Bell's Palsy and Herpes Simplex Virus: Fact or Mystery?

2007 ◽  
Vol 2007 ◽  
pp. 126-127
Author(s):  
J.R. Berger
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.


2002 ◽  
Vol 111 (7) ◽  
pp. 616-622 ◽  
Author(s):  
Naohito Hato ◽  
Hisanobu Kisaki ◽  
Nobumitu Honda ◽  
Hirotaka Takahashi ◽  
Shingo Murakami ◽  
...  

Herpes simplex virus type 1 (HSV-1) has been proven to be a cause of Bell's palsy; however, the underlying pathophysiology of the facial nerve paralysis is not fully understood. We established a mouse model with facial nerve paralysis induced by HSV-1 infection simulating Bell's palsy and investigated the pathophysiology of the facial nerve paralysis. The time course of the R1 latency in the blink reflex tests paralleled the recovery of the facial nerve paralysis well, whereas electroneurographic recovery tended to be delayed, compared to that of the paralysis; these responses are usually seen in Bell's palsy. On histopathologic analysis, intact, demyelinated, and degenerated nerves were intermingled in the facial nerve in the model. The similarity of the time course of facial nerve paralysis and the electrophysiological results in Bell's palsy and the model strongly suggest that the pathophysiological basis of Bell's palsy is a mixed lesion of various nerve injuries.


1991 ◽  
Vol 105 (8) ◽  
pp. 625-627 ◽  
Author(s):  
P. J. Wormald ◽  
S. L. Sellars ◽  
J. C. de Villiers

AbstractBilateral facial nerve palsies are rare. This article details the Cape Townexperience of 24 patients with this condition seen over the past 20 years and highlights the three main groups in which these bilateral facial nerve palsies occurred. These are Bell's palsy, fracture of the temporal bones and sclerosteosis. Avariety of other rare causes was also found. Bell's palsy remains a diagnosis of exclusion though there has been some evidence to suggest implication of the Herpes simplex virus. The mechanism whereby temporal bone fractures cause bilateral facial nerve palsies is discussed. The clinical presentation and management of sclerosteosis is also discussed


1988 ◽  
Vol 97 (6_suppl3) ◽  
pp. 18-21 ◽  
Author(s):  
Koshiro Nakamura ◽  
Naoaki Yanagihara

In 45 patients with Bell's palsy of recent onset, the neutralization antibody titers to herpes simplex virus type 1 (HSV-1) were assayed by a microtiter technique. As a control, the neutralization antibody titers of 50 normal subject were assayed. Complement fixation tests also were performed. The geometric means of the neutralization antibody titers of the patients appeared higher at all times than those of the normal subjects. Significant change in the neutralization antibody titer suggesting a recent infection of HSV-1 was seen in seven patients (15.6%), while the complement fixation test demonstrated significant change in only one patient (2.2%). The higher geometric means of the neutralization antibody titers in the patients was thought to indicate that reactivation of the HSV-1 infection was responsible for the onset of Bell's palsy.


1981 ◽  
Vol 107 (2) ◽  
pp. 79-81 ◽  
Author(s):  
A. Vahlne ◽  
S. Edstrom ◽  
P. Arstila ◽  
M. Beran ◽  
H. Ejnell ◽  
...  

2003 ◽  
Vol 19 (1) ◽  
pp. 6-10
Author(s):  
Susan M Miller

Objective: To examine the role of acyclovir in the treatment of Bell's palsy. Data Sources: A search was performed using MEDLINE (1966–September 2002) and the Cochrane Database of Systematic Reviews with the search terms acyclovir, antiviral, idiopathic facial paralysis, Bell's palsy, herpes simplex virus, and corticosteroids. Data Synthesis: Treatment of Bell's palsy is controversial. Recent research has indicated that herpes simplex virus type 1 may be the likely causative agent. Clinical trials and review articles focusing on the use of acyclovir in the treatment of Bell's palsy were reviewed and evaluated. Conclusions: More solid evidence is necessary to validate whether herpes simplex virus type 1 causes Bell's palsy. Limited published clinical studies exist that have used acyclovir for the treatment of Bell's palsy. The results of available trials are contradictory. The American Academy of Neurology's practice parameter states that acyclovir, in combination with steroids, is safe and possibly effective for Bell's palsy treatment. Further information is needed from larger prospective, randomized, placebo-controlled trials to clarify the ultimate therapeutic role of acyclovir for Bell's palsy.


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