Bell palsy is idiopathic paralysis of the facial nerve (cranial nerve VII) that leads to unilateral paralysis of upper and lower facial muscles. In contrast, upper facial muscles are spared in central facial weakness (stroke) because of their bilateral innervation. Altered taste and hyperacusis also may occur in Bell palsy because of involvement of chorda tympani and stapedius muscles.
In classic Bell palsy, initial brain imaging and laboratory testing are not required.
Head MRI is indicated in patients with atypical symptoms/signs, facial twitching or spasm preceding weakness (suggests malignancy), slow progression of symptoms after 3 weeks, or no symptom improvement after 4 months.
If a secondary cause is suspected on the basis of history (subacute onset over days, comorbidities, rash) or clinical examination (deficits unrelated to the facial nerve), additional testing is indicated and prednisone is typically avoided. Brain MRI with contrast also is recommended in patients with lingering or worsening weakness after 2 months.
Between 70% and 90% of patients with Bell palsy fully recover within a few weeks. Treatment with a 10-day course of oral prednisone, started within 72 hours of onset, is recommended to expedite both the rate and speed of full recovery. The utility of adding antiviral treatment to prednisone is controversial, and guidelines differ in their recommendations. There may be a small benefit to adding antiviral (valacyclovir) treatment in patients with severe palsy. Use of an eye patch and artificial tears to prevent corneal dryness are recommended. Synkinesis (concomitant movement of perioral and periorbital muscles) may result from aberrant reinnervation after Bell palsy.