Bell Palsy
Idiopathic acute unilateral lower motor neuron facial nerve paralysis.
- Sparing of the forehead (suggests central lesion).
- Bilateral presentation (consider Guillain-Barré or Lyme).
Emergency Management: Facial palsy accompanied by aphasia or hemiparesis requires stroke code.
Acute, unilateral, lower motor neuron facial nerve (CN VII) paralysis. It causes facial muscle weakness and is typically considered idiopathic, though HSV-1 reactivation is heavily implicated.
Detailed Overview
Bell palsy accounts for most facial nerve palsies, presenting with rapid onset weakness over 48-72 hours. Inflammation and edema of the facial nerve within the narrow fallopian canal lead to compression and demyelination. Timely oral corticosteroids within 72 hours improve recovery rates.
Epidemiology & Demographics
Incidence 15-30 per 100,000 annually. Affects sexes equally. 3x higher risk during the 3rd trimester of pregnancy and early postpartum.
Etiological Mechanism
Idiopathic; strong evidence points to reactivation of Herpes Simplex Virus 1 (HSV-1) or Varicella Zoster Virus (VZV) in the geniculate ganglion.
Primary Causes
Primary: Idiopathic. Secondary triggers: URI, stress, cold exposure.
- Pregnancy: 3x higher risk, especially in the 3rd trimester or 1st week postpartum.
- Diabetes Mellitus: 4x higher risk compared to the general population.
Latent HSV-1 in the geniculate ganglion reactivates, causing neural edema. The facial nerve traverses the rigid temporal bone; edema causes ischemia and demyelination. Severe compression can cause Wallerian degeneration.
Characteristic Clinical Presentation
- Facial Weakness: Sudden onset unilateral upper and lower facial paralysis.
- Hyperacusis: Ipsilateral sensitivity to sound due to stapedius muscle denervation.
- Dysgeusia: Loss of taste on the anterior 2/3 of the tongue (chorda tympani involvement).
Physical Examination Signs
- Forehead Involvement
- Bell Phenomenon
- Exposure Keratitis: Corneal ulceration due to incomplete eye closure.
- Synkinesis: Involuntary facial movement during voluntary movement due to aberrant nerve regeneration.
Diagnostic Criteria & Guidelines
Clinical diagnosis: sudden onset unilateral LMN facial palsy involving forehead, absent other focal neurologic deficits.
Differential Diagnosis
- Ischemic Stroke (spares forehead)
- Lyme Disease (often bilateral)
- Ramsay Hunt Syndrome (VZV with ear vesicles)
Laboratory Tests & Biomarkers
- Lyme Serology: If bilateral or in endemic areas, expect positive IgM/IgG.
- HbA1c: Check for undiagnosed DM; >6.5%.
Imaging Modalities & Findings
- MRI Brain with Contrast:
-
House-Brackmann I
Normal facial function.
-
House-Brackmann VI
No facial movement.
Prednisone 60 mg PO daily for 5 days, then 5-day taper. Eye lubrication with artificial tears q1-2h and nightly ophthalmic ointment.
Second-Line & Adjunctive Therapy
Valacyclovir 1000 mg PO TID for 7 days (added for severe cases HB grade IV or higher).
Surgical & Procedural Management
Surgical facial nerve decompression via middle cranial fossa approach if >90% degeneration on ENoG within 14 days.
Recommended Lifestyle Changes
- Tape affected eye closed at night to prevent corneal abrasions.
- Chew on the unaffected side.
Patient Counseling & Advice
Reassure that a stroke has been ruled out. Symptoms peak in 72 hours; improvement takes 3-4 weeks.
Follow-Up & Monitoring Schedule
Re-evaluate in 48-72 hours for eye care, then at 1 month to assess motor recovery.
Preventive Strategies
No proven prevention; early treatment of triggers like shingles.
71% recover completely without treatment; >80% recover completely with early steroids.
Frequently Asked Questions
View Official Guideline