating disease	Multiple sclerosis
Vascular malformations	AVMs, aneurysms

Cause	Notes
Brainstem stroke	Lateral pontine stroke → may combine with CN VI palsy (Millard-Gubler)
Tumour, demyelinating disease ^[1]	Pontine glioma, MS plaques
Syringobulbia	Extension of syrinx into the medulla/pons

Cause	Notes
Acoustic neuroma (vestibular schwannoma) ^[1]	Most common CPA tumour. Compresses CN VII and CN VIII → gradual unilateral SNHL + facial weakness
Meningioma ^[1]	Second most common CPA lesion

Cause	Notes
Temporal bone fracture ^[1]	Transverse fractures (perpendicular to petrous ridge) → damage labyrinthine segment/geniculate ganglion. Longitudinal fractures can also damage the tympanic/mastoid segments.
Facial nerve schwannoma ^[1]	Primary tumour of the facial nerve itself. Can occur anywhere along its course.

Cause	Notes
Acute otitis media ^[1]	Infection may erode the thin bony canal (especially where dehiscent) and inflame the nerve
Chronic otitis media — cholesteatoma ^[1]	Erosion of bony facial canal by keratin squamous epithelium → direct compression/invasion
Herpes zoster oticus — Ramsay Hunt syndrome ^[1]	VZV reactivation in the geniculate ganglion. Classic triad: ipsilateral facial paralysis + otalgia + vesicles in the auditory canal/auricle ^[2]. Poorer prognosis than Bell's palsy.
Tumour in middle ear — glomus tumour, carcinoma ^[1]	Glomus tympanicum/jugulare can invade facial canal
Bell's palsy ^[1]	Nerve swollen in the facial nerve canal causing neuropraxia ^[1] — see detailed section below

Cause	Notes
Facial trauma — blunt or penetrating ^[1]	May only affect a single branch ^[1] — e.g. isolated marginal mandibular branch injury from a knife wound
Malignant tumour in parotid gland ^[1]	Facial nerve runs through the parotid. Malignant parotid tumours (e.g. mucoepidermoid carcinoma, adenoid cystic carcinoma) can invade the nerve. A parotid mass with facial weakness = malignant until proven otherwise
Metastatic intraparotid lymph node ^[1]	E.g. cutaneous SCC of scalp/ear metastatic to parotid nodes
Surgical injury — common ^[1]	Parotidectomy, mastoidectomy, otological surgery

Cause	Key features
Guillain-Barré syndrome	Bilateral facial palsy in > 50% of GBS; ascending weakness, areflexia, albuminocytologic dissociation in CSF
Sarcoidosis	Heerfordt syndrome (uveoparotid fever): bilateral parotid enlargement, uveitis, facial palsy, fever. ACE ↑, non-caseating granulomas on biopsy
Lyme disease	Tick-borne Borrelia spirochaete. Facial palsy is the most common cranial neuropathy. Can be bilateral. Erythema migrans + arthralgia. (Less relevant in Hong Kong but important for differential)

Bell's palsy is an idiopathic facial nerve palsy and the commonest cause of facial nerve palsy. ^[1]

Key points:

? Herpes reactivation neuritis ^[1] — HSV-1 reactivation is the most likely aetiology; labelled "idiopathic" because there is no established clinical method to confirm HSV in routine practice ^[2]
Pathophysiology: viral reactivation → inflammation and oedema of the nerve within the rigid labyrinthine segment (narrowest part of the facial canal) → compression → neuropraxia (conduction block without axonal disruption in mild cases; axonotmesis in severe cases) ^[1]
Nerve swollen in the facial nerve canal causing neuropraxia ^[1]
> 90% good recovery ^[1]

5. Pathophysiology

The facial nerve travels through a rigid bony canal in the temporal bone for ~30 mm. The labyrinthine segment is the narrowest (~0.68 mm diameter). Any process causing nerve oedema (inflammation, viral reactivation, vascular congestion) within this non-expansile tube leads to a compartment-syndrome-like situation:

Oedema → compression of nerve against bone → ischaemia of vasa nervorum → further oedema → more compression (vicious cycle) → conduction block (neuropraxia) or, if severe, axonal degeneration (axonotmesis/neurotmesis).

This explains:

Why Bell's palsy recovers well (most are neuropraxia → remyelination within weeks)
Why temporal bone fractures can cause immediate or delayed palsy (direct axonal injury vs. post-traumatic oedema)
Why cholesteatoma/tumour causes slowly progressive palsy (gradual erosion + compression)

This is one of the most tested concepts in clinical medicine.

The upper face (frontalis, upper orbicularis oculi) receives corticobulbar input from both hemispheres → a unilateral UMN lesion (e.g. stroke) leaves upper face relatively spared because the intact contralateral hemisphere compensates.
The lower face receives corticobulbar input from the contralateral hemisphere only → a UMN lesion causes contralateral lower face weakness.
A LMN lesion (anywhere from the facial nucleus onwards) affects all ipsilateral facial muscles — both upper and lower face — because the final common pathway is destroyed.

UMN lesion → frontalis spared (bilateral innervation) ^[1]

Important Exception

A partial lesion at the pes anserinus (the point of bifurcation of the facial nerve between the deep and superficial lobes of the parotid) may spare the temporal branch → mimicking UMN palsy. Always correlate with other UMN signs (hyperreflexia, Babinski, spasticity) or look for a parotid mass ^[2].

Conversely, a brainstem lesion affecting the facial nucleus or fascicles will produce an LMN pattern (all facial muscles affected) despite being a "central" lesion — because the damage is at the LMN level ^[2].

The location of the lesion determines which functions are lost ^[1]:

Lesion site	Motor	Taste (anterior 2/3)	Lacrimation	Stapedial reflex / Hyperacusis	Salivation
Proximal to geniculate ganglion	✗ All ipsilateral	✗ Lost	✗ Decreased ^[1]	✗ Absent / Hyperacusis present	✗ Decreased
Between geniculate ganglion and stylomastoid foramen	✗ All ipsilateral	✗ Affected ^[1]	✓ Normal ^[1]	✗ Hyperacusis present, stapedial reflex affected ^[1]	✗ Decreased (if proximal to chorda tympani takeoff)
Beyond stylomastoid foramen	✗ All ipsilateral (or single branch if distal)	✓ Normal	✓ Normal	✓ Normal stapedial reflex ^[1]	✓ Normal

Why each feature:

Lacrimation lost = greater petrosal nerve (parasympathetic to lacrimal gland) is damaged → lesion proximal to geniculate ganglion
Hyperacusis = nerve to stapedius damaged → stapedius cannot dampen ossicular vibration → sounds perceived as abnormally loud. Lesion proximal to departure of nerve to stapedius (mastoid segment)
Taste lost (anterior 2/3) = chorda tympani damaged → lesion proximal to chorda tympani departure (middle of mastoid segment)
Only motor = lesion beyond stylomastoid foramen (all sensory and parasympathetic branches have already departed)

6. Classification

Type	Upper Motor Neuron (UMN)	Lower Motor Neuron (LMN)
Lesion site	Cortex → facial nucleus	Facial nucleus → face
Forehead	Spared	Involved
Lower face	Contralateral weakness	Ipsilateral weakness
Associated signs	Hyperreflexia, spasticity, Babinski	Hyporeflexia, atrophy, fasciculations
Common causes	Stroke, tumour, MS	Bell's palsy, Ramsay Hunt, CPA tumour, trauma

Onset	Causes
Acute (hours–days)	Bell's palsy, Ramsay Hunt, stroke, trauma
Subacute (days–weeks)	Otitis media, Lyme, GBS
Chronic/Progressive (weeks–months)	Tumour (parotid, CPA, cholesteatoma, facial nerve schwannoma) — any progressive facial palsy must be investigated for malignancy

This is the standard clinical grading of facial nerve function:

Grade	Description	Gross	At rest	Motion
I	Normal	Normal function in all areas	Normal symmetry	Normal
II	Mild dysfunction	Slight weakness noticeable on close inspection	Normal symmetry and tone	Forehead: moderate-good; Eye: complete closure with effort; Mouth: slight asymmetry
III	Moderate dysfunction	Obvious but not disfiguring difference; synkinesis may be present	Normal symmetry and tone	Forehead: slight-moderate; Eye: complete closure with effort; Mouth: slightly weak with maximum effort
IV	Moderately severe	Obvious weakness and/or disfiguring asymmetry	Normal symmetry and tone	Forehead: none; Eye: incomplete closure; Mouth: asymmetric with maximum effort
V	Severe dysfunction	Only barely perceptible motion	Asymmetry	Forehead: none; Eye: incomplete closure; Mouth: slight movement
VI	Total paralysis ^[2]	NO movement	Asymmetry	None

7. Clinical Features

Symptom	Pathophysiological Basis
Facial weakness / asymmetry	Loss of motor innervation to ipsilateral facial muscles. The patient notices difficulty smiling, eating (food collects in the buccal sulcus), drinking (fluid dribbles from the corner of the mouth), or closing the eye.
Inability to close the eye	Weakness of orbicularis oculi → failure of lid closure → exposure keratitis risk. The eye may water paradoxically (reflex tearing from corneal exposure, despite reduced basal lacrimation in proximal lesions).
Drooping of the mouth	Weakness of the lower facial muscles (orbicularis oris, depressor anguli oris) → the mouth is pulled to the opposite (normal) side due to unopposed contraction.
Drooling	Loss of orbicularis oris tone → incompetent oral sphincter → saliva leaks from the affected side.
Difficulty speaking / pronouncing labials	Orbicularis oris and buccinator weakness → difficulty with bilabial consonants (b, p, m) and plosives.
Dry eye	Lesion proximal to geniculate ganglion → loss of greater petrosal nerve → reduced parasympathetic stimulation of lacrimal gland → decreased tearing ^[2]
Dry mouth	Loss of chorda tympani → reduced parasympathetic stimulation of submandibular and sublingual glands → decreased salivary secretion ^[2]
Hyperacusis ^[2]	Loss of nerve to stapedius → stapedius muscle paralysis → cannot dampen oscillation of stapes → sounds perceived as painfully loud on ipsilateral side
Loss of taste on anterior 2/3 of tongue ^[2]	Loss of chorda tympani → loss of special sensory (gustatory) fibres from fungiform papillae on the anterior tongue
Ear pain (otalgia)	Common in Bell's palsy and especially prominent in Ramsay Hunt syndrome (VZV geniculate ganglionitis → severe deep ear pain). Also occurs because CN VII has a small somatic sensory territory around the ear.
Post-auricular pain	Thought to be related to inflammation around the stylomastoid foramen — present in ~50% of Bell's palsy patients
Numbness around the ear	Involvement of the small somatic sensory component of CN VII (Hitselberger sign in acoustic neuroma)

Clinical assessment: 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]

Sign	How to elicit	Pathophysiological Basis
Eyebrow sagging / loss of forehead wrinkles	"Raise your eyebrows" (tests frontalis → temporal branch)	Loss of temporal branch innervation. If preserved → UMN lesion (bilateral cortical input to upper face nucleus). If lost → LMN lesion.
Inability to close eye / incomplete eye closure	"Close your eyes tightly; I'll try to open them" (tests orbicularis oculi → zygomatic branch)	Loss of zygomatic branch → orbicularis oculi weakness. Graded by whether examiner can overcome closure.
Bell's phenomenon	When patient attempts to close the eye, the eyeball rolls upward and outward, exposing the sclera. This is a normal synkinetic reflex, but it becomes visible only when orbicularis oculi is too weak to close the lid.	Normal brainstem reflex (superior rectus + inferior oblique co-contraction during lid closure) that is masked by normal lid closure but unmasked by facial weakness. Protective mechanism — cornea rotates away from exposure.
Disappearance of nasolabial fold	Observe at rest and during smiling	Loss of tone in zygomaticus, levator labii superioris, orbicularis oris → the fold on the affected side is flattened
Drooping of corner of mouth	"Show me your teeth" / "Smile widely" (tests buccal, marginal mandibular branches)	Lower facial muscle weakness → mouth deviates towards the normal side on smiling (normal side pulls)
Unable to puff cheeks / whistle	"Puff out your cheeks" (tests buccinator → buccal branch)	Buccinator weakness → air escapes from the affected side
Platysma weakness	"Tense your neck" (tests cervical branch)	Cervical branch weakness
Vesicles on ear / auditory canal	Inspect the pinna and EAC with an otoscope	Pathognomonic for Ramsay Hunt syndrome — VZV reactivation in the geniculate ganglion with cutaneous eruption in CN VII dermatome
Parotid mass	Palpate both parotid glands and neck	A parotid mass with associated facial weakness = malignant parotid tumour until proven otherwise
Other CN deficits (especially CN V, VI, VIII)	Full cranial nerve examination	CPA lesions compress multiple nerves (V → facial numbness, VI → diplopia, VIII → hearing loss, tinnitus, vertigo). Pontine lesions → CN VI palsy.
Ear examination: middle ear pathology	Otoscopy	Cholesteatoma (retraction pocket with squamous debris), acute otitis media (bulging red TM), or glomus tumour (pulsatile red mass behind TM)

Bell's Phenomenon vs Bell's Palsy

Don't confuse these! Bell's phenomenon is the upward rolling of the eye on attempted eye closure — it is a normal reflex present in ~75% of the population, but only visible when orbicularis oculi is weak. Bell's palsy is the idiopathic LMN facial palsy. They are named after the same Sir Charles Bell but are different concepts.

