Medicine – Facial Nerve (Cranial Nerve VII)

The facial nerve, cranial nerve VII, is a mixed cranial nerve with motor, sensory, special sensory, and parasympathetic functions. A useful way to remember its major functions is:

Face + Ear + Taste + Tears + Saliva.

Its most obvious function is controlling the muscles of facial expression, but it also supplies the stapedius muscle, carries taste from the anterior two-thirds of the tongue, and provides parasympathetic fibres to the lacrimal and salivary glands.

1. Motor Supply to the Face

The facial nerve provides motor innervation to the muscles of facial expression.

These muscles allow a person to:

Raise the eyebrows.

Close the eyes tightly.

Smile.

Show the teeth.

Puff out the cheeks.

Frown.

Weakness of these movements is therefore an important sign of facial nerve dysfunction.

2. Upper versus Lower Facial Muscles

The cortical control of the facial nucleus is clinically important.

The part of the facial nucleus controlling the upper face receives corticobulbar input from both cerebral hemispheres.

The part controlling the lower face receives predominantly contralateral cortical input.

This explains the major difference between upper motor neurone and lower motor neurone facial palsy.

3. Motor Supply to Stapedius

The facial nerve supplies the stapedius muscle in the middle ear.

Stapedius normally reduces excessive movement of the stapes in response to loud sounds.

Facial nerve damage proximal to the stapedius branch can therefore cause hyperacusis, meaning that ordinary sounds are perceived as abnormally loud or uncomfortable.

Therefore:

CN VII lesion → stapedius paralysis → hyperacusis.

4. Sensory Supply to the Ear

The facial nerve carries a small amount of general somatic sensation from part of the external auditory canal and external ear.

This sensory territory is small because most sensation around the ear is supplied by other nerves.

Nevertheless, the association of CN VII with the external auditory canal becomes particularly relevant in Ramsay Hunt syndrome.

5. Taste

Taste fibres from the anterior two-thirds of the tongue travel through the chorda tympani, a branch associated with the facial nerve.

Therefore, a facial nerve lesion proximal to the origin of the chorda tympani can produce:

Reduced or absent taste from the anterior two-thirds of the tongue on the affected side.

6. Chorda Tympani

The chorda tympani has two particularly important functions.

It carries:

Taste fibres from the anterior two-thirds of the tongue.

and

Parasympathetic secretomotor fibres to the submandibular and sublingual salivary glands.

Therefore, CN VII is involved not only in taste but also in salivation.

7. Lacrimal Gland

Parasympathetic fibres associated with the facial nerve supply the lacrimal gland through the greater petrosal nerve and associated pathways.

These fibres stimulate tear production.

A sufficiently proximal facial nerve lesion can therefore impair lacrimation and contribute to dryness of the eye.

8. Salivary Glands

The facial nerve also provides parasympathetic secretomotor fibres to:

Submandibular gland.

Sublingual gland.

The parotid gland is not supplied parasympathetically by the facial nerve.

Its secretomotor parasympathetic supply comes from the glossopharyngeal nerve, CN IX.

This distinction is clinically important because the facial nerve passes through the parotid gland but does not provide its secretomotor innervation.

9. Facial Nerve Branches

After leaving the stylomastoid foramen, the facial nerve enters the parotid gland and divides into five major terminal motor branches.

These are:

Temporal.

Zygomatic.

Buccal.

Marginal mandibular.

Cervical.

10. Correction to the Original Branch List

The original list gives:

Temporal, ophthalmic, maxillary, mandibular and cervical.

This mixes the branches of the facial nerve with divisions of the trigeminal nerve, CN V.

The correct five terminal branches of CN VII are:

Temporal → Zygomatic → Buccal → Marginal mandibular → Cervical.

11. Easy Memory for the Five Branches

A traditional mnemonic is:

To Zanzibar By Motor Car

T → Temporal

Z → Zygomatic

B → Buccal

M → Marginal mandibular

C → Cervical

These are motor branches supplying the muscles of facial expression.

