# Facial Nerve Paralysis: Evaluation and Management

## Overview
Facial nerve (CN VII) paralysis is a common and distressing condition encountered in otolaryngology. Etiologies range from idiopathic (Bell palsy) to traumatic, infectious, and neoplastic. Systematic evaluation with topographic diagnosis and electrodiagnostic testing guides management. Timely intervention can significantly improve outcomes.

## Facial Nerve Anatomy

### Intracranial Segment
Motor nucleus in the pons; upper face receives bilateral cortical input, lower face receives contralateral input only. Nerve root exits the brainstem at the pontomedullary junction. Courses through the cerebellopontine angle (CPA) with CN VIII.

### Intratemporal Segments
**Meatal (IAC) segment**: 8-10 mm; within the internal auditory canal; narrowest portion at the meatal foramen (fundus) -- most susceptible to compression. **Labyrinthine segment**: 3-5 mm; shortest and narrowest bony segment; from fundus to geniculate ganglion; contains the greater superficial petrosal nerve (GSPN) branch (lacrimation). **Tympanic (horizontal) segment**: 8-11 mm; from geniculate ganglion across the medial wall of the middle ear, superior to the oval window, inferior to the lateral SCC. **Mastoid (vertical) segment**: 10-14 mm; descends from the second genu to the stylomastoid foramen; gives off the nerve to stapedius and chorda tympani.

### Extratemporal Segment
Exits stylomastoid foramen. Gives off posterior auricular nerve (occipitalis, posterior auricular muscles), nerve to posterior belly of digastric, nerve to stylohyoid. Enters the parotid gland; divides at pes anserinus into upper (temporozygomatic) and lower (cervicofacial) divisions. Terminal branches: temporal, zygomatic, buccal, marginal mandibular, cervical.

### Topographic Diagnosis
**Above geniculate ganglion**: loss of lacrimation (Schirmer test), taste (chorda tympani), stapedial reflex, and motor function. **Below GSPN, above nerve to stapedius**: preserved lacrimation; absent stapedial reflex, taste, motor. **Below stapedius nerve, above chorda tympani**: preserved lacrimation and stapedial reflex; absent taste and motor. **Below chorda tympani**: motor loss only.

## Grading Systems

### House-Brackmann Scale (most widely used)

| Grade | Description | Key Features |
|-------|-------------|--------------|
| I | Normal | Normal function in all areas |
| II | Slight dysfunction | Normal symmetry at rest; complete eye closure with effort |
| III | Moderate dysfunction | Obvious but not disfiguring weakness; incomplete eye closure |
| IV | Moderately severe | Obvious disfiguring weakness; incomplete eye closure; asymmetric mouth |
| V | Severe dysfunction | Barely perceptible motion; incomplete eye closure; slight mouth movement |
| VI | Total paralysis | No movement |

**Grade I**: Normal. **Grade II**: Slight weakness; normal symmetry at rest; complete eye closure with effort. **Grade III**: Obvious weakness, not disfiguring; incomplete eye closure; slight mouth asymmetry. **Grade IV**: Obvious disfiguring weakness; incomplete eye closure; asymmetric mouth movement. **Grade V**: Barely perceptible motion; incomplete eye closure; slight mouth movement. **Grade VI**: No movement (complete paralysis).

### Sunnybrook Facial Grading System
More detailed; assesses resting symmetry, voluntary movement, and synkinesis separately. Composite score 0-100; more sensitive to change over time, Increasingly used in research and clinical practice.

## Etiologies

### Bell Palsy (Idiopathic)
Most common cause (~70% of acute facial paralysis). Presumed viral etiology (HSV-1 reactivation in geniculate ganglion). Acute onset over 24-72 hours; unilateral, Peak incidence 15-45 years; slight female predominance. Risk factors: pregnancy (3rd trimester/postpartum), diabetes, upper respiratory infection.

