An MRI of the brain should be obtained in this patient who has limited recovery despite appropriate treatment 3 months after onset of complete facial nerve (cranial nerve VII) palsy to rule out an underlying structural abnormality. He has acute weakness involving both upper and lower facial muscles, which favors a peripheral rather than central weakness. The initial presence of hyperacusis and the impaired taste noted on examination are also consistent with facial nerve involvement. In patients with typical isolated facial nerve paralysis, immediate brain imaging is unnecessary. Most of these patients have idiopathic Bell palsy, and 70% to 90% achieve complete recovery within 3 months. Severe residual weakness occurs in a minority of patients with Bell palsy, but the persistence of significant deficits at 3 months should prompt further investigation, including evaluation for alternative causes of facial nerve paralysis (such as diabetes mellitus, Lyme disease, vasculitis, HIV infection, sarcoidosis, paraproteinemia, and Sjögren syndrome) and an MRI of the brain to rule out structural causes. If results of this evaluation do not reveal a cause of the persistent symptoms, the diagnosis is incomplete recovery after Bell palsy, and clinical monitoring is then recommended.

Acute monotherapy with antiviral medications, such as acyclovir, does not improve prognosis. Early adjunctive use of antiviral therapy in addition to prednisone is favored by some experts, but the evidence supporting this treatment is inconsistent.

Evidence supporting the benefit of physical therapy for rehabilitation after facial nerve palsy is insufficient. In this patient, a structural cause of the deficits should first be excluded.