Origin - Nucleus in the pons

Exit → Stylomastoid foramen

Upper part of VIIth nucleus supply upper face (principally frontalis) bilaterally

Largely motor

Supplies muscles of facial expression

Chorda tympani◦ Motor fibres to the stapedius muscle◦ Sensory taste fibres from the anterior two-thirds

of the tongue

Upper motor neuron (UMN lesions)◦ Facial Nucleus and above

Lower motor neuron (LMN) lesions◦ Below facial nucleus

Upper motor neurone (UMN lesions)

Lower motor neurone (LMN) lesions

Contralateral IpsilateralLower part Entire faceFrontalis (frowning) spared Frontalis (frowning) affectedEye closure/blinking present Eye closure/blinking absentNo corneal exposure and ulceration

Corneal exposure and ulceration

Angle of the mouth falls; unilateral dribbling

Relative preservation of spontaneous emotional movement

Taste sensation is frequently also impaired

UMN-◦ Cerebrovascular accident (stroke)

LMN

LMN-◦ Pons

Tumours (e.g. glioma) Multiple Sclerosis Infarction

◦ Cerebellopontine angle (CPA) – V+VI+VII+VIIIA Acoustic neuroma Meningioma Metastasis Cholesteatoma

◦ Petrous temporal bone Bell’s palsy Trauma Middle ear infection Herpes zoster

LMN-◦ Beyond the skull

Skull base tumours Paget’s disease of bone Parotid gland tumours Sarcoidosis Trauma.

Acute isolated facial palsy Why?

?Viral infection (often herpes simplex) Lyme disease HIV seroconversion

Nerve swollen - petrous bone facial canal Unilateral LMN

Evolves over 24–48 hours Taste on the tongue may be lost/altered Hyperacusis Pain behind the ear is common at onset Suspect a stroke Vague altered facial sensation Examination of facial sensation - normal.

Prognosis good Recurrence unlikely Recovery-

◦ 3–8 weeks◦ At least 85%◦ Complete/near complete

Eye care◦ Lubricants◦ Taping, lateral tarsorrhaphy, gold weight

Drugs◦ Steroids early◦ Prednisolone 1mg/kg/day X 7 days

Rare Often less obviously apparent - no facial asymmetry Causes:

◦ Infections: Lyme (bilateral in 25% – Bannwarth’s syndrome) Viral: HIV seroconversion, EBV Mastoiditis (bilateral) Diphtheria and botulism (rare)

◦ Sarcoidosis◦ Skull base trauma and tumours◦ Pontine lesions, e.g. gliomas◦ Neuromuscular disorders:

Guillain–Barré syndrome Myasthenia Myotonic dystrophy and facioscapulohumeral dystrophy

◦ Congenital and genetic causes

Teeth Gums Paranasal sinuses Temporomandibular joints Jaw Eyes Neurological conditions

Trigeminal◦ Autonomic cephalgias◦ Neuralgia

Migraine Carotid dissection Giant cell arteritis (temporal arteritis) Atypical facial pain (somatisation?)

6th and 7th decades Hypertension - main risk factor

Compression At or near the pons Ectatic vascular loop High res MRI

Younger patients Multiple sclerosis CP angle tumours

◦ Acoustic schwannomas◦ Meningiomas◦ Epidermoids

Paroxysms pain Knife-like/electric shock-like Lasting seconds Vth nerve distribution Starts in mandibular division (V3) →

maxillary (V2) → occasionally ophthalmic divisions (V1).

Bilateral ◦ Rare (3%)◦ Intrinsic brainstem pathology (demyelination)

Many times a day Trigger

◦ Trigger zones in the face◦ Washing, shaving, cold wind, chewing

Drugs:-◦ Carbamazepine (600–1200 mg daily)◦ Oxcarbazepine, lamotrigine, gabapentin

Surgical:-◦ Percutaneous radiofrequency selective ablation of

the trigeminal ganglion◦ Microvascular decompression

Spontaneous remissions◦ Months or years

BUT almost invariably recur