### Ramsay Hunt Syndrome (Herpes Zoster Oticus)
Varicella-zoster virus (VZV) reactivation in geniculate ganglion. Triad: facial paralysis, otalgia, vesicular eruption on ear (concha, EAC) or palate. Vesicles may appear before, during, or after paralysis (zoster sine herpete: paralysis without vesicles). Worse prognosis than Bell palsy: complete recovery in only ~50-70% vs. 85% for Bell palsy. May involve CN VIII (sensorineural hearing loss, vertigo).

### Traumatic
Temporal bone fractures: transverse (otic capsule disrupting) > longitudinal (otic capsule sparing). Iatrogenic: mastoid surgery, parotid surgery, facial cosmetic surgery. Penetrating trauma, Birth trauma (forceps delivery).

### Neoplastic
Facial nerve schwannoma, hemangioma. Parotid malignancy (mucoepidermoid carcinoma, adenoid cystic carcinoma). CPA tumors (vestibular schwannoma, meningioma), Temporal bone malignancy (SCC). Red flags: slowly progressive paralysis, recurrent ipsilateral paralysis, associated mass.

### Other Etiologies
Acute otitis media (dehiscent fallopian canal), Cholesteatoma, Lyme disease (bilateral facial paralysis in endemic areas). Sarcoidosis (Heerfordt syndrome: parotid enlargement, uveitis, facial palsy, fever). Melkersson-Rosenthal syndrome (recurrent facial paralysis, facial edema, fissured tongue). Autoimmune: Guillain-Barre syndrome, multiple sclerosis. Congenital: Mobius syndrome, birth trauma.

## Electrodiagnostic Testing

### Electroneurography (ENoG)
Supramaximal electrical stimulation of the facial nerve at stylomastoid foramen; compound muscle action potential (CMAP) recorded at nasolabial fold. Compares amplitude of affected to unaffected side. >90% degeneration within 14 days = poor prognosis; consider surgical decompression [CONTROVERSY]. Most useful between days 3-14 after onset (Wallerian degeneration takes 72 hours). Not useful after 3 weeks (nerve too degenerated for stimulation).

### Electromyography (EMG)
Needle electrode in facial muscles records motor unit potentials. Fibrillation potentials: spontaneous activity from denervated muscle (appears 2-3 weeks after injury). Polyphasic potentials: sign of reinnervation. Useful after 3 weeks when ENoG is no longer informative. Voluntary motor unit potentials = intact axons (good prognostic sign).

## Management of Bell Palsy

### Medical Treatment
**Corticosteroids**: strong evidence (multiple RCTs); prednisone 1 mg/kg/day (max 60-80 mg) for 7-10 days, started within 72 hours of onset. **Antivirals**: valacyclovir 1000 mg TID or acyclovir 400 mg 5x/day for 7-10 days; modest benefit when combined with steroids; debated as monotherapy. Combined corticosteroid + antiviral therapy is standard practice, though antiviral benefit is controversial.

### Eye Protection
Critical to prevent exposure keratopathy in incomplete eye closure. Artificial tears during the day, Lubricating ointment and taping/patching at night, Moisture chamber or swim goggles, Ophthalmology referral if corneal exposure.

### Prognosis
85% of untreated Bell palsy patients recover completely. Grade VI paralysis with >90% degeneration on ENoG: ~50% have poor recovery. Synkinesis (aberrant regeneration) is the most common long-term sequela.

## Management of Ramsay Hunt Syndrome
Corticosteroids + antivirals (valacyclovir 1000 mg TID for 7 days). Higher antiviral doses than Bell palsy, Earlier treatment correlates with better outcomes, Worse baseline prognosis than Bell palsy.

## Management of Traumatic Facial Nerve Injury

### Temporal Bone Fractures
Immediate-onset complete paralysis: suggestive of nerve transection or severe compression; consider surgical exploration. Delayed-onset paralysis: likely edema or intraneural hemorrhage; observe with steroids. High-resolution CT temporal bone to localize fracture and relation to fallopian canal. Surgical decompression via transmastoid or middle cranial fossa approach if ENoG shows >90% degeneration.

