Definition
This is an isolated acute unilateral seventh cranial nerve palsy of peripheral (lower motor neuron) type. It is not associated with other cranial nerve neuropathies or brain stem dysfunction. Age is not a bar.
Etiopathogenesis
Usually, it develops abruptly about 2 weeks after a viral infection, e.g. Epstein-Barr virus (most common), herpes simplex virus, mumps virus, HIV, etc. and Lyme disease. Infection with toxocara, rickettsia and mycoplasma may also precede development of the lower motor neuron lesion of the facial nerve.
Clinical Features
It usually develops abruptly about 2 weeks after a systemic viral infection.
Manifestations include:
- Deviation of the upper and lower face to opposite side
- Drooling at the angle of the mouth
- Inability to close the eye, on affected side (Fig. 30.7)
- Loss of taste in anterior two thirds of the tongue.
Fig. 30.7: Bell palsy. Note the inability to close the right eye, by deviating the mouth to the left.
Diagnosis
- It is more or less clinical.
- Electrophysiological examination of the facial nerve may help to find out the extent of neuropathy and degeneration.
- In chronic cases (not recovering in few weeks), causes of facial nerve involvement such as leukemia, tumors, brain stem infarct and injury must be ruled out.
Treatment
Treatment in acute cases is more or less supportive. An ocular lubricant, especially at night, is needed for protection of the cornea. A short course of low-dose steroids (prednisolone, 1 mg/kg/day) is justified. It is best started within 3–5 days of onset and tapered after a therapy of 1 week.
Prognosis and Outcome
Usually (over 85% cases) Bell’s palsy resolves fully within a few weeks to several months. It shows full recovery spontaneously. In some 10% cases, the patient may be left with slight weakness. In the remaining 5% cases, permanent severe facial weakness may persist.
Author