Acute onset over 1–2 days → progressive course reaching maximal clinical weakness within 3 weeks → recovery of some degree of function within 6 months ^[2].

If weakness is still progressing after 3 weeks, reconsider the diagnosis — may be a tumour
Incomplete palsy (House-Brackmann II–IV) → > 95% full recovery
Complete palsy (House-Brackmann VI) → ~60–70% achieve satisfactory recovery; 30% may have residual synkinesis or weakness
> 90% good recovery ^[1]

If axonal degeneration occurs and regeneration is aberrant:

Synkinesis — involuntary movement of one facial muscle group when another is activated (e.g. mouth twitches when closing eye) → misdirected axonal regrowth
Crocodile tears (gustatory lacrimation) — tearing while eating → regenerating fibres originally destined for the submandibular gland reach the lacrimal gland instead (via greater petrosal nerve pathway)
Contracture — chronic increased tone in facial muscles

Nasopharyngeal carcinoma (NPC) is endemic in Southern China/Hong Kong. Skull base extension or perineural spread of NPC can involve CN VII (and commonly CN V, VI). Always check post-nasal space in any unexplained cranial neuropathy in a Hong Kong patient.
Ramsay Hunt syndrome is not uncommon — always inspect the ear for vesicles in any patient presenting with facial palsy + severe ear pain.
Parotid malignancy — any parotid mass + facial weakness = high suspicion for malignancy. In Hong Kong, mucoepidermoid carcinoma and adenoid cystic carcinoma are the most important differentials.

High Yield Summary

Facial nerve (CN VII) is a mixed nerve (motor, sensory/taste, parasympathetic, somatic sensory) with a very complex course through the temporal bone.
LMN palsy → entire ipsilateral face weak (forehead included). UMN palsy → forehead spared (bilateral cortical innervation to upper face nucleus).
Bell's palsy is the commonest cause (~50%), is idiopathic (? HSV reactivation), and > 90% recover well. It is a diagnosis of exclusion.
Localise the lesion using associated features: lacrimation (greater petrosal nerve), stapedial reflex/hyperacusis (nerve to stapedius), taste (chorda tympani).
Red flags requiring urgent investigation: progressive palsy > 3 weeks, bilateral palsy, associated CN deficits, parotid mass, history of malignancy, no recovery by 6 weeks.
Ramsay Hunt syndrome = VZV reactivation in geniculate ganglion → triad of facial palsy + otalgia + vesicles in ear.
House-Brackmann scale grades I (normal) to VI (total paralysis).
Management of Bell's palsy: prednisolone 1mg/kg/day for 5 days then taper + acyclovir/famciclovir for 5 days + eye protection + facial physiotherapy. Reconsider diagnosis if no improvement after 6 weeks.

Active Recall - Facial Nerve Palsy

^[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p1–p9, p17, p19, p81) ^[2] Senior notes: felixlai.md (sections on Facial nerve palsy, pp. 206–212, 220)

Differential Diagnosis of Facial Nerve Palsy

The differential diagnosis of facial nerve palsy is one of those clinical exercises where anatomy is your best friend. The approach is straightforward: trace the nerve from cortex to face, and at each anatomical level, list what could go wrong. Then separately consider systemic and bilateral causes. The whole point of the differential is to avoid slapping the label "Bell's palsy" on something sinister — remember, Bell's palsy is a diagnosis by exclusion ^[1].

Before diving into lists, let's establish the thinking process. When a patient walks in with facial weakness, you need to answer three questions in sequence:

Is it UMN or LMN? → Forehead sparing (UMN) vs. forehead involved (LMN)
If LMN, where along the nerve is the lesion? → Use associated features (lacrimation, taste, hyperacusis, other CNs) to localise
What is the cause at that anatomical level? → Tumour, infection, trauma, inflammatory, idiopathic?

DDx Organised by Anatomical Level

This is the approach emphasised in the lecture ^[1] and senior notes ^[2].

These cause contralateral lower face weakness with forehead sparing.

Cause	Why it causes facial weakness	Distinguishing features
CVA (stroke) — commonest cause of UMN facial palsy ^[1]	Ischaemia/haemorrhage of the motor cortex or corticobulbar tract → loss of contralateral input to the lower facial nucleus (upper face nucleus is spared because it gets bilateral cortical input)	Acute onset, associated hemiparesis/hemiplegia, hemisensory loss, speech/language deficits, stroke risk factors. UMN signs (hyperreflexia, upgoing plantars).
Tumour ^[1]	Mass effect compresses or infiltrates corticobulbar fibres	Subacute/progressive onset, headache, seizures, other focal neurological deficits. Raised ICP signs.
Demyelinating disease (e.g. MS) ^[1]	Demyelinating plaques in the cerebral white matter disrupt corticobulbar conduction	Relapsing-remitting course, young female, optic neuritis, Lhermitte's sign, other white matter lesion symptoms
Vascular malformations	AVM or aneurysm compresses cortical motor areas	May present with haemorrhage, seizures

Key Point

The moment you see forehead sparing, you should be thinking "UMN" and the differential immediately shifts to stroke, tumour, and demyelination — NOT Bell's palsy. The single most common cause is CVA.

This is the exception that catches students out — the lesion is in the brainstem (central), but produces an LMN pattern because it destroys the facial nucleus itself or its fascicles (the final common pathway starts here) ^[2].

Cause	Why it causes facial weakness	Distinguishing features
Brainstem stroke	Infarction of the lateral pons destroys the facial nucleus/fascicles	Millard-Gubler syndrome: ipsilateral CN VI + CN VII palsy + contralateral hemiplegia (lesion damages facial nucleus, abducens nucleus, and corticospinal tract in the pons). Foville syndrome: adds conjugate gaze palsy.
Tumour (pontine glioma) ^[1]	Infiltrative growth destroys the facial nucleus	Progressive course, other brainstem signs (long tract signs, other CN palsies), common in children
Demyelinating disease (MS) ^[1]	Demyelinating plaque in the pons affects facial nucleus or fascicles	Relapsing course, young patient, MRI shows periventricular/pontine plaques
Syringobulbia	Extension of a syrinx cavity into the lower pons/medulla damages the facial nucleus	Associated lower CN palsies, dissociated sensory loss, often with syringomyelia history

Why does a pontine lesion give LMN facial palsy? Because the lower motor neuron for CN VII starts at the facial nucleus in the pons. Destroying the nucleus itself is identical in effect to cutting the peripheral nerve — all ipsilateral facial muscles are affected. The distinction from peripheral causes is the presence of associated brainstem signs: long tract signs (contralateral hemiplegia, hemisensory loss), other CN palsies (especially CN VI which is right next door), and cerebellar signs.

Cause	Why it causes facial weakness	Distinguishing features
Acoustic neuroma (vestibular schwannoma) ^[1]	Schwannoma arising from CN VIII in the IAM expands and compresses CN VII (which runs alongside in the anterosuperior compartment)	Gradual unilateral SNHL (the earliest and most common symptom), tinnitus, unsteadiness. Facial weakness is actually a late finding — by the time facial palsy appears, the tumour is usually large. Asymmetrical sensorineural hearing loss of gradual onset ^[3]. Also: CN V numbness (large tumour compresses trigeminal), cerebellar signs.
Meningioma ^[1]	CPA meningioma compresses CN VII and CN VIII at the CPA	Similar presentation to acoustic neuroma but may involve CN V earlier; typically enhances homogeneously on MRI with dural tail
Epidermoid cyst	Congenital inclusion cyst at CPA compresses CNs	Recurrent aseptic meningitis, CN palsies, DWI restriction on MRI
Metastasis (leptomeningeal)	Malignant cells seed the meninges around the CPA	Known primary malignancy, multiple CN palsies, headache

Cause	Why it causes facial weakness	Distinguishing features
Temporal bone fracture ^[1]^[3]	Direct injury to the facial nerve within the bony canal. Transverse fractures (perpendicular to petrous ridge) are more likely to damage the nerve (labyrinthine segment/geniculate ganglion) — 50% incidence of facial palsy. Longitudinal fractures (parallel to petrous ridge) — ~20% incidence, usually in the tympanic/mastoid segment.	History of head trauma, facial nerve function — immediate vs. delayed onset ^[3]. Immediate = probable nerve transection → needs exploration. Delayed = oedema/haematoma → may observe. Haemotympanum, CSF otorrhoea, hearing loss.
Facial nerve schwannoma ^[1]	Primary schwannoma arising from the nerve itself (can occur anywhere along its course but especially geniculate ganglion and tympanic segment)	Very slow progression of facial weakness (months–years), may have conductive or sensorineural hearing loss depending on location, middle ear mass on otoscopy

Cause	Why it causes facial weakness	Distinguishing features
Acute otitis media (AOM) ^[1]	The bony wall of the facial canal in the tympanic segment is very thin (< 0.1 mm) and dehiscent in ~50% of people — bacterial infection and inflammation in the middle ear can directly inflame or compress the exposed nerve	Ear pain, fever, conductive hearing loss, bulging erythematous TM on otoscopy. Facial palsy develops during active infection.
Chronic otitis media — cholesteatoma ^[1]^[3]	Cholesteatoma (aberrant keratinising squamous epithelium in the middle ear) progressively erodes bone, including the bony facial canal → direct compression and invasion of the nerve. Extracranial complication of CSOM: facial nerve paralysis ^[3].	Chronic foul-smelling otorrhoea, conductive hearing loss, retraction pocket or attic crust on otoscopy, management of "unsafe" CSOM: mastoidectomy ^[3]
Herpes zoster oticus — Ramsay Hunt syndrome ^[1]	VZV reactivation in the geniculate ganglion → intense inflammation and neural destruction. The nerve is damaged at its most vulnerable narrow segment.	Classic triad: ipsilateral facial paralysis + otalgia + vesicles in the auditory canal/auricle ^[2]. Often more severe than Bell's palsy with poorer recovery (~50–70% vs > 90%). May also have CN VIII involvement (SNHL, vertigo).
Tumour in middle ear — glomus tumour, carcinoma ^[1]^[3]	Glomus tympanicum or glomus jugulare: highly vascular paraganglioma that erodes into the facial canal. Middle ear carcinoma (SCC) can also invade the nerve. Glomus tumour middle ear ^[3].	Pulsatile tinnitus (the classic symptom of glomus tumours), conductive hearing loss, red pulsatile mass behind the TM ("rising sun" sign), may have other lower CN palsies (IX, X, XI for glomus jugulare)
Bell's palsy — nerve swollen in the facial canal ^[1]	Idiopathic facial nerve palsy. ? Herpes reactivation neuritis ^[1]. HSV-1 reactivation → inflammation → oedema of the nerve within the rigid labyrinthine segment → neuropraxia ^[1]. The labyrinthine segment is the narrowest part (~0.68 mm), so even mild oedema causes a compartment-syndrome-like compression.	Commonest cause of facial nerve palsy ^[1]. Acute onset 1–2 days. Diagnosis by exclusion ^[1]. Physical exam to rule out other causes like CVA, parotid tumour, middle ear infection etc. ^[1]. > 90% good recovery ^[1]. May progress in the first 3 weeks ^[1]. Consider imaging if no improvement or deterioration after 6 weeks ^[1].

Bell's Palsy is a Diagnosis of Exclusion

You must actively rule out other causes before labelling a patient as Bell's palsy. The lecture explicitly states: "Physical exam to rule out other causes like CVA, parotid tumour, middle ear infection etc." ^[1]. A progressive facial palsy beyond 3 weeks, bilateral palsy, parotid mass, or associated CN deficits should make you reconsider the diagnosis. "Consider other causes of facial nerve palsy if no improvement after 6 weeks" ^[1].

