Definition: Acute, idiopathic peripheral facial nerve (CN VII) palsy

The Facial Nerve (CN VII):

  • Provides parasympathetic innervation to the submandibular salivary glands, sublingual salivary glands, and lacrimal glands
  • Conveys taste sensations from the anterior two-thirds of the tongue via sensory fibers
  • Controls the muscles of facial expression
  • Pearls:
    • The right facial nerve controls the right face, and the left facial nerve controls the left face
    • The upper muscles of facial expression are innervated by fibers from both the ipsilateral as well as contralateral cortex; in other words, innervation to each side of the forehead is from both motor cortices
    • Therefore, a peripheral lesion should completely affect one side of the face, while a central lesion should spare the motor function of the forehead, since the contralateral cortex supplies fibers to the affected side


  • Idiopathic by definition
  • See differential for possible etiologies
  • Mechanism: edema, inflammation, and nerve degeneration at the geniculate ganglion within stylomastoid foramen which can lead to compression and possible ischemia and demyelination


  • Incidence of 15-40 / 100,000
  • Affects men and women equally
  • All ages are affected, with peak incidence in the 30s to 50s
  • Risk factors include pregnancy, diabetes, and previous episode(s) of Bell’s palsy


  • Sudden onset unilateral facial droop, incomplete eyelid closure, and loss of forehead muscle tone
  • Onset over the course of hours and peaks within three to seven days
  • Facial asymmetry with disappearance of nasolabial fold and facial creases
  • Eye irritation from decreased tearing and inability to close the affected eye
  • Abnormal taste and drooling from the affected side
  • Subjective “numbness” of the affected side due to paralysis but preserved facial sensation


  • Unilateral eyebrow sagging and inability to close the eye
  • Disappearance of unilateral facial creases, especially nasolabial fold and forehead furrows
  • Drooping at the corner of the mouth
  • Although absolute tear production may be decreased, the inability to blink may allow tears to spill from the eye
  • Preservation of the upper muscles of facial expression suggests a central cause
  • Assess bilateral ear canals with otoscopy
  • Assess parotid gland for masses
  • Perform a full neurological exam: should expect an otherwise normal neurological exam including all other cranial nerves and extremity motor function


  • Bell’s palsy is a diagnosis of exclusion
  • Herpes Zoster (Ramsay Hunt syndrome): evaluate for vesicles, tinnitus, or vertigo
  • Infectious mononucleosis: evaluate for pharyngitis, posterior cervical adenopathy, or viral prodrome
  • Guillain-Barré Syndrome: usually presents with ascending motor weakness
  • Lyme Disease: history of rash or tick bite in endemic area
  • Otitis Media
  • Cholesteatoma
  • Parotid gland masses
  • Multiple Sclerosis: usually bilateral peripheral CN VII palsy
  • Sarcoidosis: usually bilateral peripheral CN VII palsy
  • Brainstem events (mass, bleed, infarct): will usually present with other cranial nerve palsies
  • Basilar artery aneurysm
  • Stroke
  • Tumors: consider parotid, bone, metastatic masses, or acoustic neuroma
  • Trauma: skull fracture or penetrating facial injury


  • For high pre-test probability of Bell’s Palsy, there is no indication for labs or imaging: diagnosis is based on history and physical
  • If you suspect another cause of facial nerve palsy, order targeted labs and/or imaging (e.g. Lyme titers or monospot if high suspicion for viral etiology)
  • Consider blood glucose in Bell’s Palsy patients with other diabetic risk factors as 10% of Bell’s Palsy patients have diabetes

ED Management:

  • Glucocorticoids may hasten recovery if started within 72 hours of symptom onset: 1mg/kg prednisone (or 60 to 80 mg) PO daily for 7 days (pediatric dose: 2mg/ kg/ day PO [max 60mg])
    • NNT to prevent one incomplete recovery = 10
    • No clear regimen, most studies use 7-10 days of PO prednisone
  • Anti-viral therapy with steroids may improve functional nerve recovery if started within 72 hours of symptom onset: valacyclovir 1000 mg PO daily for 7 days (pediatric dose: 20mg/ kg TID PO)
    • Low quality evidence that antivirals with glucocorticoids is superior to glucocorticoids alone
    • American Academy of Neurology recommends offering antivirals while explaining limited evidence but also limited harm
  • Corneal damage may occur due to incomplete eye closure
    • prescribe lubricating and hydrating ophthalmic ointment and/ or drops (artificial tears qhs and prn dryness/ irritation in affected eye)
    • instruct patient on wearing eye patch at night on affected eye


  • In the Copenhagen Facial Nerve Study (2002), 2,570 cases of untreated peripheral facial nerve palsy were studied during a period of 25 years (1,701 cases of Bell’s palsy)
  • 71% of Bell’s palsy patients returned to baseline function in three weeks without treatment
  • Almost all patients noticed some improvement in three to four months
  • Prognosis is related to initial severity: with incomplete lesions, 94% returned to baseline whereas of those with complete lesions, 60% returned to baseline

Patient Education and Discharge Instructions:

  • While not life threatening, Bell’s palsy can cause significant distress
  • Symptoms peak within three to seven days, and almost always improve somewhat by 3 months
  • With incomplete lesions, ~95% return to baseline; with complete lesions, ~60% return to baseline
  • Prescribe artificial tears during the day and ointments with eye patch at night
  • 1 week follow-up with outpatient neurologist for management of symptoms and to monitor recovery

Take Home Points:

  • Bell’s palsy is acute, peripheral, and idiopathic
  • A non-acute onset of symptoms (gradual onset of more than two weeks duration) should suggest a mass lesion
  • Perform a very careful thorough exam, including full neurological exam, dermatological exam (evaluate for vesicles or rash), and ENT exam (evaluate for pharyngitis, posterior cervical adenopathy, otitis media, deafness)
  • No role for labs or imaging, but deviation from the typical history and physical should prompt further workup
  • Start glucocorticoids and antivirals in the ED if symptoms started within 72 hours and if there are no contraindications
  • Provide patient education about the prognosis and eye care to prevent corneal abrasions
  • Arrange for close neurology follow-up


Zhang W, Xu L, Luo T, Wu F, Zhao B, Li X. The etiology of Bell’s palsy: a review. Journal of Neurology. 2019. doi:10.1007/s00415-019-09282-4.

Tiemstra JD, Khatkhate N. Bell’s Palsy: Diagnosis and Management. American Family Physician. Published October 1, 2007. Accessed May 22, 2019.

Gronseth GS, Paduga R. Evidence-based guideline update: Steroids and antivirals for Bell palsy: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2012;79(22):2209-2213. doi:10.1212/wnl.0b013e318275978c.

Madhok VB, Gagyor I, Daly F, et al. Corticosteroids for Bells palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews. 2016. doi:10.1002/14651858.cd001942.pub5.

Gagyor I, Madhok VB, Daly F, et al. Antiviral treatment for Bells palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews. 2015. doi:10.1002/14651858.cd001869.pub6.

Loomis C, Mullen MT. Differentiating Facial Weakness Caused by Bell’s Palsy vs. Acute Stroke. Journal of Emergency Medical Services. Published May 7, 2014. Accessed May 22, 2019.

Peitersen E. Bell’s palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiologies.  Acta Otolaryngol Suppl.  2002:4-30.

Schaider et al. Rosen & Barkin’s 5-Minute Emergency Medicine Consult, 5th Edition.  Wolters Kluwer.