Facial Nerve Palsy

Anatomy of the Facial Nerve (CN VII)

• Greater superficial petrosal nerve - carries parasympathetic fibers to the lacrimal gland
• Nerve to stapedius - stapedius reflex
• Chorda tympani - taste to anterior 2/3 of tongue; submandibular/sublingual salivary glands

Upper vs. Lower Motor Neuron Lesion

Causes by Anatomical Level

Supranuclear (UMN)

• Stroke (most common in older adults)
• Brain tumor
• Multiple sclerosis

Nuclear / Fascicular (Brainstem)

• Demyelination (MS)
• Ischemia, hemorrhage
• Neoplasm
• Millard-Gubler syndrome (ipsilateral CN VI + VII palsy, contralateral hemiplegia)

Cerebellopontine Angle

• Acoustic schwannoma (hearing loss is usually the primary feature; facial weakness suggests facial schwannoma with a "labyrinthine tail" on MRI)
• Meningioma
• Facial nerve schwannoma

Intratemporal (Geniculate Ganglion and Below)

• Bell's palsy (idiopathic - most common cause of LMN facial palsy overall)
• Ramsay Hunt syndrome (herpes zoster oticus - VZV reactivation in geniculate ganglion)
• Acute otitis media / mastoiditis
• Temporal bone fracture
• Cholesteatoma, glomus tumor
• Lyme disease (Borrelia burgdorferi - can cause bilateral facial palsy)
• Sarcoidosis

Extracranial (Parotid, Face)

• Parotid gland tumors (malignant) - can track along the nerve perineural spread
• Trauma, surgery
• Parotiditis

Bell's Palsy

• Acute-subacute onset, maximal within 72 hours
• Ipsilateral weakness of the entire face (forehead included)
• Pain in/around the ear (60% of patients)
• Impaired lacrimation (60%)
• Taste changes - anterior 2/3 tongue (30-50%)
• Hyperacusis (15-30%)
• Ipsilateral facial sensory symptoms (via trigeminal-facial nerve connection via greater superficial petrosal nerve)
• MRI may show enhancement of the facial nerve, most commonly at the geniculate ganglion

Ramsay Hunt Syndrome (Herpes Zoster Oticus)

• Triad: LMN facial palsy + herpetic vesicles in the ear (auricle/external auditory canal) + sensorineural hearing loss/vertigo
• Otalgia is often severe
• Treatment: prednisolone + acyclovir/valacyclovir (combination superior to steroids alone in this condition)
• Recovery rate is lower than Bell's palsy

Grading - House-Brackmann Scale

Key Clinical Red Flags

• Progressive palsy over >3 weeks - suspect underlying neoplasm
• Incomplete palsy not recovering after 3-6 weeks - suspect neoplasm
• Ipsilateral recurrence - 6 of 20 patients in one series had a tumor as the cause
• Bilateral concurrent palsy - think systemic: Guillain-Barré syndrome, sarcoidosis, Lyme disease, lymphoma, leukemia, Moebius syndrome
• Other cranial nerve signs (e.g., CN VI + VII = Gradenigo syndrome from petrous apex inflammation)

Investigations

Management

Bell's Palsy

• First-line: Prednisolone (e.g., 50-60 mg/day x 10 days)
• Started within 72 hours of onset (ideally within 48 hours) for best outcomes
• Meta-analyses show 17% better chance of complete recovery compared to placebo; recovery rates 49-97% with steroids vs 23-64% untreated
• Evidence is less clear in children

• Combined with steroids for severe Bell's palsy
• A Cochrane review found combination therapy (antivirals + steroids) reduces synkinesis and excessive tearing compared to steroids alone
• However, the AAN guideline (2012) concluded antivirals alone add at most a 7% improvement in recovery; benefit, if any, is modest
• Benefit is clearer in Ramsay Hunt syndrome

• Lubricating eye drops/ointment
• Taping the eye closed at night
• Moisture chamber spectacles
• Tarsorrhaphy if permanent lagophthalmos (gold weight upper lid insertion for paralytic ectropion/facial nerve palsy is another option)

• Transmastoid decompression of tympanic/mastoid segments: abandoned (randomized trials showed no benefit; lesion is in the proximal labyrinthine segment, which this approach cannot reach)
• Decompression of the meatal foramen and labyrinthine segment (middle fossa approach): remains controversial; limited high-quality evidence
• In AOM-related palsy: ventilation tube insertion + IV antibiotics resolves ~80% of cases; cortical mastoidectomy for the remainder