Cause	Why it causes facial weakness	Distinguishing features
Facial trauma — blunt or penetrating ^[1]	Direct injury to the extratemporal nerve or its branches after they exit the skull. Because the nerve has already divided into branches at this level, may only affect a single branch ^[1] (e.g. isolated marginal mandibular palsy from a knife wound or mandible fracture).	History of trauma, laceration or fracture in the parotid/mandibular region, may see isolated branch deficit
Malignant tumour in parotid gland ^[1]	CN VII runs through the parotid gland (dividing it into superficial and deep lobes). Malignant parotid tumours (mucoepidermoid carcinoma, adenoid cystic carcinoma) can directly invade the nerve. Facial weakness = high suspicion of malignant involvement of parotid gland ^[2].	Parotid mass + facial weakness = malignant until proven otherwise. May be painless initially. Parotid tumour must be distinguished from Bell's palsy ^[2]. Progressive course. Firm, fixed mass.
Metastatic intraparotid lymph node ^[1]	The parotid contains lymph nodes (the only salivary gland that does, because the lymph nodes were encapsulated within the gland during embryonic development). Metastatic disease (e.g. cutaneous SCC of scalp/ear, melanoma) can invade the nerve.	Known primary (usually skin cancer of scalp/ear), firm node in parotid region, may have other cervical lymphadenopathy
Surgical injury — common ^[1]	Iatrogenic injury during parotidectomy, mastoidectomy, facelift surgery, TMJ surgery, or neck dissection. The marginal mandibular branch is at particular risk during submandibular gland excision (runs superficial to the facial artery).	Onset temporally related to surgery. May be immediate (nerve cut/cauterised) or delayed (oedema, traction injury).

These are critical because bilateral facial palsy is a red flag — it should NEVER be labelled as bilateral Bell's palsy without thorough investigation.

Cause	Key features	Why it causes facial palsy
Guillain-Barré syndrome (GBS) ^[2]	Occurs in > 50% of GBS patients. Typically bilateral and symmetrical involvement ^[2]. Ascending weakness, areflexia, albuminocytologic dissociation in CSF (raised protein, normal cell count).	Autoimmune demyelinating polyradiculoneuropathy → immune attack on myelin of peripheral nerves including CN VII. Often post-infectious (Campylobacter, CMV). The facial nerve is a peripheral nerve, so it is affected like any other.
Sarcoidosis ^[2]	Cranial neuropathy including peripheral facial nerve palsy is a frequent manifestation of neurosarcoidosis ^[2]. Heerfordt syndrome (uveoparotid fever): bilateral parotid swelling + uveitis + facial palsy + fever. ACE ↑, bilateral hilar lymphadenopathy on CXR, non-caseating granulomas on biopsy.	Granulomatous inflammation infiltrates and compresses the facial nerve, either at the skull base or within the parotid gland. Sarcoidosis has a predilection for cranial nerves (CN VII is the most commonly affected).
Lyme disease ^[2]	Tick-borne illness caused by Borrelia spirochaete. Facial nerve palsy is the most common cranial neuropathy associated with Lyme disease ^[2]. Can be bilateral (25% of Lyme-associated facial palsy). Erythema migrans, arthritis, cardiac conduction abnormalities.	Direct spirochaetal invasion and immune-mediated inflammation of the nerve. Less relevant in Hong Kong (Lyme is endemic in North America and Europe) but important for the differential, especially if travel history present.
Diabetes mellitus	Increased risk of Bell's palsy. More likely to have recurrent episodes and incomplete recovery.	Microvascular disease (diabetic microangiopathy) affecting the vasa nervorum → ischaemic neuropathy of CN VII, similar mechanism to diabetic mononeuropathy of CN III.
Pregnancy	Third trimester/immediate postpartum. 3× higher incidence than age-matched non-pregnant women.	Fluid retention → oedema within the rigid facial canal → compression. Also possible immune modulation.
HIV/AIDS	Facial palsy can occur at seroconversion or with advanced disease.	Direct viral neurotropism, immune-mediated demyelination, or opportunistic infections (VZV, CMV).
Melkersson-Rosenthal syndrome	Rare. Triad: recurrent facial palsy + facial oedema (especially lip swelling) + fissured tongue (lingua plicata).	Unknown; thought to be a granulomatous inflammatory condition affecting the facial nerve.
Acute/chronic otitis media as bilateral	Rare but possible, especially in children	Bilateral middle ear infection → bilateral nerve inflammation
Leukaemia/lymphoma	Leukaemic or lymphomatous infiltration of CN VII	Malignant cells infiltrate the nerve directly (neuroleukaemia)
Möbius syndrome	Congenital bilateral CN VI + CN VII palsy. Child cannot smile or abduct the eyes.	Developmental failure/aplasia of CN VI and CN VII nuclei in the brainstem.

Sometimes it's more practical to think about the DDx based on the pattern of presentation:

Pattern	Think of...
Acute onset (hours), LMN, no other features	Bell's palsy (most likely), Ramsay Hunt (check ear for vesicles)
Acute onset, LMN, vesicles in ear	Ramsay Hunt syndrome
Acute onset, UMN, other neurological deficits	Stroke (CVA)
Acute onset after head trauma	Temporal bone fracture
Progressive (weeks–months), LMN	Tumour until proven otherwise — parotid malignancy, acoustic neuroma, facial nerve schwannoma, cholesteatoma, NPC with skull base extension
Bilateral facial palsy	GBS, sarcoidosis, Lyme disease, bilateral Bell's (rare — diagnosis of exclusion), leukaemia, HIV
Recurrent ipsilateral facial palsy	Facial nerve schwannoma, Melkersson-Rosenthal syndrome, recurrent Bell's (uncommon), tumour
Facial palsy + parotid mass	Malignant parotid tumour ^[1] — must be investigated
Facial palsy + foul ear discharge	Cholesteatoma (unsafe CSOM) ^[3]
Facial palsy + pulsatile tinnitus	Glomus tumour (paraganglioma) ^[1]^[3]
Facial palsy + unilateral SNHL	CPA lesion — acoustic neuroma, meningioma ^[1]
Facial palsy + CN VI palsy	Pontine lesion (Millard-Gubler), CPA tumour, raised ICP with CN VI false localising sign

Nasopharyngeal carcinoma (NPC): Endemic in southern China/Hong Kong. Arises most commonly in the fossa of Rosenmüller ^[4]. Advanced NPC can spread to the skull base and involve multiple cranial nerves, including CN VII. More commonly affects CN V (facial numbness) and CN VI (diplopia) first, but CN VII can be involved with extensive disease. Always check post-nasal space in any unexplained cranial neuropathy in a Hong Kong patient.
Cholesteatoma: Relatively common in Hong Kong ENT practice. Any patient with chronic ear discharge and facial weakness should have urgent CT temporal bone and surgical management (mastoidectomy) ^[3].
Parotid malignancy: Mucoepidermoid carcinoma is the most common malignant parotid tumour; adenoid cystic carcinoma is notorious for perineural invasion and distant metastasis ^[2]. In Hong Kong, cutaneous SCC metastatic to intraparotid nodes is also seen, particularly from scalp/ear primaries in elderly patients.

High Yield Summary — Differential Diagnosis of Facial Nerve Palsy

Progressive weakness > 3 weeks → Tumour (parotid, CPA, facial nerve schwannoma, NPC)
No improvement after 6 weeks → Consider imaging ^[1]
Bilateral palsy → GBS, sarcoidosis, Lyme, leukaemia
Parotid mass → Malignant parotid tumour
Other CN deficits → CPA tumour, brainstem lesion, skull base pathology
Vesicles in ear → Ramsay Hunt (not Bell's)
History of head trauma → Temporal bone fracture
Chronic ear discharge → Cholesteatoma
Recurrent episodes → Facial nerve schwannoma, Melkersson-Rosenthal, recurrent Bell's (rare)
History of malignancy → Metastasis (leptomeningeal, intraparotid LN)

Active Recall - DDx of Facial Nerve Palsy

References

^[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p4–p7, p8, p9, p11, p17, p18, p19) ^[2] Senior notes: felixlai.md (sections on Facial nerve palsy etiology pp. 210–212, clinical manifestation, salivary gland tumours pp. 231–232) ^[3] Lecture slides: GC 214. Common ear diseases and hearing loss (1).pdf (p12, p14) ^[4] Lecture slides: GC 215. Common nasal conditions and nasopharyngeal carcinoma (1).pdf (p51)

Diagnostic Criteria, Algorithm and Investigations for Facial Nerve Palsy

Unlike conditions such as rheumatic fever (Jones criteria) or SLE (ACR/EULAR criteria), facial nerve palsy does not have a formal set of diagnostic criteria with sensitivity/specificity validation. The diagnosis is clinical — you see facial weakness, you confirm which muscles are affected, you determine UMN vs LMN, you localise the lesion, and then you either identify a cause or, by exclusion, label it Bell's palsy.

Bell's palsy is a diagnosis by exclusion ^[1]. This means the "diagnostic criteria" for Bell's palsy are really a checklist of things you must rule out before you can apply the label.

All of the following must be present to diagnose Bell's palsy:

Criterion	Rationale
1. Acute onset of unilateral facial weakness (over 1–2 days)	Gradual/progressive onset over weeks → think tumour. Bilateral → think GBS, sarcoidosis, Lyme.
2. LMN pattern — upper AND lower face involved ipsilaterally	Forehead sparing → UMN → stroke, tumour.
3. No identifiable cause on clinical examination	Physical exam to rule out other causes like CVA, parotid tumour, middle ear infection etc. ^[1]
4. No other cranial nerve deficits	CN V/VI/VIII involvement → CPA lesion, brainstem pathology, skull base disease.
5. No vesicles on the ear	Vesicles → Ramsay Hunt syndrome (VZV), not Bell's. Vesicles in herpes may not show up in first 2 days ^[1] — so re-examine the ear!
6. No parotid mass	Parotid mass + facial weakness → malignant parotid tumour.
7. No history of trauma	Recent head injury → temporal bone fracture.
8. No otological pathology on otoscopy	Bulging TM → AOM. Retraction pocket/debris → cholesteatoma. Pulsatile red mass → glomus tumour.
9. Maximal weakness within 3 weeks	May progress in the first 3 weeks — warn patient ^[1]. If still progressing beyond 3 weeks → not Bell's → investigate for tumour.

The 6-Week Rule

Remember to consider other causes of facial nerve palsy if no improvement after 6 weeks ^[1]. Similarly, consider imaging if no improvement or deterioration after 6 weeks ^[1]. If a patient you've labelled as "Bell's palsy" isn't getting better by 6 weeks, you must step back and reconsider the differential — especially tumour.

This is the standard grading system used worldwide to document severity and track recovery. It's not a "diagnostic criterion" per se, but it's essential for clinical documentation, prognostication, and deciding on surgical intervention.

House and Brackmann facial paralysis grading system ^[1]:

Grade	Description	Key Landmarks	Clinical Significance
I	Normal facial function in all areas ^[1]	Symmetric at rest and during movement	Normal
II	Mild dysfunction ^[1]	Slight weakness noticeable on close inspection. Forehead: moderate-to-good function. Eye: complete closure with minimal effort. Mouth: slight asymmetry ^[1]	Good prognosis — nearly all recover fully
III	Moderate dysfunction ^[1]	Obvious but not disfiguring difference between the two sides. First time you can notice a difference at rest. Forehead: slight-to-moderate movement. Eye: complete closure with maximum effort. Mouth: slightly weak with maximum effort ^[1]
IV	Moderately severe dysfunction ^[1]	Obvious weakness and/or disfiguring asymmetry. First time you have incomplete eye closure. No forehead movement. Forehead: no motion. Eye: incomplete closure. Mouth: asymmetric with maximum effort ^[1]	First grade with incomplete eye closure → corneal protection becomes critical
V	Severe dysfunction ^[1]	Only barely perceptible motion. At rest, asymmetry. Forehead: no movement. Eye: incomplete closure. Mouth: slight movement ^[1]	Poor spontaneous recovery
VI	Total paralysis ^[1]^[2]	No movement ^[1]^[2]	Worst prognosis. Consider electrophysiological testing to determine if surgical decompression is indicated.

Why does grading matter clinically? It determines prognosis (Grade II–III → excellent recovery; Grade V–VI → 30–40% may have permanent residual weakness), guides the urgency of eye protection (Grade IV+ need aggressive corneal care), and serves as baseline for monitoring treatment response.

The approach is stepwise and anatomy-driven. Think of it as a funnel: start broad (UMN vs LMN), then narrow down based on clinical features, and only order investigations when clinically indicated. Investigations for facial nerve palsy depend on clinical findings ^[1].

Investigation Modalities

The lecture is very clear: investigations for facial nerve palsy depend on clinical findings ^[1]. You do NOT shotgun-investigate every Bell's palsy patient. Investigations are indicated when:

Clinical features suggest a specific cause (trauma, infection, tumour, CPA lesion)
The presentation is atypical
There is progression beyond 3 weeks
There is no improvement or deterioration after 6 weeks
Complete palsy (HB Grade VI) where electrophysiological testing guides surgical decision

Let's systematically go through each investigation.

