A complete interruption of the facial nerve at the stylomastoid foramen paralyzes all muscles of facial expression on the same side. The corner of the mouth droops, the creases and skin folds are effaced, the forehead is unfurrowed, the palpebral fissure is widened and the eyelids will not close completely. Upon attempted closure of the lids, both eyes roll upward (Bell phenomenon), but the one on the paralyzed side remains visible because of lack of eyelid closure. The lower lid sags also, and the punctum falls away from the conjunctiva, permitting tears to spill over the cheek. (In contrast, the paralyzed frontalis muscle in patients of Asian origin sometimes lowers the eyelid and makes the palpebral fissure appear narrowed.) Food and secretions collect between the teeth and cheek, and saliva may dribble from the corner of the mouth. The patient complains of heaviness or numbness and sometimes an aching pain in the face, but sensory loss can usually not be demonstrated. Taste, however, is intact because the chorda tympani has separated from the main trunk of the facial nerve proximal to the stylomastoid foramen.
If the lesion is in the facial canal above the junction with the chorda tympani but below the geniculate ganglion, all the preceding symptoms are present but in addition, taste is lost over the anterior two-thirds of the tongue on the same side. The nerve to the stapedius muscle is also usually involved with a lesion at this site and there is hyperacusis (sensitivity to sudden loud sounds). If the geniculate ganglion or the motor root proximal to it is damaged, lacrimation and salivation may be reduced. Lesions at this point may also affect the adjacent eighth nerve, causing deafness, tinnitus, or dizziness.
The most common disease of the facial nerve is Bell’s palsy (incidence rate of 23 per 100,000 people annually according to Hauser et al). The disorder affects men and women more or less equally and occurs at all ages and all times of the year. There is controversy regarding an increased incidence in women during the third trimester of pregnancy, particularly in the 2 weeks preceding delivery and in the first 2 weeks postpartum; up to a threefold increase has been cited by some authors, but others have failed to find this disproportion. Bell’s palsy is probably more common in diabetic patients and possibly in those with hypertension than in the healthy population.
Regarding the causation of Bell’s palsy, a viral agent has long been suspected, as was discussed by Baringer, and such a mechanism has been established with reasonable certainty for the majority of cases. Burgess and colleagues identified the DNA of herpes simplex virus (HSV) in the geniculate ganglion of an elderly man who died 6 weeks after the onset of Bell’s palsy. Murakami and coworkers (1996), using the polymerase chain reaction, found HSV type I in the endoneurial fluid surrounding the seventh nerve in 11 of 14 cases of Bell’s palsy; the fluid was obtained during surgical decompression of the nerve in severe cases. The same investigators produced facial paralysis by inoculating HSV into the ears and tongues of mice; virus antigens were then found in the facial nerve and geniculate ganglion. Varicella zoster virus (VZV) was not found in any of their patients but was isolated from patients with the Ramsay Hunt syndrome, which refers to facial palsy associated with VZV reactivation causing a vesicular rash on the pinna of the ear, palate, and/or tongue (discussed further on). Patients with fracture or other infections of the temporal bone yielded neither HSV nor VZV gene sequences. As one might expect, the opportunity to examine the facial nerve in the course of Bell’s palsy occurs very rarely. Only a handful of such cases are on record, all showing varying degrees of degeneration of nerve fibers. One case was said to show inflammatory changes, but these may have been misinterpreted (see Karnes).