The role of the facial nerve latency test in the prognosis of Bell's Palsy

1990 ◽  
Vol 100 (10) ◽  
pp. 1083-1085 ◽  
Author(s):  
Antonios Th. Skevas ◽  
Vasilios G. Danielides ◽  
Dimitrios A. Assimakopoulos
1992 ◽  
Vol 8 (3) ◽  
pp. 126-128 ◽  
Author(s):  
Vassillios G. Danielides ◽  
Antonios T. Skevas ◽  
Kanaris Panagopoulos ◽  
Ioannis Kastanioudakis

Author(s):  
M Khateri ◽  
S Cheraghi ◽  
A Ghadimi ◽  
H Abdollahi

Bell’s palsy is an idiopathic peripheral nerve palsy involving the facial nerve. It accounts for 60 to 75% of all cases of unilateral facial paralysis. The main mechanisms to induce BP remain unclear, but infection, ischemic condition and immunodeficiency may contribute to the development of Bell’s palsy. Accumulating evidence has shown several factors can trigger the reactivation of latent HSV including psychological stressors, physical stressors and immunosuppression. Ionization and non-ionization radiations are of importance of physical stressors. Some data have shown radiation can reactivate HSVs. Based on preliminary studies showing radiation reactivation of HSVs, we aimed to hypothesize radiation (in both forms of ionization and non-ionization) may cause Bell’s palsy. In the future, the role of radiotherapy, radiofrequency radiation from mobile phones and wireless devices in HSV reactivation and Bell’s palsy should be investigated.


1994 ◽  
Vol 108 (11) ◽  
pp. 940-943 ◽  
Author(s):  
Tarek S. Shafshak ◽  
Aymen Y. Essa ◽  
Fathy A. Bakey

AbstractIncomplete recovery from Bell's palsy was observed in some patients even after the intake of corticosteroids. This prospective study was performed on 160 patients with unilaterial nonrecurrent Bell's palsy in order to investigate the role of prednisolone on the prognosis of Bell's palsy. Ninety-three patients were given prednisolone tablets (1 mg/kg body wt/day up to 70 mg) for six successive days, then the dose was reduced gradually over the next four days. The remaining 67 patients were not given prednisolone (control group). Facial nerve recovery was assessed clinically and electrophysiologically for up to one year. The results of this study suggested that the most probable contributing factor for the success of prednisolone in improving the prognosis of Bell's palsy was its early intake (within the first 24 hours following onset).


2012 ◽  
Vol 73 (S 02) ◽  
Author(s):  
L. M. Marques ◽  
J. Pimentel ◽  
P. Escada ◽  
G. Neto D'Almeida

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Akira Inagaki ◽  
Sachiyo Katsumi ◽  
Shinji Sekiya ◽  
Shingo Murakami

AbstractIn Bell’s palsy, electrodiagnosis by electroneurography (ENoG) is widely used to predict a patient’s prognosis. The therapeutic options for patients with poor prognostic results remain controversial. Here, we investigated whether early intervention with intratympanic steroid therapy (ITST) is an effective treatment for Bell’s palsy patients with poor electrodiagnostic test results (≤ 10% electroneurography value). Patients in the concurrent ITST group (n = 8) received the standard systemic dose of prednisolone (410 mg total) and intratympanic dexamethasone (16.5 mg total) and those in the control group (n = 21) received systemic prednisolone at the standard dose or higher (average dose, 605 ± 27 mg). A year after onset, the recovery rate was higher in the ITST group than in the control group (88% vs 43%, P = 0.044). The average House-Brackmann grade was better in the concurrent ITST group (1.13 ± 0.13 vs 1.71 ± 0.16, P = 0.035). Concurrent ITST improves the facial nerve outcome in patients with poor electroneurography test results, regardless of whether equivalent or lower glucocorticoid doses were administered. This may be ascribed to a neuroprotective effect of ITST due to a higher dose of steroid reaching the lesion due to dexamethasone transfer in the facial nerve.


1995 ◽  
Vol 104 (7) ◽  
pp. 574-581 ◽  
Author(s):  
Toshiaki Sugita ◽  
Yasuo Fujiwara ◽  
Shingo Murakami ◽  
Yoshinari Hirata ◽  
Naoaki Yanagihara ◽  
...  

We have been the first to succeed in producing an acute and transient facial paralysis simulating Bell's palsy, by inoculating herpes simplex virus into the auricles or tongues of mice. The KOS strain of the virus was injected into the auricle of 104 mice and the anterior two thirds of the tongue in 30 mice. Facial paralysis developed between 6 and 9 days after virus inoculation, continued for 3 to 7 days, and then recovered spontaneously. The animals were painlessly sacrificed between 6 and 20 days after inoculation for histopathologic and immunocytochemical study. Histopathologically, severe nerve swelling, inflammatory cell infiltration, and vacuolar degeneration were manifested in the affected facial nerve and nuclei. Herpes simplex virus antigens were also detected in the facial nerve, geniculate ganglion, and facial nerve nucleus. The pathophysiologic mechanisms of the facial paralysis are discussed in light of the histopathologic findings, in association with the causation of Bell's palsy.


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