A. Clinical Examination (The Most Important "Investigation")

Clinical assessment of facial nerve: 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]

Branch tested	Action to request	Muscle tested
Temporal	"Raise your eyebrows" / "Wrinkle your forehead"	Frontalis
Zygomatic	"Close your eyes tightly — don't let me open them"	Orbicularis oculi
Buccal	"Show your teeth" / "Puff out your cheeks"	Levator anguli oris, buccinator, zygomaticus
Marginal mandibular	"Show your bottom teeth" / "Evert your lower lip"	Depressor anguli oris, depressor labii inferioris, mentalis
Cervical	"Tense your neck"	Platysma

Why test each branch separately? Because a lesion beyond the stylomastoid foramen (e.g. parotid tumour, penetrating trauma) may only affect a single branch ^[1]. If only one branch is affected, the lesion is almost certainly extratemporal.

UMN: frontalis spared (bilateral innervation) ^[1] — lower face weak contralateral to lesion
LMN: entire ipsilateral face weak including forehead
Exception: Partial lesion at pes anserinus (parotid bifurcation) may spare temporal branch → mimics UMN ^[2]
Exception: Brainstem lesion involving facial nucleus → LMN pattern despite "central" location ^[2]

Tests that attempt to localise the site of lesion include Schirmer test for lacrimation, stapedial reflex and evaluation of taste and salivation ^[2]. The lecture organises localisation as follows ^[1]:

Lesion site	Lacrimation	Taste	Stapedial reflex	Motor
Proximal to geniculate ganglion	Decreased ^[1]	Affected ^[1]	Absent (hyperacusis)	All ipsilateral
Between geniculate ganglion and stylomastoid foramen	Normal ^[1]	May be affected (depends on whether proximal or distal to chorda tympani)	Affected, hyperacusis present ^[1]	All ipsilateral
Beyond stylomastoid foramen	Normal ^[1]	Normal	Normal stapedial reflex ^[1]	Only motor affected (may be single branch)

Schirmer test: A strip of filter paper is placed in the lower conjunctival fornix of both eyes. After 5 minutes, the length of wetting is measured. Reduced wetting on the affected side indicates reduced lacrimation → lesion proximal to geniculate ganglion (greater petrosal nerve involvement). Why does this work? Because the greater petrosal nerve carries parasympathetic fibres to the lacrimal gland. If the lesion is proximal to where this nerve branches off (at the geniculate ganglion), parasympathetic supply is lost and the gland produces less tears.

Stapedial reflex (acoustic reflex): Tested with impedance audiometry/tympanometry. A loud sound is delivered, and the contraction of the stapedius muscle (which stiffens the ossicular chain) is measured as a change in middle ear compliance. If the nerve to stapedius is damaged (lesion in the mastoid segment, proximal to the nerve to stapedius branch), the reflex is absent on the affected side. Clinically, the patient may complain of hyperacusis — sounds perceived as uncomfortably loud because the stapedius cannot dampen stapes oscillation.

Taste testing: Cotton swab with sugar, salt, citric acid, or quinine is applied to the anterior 2/3 of the tongue unilaterally while the tongue is protruded. Loss of taste on the affected side indicates chorda tympani involvement → lesion proximal to chorda tympani departure (mastoid segment).

Practical Note on Localisation Tests

The senior notes wisely point out that these localisation tests only have moderate accuracy and are of little practical benefit ^[2]. Why? Because (a) the tests have significant inter-observer variability, and (b) only a limited number of patients have lesions distal to the geniculate ganglion — most Bell's palsy lesions are at or proximal to the labyrinthine segment, so these tests won't differentiate much ^[2]. In practice, imaging (MRI) has largely replaced these bedside tests for precise localisation.

Otoscopy: Looking for AOM (bulging red TM), cholesteatoma (retraction pocket, squamous debris), glomus tumour (pulsatile red mass), vesicles (Ramsay Hunt), haemotympanum (temporal bone fracture)
Other CNs: Especially CN V (corneal reflex, facial sensation), CN VI (lateral gaze), CN VIII (hearing — tuning fork tests, whispered voice). CPA lesions compress multiple nerves.
Parotid palpation: Mass → urgent investigation for malignancy
Neck palpation: Cervical lymphadenopathy → metastatic disease, lymphoma

B. Electrophysiological Testing

This is where the lecture dedicates significant attention. Investigations: electrophysiological testing and imaging ^[1].

Thought to be the most accurate of the electrodiagnostic tests ^[1].

How it works ^[1]:

Stimulate the facial nerve at the stylomastoid foramen ^[1]
Summation potential is recorded in the nasal alar ^[1] (i.e. surface electrode over the nasalis muscle)
The peak to peak amplitude is proportional to the number of intact axons ^[1]
The two sides are compared as a percentage of response ^[1]

Interpretation ^[1]^[2]:

The CMAP amplitude on the paralysed side is compared with the normal side
A CMAP value of 10% of normal corresponds to a loss/degeneration of 90% of motor axons on that side ^[2]
90% degeneration — surgical decompression should be performed ^[1]
Less than 90% degeneration within 3 weeks predicts 80–100% spontaneous recovery ^[1]

Disadvantages: discomfort, cost, and test-retest variability ^[1]

Why is 10 days post-onset the optimal timing? Because Wallerian degeneration takes approximately 3–5 days to reach the distal stump after axonal injury. Before this, the distal nerve segment can still conduct (even though it's been disconnected from the cell body). Testing before 3 days post-onset may give falsely reassuring results because the distal axons haven't degenerated yet and will still conduct. By 10–14 days, all fibres that are going to degenerate have done so, giving a true picture of axonal loss ^[2].

Key Clinical Decision Point

ENoG < 10% response (i.e. > 90% degeneration) is the indication for considering surgical decompression ^[1]. This is a critical cut-off. If > 90% of axons are degenerated within the first 2 weeks, spontaneous recovery is poor and decompression may salvage the remaining fibres. If < 90% degeneration, the prognosis is excellent and surgery is not needed.

A needle electrode is inserted into the facial muscles and recordings are made during rest and voluntary contraction.

Interpretation ^[2]:

Finding	Timing	Meaning
Normal biphasic/triphasic motor unit potentials	Normal	Intact nerve-muscle unit
Fibrillation potentials	10–21 days post-injury	Indicates denervation — muscle fibres are spontaneously depolarising because they have lost their nerve supply. This confirms axonal loss (not just neuropraxia).
Polyphasic reinnervation potentials	6–12 weeks before clinical recovery	Earliest evidence of nerve recovery ^[2]. These are nascent motor units — regenerating axons are starting to re-innervate muscle fibres. Each axon innervates only a few fibres initially, hence the polyphasic morphology.

Why is EMG useful? It can detect reinnervation (polyphasic potentials) before any clinical movement is visible — this is reassuring and means the nerve is recovering. It also helps confirm complete denervation (fibrillation only, no voluntary potentials) which has prognostic implications.

Technique ^[2]:

Facial nerve is supramaximally stimulated near the parotid gland
Evoked potential (CMAP) is measured by surface electrodes over orbicularis oculi, nasalis, or lower facial muscles
CMAP amplitude reflects the number of functioning motor axons
Amplitude on paralysed side is compared with normal side at 10 days post-onset

This is essentially the same principle as ENoG. In practice, ENoG and NCS are often used interchangeably, though ENoG specifically refers to the standardised protocol of stimulating at the stylomastoid foramen and recording at the nasal alar.

C. Imaging

Investigations depend on clinical findings ^[1]. Here is when to order what:

When to order	What you're looking for	Key findings
UMN facial palsy	Stroke, tumour, demyelination	Acute infarct on DWI (bright signal), enhancing mass, periventricular white matter plaques (MS)
Other CN deficits suggesting CPA/brainstem lesion	Acoustic neuroma, meningioma, pontine glioma	Enhancing CPA mass (schwannoma: heterogeneous; meningioma: homogeneous with dural tail), brainstem lesion
No improvement after 6 weeks (re-evaluation of Bell's palsy)	Occult tumour, inflammatory process	Enhancing lesion along facial nerve course

MRI with gadolinium contrast is the gold standard for soft tissue imaging of the brain, CPA, and course of the facial nerve. In Bell's palsy, MRI may show enhancement of the facial nerve (especially at the fundus of the IAM and labyrinthine segment) — this confirms inflammation but is not routinely needed unless the diagnosis is uncertain.

MRI: best soft tissue differentiation. Still cannot image the facial nerve or lingual nerve ^[1] — this refers specifically to direct visualisation of the normal thin nerve itself. However, MRI CAN detect pathological enhancement, thickening, or mass lesions along the nerve's course. The point is that a normal-appearing MRI doesn't exclude nerve pathology (e.g. early Bell's palsy).

When to order	What you're looking for	Key findings
Cholesteatoma	Bone erosion, soft tissue mass in middle ear/mastoid	CT: opacification of middle ear/mastoid, erosion of scutum, tegmen tympani, or facial canal. MRI (DWI): restricted diffusion in cholesteatoma (distinguishes it from granulation tissue/fluid)
Facial nerve schwannoma	Expansion and enhancement along facial canal	Enhancing, fusiform mass expanding the facial canal, often at geniculate ganglion
Glomus tumour	Vascular mass in middle ear or jugular foramen	"Salt and pepper" enhancement on MRI; CT shows bone erosion at jugular foramen
AOM with complications	Extension of infection	Opacification of middle ear, possible abscess formation

When to order	What you're looking for	Key findings
Head trauma + facial palsy	Fracture line involving the facial canal	Longitudinal fracture: parallel to long axis of petrous bone (~80% of temporal bone fractures), may involve tympanic or mastoid segment. Transverse fracture: perpendicular to petrous ridge (~20%), more likely to involve labyrinthine segment/geniculate ganglion → higher incidence of facial palsy and SNHL. Look for: fracture line crossing the facial canal, haemotympanum, ossicular disruption.

Why CT and not MRI for trauma? CT is far superior for bone detail. It's fast, readily available, and exquisitely demonstrates the fine bony anatomy of the temporal bone, the fracture line, and its relationship to the facial canal. MRI is poor for bone.

When to order	What you're looking for	Key findings
Palpable parotid mass + facial weakness	Malignant parotid tumour, metastatic intraparotid node	MRI: defines extent of mass, relationship to facial nerve (though nerve itself may not be directly visualised), deep lobe extension. CT: bone involvement if advanced. USG: readily available, guides FNA. FNA cytology: can discriminate benign from malignant tumours ^[2], though less specific for exact tumour subtype.

Investigation	Indication	Rationale
CT/MRI brain + nasopharynx	Suspected NPC (Hong Kong endemic)	NPC at fossa of Rosenmüller can extend to skull base → multiple CN palsies
PET-CT scan ^[2]	Known malignancy, suspected metastatic disease	Identify primary disease or detect distant metastatic disease ^[2]
CT angiography	Glomus tumour	Vascular tumour — need to assess feeding vessels and relationship to carotid before surgery

Blood tests are NOT routinely indicated in straightforward Bell's palsy but are important for specific differentials:

Test	Indication	What you're looking for
FBC + ESR/CRP	Infection (AOM, mastoiditis), inflammation	Leucocytosis, raised inflammatory markers
Blood glucose / HbA1c	All patients	Screen for diabetes mellitus (risk factor for Bell's palsy, affects prognosis)
Lyme serology (anti-Borrelia IgM/IgG)	Endemic area or travel history, bilateral palsy, erythema migrans	Positive serology confirms Lyme disease
ACE level, calcium	Suspected sarcoidosis (bilateral palsy, parotid swelling, uveitis)	Elevated ACE (non-specific), hypercalcaemia
HIV serology	Risk factors, bilateral palsy, atypical presentation	Seroconversion illness or immunosuppression
VZV IgM / PCR	Suspected Ramsay Hunt (but vesicles may be absent — "zoster sine herpete")	Confirms VZV reactivation
Anti-ganglioside antibodies, CSF analysis	Suspected GBS (bilateral palsy, ascending weakness, areflexia)	CSF: albuminocytological dissociation (raised protein, normal cells). Anti-GM1/GQ1b antibodies.
CXR	Sarcoidosis	Bilateral hilar lymphadenopathy

Scenario	Investigations needed
Classic Bell's palsy (acute onset, LMN, no red flags)	None routinely. Consider blood glucose. Start treatment empirically.
No improvement or deterioration by 6 weeks	Consider imaging ^[1] — MRI brain + temporal bone + parotid
Complete palsy (HB Grade VI)	ENoG at 10–14 days to assess degree of degeneration and guide surgical decision
UMN pattern	Urgent CT/MRI brain — stroke workup
Ear pathology on otoscopy	CT temporal bone (cholesteatoma, glomus) ± MRI with DWI
Post-traumatic	CT temporal bone ^[1]
Parotid mass	MRI/CT parotid + USG FNA ^[1]
Other CN deficits	MRI brain with gadolinium — CPA lesion, brainstem pathology
Bilateral palsy	Lyme serology, ACE level, CXR, HIV serology, consider LP (GBS)
Recurrent palsy	MRI temporal bone (facial nerve schwannoma), consider Melkersson-Rosenthal
Progressive palsy > 3 weeks	MRI brain + temporal bone + parotid — tumour until proven otherwise

Surgical decompression of nerve ^[1]:

Indications ^[1]:

Traumatic cause ^[1]
Middle ear infection ^[1]
Iatrogenic injury (middle ear or parotid surgery) ^[1]

Bell's palsy — no proven benefits ^[1] (this is important — despite theoretical rationale, RCT evidence does not support routine surgical decompression for Bell's palsy)

Earlier the better ^[1] — if decompression is indicated (e.g. traumatic cause with immediate complete palsy), do it as soon as possible before irreversible Wallerian degeneration sets in.