### Iatrogenic Injury
If injury recognized intraoperatively: primary neurorrhaphy (tension-free) if transected; nerve grafting (greater auricular nerve, sural nerve) if gap present. If noted postoperatively: CT to assess; explore if complete paralysis and no recovery by 3-6 months.

### Surgical Decompression [CONTROVERSY]
Controversial in Bell palsy: some centers advocate middle cranial fossa decompression for complete paralysis with >90% ENoG degeneration within 14 days. Evidence is limited; only one small RCT (Gantz et al.) showed benefit. More widely accepted for traumatic injuries with complete immediate paralysis.

## Reanimation Procedures
Discussed in detail in Topic 49 (Facial Reanimation After Nerve Injury). Early: nerve repair, nerve grafting, nerve transfer (hypoglossal-facial, masseteric-facial). Late (>18-24 months): free muscle transfer (gracilis), static procedures (gold weight, fascia lata sling).

<image>Detailed anatomical diagram of the intratemporal course of the facial nerve showing the four segments: meatal (IAC), labyrinthine, tympanic (horizontal), and mastoid (vertical). Key branches are labeled at their takeoff points: greater superficial petrosal nerve at the geniculate ganglion, nerve to stapedius in the mastoid segment, and chorda tympani near the stylomastoid foramen. The relationship to the oval window, lateral semicircular canal, and cochlea is shown. Cross-sectional inset at the meatal foramen showing the nerve in its narrowest bony canal.</image>

<image>Clinical photograph series showing House-Brackmann grading of facial nerve function from Grade I (normal) to Grade VI (complete paralysis). Each grade shows the face at rest and with attempted eye closure and smile. Key features highlighted: Grade II slight asymmetry with smile, Grade III forehead movement present but incomplete eye closure, Grade IV obvious asymmetry and no forehead movement, Grade V barely perceptible movement, Grade VI total flaccid paralysis.</image>

<image>Flowchart for the evaluation and management of acute unilateral facial paralysis. Starting with history and physical exam, branching based on onset (acute vs. gradual), presence of vesicles (Ramsay Hunt vs. Bell palsy), history of trauma, or progressive course suggesting neoplasm. For Bell palsy: steroids plus antivirals within 72 hours, serial ENoG if complete paralysis, decision point at >90% degeneration for possible surgical decompression. Eye protection emphasized at all stages.</image>

## Clinical Pearls
Always consider neoplasm in gradually progressive facial paralysis, recurrent ipsilateral paralysis, or facial paralysis with an associated mass -- these are not Bell palsy. Steroids started within 72 hours are the strongest evidence-based treatment for Bell palsy; the evidence for antivirals is weaker but they are routinely added. Eye protection is the most critical intervention regardless of etiology -- corneal ulceration can lead to permanent vision loss. ENoG is most useful between days 3-14; EMG is more useful after 3 weeks. In a child with bilateral facial paralysis, strongly consider Lyme disease in endemic areas. Ramsay Hunt syndrome without visible vesicles (zoster sine herpete) can be diagnosed via VZV PCR of saliva or serology. The labyrinthine segment is the narrowest bony canal and most common site of compression in Bell palsy. House-Brackmann Grade III is the critical threshold: Grade III and above generally have good outcomes; Grade IV and below warrant closer monitoring and possible intervention.

## References
- Baugh RF, Basura GJ, Ishii LE, et al. "Clinical Practice Guideline: Bell's Palsy." *Otolaryngol Head Neck Surg*. 2013;149(3 Suppl):S1-S27.
- Gantz BJ, Rubinstein JT, Gidley P, Woodworth GG. "Surgical management of Bell's palsy." *Laryngoscope*. 1999;109(8):1177-1188.
- de Almeida JR, Guyatt GH, Sud S, et al. "Management of Bell palsy: clinical practice guideline." *CMAJ*. 2014;186(12):917-922.
- Murakami S, Mizobuchi M, Nakashiro Y, et al. "Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle." *Ann Intern Med*. 1996;124(1 Pt 1):27-30.