Traumatic Facial Palsy

• Immediate palsy after trauma (complete, no chance of recovery without intervention): consider early exploration and decompression
• Delayed palsy: generally favorable prognosis; managed conservatively initially
• Facial nerve injury is usually at/just distal to the geniculate ganglion in longitudinal temporal bone fractures, and just proximal to the geniculate ganglion in transverse fractures

Sequelae and Aberrant Regeneration

• Synkinesis: involuntary co-contraction (e.g., eye closure when smiling) - affects ~17% after Bell's palsy; can worsen for up to 1 year
• "Crocodile tears" (gustatory lacrimation): aberrant regeneration of salivary fibers into lacrimal gland - tearing occurs during eating
• Hemifacial spasm: involuntary episodic contractions, often caused by vascular compression at the brainstem exit of CN VII; treat with botulinum toxin or microvascular decompression
• Contracture: hypertonia and shortening of the affected side, causing the nasolabial fold to deepen and palpebral fissure to narrow (paradoxically looks "normal" compared to the unaffected side at rest)

Recent Evidence (2024-2026)

• Laser therapy for Bell's palsy (2024) found some evidence for low-level laser therapy in randomized trials, though quality of evidence remains limited [PMID: 39546047]
• Physical therapy for idiopathic facial paralysis (2025) supports neuromuscular retraining, mime therapy, and facial exercise in recovery [PMID: 39647183]
• Traumatic facial palsy management (2025) systematic review confirms outcomes vary by mechanism and timing of intervention [PMID: 40287586]

Demyelination

Definition

• Oligodendrocytes - in the CNS (each oligodendrocyte myelinates multiple axons)
• Schwann cells - in the PNS (each Schwann cell myelinates one internode of one axon)

The Normal Myelin System

• The axon is wrapped in segments called internodes (between consecutive nodes of Ranvier)
• Voltage-gated Na⁺ channels are concentrated at the nodes of Ranvier, not in the internodal membrane
• An action potential at one node generates ionic current that flows under the myelin to the next node and fires it - this is saltatory conduction
• K⁺ channels help terminate the current and repolarize the axon
• Safety factor for transmission is normally 5-7 times above threshold - highly reliable

What Happens When Myelin is Lost

1. Current leaks out through the now-exposed internodal axon membrane instead of jumping to the next node
2. Conduction slows dramatically or fails altogether (conduction block)
3. The widening of nodes of Ranvier is the earliest change, causing initial slowing of conduction velocity
4. More severe demyelination causes conduction block - complete failure of impulse transmission across the affected segment
5. Asynchronous conduction in different fibers within the same nerve bundle can abolish functions that depend on synchronized firing (e.g., deep tendon reflexes, vibration sense), causing paresthesias

"The main physiologic effect of demyelination is to impede saltatory electrical conduction of nerve impulses from one node of Ranvier... to the next node." - Adams and Victor's Principles of Neurology

The Key Diagram: Three Types of Nerve Pathology

Segmental Demyelination (Classic Form)

• The myelin sheath disappears over segments of variable length, bounded on each end by a node of Ranvier
• The axon is spared - this is what distinguishes it from Wallerian degeneration
• Schwann cells (or oligodendrocytes) survive and can attempt remyelination, but new myelin sheaths are thinner and shorter - yielding permanently slower conduction velocity even after "recovery"
• Adams and Victor's Principles of Neurology

Demyelination vs. Other Nerve Pathology

Physiological Consequences

• Uhthoff phenomenon (classic in MS): temporary worsening of symptoms with increased body temperature or exercise, because a partially demyelinated axon's safety margin drops below threshold when temperature rises slightly
• Evoked potential delays: demyelination of the optic nerve causes prolonged visual evoked potential latencies - a key diagnostic finding in MS
• Recovery after acute demyelination: in the short term (days), recovery reflects subsidence of edema and inflammation, not true remyelination. Remyelination is a slower, partial process

Causes of Demyelination

CNS Demyelination

PNS Demyelination

Key Difference: Demyelination vs. Axonal Loss

• Demyelination → Slowed conduction velocity + prolonged distal latency + conduction block on NCS; muscle bulk and power relatively preserved early; good recovery potential
• Axonal loss → Reduced amplitude of compound muscle/sensory action potentials on NCS; muscle wasting and weakness more prominent; poorer recovery