Bell’s Palsy

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

Etiology:

• 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

Epidemiology:

• 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

History:

• 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

Physical:

• 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

Differential:

• 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

Diagnosis:

• 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

Prognosis:

• 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

References:

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. https://www.aafp.org/afp/2007/1001/p997.html. 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. https://www.jems.com/articles/print/volume-39/issue-5/features/differentiating-facial-weakness-caused-b.html. 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.