Electrical testing as indication for decompression — ENoG < 10% ^[1]

Imaging for site of decompression ^[1] — you need to know WHERE the nerve is compressed (CT temporal bone) to plan the surgical approach.

Surgical decompression should NOT be undertaken if facial paralysis has been present for 14 days or more since severe degeneration of facial nerve is probably irreversible after 2–3 weeks ^[2].

High Yield Summary — Diagnosis of Facial Nerve Palsy

Bell's palsy is a diagnosis of exclusion — you must rule out stroke (UMN), trauma, infection (AOM, cholesteatoma, Ramsay Hunt), and tumour (parotid, CPA) by clinical examination before applying the label.
Investigations depend on clinical findings — do NOT shotgun-investigate uncomplicated Bell's palsy.
House-Brackmann grading (I–VI) documents severity and tracks recovery. Grade IV is the first with incomplete eye closure; Grade VI is total paralysis.
ENoG is the most accurate electrodiagnostic test: stimulate at stylomastoid foramen, record at nasal alar. > 90% degeneration (< 10% response) → consider surgical decompression. < 90% degeneration → 80–100% spontaneous recovery.
Imaging:
- MRI brain → intracranial/CPA lesion
- MRI/CT temporal bone → middle ear pathology
- CT temporal bone → trauma
- MRI/CT parotid + USG FNA → parotid mass
Surgical decompression indications: traumatic cause, middle ear infection, iatrogenic injury. NOT indicated for Bell's palsy (no proven benefit). Earlier is better. ENoG < 10% guides the decision.
Red flag timeline: progress beyond 3 weeks → investigate. No improvement by 6 weeks → image.

Active Recall - Diagnosis of Facial Nerve Palsy

References

^[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p9, p10, p11, p14, p16, p17, p18, p19, p20, p47, p81) ^[2] Senior notes: felixlai.md (sections on Facial nerve palsy diagnosis pp. 206, 212–214)

Management of Facial Nerve Palsy

The management of facial nerve palsy follows a simple logical hierarchy:

Identify the cause ^[1] → Remove the causative agent ^[1] → Protect the eye → Rehabilitate the nerve.

The specific management depends entirely on the aetiology. Bell's palsy (idiopathic) is managed medically. Secondary causes are managed by treating the underlying pathology. Surgical intervention is reserved for specific indications. Let's build this from first principles.

I. Management of Bell's Palsy (The Commonest Scenario)

Bell's palsy: Idiopathic facial nerve palsy. Commonest cause of facial nerve palsy. > 90% good recovery. ^[1]

Management of Bell's palsy: Diagnosis by exclusion. Physical exam to rule out other causes like CVA, parotid tumour, middle ear infection etc. ^[1]

Before you treat, you must be confident this IS Bell's palsy:

Physical exam to rule out other causes like CVA, parotid tumour, middle ear infection etc. ^[1]
Diagnosis by exclusion ^[1]
May progress in the first 3 weeks — warn patient ^[1]

Reduce swelling with steroids — prednisolone 1mg/kg/day in daily dose for 5 days then taper if no contraindications ^[1]

Parameter	Detail
Drug	Prednisolone (or prednisone — equivalent)
Dose	1 mg/kg/day ^[1] (typically 60 mg/day for an average adult)
Duration	5 days at full dose, then taper ^[1] over the next 5 days (total course ~10 days)
Timing	Must start within 72 hours of onset for maximum benefit. Evidence shows benefit diminishes if started after 72 hours.
Contraindications	Active peptic ulcer disease, uncontrolled diabetes mellitus (steroids cause hyperglycaemia — still give steroids but monitor glucose closely and adjust diabetic medications), active TB, systemic fungal infections, psychosis. Pregnancy — use with caution (discuss risk-benefit).

Why steroids? The pathophysiology of Bell's palsy is nerve oedema within the rigid bony facial canal → compression → ischaemia. Corticosteroids are potent anti-inflammatory agents that reduce oedema, suppress the inflammatory cascade (inhibit phospholipase A2 → ↓ prostaglandins and leukotrienes), and reduce capillary permeability. By reducing swelling, you decompress the nerve pharmacologically and break the vicious cycle of oedema → ischaemia → more oedema.

Evidence: The landmark Scottish Bell's Palsy Study (Sullivan et al., NEJM 2007) demonstrated that early prednisolone significantly improved complete recovery rates at 3 and 9 months. This is Level 1 evidence and forms the basis of current guidelines worldwide.

High Yield

Steroids are the single most important medical treatment for Bell's palsy. If you remember nothing else about Bell's palsy management, remember: prednisolone 1 mg/kg/day for 5 days then taper, started within 72 hours.

Antiviral — acyclovir or famciclovir for 5 days ^[1]

Parameter	Detail
Drugs	Acyclovir 400 mg 5×/day for 5–7 days, OR Famciclovir 500 mg TDS for 5–7 days, OR Valacyclovir 1 g TDS for 5–7 days
Rationale	? Herpes reactivation neuritis ^[1] — if HSV-1 reactivation is the underlying cause, antivirals inhibit viral DNA polymerase and halt viral replication
Evidence	Antivirals alone do not significantly improve outcomes. Combined with steroids, they may provide modest additional benefit, particularly in severe palsy (HB Grade V–VI) ^[2]. The benefit is debated, but the side effect profile is very favourable, so most protocols include them.
Timing	Start within 72 hours of symptom onset, ideally simultaneously with steroids
Special note	Vesicles in herpes may not show up in first 2 days ^[1] — this is why we give antivirals empirically even without vesicles. If vesicles subsequently appear, the diagnosis shifts to Ramsay Hunt syndrome, and antiviral dose should be escalated.

Why acyclovir/famciclovir/valacyclovir? These are all guanosine analogues. "Acyclovir" = "a-cyclic" guanosine → lacks the sugar ring of normal nucleosides. Once phosphorylated (first by viral thymidine kinase, then by cellular kinases), it is incorporated into the growing viral DNA chain and acts as a chain terminator because it lacks the 3'-OH group needed for the next nucleotide to attach. This is selective for virus-infected cells because only cells with active viral thymidine kinase can perform the first phosphorylation step. Famciclovir is a prodrug of penciclovir (similar mechanism, better oral bioavailability). Valacyclovir is a prodrug of acyclovir (better bioavailability = higher plasma levels = can use less frequent dosing).

Contraindications: Renal impairment (acyclovir is renally cleared and can cause crystalline nephropathy — adjust dose for eGFR). Ensure adequate hydration.

Eye protection and eye drops ^[1]

This is critical and often underemphasised. The eye is at risk because:

Orbicularis oculi weakness → incomplete lid closure (lagophthalmos) → corneal exposure
Loss of greater petrosal nerve function (in proximal lesions) → decreased lacrimation → dry cornea
Loss of corneal blink reflex (afferent CN V is intact, but efferent CN VII is weak) → cornea is exposed to desiccation, foreign bodies, and trauma

Untreated exposure keratitis can progress to corneal ulceration → corneal scarring → permanent visual impairment. This is the most important preventable complication of facial nerve palsy.

Measure	Details	When
Artificial tears / lubricating eye drops	Hypromellose or carboxymethylcellulose drops, applied frequently during the day (every 1–2 hours)	All patients with incomplete eye closure ^[1]^[2]
Lubricating eye ointment	Thicker than drops (e.g. lacrilube, chloramphenicol ointment), provides longer-lasting corneal coverage	At night (blurs vision, so not practical during the day)
Protective glasses / moisture chamber glasses	Prevents evaporation, protects from wind and debris	Outdoors, during the day
Taping the eyelid shut	Micropore tape applied to close the eye	At night to prevent nocturnal lagophthalmos
Gold weight implantation into upper eyelid ^[2]	A small gold weight (0.8–1.6 g) is surgically inserted into the upper eyelid → gravity assists lid closure; uses the weight of gold to enable passive closure. Reversible if nerve recovers.	Prolonged incomplete eye closure (usually considered after 3–6 months if no recovery)
Tarsorrhaphy ^[2]	Surgical partial closure of the palpebral fissure by suturing the lateral eyelid margins together. Effective but poor cosmetic outcomes ^[2].	Last resort for corneal protection if other measures fail

Never Forget the Eye

In the acute management of facial nerve palsy, students (and doctors) often focus on steroids and antivirals while neglecting eye care. Corneal damage from exposure is the most important acute complication and is entirely preventable. Every patient with HB Grade III or worse needs explicit eye protection instructions. Document that you've counselled the patient.

Facial nerve physiotherapy — maintain muscle tone and hasten recovery ^[1]

Modality	Rationale
Facial exercises (active and passive)	Maintain muscle bulk and tone; prevent disuse atrophy during the period of denervation. Includes exercises like raising eyebrows, closing eyes, puffing cheeks, smiling.
Mime therapy	Structured programme of facial expression exercises. Evidence suggests it improves outcomes and reduces synkinesis.
Massage	Improves blood flow to facial muscles, reduces stiffness
Electrical stimulation	Controversial — some evidence that neuromuscular electrical stimulation maintains muscle bulk, but may promote synkinesis if started too early. Usually reserved for complete denervation.
Acupuncture	Popular in Hong Kong. Limited evidence from RCTs, but commonly used as adjunctive therapy ^[2].

Remember to consider other causes of facial nerve palsy if no improvement after 6 weeks ^[1] Consider imaging if no improvement or deterioration after 6 weeks ^[1]

Timepoint	Action
1–2 weeks	Review: is the palsy progressing? Re-examine ear for vesicles (Ramsay Hunt). Grade with House-Brackmann. Eye check.
3 weeks	Maximal weakness should have been reached by now. If still progressing → investigate (not Bell's).
6 weeks	If no improvement → re-image (MRI brain + temporal bone + parotid). Reconsider diagnosis.
3–6 months	Most Bell's palsy patients recover by this time. If residual weakness → consider rehabilitation.
> 6 months	If no recovery → consider surgical reanimation (see below).

II. Management of Specific Causes

Treatment of facial palsy: Identify the cause. Remove the causative agent e.g. mastoid surgery to remove the cholesteatoma. Consider nerve exploration and decompression in traumatic cause with immediate complete palsy. ^[1]

Treatment	Details
High-dose antiviral	Acyclovir 800 mg 5×/day for 7–10 days (higher dose and longer course than Bell's palsy because confirmed VZV reactivation), OR valacyclovir 1 g TDS for 7 days
Corticosteroids	Prednisolone 1 mg/kg/day tapering over 10–14 days (same rationale as Bell's — reduce oedema)
Analgesia	Severe otalgia is common — may need neuropathic pain agents (gabapentin, pregabalin) in addition to simple analgesics
Eye care	As above
Prognosis	Worse than Bell's palsy — only ~50–70% achieve satisfactory recovery

Why higher antiviral dose? VZV is inherently less sensitive to acyclovir than HSV (higher IC50), so you need higher drug concentrations to achieve adequate viral suppression. VZV also tends to cause more extensive neural destruction (geniculate ganglionitis), hence the worse prognosis.

Treatment	Details
IV antibiotics	Target middle ear pathogens (S. pneumoniae, H. influenzae, M. catarrhalis). IV amoxicillin-clavulanate or ceftriaxone.
Myringotomy ± grommet	Drainage of middle ear pus reduces pressure and removes the inflammatory milieu around the exposed nerve
Corticosteroids	May be given to reduce nerve oedema
Prognosis	Generally good if infection is treated promptly — facial palsy usually resolves with infection control

Why does treating the infection help the nerve? The facial canal's tympanic segment is often dehiscent (~50% of people). Infection and pus in the middle ear directly bathe and compress the exposed nerve. Draining the infection and killing bacteria removes the inflammatory stimulus.

