Idiopathic Bell's Palsy Research Articles

Angiographic study of facial paralyses (author's transl)

Many arguments lead us to think that a possible etiologic factor in idiopathic Bell's palsy is the ischemia of the facial nerve and that angiography could help in diagnosis: (1) the rapid progress of the paralysis; (2) the correlation between Bell's palsy occurring after embolization of the internal maxillary artery, the middle meningeal artery, the occipital or posterior auricular artery, and their participation in the blood supply of the facial nerve; (3) the already known ischemic third nerve paralysis reported in diabetes and extending further to the facial nerve. Even if it is technically impossible to study Bell's palsy by angiography, it is interesting to understand and consider some complications of embolization and perhaps to envisage a new kind of treatment.

Recurrent Bell's palsy. Etiology, frequency, prognosis.

The etiology, frequency and prognosis of recurrent Bell's palsy were studied in patients with peripheral paresis of n.facialis of various etiology. Fourteen (11.9%) of 117 patients with Bell's palsy had a recurrent paresis of n.facialis. Nine of these were of homolateral and five contralateral type. Seven recurrent facial paralyses in idiopathic Bell's palsy (i.e. 10.4% of the patients with idiopathic facial palsy), 3 facial palsies of viral origin (i.e. 8.8% of the patients with viral facial palsy), one in association with diabetes mellitus, one during pregnancy, one combined with positive rheumatic serological tests, and one in a case of Melkersson-Rosenthal syndrome were found. The frequency and heterogenity of etiology of recurrent facial palsies suggest a predisposing factor or immune mechanisms. In eight patients there was within 6 to 8 weeks a good, in two patients a moderate and in four patients a poor recovery of function. The greater reduction of the compound action potential of the m.orbicularis oris in recurrent homolateral facial palsy in relation to patients with single manifestation point out the greater denervation and therefore the poorer prognosis of recurrent palsies. A prophylactic decompression to prevent a third attack of recurrent facial paresis is considered.

Bell's palsy: diagnosis, management and results of treatment.

AbstractA series of 100 consecutive cases of idiopathic Bell's palsy treated by facial nerve decompression are presented. These procedures were accomplished without injury to the facial nerve, hearing or balance and without the production of a mastoid cavity. One hundred percent normal facial function was the result in 22 patients with normal excitability subjected to facial nerve decompression. Sixty‐eight patients who had surgery after loss of nerve excitability obtained an average of 80 percent return of function with varying degrees of synkinesis in most cases. The decision regarding the nature and timing of treatment should be a subjective one, made after a careful analysis of the available facts and each patient's own circumstance. The availability of a promptly accomplished and precisely performed facial nerve decompression allows every patient to have a minimal risk of permanent facial deformity.

Treatment of Bell's palsy.

Facial paralysis of abrupt onset is common. Few cases are associated with otic infection, and there is debate about possibly causal relations with diabetes, hypertension and pregnancy. Almost all cases are idiopathic (Bell's palsy).One theory ascribes the initial insult to unstable blood vessels, susceptible to excessive vasoconstriction on exposure to cold or other stimuli. Ischemia leads to swelling and compression of the nerve within its bony canal, thus aggravating the ischemia. But the relation to cold is uncertain; there is doubt about liability to compression since the nerve occupies less than 50 per cent of the canal; the postulated . . .

Pathology of Bell's Palsy

Segmental herniation of the facial nerve after epineural incision is regarded as proof that idiopathic Bell's palsy is due to elevated pressure caused by anoxia secondary to local vasospasm. However, epineural biopsies—taken at decompressions—have failed to reveal edema or other lesions. The nerve itself was observed to bulge through its entire intratympanic course. Idiopathic Bell's palsy often shows epidemiologic features and sometimes follows viral infections. Diabetes, especially latent diabetes, and arteriosclerosis are often associated with Bell's palsy—and could account for hemorrhages reported at the geniculate ganglion region. Bell's palsy is probably not one pathological entity—among its plausible causes are viral infections and vascular assaults both above the tympanic part of the facial nerve. The classical entrapment theory still awaits confirmation especially as myelin bulging is a normal phenomenon which becomes more pronounced in reaction to various injuries which are not necessarily local intratympanic ones.

Prognosis of idiopathic Bell's palsy.

Based on 54 cases of idiopathic facial paralysis of which 44 cases were followed for one year, we have found it is possible to determine the prognosis in every case at an early stage of the disease by using mainly the chorda function-test and an electromyogram. A bad prognosis is indicated by low submandibular secretion and impaired taste ability as measured by electrogustometry and semiquantitative taste examination. Therapeutic endeavors should be directed toward the prognostically poor cases as the others will recover completely without treatment.

Varicella-Zoster Virus

The complement fixing (C-F) antibody titers to varicella-zoster and herpes simplex virus in 80 cases of peripheral facial nerve paralysis were determined in association with the inflammatory findings in the increased antibody group. Of 22 patients with Ramsay-Hunt's syndrome, 18 (81%) showed more than eightfold increases in complement fixing antibody titer to the varicella-zoster virus. Significant differences between this group and the normal control group were recognized. On the other hand, 11 (25%) of 44 cases initially diagnosed as idiopathic Bell's Palsy in the acute stage showed increased antibody titer. It was found that serological testing of paired sera was necessary to differentiate idiopathic Bell's palsy from Ramsay-Hunt's syndrome. The clinical findings in these cases were analyzed for relative symptoms and signs of viral infections.

Electrogustometry in facial palsy.

Gustatory function was examined in the early stages of idiopathic Bell's palsy (74 cases) and Ramsay Hunt's syndrome (21 cases). It was found that electrogustometry, used to estimate the degree of gustatory disturbance and to follow its development in these cases, contributes not only to determining lesion location but to establishing prognosis of the paralysis. Our study to date allows no optimism concerning cases of complete facial paralysis associated with severe disturbance of the gustatory function. Moreover, as recovery of the gustatory function precedes that of facial movement in most cases, and as the motor nerve fibers usually begin to degenerate two weeks after onset, it was determined that patients should be examined within at least one week after onset.