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Murakami and coworkers, using the polymerase chain reaction (PCR) technique to amplify viral genomic sequences, identi ed HSV type I in the endoneurial uid surrounding the seventh nerve in 11 of 14 cases of Bell s palsy; the uid was obtained during surgical decompression of the nerve in ostensibly severe cases The same investigators have 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 the Bell s palsy patients but was isolated from patients with the Ramsay Hunt syndrome (page 642 and further on, page 1183) Control patients with fracture or infections of the temporal bone yielded neither HSV or VZV gene sequences.

In addition to 1 week of restricted activities and supportive care, the patients should wear compressive chin/neck strap dressings for 2 to 3 weeks postoperatively to promote healing and recontouring in the submental region. Pain is minimal and there are no dietary restrictions. Sleeping with the head of the bed elevated will promote lymphatic drainage and help with postoperative edema. Most patients return to work after 1 week.

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In the light of these ndings, the term idiopathic facial paralysis, until now the accepted synonym for Bell s palsy, is not entirely appropriate and perhaps herpes simplex or herpetic facial paralysis should be adopted The onset of Bell s palsy is acute; about one-half of the cases attain maximum paralysis in 48 h and practically all within 5 days Pain behind the ear may precede the paralysis by a day or two and in a few patients is quite intense and persistent In only a small proportion of patients, a hypesthesia in one or more branches of the trigeminal nerve can be demonstrated The explanation of this nding is not clear Impairment of taste is present to some degree in most patients but rarely persists beyond the second week of paralysis.

its status must remain ambiguous A more detailed discussion of this subject and of so-called alcoholic cerebral atrophy (see later) can be found in the review by Victor (1994), listed in the References Cerebral atrophy, like the alcoholic deteriorated state, does not constitute a well-de ned entity The concept of alcoholic cerebral atrophy was the product originally of pneumoencephalographic studies Relatively young alcoholics, some with and some without symptoms of cerebral disease, were often found to have enlarged cerebral ventricles and widened sulci, mainly of the frontal lobes (see, for example, reports of Brewer and Perrett and of Haug) Similar ndings have been reported in chronic alcoholics examined by CT scanning and MRI (see review by Carlen et al) The clinical correlates of these radiologic ndings are quite unclear.

Fig. 12-6

Most often, the nding of large ventricles comes as a surprise, no symptoms or signs of neuropsychiatric disease having been noted in the course of the usual neurologic testing In this connection, the ndings of Wilkinson are of particular importance He demonstrated that in clinically normal alcoholics, the radiologic measures of brain atrophy were age-related; once the age factor was removed, the CT ndings in these subjects did not differ signi cantly from those in nonalcoholic controls The term alcoholic cerebral atrophy implies that chronic exposure of the brain to alcohol causes an irreversible loss of cerebral tissue From the study by Harper and colleagues this may indeed be true, but it requires con rmation.

The idea of alcoholic atrophy is open to criticism mainly on the grounds that dilated ventricles have in fact been reversible to a considerable extent when abstinence is maintained (Carlen et al, Lishman, Zipursky et al, Schroth et al) Until this matter has been studied further, it would be preferable to refer to this condition as an asymptomatic ventricular enlargement and sulcal widening in alcoholics, rather than as cerebral atrophy..

As indicated earlier, this indicates that the lesion has extended to or above the point where the chorda tympani bers join the facial nerve Hyperacusis or distortion of sound in the ipsilateral ear indicates paralysis of the stapedius muscle Unlike the fth nerve in cases of idiopathic trigeminal neuritis, the facial nerve in Bell s palsy often displays enhancement on the gadolinium-enhanced MRI Correspondingly, there is a mild increase of lymphocytes and mononuclear cells in the CSF in a few instances Cases with more pronounced contrast enhancement of the facial nerve have a worse prognosis (Kress) Presumably, the enhancement re ects in ammation and swelling within the course of the facial nerve Fully 80 percent of patients recover within a month or two..

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