Remove the causative agent e.g. mastoid surgery to remove the cholesteatoma ^[1]

Treatment	Details
Mastoidectomy	Definitive surgical removal of the cholesteatoma. The eroding keratinising epithelium must be completely excised to prevent recurrence and further bone destruction.
Facial nerve decompression	If the cholesteatoma has eroded the facial canal and compressed the nerve, the surgeon will decompress the nerve at the same time as removing the cholesteatoma.
Timing	Semi-urgent — cholesteatoma is a slowly progressive but destructive process. Once facial palsy has developed, surgery should not be delayed.

Consider nerve exploration and decompression in traumatic cause with immediate complete palsy ^[1]

Scenario	Management	Rationale
Immediate complete palsy	Nerve exploration and decompression ^[1] → consider within 2–3 weeks (before irreversible degeneration). CT temporal bone to locate fracture site. ENoG to guide decision.	Immediate onset suggests nerve transection or severe compression by bone fragment. Early surgical exploration can decompress or repair the nerve. Earlier the better ^[1].
Delayed palsy (develops days after injury)	Steroids within 48–72 hours ^[2] → observe. ENoG if complete palsy.	Delayed onset suggests post-traumatic oedema or haematoma rather than transection. Most cases recover with conservative management. Failure to respond to steroids can be considered for surgical decompression of petrous portion of facial nerve ^[2].
Incomplete palsy (any onset)	Conservative — steroids, observation	Incomplete palsy means some axons are intact → excellent prognosis

Treatment	Details
Parotidectomy	Complete surgical excision is the cornerstone ^[2]. If the nerve is encased/invaded by tumour, nerve sacrifice may be necessary — this is one of the few situations where the facial nerve is deliberately cut.
Nerve grafting (if nerve sacrificed)	See nerve repair section below
Adjuvant radiotherapy	For high-grade malignancy, positive margins, perineural invasion, lymph node involvement
Specific examples	Adenoid cystic carcinoma: complete local excision; tendency for perineural invasion → ? facial nerve sacrifice; postoperative XRT. Prognosis: local recurrence 40%, distant metastasis common (lung), indolent course — 5-year survival 75%, 20-year survival 13% ^[1]

Treatment	Details
Surgical excision	Microsurgical removal via translabyrinthine, retrosigmoid, or middle cranial fossa approach. Facial nerve preservation is a primary surgical goal.
Stereotactic radiosurgery (Gamma Knife)	Alternative for small tumours ( < 3 cm) or patients unfit for surgery. Controls tumour growth in ~90%.
Observation + serial MRI	For small, asymptomatic tumours (especially in elderly patients) — "watch, wait, and rescan"

III. Surgical Management — Nerve Repair and Reanimation

When the facial nerve is irreversibly damaged (transection, resection for malignancy, or failed recovery after > 12–18 months), surgical options exist to restore some facial function. The lecture covers this in detail ^[1].

Facial nerve grafting ^[1]:

Technique	Details	Indication
Primary anastomosis ^[1]	Direct end-to-end repair of the cut nerve stumps	Only if tension-free ^[1]. If you can bring both ends together without stretching, this gives the best result. Usually possible only if a very short segment is missing.
Sural nerve or great auricular nerve grafting ^[1]	A segment of a sensory nerve is harvested and used as a cable graft to bridge the gap between proximal and distal facial nerve stumps	Primary resection of nerve in parotid cancer. Damage of a segment of nerve in traumatic cases ^[1]. Sural nerve is from the posterior calf (purely sensory — no motor deficit from harvest). Great auricular nerve is conveniently in the same surgical field during parotidectomy.
Facial-hypoglossal anastomosis ^[1]	The distal stump of the facial nerve is anastomosed to the hypoglossal nerve (CN XII)	If grafting not feasible ^[1]. This "borrows" motor axons from CN XII to reinnervate the face. Disadvantage: sacrifice of CN XII → ipsilateral tongue weakness and atrophy. Patient needs to "think about moving their tongue" to move their face initially, but cortical plasticity eventually allows more natural movement.
Cross-facial nerve grafting ^[1]	Anastomosis of normal contralateral buccal branch to the defective side ^[1]	When the proximal facial nerve stump is unavailable (e.g. destroyed by tumour near brainstem). A sural nerve graft is tunnelled across the face from the functioning buccal branch on the normal side to the defective side. Provides some voluntary symmetric movement. Takes 6–12 months for axons to grow across the graft.

Why sural nerve for grafting? It is long (up to 40 cm can be harvested), purely sensory (no motor deficit from loss), easily accessible at the posterior calf, and has a consistent anatomy. The great auricular nerve is an alternative — it's shorter but is already in the surgical field during parotidectomy, saving a second incision.

Why does nerve grafting work? After the graft is placed, the proximal axons undergo Wallerian degeneration of the distal graft segment first, then regenerating axons from the proximal stump grow through the graft's Schwann cell tubes (which act as scaffolding) at a rate of ~1 mm/day. The graft provides a structural conduit (the endoneurial tubes) that guides regenerating axons to the distal target muscles.

When nerve repair/grafting is not possible or has failed, static and dynamic reanimation procedures can improve aesthetics and function ^[1].

Surgery for facial reanimation ^[1]:

Technique	Details	Outcome
Fascial sling ^[1]	Aesthetic correction. Static sling to correct drooping of angle of mouth ^[1]. A strip of fascia lata (from the thigh) is tunnelled from the oral commissure to the zygomatic arch or temporal fascia to support the drooping mouth corner.	Restores facial symmetry at rest but does NOT provide movement.
Muscle sling — temporalis transfer ^[1]	Suture temporalis muscle to angle of mouth, can have voluntary movement ^[1]. The temporalis muscle (innervated by CN V3, trigeminal nerve) is detached from the coronoid process and its tendon is rerouted to the oral commissure.	Patient can achieve a smile by clenching their jaw (activating temporalis). Over time, cortical plasticity may allow more natural activation.
Free gracilis muscle graft with neurovascular bundle ^[1]	A segment of gracilis muscle (from the medial thigh) is transferred to the face as a free flap with its artery, vein, and obturator nerve. The nerve is anastomosed to either the cross-facial nerve graft or the masseteric nerve (CN V3).	Gold standard for facial reanimation in long-standing complete palsy. Provides dynamic, voluntary smile. Two-stage procedure if using cross-facial nerve graft.

Cause	Key Management	Special Notes
Bell's palsy	Prednisolone 1mg/kg/day × 5d + taper. Acyclovir/famciclovir × 5d. Eye care. Physiotherapy.	> 90% good recovery ^[1]. No proven benefit of surgical decompression ^[1].
Ramsay Hunt	High-dose acyclovir (800 mg 5×/d) × 7–10d + prednisolone. Eye care.	Worse prognosis than Bell's (~50–70% recovery).
AOM	IV antibiotics, myringotomy. Steroids.	Facial palsy usually resolves with infection control.
Cholesteatoma	Mastoid surgery to remove cholesteatoma ^[1]. Facial nerve decompression.	Semi-urgent surgical indication.
Temporal bone fracture	Immediate complete palsy → nerve exploration and decompression ^[1]. Delayed → steroids, observe.	Earlier the better ^[1]. ENoG < 10% → decompression ^[1].
Parotid malignancy	Parotidectomy ± nerve sacrifice + adjuvant RT. Nerve grafting if resected.	Sural nerve or great auricular nerve grafting ^[1].
CPA tumour	Microsurgical excision or stereotactic radiosurgery.	Facial nerve preservation is primary surgical goal.
GBS	IVIG or plasmapheresis. Supportive care.	Bilateral palsy; treat underlying cause.
Sarcoidosis	Systemic corticosteroids ± steroid-sparing agents.	Heerfordt syndrome: bilateral parotid + uveitis + facial palsy.

Since parotidectomy is one of the most common operations where facial nerve injury occurs, and the lecture explicitly covers this ^[1]:

Parotidectomy — Complications ^[1]:

Early ^[1]:

Bleeding / haematoma ^[1]
Facial nerve palsy ^[1]
- Transient ~5% ^[1] — due to traction, oedema, or cautery near the nerve. Usually recovers in weeks to months.
- Permanent ~1% ^[1] — due to transection, excessive cautery, or entrapment. Requires nerve repair/grafting.
Wound infection ^[1]
Salivary fistula ^[1] — saliva leaks through the wound because residual parotid tissue continues to secrete. Usually self-limiting. Can be managed with pressure dressings and anticholinergics.

Late (from the senior notes) ^[2]:

Frey syndrome (auriculotemporal syndrome / gustatory sweating) — sweating and flushing of the cheek during eating. Caused by aberrant regeneration of parasympathetic secretomotor fibres: after the auriculotemporal nerve is cut during parotidectomy, regenerating parasympathetic fibres (originally destined for salivary glands) grow into the severed sympathetic fibres that innervate sweat glands and cutaneous blood vessels. When the patient eats (triggering parasympathetic salivatory response), sweat glands and vessels in the parotid bed are stimulated instead → gustatory sweating and flushing. Affects ~30–50% of parotidectomy patients. Treatment: topical antiperspirant (glycopyrrolate cream), botulinum toxin injection.
Numbness of ear lobe — great auricular nerve is often sacrificed during parotidectomy.

Surgical decompression of nerve ^[1]:

	Details
Indications	Traumatic cause ^[1]; Middle ear infection ^[1]; Iatrogenic injury — middle ear or parotid surgery ^[1]
Bell's palsy	No proven benefits ^[1] — RCTs have not demonstrated significant improvement with decompression in Bell's palsy over medical therapy alone
Timing	Earlier the better ^[1]. Should NOT be undertaken if paralysis has been present for 14 days or more ^[2] — by this time, severe Wallerian degeneration is likely irreversible
Electrophysiological guidance	Electrical testing as indication for decompression — ENoG < 10% ^[1]
Imaging	Imaging for site of decompression ^[1] — CT temporal bone to localise the fracture line or area of compression, so the surgeon knows where to decompress
Approach	Transmastoid approach (most common) — opens the mastoid, identifies the nerve in the mastoid segment, and removes bone over the compressed segment. Middle cranial fossa approach — for labyrinthine segment decompression (more technically demanding).
Contraindications	Paralysis > 14 days (probably irreversible); patient unfit for general anaesthesia; incomplete palsy with good prognosis (doesn't need surgery)

High Yield Summary — Management of Facial Nerve Palsy

Bell's palsy: Prednisolone 1 mg/kg/day × 5 days then taper + acyclovir/famciclovir × 5 days + eye protection + physiotherapy. > 90% recover. Warn patient it may progress in first 3 weeks. Re-investigate if no improvement by 6 weeks.
Eye care is critical — lagophthalmos → exposure keratitis → corneal ulceration. All patients with incomplete eye closure need artificial tears (day), ointment + taping (night), and consideration of gold weight implantation if prolonged.
Identify and treat the cause: mastoid surgery for cholesteatoma, nerve exploration for traumatic immediate complete palsy, parotidectomy for malignancy.
Surgical decompression is indicated for traumatic, infective, and iatrogenic causes. NOT for Bell's palsy (no proven benefit). Earlier is better. ENoG < 10% guides the decision.
Nerve repair options: primary anastomosis (tension-free), sural/great auricular nerve grafting, facial-hypoglossal anastomosis (if grafting not feasible), cross-facial nerve grafting.
Facial reanimation for long-standing palsy: fascial sling (static), temporalis muscle transfer (dynamic), free gracilis muscle graft (gold standard for dynamic reanimation).
Parotidectomy complications: transient facial palsy ~5%, permanent ~1%, Frey syndrome (gustatory sweating from aberrant parasympathetic regeneration).

Active Recall - Management of Facial Nerve Palsy

References

^[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p14, p16, p17, p18, p19, p20, p21, p24, p62, p69, p79) ^[2] Senior notes: felixlai.md (sections on Facial nerve palsy treatment pp. 213–214, temporal bone fracture management p. 1124, parotidectomy complications p. 234)

Complications of Facial Nerve Palsy

Complications of facial nerve palsy arise from two broad sources: (A) consequences of the facial weakness itself — the direct functional losses from having a paralysed face; and (B) sequelae of aberrant nerve recovery — what happens when the nerve regenerates improperly. We also cover (C) complications of the surgical treatments (especially parotidectomy, the most commonly examined surgical complication set). Understanding each complication from its pathophysiological basis makes them easy to remember and predict.

