Facial Nerve Paralysis Induced by Herpes Simplex Virus in Mice: An Animal Model of Acute and Transient Facial Paralysis

Abstract

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.

Comparison of hearing results following the use of NiTiBOND versus Nitinol prostheses in stapes surgery: a retrospective controlled study reporting short-term postoperative results

“…To date we have observed 1 delayed facial paralysis with NiTiBOND piston, and 1 with Nitinol; both patients subsequently recovered completely. Recent publications suggest the reactivation of dormant viruses in the background of delayed facial nerve palsy [23,24]. Both patients received 60 mg methylprednisolone (Medrol, Pfizer) daily, which was gradually tapered off in 3 weeks, and 5 9 200 mg oral acyclovir (Zovirax, Sanofi Aventis) which was administered daily for 2 weeks [25].…”

Is There a Relationship Between Bell’s Palsy and Internal Auditory Canal?

“…In animals with facial paralysis, histopathologic examination revealed massive infiltration of inflammatory cells in the facial nerve. In addition, vacuolar degeneration, demyelination, and edematous swelling of the facial nerve were also observed [11]. MRI enhancement of the facial nerve in Bell's palsy after administration of gadopentetate dimeglumine has been explained by hypervascularity of the perineural structures and formation of an increased vascular pool of contrast material, and/or disruption of the blood-nerve barrier by acute inflammation [12].…”

Hepatocyte growth factor incorporated into herpes simplex virus vector accelerates facial nerve regeneration after crush injury

“…A similar discrepancy between CMAP amplitude and recovery of facial nerve paralysis in the recovery phase was also reported in a mouse model of HSV neuritis 40 and in a human study of Bell's palsy. 41 Wild-type HSV type 1 is known to have affinity for neurons of the facial nerve and cause pathology in an animal model, 42 and the majority of Bell's palsy is caused by reactivation of HSV type 1 latently infected in the geniculate ganglion. 43 Therefore, the question facing gene transfer using the HSV vector is how to transfer genes effectively while avoiding neuropathogenesis.…”