Craniofacial Muscles

15 Facial Nerve Innervation and Facial Palsies
273
15.5 Bell’s Palsy
The natural history of Bell’s palsy is fascinating yet frustrating. It is the most
common cause of facial paralysis, and yet there is considerable uncertainty as to its
underlying pathology. Despite being a diagnosis of exclusion, it is a convenient
place to start to think about facial palsy as a whole. The theories to explain the cause
of idiopathic palsy began in the 1800s with the concept of “rheumatism” as the
condition seemed to be associated with fevers, chills, and localized pain and swelling
in the neck region. In fact, Freidrich initially published his account as the paralysis
musculorum faciei rheumatica . The idea of swelling, combined with the
anatomical knowledge that the nerve had a signi fi cant petrous course in the temporal
bone gave rise to the hypothesis that the nerve might become thickened and
edematous, resulting in compression around the stylomastoid foramen. This compression
was believed to have secondary ischemic effects due to disturbance of the
vasa nervorum accompanying the nerve. This gave rise in the 1930s to the school of
thought advocating mastoid decompression surgery, which was in vogue for some
30 or more years (Cawthorne 1951 ; Jonkees 1957 ) . In 1972, McGovern postulated
that an immunological source may be responsible for the in fl ammation and edema
causing the nerve damage; later that year McCormick suggested herpes simplex
(HSV-1) as a possible culprit (McGovern et al. 1972 ; McCormick 1972 ) . There is
still no conclusive evidence that HSV-1 is the de fi nitive cause, but polymerase chain
reaction techniques seem to be supportive (Murakami et al. 1996 ) .
Peitersen began a very thorough prospective study of the natural course of facial
palsy in the early 1970s, following over 2,500 patients around Copenhagen for 30
years (Peitersen 2002 ) . Emphasis was placed on the speci fi c details surrounding the
onset of the condition (e.g., time, other cranial nerve symptoms, pregnancy, comorbidities,
trauma, ocular, and auricular symptoms, etc.), any previous or familial episodes,
completeness vs. incomplete and the nature of branch involvement, as well
as the timing and completeness of remission. At the fi rst visit this was coupled to a
full ENT and cranial nerve examination, acoustic and vestibular tests, taste, nasolacrimal
and stapedial re fl ex examination, and baseline laboratory tests to rule out
diabetes, hypertension, serum antibodies to HSV, HZV, and borreliosis. Patients
were then seen weekly until function was observed to be returning. After 6 months,
this reduced to monthly and then discontinued after full recovery or after 1 year. If
patients suffered a second episode or had not recovered in 4 months, they underwent
further testing with CSF analysis and CT and MRI scanning. The Copenhagen
Facial Nerve Study is particularly useful in both its size and completeness of follow
up (98%). Of 2,570 cases, 1,701 were idiopathic or Bell’s palsies, an incidence of
32/100,000 per year. Seventy percent of these were complete paralyses. There was
a 6.8% recurrence rate and 4.1% represented familial cases. There was no indication
of a seasonal or decade variation, and there was no statistical connection with gender
or laterality. Bell’s palsy was uncommon under the age of 15 and above 60 years
with a maximum incidence between 15 and 45 years ( P < 0.001 in comparison with
the underlying population).