Bell’s palsy is an acute, idiopathic peripheral facial nerve palsy resulting from inflammation and dysfunction of the seventh cranial nerve. It is characterized by sudden-onset unilateral facial weakness involving both the upper and lower face. Bell’s palsy is the most common cause of acute facial paralysis and is typically diagnosed clinically after exclusion of alternative etiologies.

Patients often present with rapid progression of facial weakness over hours to days. Clinical features include facial drooping, inability to close the eye, impaired facial expression, altered taste sensation, hyperacusis, and reduced tear or saliva production. Pain around the ear or mastoid region may precede weakness. The involvement of the forehead distinguishes peripheral facial palsy from central causes.

Neurological assessment focuses on confirming peripheral nerve involvement and excluding secondary causes such as stroke, infection, trauma, or neoplastic compression. A thorough cranial nerve examination is essential. Neuroimaging is reserved for atypical presentations, recurrent palsy, or cases with progressive neurological signs.

Management of Bell’s palsy aims to reduce nerve inflammation, preserve nerve function, and prevent ocular complications. Early initiation of therapy significantly improves outcomes. Eye protection is critical to prevent corneal injury due to incomplete eyelid closure. Facial rehabilitation may support functional recovery.

Most patients experience gradual improvement over weeks to months, with a high rate of complete or near-complete recovery. However, a subset develops residual weakness, synkinesis, or facial contractures. Long-term neurological follow-up allows monitoring of recovery and management of complications.

Bell’s palsy represents an acute mononeuropathy requiring prompt neurological recognition and supportive care to optimize functional recovery and minimize long-term sequelae.