The onset is usually acute, with maximal deficit developing within a few hours. The motor deficit is almost always unilateral, and in two thirds of cases, it may be accompanied by pain in or behind the ear. Fever, tinnitus, and mild hearing diminution may be present during the first few hours. Symptoms may fluctuate during the first few days after onset. Voluntary and involuntary motor responses are lost. Both upper and lower parts of the face are affected, a feature that distinguishes this peripheral facial nerve lesion from a central supranuclear lesion, in which only lower facial muscles are affected. Patients may report facial weakness with difficulty closing the eyelid or drooling, preauricular pain, and alterations in taste or hearing (hyperacusis or sensitivity to loud sounds).

On examination, there is facial asymmetry. The palpebral fissure appears widened, the forehead is smooth, and the nasolabial fold is flattened on the involved side. The Bell phenomenon (the normal upward deviation of the eye with lid closure) is exaggerated because of weakness of the orbicularis oculi. The corneal reflex may be decreased on the involved side. Lacrimation is only rarely defective, and if the injury involves the nervus intermedius proximal to the geniculate ganglion, loss or perversion of taste on the anterior two thirds of the tongue may occur, as may altered sensitivity to sound (hyperacusis) due to involvement of the stapedius muscle.

Causes of facial paralysis other than straightforward Bell palsy are suggested by the presence of associated cranial nerve abnormalities. Lesions in the internal auditory meatus may affect nerve VIII causing dearness, tinnitus, or dizziness, while pontine lesions paralyzing the face may affect nerve VI (abducens) and have corticospinal and sensory tract symptoms.

In 75% to 85% of cases, patients recover to a cosmetically acceptable level without treatment. Most do so within 3 weeks. Recovery is best in children; a poor prognosis has been associated with increasing age, hyperacusis, diminished taste, and severity of the initial motor deficit. The prognosis can be assessed by electromyographic (EMG) testing of the involved muscles at least 72 hours after the clinical nadir. Those with EMG evidence of extensive axonal degeneration 2 weeks after the onset of the weakness have a poorer prognosis. Those with partial or complete preservation of the compound muscle action potential amplitude have anatomic continuity of the facial nerve, partial axonal preservation, and a better prognosis. EMG is indicated only for patients with severe clinical involvement that has not improved by 7 to 10 days after onset.

Other poor outcomes in Bell palsy result from abnormal regeneration of damaged nerve fibers. Lacrimation during eating or “crocodile tears” appear when fibers regrow and connect with lacrimal ducts instead of salivary glands. Abnormal movements such as hemifacial spasm or facial synkinesis with jaw winking may occur if regenerating motor fibers innervate inappropriate muscles. Contracture of the involved site may be noted during voluntary movement. Seven percent of patients experience recurrent facial paralysis.