A. Complications of Facial Weakness Itself

These occur because the facial nerve controls a remarkably wide range of functions — not just smiling. When any of these are lost, specific complications follow.

This is the number one clinical concern in any patient with facial palsy, regardless of cause.

Complication	Pathophysiological Basis	Details
Exposure keratitis	Orbicularis oculi weakness → lagophthalmos (inability to fully close the eye) → cornea is exposed to air, desiccation, and foreign bodies. Additionally, in proximal lesions, loss of greater petrosal nerve → ↓ lacrimation → ↓ tear film → cornea dries out even faster. Finally, the blink reflex (afferent CN V, efferent CN VII) is disrupted on the efferent limb, so the eye cannot blink protectively.	The corneal epithelium relies on the tear film for oxygen, nutrients, and mechanical protection. Without adequate coverage, epithelial cells desiccate and slough → punctate epithelial erosions → frank epithelial defect.
Corneal ulceration	Untreated exposure keratitis progresses. The denuded corneal stroma is vulnerable to secondary bacterial infection (Pseudomonas, Staphylococcus) → infectious corneal ulcer.	Can progress rapidly (hours) to corneal perforation, endophthalmitis, and permanent visual loss. This is why cornea is at risk due to poor eyelid closure and reduced tearing which may result in drying and abrasions ^[2] and why eye protection and eye drops ^[1] are non-negotiable.
Corneal scarring / opacification	Healed corneal ulcer leaves a scar (leucoma) → permanent visual impairment	Even with treatment, deep ulcers may leave visually significant scars
Epiphora (paradoxical tearing)	Despite reduced basal lacrimation (in proximal lesions), the exposed cornea triggers reflex tearing via CN V afferents → lacrimal gland oversecretion. Combined with lower lid laxity (orbicularis weakness) → tears overflow instead of draining into the punctum.	Patients complain "my eye is always watering" — this is NOT because they have too many tears, but because (a) reflex hypersecretion and (b) the lower lid sags away from the globe (ectropion) so tears don't reach the punctum.
Ectropion	Orbicularis oculi weakness → loss of tone in the lower lid → the lower lid falls away from the globe → exposure of conjunctiva, improper tear drainage	Contributes to both exposure keratitis (lower cornea exposed) and epiphora (tears miss the punctum)

Most Important Complication

Corneal damage is the most important acute complication of facial nerve palsy and the one most likely to cause permanent morbidity. Every patient with HB Grade III or worse must receive explicit eye protection instructions. The management was covered in the previous section: artificial tears (day), lubricating ointment + taping (night), protective glasses, and consideration of gold weight implantation or tarsorrhaphy for prolonged cases ^[2].

Complication	Pathophysiological Basis
Difficulty eating	Buccinator weakness → food accumulates in the buccal sulcus on the affected side because the buccinator normally pushes food medially back onto the occlusal surface. Orbicularis oris weakness → poor oral seal → difficulty containing food and liquid.
Drooling	Orbicularis oris weakness → incompetent oral sphincter → saliva dribbles from the affected corner of the mouth. This is NOT because of excess saliva production — it's a mechanical sealing problem.
Biting of the buccal mucosa	Without buccinator tone, the cheek falls inward between the teeth during chewing → repeated traumatic biting → mucosal ulceration
Aspiration risk	More relevant in bilateral palsy or when combined with other bulbar cranial neuropathies. The loss of oral competence means liquids may spill posteriorly into the pharynx before the swallow reflex is triggered.

Complication	Pathophysiological Basis
Speech difficulty	Orbicularis oris and buccinator weakness → difficulty with bilabial consonants (b, p, m, w) and labiodental consonants (f, v). The patient sounds "slushy" or mumbles. Not a dysarthria in the neurological sense (that involves tongue, palate, larynx) but a mechanical articulation problem.
Inability to whistle or blow	Orbicularis oris cannot form the tight seal needed
Facial disfigurement and psychosocial impact	The face is the primary vehicle for human social communication. Facial asymmetry → inability to smile, express emotions, or make eye contact comfortably. This leads to depression, social withdrawal, anxiety, reduced quality of life. Studies show psychosocial morbidity is often underestimated by treating physicians.
Loss of non-verbal communication	Facial expressions convey > 50% of emotional information. Loss of ability to smile, frown, or express surprise profoundly affects interpersonal relationships and professional life.

Complication	Pathophysiological Basis
Hyperacusis	Loss of nerve to stapedius → stapedius muscle paralysis → cannot dampen oscillation of the stapes → sounds (especially low-frequency) are perceived as abnormally and painfully loud on the affected side. This is functionally disabling — patients avoid noisy environments.

B. Complications of Aberrant Nerve Recovery (Sequelae of Regeneration)

These occur when axonal degeneration has happened (HB Grade V–VI initially) and the nerve regenerates, but the regenerating axons grow into the wrong Schwann cell tubes, ending up at unintended targets. Think of it as regenerating nerve fibres taking a "wrong turn" at the branching point.

Feature	Explanation
Definition	Involuntary movement of one group of facial muscles when another group is voluntarily activated
Mechanism	After axonal degeneration, regenerating motor axons from the proximal stump grow down the distal endoneurial tubes. But these tubes branch, and axons that originally innervated orbicularis oculi may instead grow down the tube leading to orbicularis oris (or vice versa). When the patient tries to close their eye, the mouth twitches — because the "eye-closing" axon now innervates mouth muscles.
Common patterns	Oral-ocular synkinesis: mouth moves when closing eye. Ocular-oral synkinesis: eye narrows when smiling. Platysmal synkinesis: neck tenses during facial expressions.
Incidence	Occurs in ~15–30% of Bell's palsy patients who had severe initial palsy (especially HB V–VI)
Management	Botulinum toxin injection to the overactive muscle group (temporarily paralyses the misdirected fibres). Mime therapy and biofeedback physiotherapy. Selective myectomy in severe cases.

Feature	Explanation
Definition	Tearing from the ipsilateral eye during eating
Mechanism	During regeneration, parasympathetic secretomotor fibres that originally ran in the chorda tympani (destined for the submandibular and sublingual glands → salivation) aberrantly regenerate into the pathway of the greater petrosal nerve (destined for the lacrimal gland → tearing). So when the patient eats (triggering a salivatory parasympathetic response), the signal reaches the lacrimal gland instead → tears flow while eating. The name "crocodile tears" comes from the myth that crocodiles weep while eating their prey.
Incidence	~6% of recovered Bell's palsy patients
Management	Botulinum toxin injection into the lacrimal gland, anticholinergic eye drops (e.g. ipratropium). Usually mild and tolerable.

Feature	Explanation
Definition	Chronic increased tone and tightness in the facial muscles on the affected side, giving a paradoxical appearance that the affected side looks "smaller" or "tighter" than the normal side
Mechanism	Aberrant reinnervation leads to co-contraction of multiple muscle groups at rest → chronic tonic contraction → fibrotic shortening of the muscles. The nasolabial fold may actually appear DEEPER on the affected side than the normal side (confusing for the examiner).
Management	Botulinum toxin to relax contracted muscles. Physiotherapy.

Feature	Explanation
Definition	Involuntary, intermittent, clonic contractions of muscles innervated by CN VII
Mechanism	Can occur as a late sequela of Bell's palsy due to aberrant regeneration and ephaptic transmission (cross-talk between adjacent demyelinated nerve fibres — an electrical impulse in one fibre jumps to a neighbouring fibre). Can also be caused by vascular compression of CN VII at the root exit zone (a different entity).
Management	Botulinum toxin injection (first-line). Microvascular decompression if caused by vascular compression.

Facial nerve palsy doesn't exist in isolation — it's often a sign of an underlying disease, and that disease can produce its own complications.

Underlying cause	Specific complications
Cholesteatoma	Extracranial complications: facial nerve paralysis, ossicular chain erosion, labyrinthitis, lateral SCC fistula, subcutaneous/subperiosteal abscess ^[3]. Intracranial complications: extradural abscess, subdural abscess, sigmoid sinus thrombophlebitis, meningitis, brain abscess — temporal lobe and cerebellum, otitic hydrocephalus ^[3]. The cholesteatoma erodes bone relentlessly, and each complication represents erosion into a different critical structure.
Temporal bone fracture	SNHL (cochlear damage), CSF otorrhoea (dural tear), meningitis (if CSF leak persists > 7 days), haemotympanum, conductive hearing loss (ossicular disruption)
Parotid malignancy	Local invasion (skin, mandible, EAC), cervical lymph node metastasis, distant metastasis (especially lung for adenoid cystic carcinoma — distant metastasis common: lung ^[1])
CPA tumour	Progressive hearing loss, trigeminal neuropathy, hydrocephalus (large tumour compresses 4th ventricle), brainstem compression

D. Complications of Surgical Treatment

This is explicitly covered in the lecture and is a favourite exam topic ^[1].

Early complications ^[1]:

Complication	Pathophysiological Basis	Incidence/Notes
Bleeding / haematoma ^[1]	Parotid bed is highly vascular (branches of external carotid artery — transverse facial, superficial temporal). Post-operative haematoma can cause airway compromise if large.	Requires urgent return to theatre for evacuation if expanding.
Facial nerve palsy ^[1]	The facial nerve runs through the parotid gland. During parotidectomy, the nerve must be identified and preserved (unless deliberately sacrificed for malignancy). Injury mechanisms: traction, cautery, inadvertent transection, oedema.	Transient ~5% ^[1] — neuropraxia from traction/oedema; recovers in weeks to months. Permanent ~1% ^[1] — transection or severe thermal injury; requires nerve grafting (sural nerve or great auricular nerve grafting ^[1]).
Wound infection ^[1]	Surgical site contamination, haematoma providing culture medium	Standard surgical wound infection management
Salivary fistula ^[1]	Residual parotid tissue (in superficial parotidectomy, the deep lobe is preserved) continues to secrete saliva → saliva tracks along the surgical wound and exits through the skin	Usually self-limiting (days to weeks). Management: pressure dressings, anticholinergic drugs (to reduce salivary secretion). Persistent fistula may require revision surgery or botulinum toxin injection.

Late complications ^[1]:

Complication	Pathophysiological Basis	Details
Recurrence ^[1]	Incomplete excision, especially for pleomorphic adenoma (which has pseudopods extending beyond the visible capsule — this is why avoid enucleation and tumour spillage ^[1])	Consider radiotherapy for recurrent tumour or prevention of recurrence in case of spillage ^[1]
Frey's syndrome — gustatory sweating ^[1]^[2]	Characterised by sweating and flushing of facial skin over parotid bed and neck during mastication ^[2]. Result of aberrant regeneration of cut parasympathetic fibres between the otic ganglion and salivary tissues which leads to innervation of sweat glands and subcutaneous vessels ^[2]. During parotidectomy, the auriculotemporal nerve (carrying parasympathetic fibres from otic ganglion to parotid) is inevitably severed. On regeneration, these parasympathetic fibres grow into the cut sympathetic fibres that innervate cutaneous sweat glands and blood vessels. When the patient eats → parasympathetic discharge → sweat glands activated and vessels dilate → sweating and flushing over the parotid bed.	Affects ~30–50% of patients. Diagnosed with Minor's starch-iodine test (paint iodine on the cheek, dust with starch, give patient something to eat → sweating areas turn blue-black). Treatment: topical glycopyrrolate cream, botulinum toxin injection into the affected skin (blocks cholinergic transmission to sweat glands).
Hypertrophic scar / keloid ^[1]	Abnormal wound healing with excessive collagen deposition	Pre-auricular incision is standard — usually heals well cosmetically, but keloid-prone individuals may develop hypertrophic scars
Sunken parotid area, cosmetic problem ^[1]	Removal of the parotid gland leaves a concavity in the pre-auricular region → facial asymmetry	Can be addressed with fat grafting, dermal fat graft, or acellular dermal matrix to fill the defect
Ear lobe numbness	The great auricular nerve (C2, C3) crosses the sternocleidomastoid and is often sacrificed or injured during parotidectomy → loss of sensation over the ear lobe and angle of mandible	Very common (almost universal); most patients adapt over time

Frey Syndrome — Exam Favourite

Frey syndrome is one of those topics that sounds exotic but is very commonly examined because it tests understanding of autonomic nerve regeneration. The key concept: parasympathetic fibres meant for salivary glands aberrantly reinnervate sympathetic targets (sweat glands, blood vessels). So eating (a parasympathetic stimulus) causes sweating and flushing (normally sympathetic responses). The diagnostic test is Minor's starch-iodine test. Treatment is botulinum toxin injection.