12. Trigeminal Nerve Branches – Important Distinction

The terms ophthalmic, maxillary and mandibular belong primarily to the trigeminal nerve, cranial nerve V.

They are:

V1 → Ophthalmic.

V2 → Maxillary.

V3 → Mandibular.

Therefore:

CN V → Ophthalmic, Maxillary, Mandibular.

CN VII → Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical.

13. Facial Nerve Palsy

Facial weakness can result from either an:

Upper motor neurone lesion.

or

Lower motor neurone lesion.

The pattern of facial weakness helps localise the lesion.

14. Upper Motor Neurone Facial Palsy

An UMN facial palsy results from damage to corticobulbar pathways above the facial nucleus.

Because the upper facial muscles receive bilateral cortical innervation, they are relatively preserved in a unilateral UMN lesion.

Therefore, an UMN lesion classically causes:

Contralateral lower facial weakness with relative forehead sparing.

15. Forehead Sparing

Suppose a patient has a left cerebral stroke affecting corticobulbar fibres.

The patient may develop:

Right lower facial weakness.

However, the patient may still be able to wrinkle the forehead and close the eyes relatively well because the upper facial nucleus receives bilateral cortical input.

Therefore:

Forehead sparing → think UMN lesion.

16. Causes of UMN Facial Weakness

Important causes include:

Stroke.

Multiple sclerosis.

Intracranial tumour or other central structural lesions.

These lesions affect the corticobulbar pathways rather than the peripheral facial nerve itself.

17. Stroke

Stroke is an important cause of acute UMN facial weakness.

The typical pattern is:

Contralateral lower facial weakness + forehead relatively spared.

Other neurological deficits may occur simultaneously, such as:

Arm or leg weakness.

Dysarthria.

Sensory abnormalities.

Aphasia, depending on the site of the stroke.

18. Multiple Sclerosis

Multiple sclerosis can produce facial weakness when demyelinating lesions involve central corticobulbar pathways or the facial nerve pathway within the brainstem.

The exact clinical pattern therefore depends on the location of the demyelinating plaque.

Other neurological manifestations of MS may coexist.

19. Lower Motor Neurone Facial Palsy

An LMN facial palsy occurs when the facial nucleus in the pons or the facial nerve itself is affected.

The lesion causes weakness of the entire ipsilateral half of the face.

Therefore, the patient may be unable to:

Wrinkle the forehead.

Close the eye tightly.

Smile normally.

Puff out the cheek.

20. LMN Facial Palsy and the Forehead

Unlike an UMN lesion, an LMN lesion does not spare the forehead.

Therefore:

Whole ipsilateral face weak → LMN facial palsy.

Contralateral lower face weak with forehead spared → UMN facial palsy.

This is one of the most useful bedside distinctions.

21. Bell Palsy

Bell palsy is an acute idiopathic peripheral facial nerve palsy and is one of the most common causes of an isolated LMN facial palsy.

It usually develops rapidly, often over hours.

The patient develops unilateral weakness involving both the upper and lower face.

22. Features of Bell Palsy

Patients may have:

Unilateral facial weakness.

Inability to close the affected eye completely.

Drooping of the corner of the mouth.

Difficulty drinking because fluid escapes from the mouth.

Reduced taste, depending on lesion location.

Hyperacusis, depending on involvement of the stapedius branch.

Some patients experience discomfort around the ear.

23. Eye Protection in Bell Palsy

Inability to close the eyelid can expose the cornea.

This may lead to:

Corneal dryness.

Exposure keratitis.

Corneal ulceration in severe cases.

Therefore, eye protection and lubrication are important when eye closure is impaired.

24. Ramsay Hunt Syndrome

Ramsay Hunt syndrome is caused by reactivation of varicella-zoster virus involving the facial nerve, usually around the geniculate ganglion.

It can produce a severe LMN facial palsy.

