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An Epidemic of Bell’s Palsy
Abstract & Commentary
Source: Mutsch M, et al. Use of the inactivated intranasal influenza vaccine and the risk of Bell’s palsy in Switzerland. N Engl J Med. 2004;350:896-903.
This paper examined the risk of Bell’s palsy after introduction of an inactivated intranasal influenza vaccine in Switzerland. Mutsch and associates used a matched case-control study and a case-series analysis. They contacted all primary care physicians; ear, nose, and throat specialists; and neurologists in German-speaking regions of Switzerland and asked them to identify cases of Bell’s palsy diagnosed in adults between October 1, 2000, and April 30, 2001. These patients were each matched with control patients according to age, date of clinic visit, and physician. The vaccination information was provided by the physicians.
Mutsch et al identified a total of 773 patients with Bell’s palsy. They enrolled 412 of the 773 patients in the study and matched them with 722 control patients. In the case-control study, they found that 68 patients with Bell’s palsy and 8 controls had received the intranasal vaccine. In contrast to parenteral vaccines, the intranasal vaccine increased the risk of Bell’s palsy with an adjusted odds ratio of 84.0. The relative risk of Bell’s palsy was estimated to be 19 times the risk in controls, with the period of highest risk being 31-60 days after vaccination.
This study raises a number of very interesting issues. Mutsch et al have unequivocally demonstrated a marked increase in Bell’s palsy following intranasal administration of an inactivated influenza vaccine. This led to a discontinuation of the clinical use of the vaccine. The risk was greatest in the second month after intranasal vaccination. About 1 in 5 patients described in this study had an incomplete recovery, consistent with other reports. The means of which an inactivated vaccine could lead to Bell’s palsy is not clear. Two possibilities have been considered concerning the mechanism of this increase. The first is that this may represent an autoimmune process. The vaccine contained adjuvant Escherichia coli heat-labile toxin that may be an inflammatory mediator, but preclinical research on its toxicologic characteristics did not support this idea. A second possibility is that the intranasal administration of the vaccine might have led to activation of herpes simplex virus, which may be latent in the geniculate ganglion. There is a substantial body of evidence implicating herpes simplex in the pathogenesis of Bell’s palsy. In particular, there was one study in which herpes simplex virus DNA was identified in endoneural fluid and muscle taken from patients with Bell’s palsy. The delayed onset of Bell’s palsy 1 month after the vaccinations could be compatible with either an autoimmune process or reactivation of latent herpes simplex virus. The results of the present study suggest that the sample size and prelicensure trials may need to be increased since no cases of Bell’s palsy were reported among 1218 initial recipients of the vaccine. M. Flint Beal
Dr. Beal, Professor and Chairman; Department of Neurology; Cornell University Medical College New York, NY is Editor of Neurology Alert.