Complication	Mechanism
Facial nerve injury	The nerve runs in the posterior wall of the middle ear (mastoid segment) — at risk during drilling
Sensorineural hearing loss	Inadvertent damage to the inner ear (especially lateral semicircular canal) during surgery
CSF leak	Inadvertent breach of the tegmen tympani (roof of the middle ear) → communication with the middle cranial fossa
Meningitis	Secondary to CSF leak
Recurrent / residual cholesteatoma	Incomplete removal → requires revision surgery. This is why long-term follow-up with MRI DWI is needed.

Complication	Mechanism
SNHL	Transmastoid or middle cranial fossa approach risks damage to the inner ear
CSF leak	Middle cranial fossa approach involves retraction of the temporal lobe dura → potential dural tear
Failure to recover	If decompression is performed too late (> 14 days ^[2]) or if the degree of neural injury was too severe (neurotmesis — complete nerve disruption)
Worsened facial palsy	Surgical manipulation of an already oedematous nerve can occasionally worsen neuropraxia

Timing	Complication
Acute (first days)	Exposure keratitis (if eye care not instituted), aspiration (bilateral/severe palsy), speech difficulty
Subacute (weeks)	Corneal ulceration (if exposure keratitis untreated), psychological impact, weight loss from eating difficulty
Chronic (months)	Synkinesis, crocodile tears, contracture, hemifacial spasm (all from aberrant regeneration). Permanent corneal scarring.
Long-term (years)	Persistent disfigurement → psychosocial morbidity. Complications of underlying disease (recurrent cholesteatoma, tumour recurrence/metastasis).

High Yield Summary — Complications of Facial Nerve Palsy

Corneal damage (exposure keratitis → ulceration → scarring → blindness) is the most important preventable acute complication. All patients with incomplete eye closure need aggressive eye protection.
Synkinesis (~15–30% of severe Bell's palsy) results from aberrant axonal regeneration — motor axons grow into wrong Schwann cell tubes. Managed with botulinum toxin and physiotherapy.
Crocodile tears (gustatory lacrimation) — parasympathetic fibres meant for salivary glands aberrantly reinnervate the lacrimal gland. Patient tears while eating.
Frey syndrome (after parotidectomy) — parasympathetic fibres meant for the parotid gland aberrantly reinnervate sweat glands and cutaneous vessels. Patient sweats and flushes over the cheek while eating. Diagnosed by Minor's starch-iodine test. Treated with botulinum toxin.
Parotidectomy complications: early — bleeding/haematoma, facial nerve palsy (transient ~5%, permanent ~1%), wound infection, salivary fistula. Late — recurrence, Frey syndrome, hypertrophic scar, sunken parotid area.
Cholesteatoma complications (the cause of the facial palsy): extracranial (ossicular erosion, labyrinthitis, LSCC fistula, subperiosteal abscess) and intracranial (extradural/subdural abscess, meningitis, brain abscess, sigmoid sinus thrombophlebitis, otitic hydrocephalus).
Psychosocial impact is profound and often underestimated — the face is our primary tool of social communication.

Active Recall - Complications of Facial Nerve Palsy

References

^[1] Lecture slides: GC 217. Facial nerve palsy and salivary gland diseases.pdf (p7, p16, p17, p19, p21, p62, p69, p79, p80) ^[2] Senior notes: felixlai.md (sections on Facial nerve palsy treatment pp. 213–214, parotidectomy complications p. 234, Frey syndrome) ^[3] Lecture slides: GC 214. Common ear diseases and hearing loss (1).pdf (p12)

High Yield Summary

Facial nerve (CN VII) is a mixed nerve (motor, sensory/taste, parasympathetic, somatic sensory) with a very complex course through the temporal bone.
LMN palsy → entire ipsilateral face weak (forehead included). UMN palsy → forehead spared (bilateral cortical innervation to upper face nucleus).
Bell's palsy is the commonest cause (~50%), is idiopathic (? HSV reactivation), and > 90% recover well. It is a diagnosis of exclusion.
Localise the lesion using associated features: lacrimation (greater petrosal nerve), stapedial reflex/hyperacusis (nerve to stapedius), taste (chorda tympani).
Red flags requiring urgent investigation: progressive palsy > 3 weeks, bilateral palsy, associated CN deficits, parotid mass, history of malignancy, no recovery by 6 weeks.
Ramsay Hunt syndrome = VZV reactivation in geniculate ganglion → triad of facial palsy + otalgia + vesicles in ear.
House-Brackmann scale grades I (normal) to VI (total paralysis).
Management of Bell's palsy: prednisolone 1mg/kg/day for 5 days then taper + acyclovir/famciclovir for 5 days + eye protection + facial physiotherapy. Reconsider diagnosis if no improvement after 6 weeks.

High Yield Summary — Differential Diagnosis of Facial Nerve Palsy

Progressive weakness > 3 weeks → Tumour (parotid, CPA, facial nerve schwannoma, NPC)
No improvement after 6 weeks → Consider imaging ^[1]
Bilateral palsy → GBS, sarcoidosis, Lyme, leukaemia
Parotid mass → Malignant parotid tumour
Other CN deficits → CPA tumour, brainstem lesion, skull base pathology
Vesicles in ear → Ramsay Hunt (not Bell's)
History of head trauma → Temporal bone fracture
Chronic ear discharge → Cholesteatoma
Recurrent episodes → Facial nerve schwannoma, Melkersson-Rosenthal, recurrent Bell's (rare)
History of malignancy → Metastasis (leptomeningeal, intraparotid LN)

High Yield Summary — Diagnosis of Facial Nerve Palsy

Bell's palsy is a diagnosis of exclusion — you must rule out stroke (UMN), trauma, infection (AOM, cholesteatoma, Ramsay Hunt), and tumour (parotid, CPA) by clinical examination before applying the label.
Investigations depend on clinical findings — do NOT shotgun-investigate uncomplicated Bell's palsy.
House-Brackmann grading (I–VI) documents severity and tracks recovery. Grade IV is the first with incomplete eye closure; Grade VI is total paralysis.
ENoG is the most accurate electrodiagnostic test: stimulate at stylomastoid foramen, record at nasal alar. > 90% degeneration (< 10% response) → consider surgical decompression. < 90% degeneration → 80–100% spontaneous recovery.
Imaging:
- MRI brain → intracranial/CPA lesion
- MRI/CT temporal bone → middle ear pathology
- CT temporal bone → trauma
- MRI/CT parotid + USG FNA → parotid mass
Surgical decompression indications: traumatic cause, middle ear infection, iatrogenic injury. NOT indicated for Bell's palsy (no proven benefit). Earlier is better. ENoG < 10% guides the decision.
Red flag timeline: progress beyond 3 weeks → investigate. No improvement by 6 weeks → image.

High Yield Summary — Management of Facial Nerve Palsy

Bell's palsy: Prednisolone 1 mg/kg/day × 5 days then taper + acyclovir/famciclovir × 5 days + eye protection + physiotherapy. > 90% recover. Warn patient it may progress in first 3 weeks. Re-investigate if no improvement by 6 weeks.
Eye care is critical — lagophthalmos → exposure keratitis → corneal ulceration. All patients with incomplete eye closure need artificial tears (day), ointment + taping (night), and consideration of gold weight implantation if prolonged.
Identify and treat the cause: mastoid surgery for cholesteatoma, nerve exploration for traumatic immediate complete palsy, parotidectomy for malignancy.
Surgical decompression is indicated for traumatic, infective, and iatrogenic causes. NOT for Bell's palsy (no proven benefit). Earlier is better. ENoG < 10% guides the decision.
Nerve repair options: primary anastomosis (tension-free), sural/great auricular nerve grafting, facial-hypoglossal anastomosis (if grafting not feasible), cross-facial nerve grafting.
Facial reanimation for long-standing palsy: fascial sling (static), temporalis muscle transfer (dynamic), free gracilis muscle graft (gold standard for dynamic reanimation).
Parotidectomy complications: transient facial palsy ~5%, permanent ~1%, Frey syndrome (gustatory sweating from aberrant parasympathetic regeneration).

High Yield Summary — Complications of Facial Nerve Palsy

Corneal damage (exposure keratitis → ulceration → scarring → blindness) is the most important preventable acute complication. All patients with incomplete eye closure need aggressive eye protection.
Synkinesis (~15–30% of severe Bell's palsy) results from aberrant axonal regeneration — motor axons grow into wrong Schwann cell tubes. Managed with botulinum toxin and physiotherapy.
Crocodile tears (gustatory lacrimation) — parasympathetic fibres meant for salivary glands aberrantly reinnervate the lacrimal gland. Patient tears while eating.
Frey syndrome (after parotidectomy) — parasympathetic fibres meant for the parotid gland aberrantly reinnervate sweat glands and cutaneous vessels. Patient sweats and flushes over the cheek while eating. Diagnosed by Minor's starch-iodine test. Treated with botulinum toxin.
Parotidectomy complications: early — bleeding/haematoma, facial nerve palsy (transient ~5%, permanent ~1%), wound infection, salivary fistula. Late — recurrence, Frey syndrome, hypertrophic scar, sunken parotid area.
Cholesteatoma complications (the cause of the facial palsy): extracranial (ossicular erosion, labyrinthitis, LSCC fistula, subperiosteal abscess) and intracranial (extradural/subdural abscess, meningitis, brain abscess, sigmoid sinus thrombophlebitis, otitic hydrocephalus).
Psychosocial impact is profound and often underestimated — the face is our primary tool of social communication.

Facial Nerve Palsy

1. Definition

2. Epidemiology

3. Anatomy and Function of CN VII

3.1 Overview

3.2 Course of CN VII — Divided into 3 parts [1]

A. Pre-temporal bone

B. Intra-temporal bone (within the facial canal)

C. Post-temporal bone

4. Aetiology

4.1 Classification by Location

I. Intracerebral (Supranuclear / UMN Lesion) [1]

II. Facial Nucleus / Pons (LMN) [1]

III. CPA / Internal Acoustic Meatus [1]

IV. Temporal Bone [1]

V. Middle Ear [1]

VI. Beyond Stylomastoid Foramen [1]

4.2 Other Systemic / Bilateral Causes [2]

4.3 Bell's Palsy — The Most Common Cause

5. Pathophysiology

5.1 Why the Facial Canal Matters

5.2 UMN vs LMN — The Forehead Paradox

5.3 Localisation by Associated Features

6. Classification

6.1 By Type of Neuron

6.2 By Onset

6.3 House-Brackmann Grading System [2]

7. Clinical Features

7.1 Symptoms

7.2 Signs

7.3 Clinical Course (Bell's Palsy)

7.4 Late Sequelae (from aberrant regeneration / synkinesis)

8. Special Considerations for Hong Kong Practice

Active Recall - Facial Nerve Palsy

References

Conceptual Framework: How to Think About the DDx

DDx Organised by Anatomical Level

I. Intracerebral / Supranuclear (UMN Lesion)

II. Brainstem / Facial Nucleus in the Pons (LMN pattern, but "central")

III. Cerebellopontine Angle / Internal Acoustic Meatus [1]

IV. Temporal Bone [1]

V. Middle Ear [1]

VI. Beyond Stylomastoid Foramen [1]

Systemic / Bilateral Causes

DDx by Clinical Presentation Pattern

Hong Kong–Specific Considerations

Summary: The "Must-Not-Miss" Differentials

Active Recall - DDx of Facial Nerve Palsy

Key Principle: There Is No Single "Diagnostic Criterion" for Facial Nerve Palsy

Diagnostic Criteria for Bell's Palsy (Clinical Diagnosis of Exclusion)

Severity Grading: House-Brackmann Classification [1][2]

Diagnostic Algorithm

Investigation Modalities

A. Clinical Examination (The Most Important "Investigation")

i. Motor Testing of CN VII [2]

ii. UMN vs LMN Distinction [1][2]

iii. Localisation Tests [2]

iv. Other Examination Components

B. Electrophysiological Testing

i. Electroneurography (ENoG)

ii. Electromyography (EMG) [2]

iii. Nerve Conduction Studies (NCS) [2]

C. Imaging

i. MRI Brain — for suspected intracranial lesion [1]

ii. MRI/CT Temporal Bone — if middle ear pathology is suspected [1]

iii. CT Temporal Bone — temporal bone trauma [1]

iv. MRI/CT Parotid and USG FNA — if parotid lesion is suspected [1]

v. Additional Imaging in Specific Scenarios

D. Blood Tests

Putting It All Together: When to Investigate

Surgical Decompression: The Decision Algorithm

Active Recall - Diagnosis of Facial Nerve Palsy

Overarching Principle

Master Management Algorithm

I. Management of Bell's Palsy (The Commonest Scenario)

Step 0: Confirm the Diagnosis

Step 1: Corticosteroids

Step 2: Antivirals

Step 3: Eye Protection

Step 4: Physiotherapy