ESSENTIALS OF DIAGNOSIS
Sudden onset of lower motor neuron facial palsy.
Hyperacusis or impaired taste may occur.
No other neurologic abnormalities.
Bell palsy is an idiopathic facial paresis of lower motor neuron type that has been attributed to an inflammatory reaction involving the facial nerve near the stylomastoid foramen or in the bony facial canal. In some instances, this may be due to reactivation of herpes simplex or varicella zoster virus infection in the geniculate ganglion. The disorder is more common in pregnant women and in persons with diabetes mellitus.
The facial paresis (Figure 24–1) generally comes on abruptly, but it may worsen over the following day or so. Pain about the ear precedes or accompanies the weakness in many cases but usually lasts for only a few days. The face itself feels stiff and pulled to one side. There may be ipsilateral restriction of eye closure and difficulty with eating and fine facial movements. A disturbance of taste is common, owing to involvement of chorda tympani fibers, and hyperacusis due to involvement of fibers to the stapedius occurs occasionally. In cases due to herpes zoster infection, vesicles may be observed in the external ear canal.
Facial palsy caused by an infection with Borrelia burgdorferi (Lyme disease). (Public Health Image Library, CDC.)
Lower motor neuron facial palsy can be differentiated from stroke by clinical examination. A stroke or other central lesion will not cause hyperacusis or disturbance of taste, generally spares the forehead, and is accompanied by other focal deficits. An isolated facial palsy may occur in patients with HIV seropositivity, sarcoidosis, Lyme disease (Figure 24–1; also see Chapter 34-11), or any process causing an inflammatory reaction in the subarachnoid space, such as meningitis. Whenever facial palsies occur bilaterally, or a facial palsy occurs in conjunction with other neurologic deficits, MRI brain imaging should be undertaken and other investigations considered.
Approximately 60% of cases of Bell palsy recover completely without treatment, presumably because the lesion is so mild that it leads merely to conduction block. Treatment with corticosteroids (prednisone 60 mg orally daily for 5 days followed by a 5-day taper, or prednisolone 25 mg orally twice daily for 10 days) increases the chance of a complete recovery at 9–12 months by 12–15%. Treatment with acyclovir or valacyclovir is only indicated when there is evidence of herpetic vesicles in the external ear canal. It is helpful to protect the eye with lubricating drops (or lubricating ointment at night) and a patch if eye closure is not possible. There is no evidence that surgical procedures to decompress the facial nerve are of benefit. Physical therapy may improve facial function.