25. Features of Ramsay Hunt Syndrome

The classic pattern includes:

Ipsilateral LMN facial weakness.

Severe ear pain.

Vesicular eruption in or around the external auditory canal or pinna.

Vestibulocochlear involvement may also produce:

Hearing loss.

Tinnitus.

Vertigo.

Therefore:

Facial palsy + painful ear vesicles → Ramsay Hunt syndrome.

26. Acoustic Neuroma

The older term acoustic neuroma generally refers to a vestibular schwannoma.

This is a benign tumour usually arising from the vestibular component of CN VIII.

As the tumour enlarges, it may compress nearby cranial nerves, including CN VII.

The more typical early presentation is:

Progressive unilateral sensorineural hearing loss.

Unilateral tinnitus.

Imbalance.

Facial weakness tends to occur with larger lesions rather than being the usual initial manifestation.

27. Parotid Tumours

The facial nerve passes through the parotid gland, where it divides into its terminal branches.

A parotid tumour can therefore compress or invade the facial nerve and produce an LMN facial palsy.

Facial weakness associated with a parotid mass is particularly concerning for malignant involvement and requires investigation.

28. Guillain–Barré Syndrome

Guillain–Barré syndrome can involve the facial nerves.

Facial weakness is frequently bilateral, although it may initially be asymmetric.

Other features may include:

Ascending limb weakness.

Areflexia.

Sensory symptoms.

Autonomic dysfunction.

Respiratory weakness.

Therefore:

Bilateral LMN facial weakness + areflexic ascending weakness → consider GBS.

29. Examination of the Facial Nerve

To examine the motor component of CN VII, ask the patient to:

Raise the eyebrows.

Wrinkle the forehead.

Close the eyes tightly.

Show the teeth.

Smile.

Puff out the cheeks.

These movements allow assessment of different facial muscle groups and help determine whether weakness involves the upper face, lower face, or both.

30. UMN versus LMN Facial Palsy – Note Form

UMN lesion: corticobulbar pathway above facial nucleus.

LMN lesion: facial nucleus or facial nerve.

UMN weakness: mainly contralateral lower face.

LMN weakness: entire ipsilateral half of face.

UMN forehead: relatively spared.

LMN forehead: weak.

UMN eye closure: relatively preserved.

LMN eye closure: impaired.

UMN causes: stroke, MS, intracranial tumour.

LMN causes: Bell palsy, Ramsay Hunt syndrome, vestibular schwannoma, parotid tumour and GBS.

31. Facial Nerve – Note Form

Cranial nerve: VII.

Motor: muscles of facial expression.

Ear: supplies stapedius.

Stapedius paralysis: may cause hyperacusis.

General sensation: small area of external auditory canal/external ear.

Taste: anterior two-thirds of tongue via chorda tympani.

Tears: parasympathetic supply to lacrimal gland.

Saliva: parasympathetic supply to submandibular and sublingual glands.

Five terminal branches: temporal, zygomatic, buccal, marginal mandibular and cervical.

Bell palsy: acute LMN facial palsy affecting the whole ipsilateral face.

Ramsay Hunt: facial palsy + painful vesicles around/in the ear ± hearing or vestibular symptoms.

Stroke: usually contralateral lower facial weakness with forehead sparing.

GBS: may produce bilateral LMN facial weakness.

Key Clinical Pattern

Remember the main functions of CN VII as:

FACE + EAR + TASTE + TEARS + SALIVA.

The five terminal branches are:

Temporal → Zygomatic → Buccal → Marginal mandibular → Cervical.

The most important localisation rule is:

UMN lesion → contralateral LOWER face weak + forehead spared.

LMN lesion → ipsilateral WHOLE face weak + forehead involved.

And remember:

Bell palsy → isolated LMN facial palsy.

Ramsay Hunt → LMN facial palsy + painful ear vesicles.

Stroke → UMN facial weakness with forehead sparing.