Herpes Simplex Virus in Idiopathic Facial Paralysis (Bell Palsy)

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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Herpes Simplex Virus and Experimental Facial Paralysis

The Facial Nerve ◽

10.1007/978-3-642-85090-5_193 ◽

1994 ◽

pp. 489-490 ◽

Cited By ~ 1

Author(s):

J. L. Llorente Pendás ◽

C. Suarez Nieto ◽

M. Oña Gutierrez ◽

A. Martinez ◽

S. Melon Garcia

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Facial Paralysis ◽

Simplex Virus

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Role of Herpes Simplex Virus Infection in the Pathogenesis of Facial Paralysis in Mice

Annals of Otology Rhinology & Laryngology ◽

10.1177/000348949610500108 ◽

1996 ◽

Vol 105 (1) ◽

pp. 49-53 ◽

Cited By ~ 20

Author(s):

Shingo Murakami ◽

Naohito Hato ◽

Takashi Doi ◽

Mutsuhiko Mizobuchi ◽

Naoaki Yanagihara

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Facial Nerve ◽

Brain Stem ◽

Facial Paralysis ◽

Antibody Titer ◽

Model Following ◽

Facial Nerves ◽

Simplex Virus ◽

Neutralization Antibody Titer

To clarify the role and site of herpes simplex virus (HSV) infection in the pathogenesis of facial paralysis, we examined the viral genome by the polymerase chain reaction and the neutralization antibody titer using microplates in an animal model. Following inoculation with HSV type 1 of the KOS strain into mouse auricles, HSV DNA appeared in the ipsilateral facial nerve on the 3rd day, and in bilateral facial nerves and the brain stem on the 10th day only in animals with facial paralysis. In animals without facial paralysis, no HSV DNA was detected in these tissues. The neutralization antibody titer was elevated between 4 and 20 days in all animals, with or without facial paralysis. Facial paralysis developed only on the inoculated side, even though HSV DNA was also present in the contralateral facial nerve. We conclude that HSV infection in the facial nerve and brain stem is prerequisite for facial paralysis, and suggest that an immunologic reaction following viral infection plays a key role in the pathogenesis.

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