Bell palsy: Clinical examination and management

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ABSTRACTBell palsy is a common neurologic disorder characterized by acute facial mononeuropathy of unclear cause presenting with unilateral facial weakness. Careful examination and a detailed history are important in making an accurate diagnosis. Early recognition is essential, as treatment with corticosteroids within 72 hours of onset has been shown to hasten recovery. Fortunately, most patients recover spontaneously within 3 weeks, even if untreated.


  • Bell palsy is an acute disorder of the facial nerve causing unilateral facial weakness, pain, abnormal taste, and reduced tearing.
  • Although herpes simplex virus reactivation is suspected in the pathogenesis, the exact cause is unknown.
  • An additional workup is warranted for abnormalities beyond isolated facial nerve palsy.
  • Guidelines recommend starting corticosteroids for patients who present within 3 days of symptom onset. There is no compelling evidence to support antiviral therapy, physical therapy, acupuncture, or surgical decompression.



Bell palsy is an idiopathic peripheral nerve disorder involving the facial nerve (ie, cranial nerve VII) and manifesting as acute, ipsilateral facial muscle weakness. It is named after Sir Charles Bell, who in 1821 first described the anatomy of the facial nerve.1 Although the disorder is clinically benign, patients can be devastated by its disfigurement.

The annual incidence of Bell palsy is 20 per 100,000, with no predilection for sex or ethnicity. It can affect people at any age, but the incidence is slightly higher after age 40.2,3 Risk factors include diabetes, pregnancy, severe preeclampsia, obesity, and hypertension.4–7


A basic understanding of the neuroanatomy of the facial nerve provides clues for distinguishing a central lesion from a peripheral lesion. This differentiation is important because the causes and management differ.

The facial nerve is a mixed sensory and motor nerve, carrying fibers involved in facial expression, taste, lacrimation, salivation, and sensation of the ear. It originates in the lower pons and exits the brainstem ventrally at the pontomedullary junction. After entering the internal acoustic meatus, it travels 20 to 30 mm in the facial canal, the longest bony course of any cranial nerve, making it highly susceptible to trauma and compression by edema.8

In the facial canal, it makes a posterior and inferior turn, forming a bend (ie, the genu of the facial nerve). The genu is proximal to the geniculate ganglion, which contains the facial nerve’s primary sensory neurons for taste and sensation. The motor branch of the facial nerve then exits the cranium via the stylomastoid foramen and passes through the parotid gland, where it divides into temporofacial and cervicofacial trunks.9

The facial nerve has five terminal branches that innervate the muscles of facial expression:

  • The temporal branch (muscles of the forehead and superior part of the orbicularis oculi)
  • The zygomatic branch (muscles of the nasolabial fold and cheek, eg, nasalis and zygomaticus).
  • The buccal branch (the buccinators and inferior part of the orbicularis oculi)
  • The marginal mandibular branch (the depressors of the mouth, eg, depressor anguli and mentalis)
  • The cervical branch (the platysma muscle).


Although the precise cause of Bell palsy is not known, one theory is that inflammation of the nerve causes focal edema, demyelination, and ischemia. Several studies have suggested that herpes virus simplex type 1 infection may be involved.10


Figure 1.

Symptoms of Bell palsy include ipsilateral sagging of the eyebrow, drooping of the face, flattening of the nasolabial fold, and inability to fully close the eye, pucker the lips, or raise the corner of the mouth (Figure 1). Symptoms develop within hours and are maximal by 3 days.

About 70% of patients have associated ipsilateral pain around the ear. If facial pain is present with sensory and hearing loss, a tumor of the parotid gland or viral otitis must be considered.11 Other complaints may include hyperacusis due to disruption of nerve fibers to the stapedius muscle, changes in taste, and dry eye from parasympathetic dysfunction. Some patients report paresthesias over the face, which most often represent motor symptoms misconstrued as sensory changes.


The clinical examination should include a complete neurologic and general examination, including otoscopy and attention to the skin and parotid gland. Vesicles or scabbing around the ear should prompt testing for herpes zoster. Careful observation during the interview while the patient is talking may reveal subtle signs of weakness and provide additional clues.

A systematic approach to the assessment of a patient with suspected Bell palsy is recommended (Table 1) and outlined below:

Does the patient have peripheral facial palsy?

In Bell palsy, wrinkling of the forehead on the affected side when raising the eyebrows is either asymmetrical or absent.

If the forehead muscles are spared and the lower face is weak, this signifies a central lesion such as a stroke or other structural abnormality and not a peripheral lesion of the facial nerve (eg, Bell palsy).

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