Viral Infection as a Cause of Acute Peripheral Facial Palsy

Djupesland, G; Berdal, P; Johannessen, Thor A.; Degré, Miklos; Stien, Ragnar; Skrede, Sverre

doi:10.1001/archotol.1976.00780120051005

Cited by 83 publications

(24 citation statements)

References 25 publications

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“…There have been few reports of CSF findings as sociated with Bell's palsy (6,22). The present study demonstrated that a relatively high incidence of CSF abnormalities accompanied facial paralysis, such as increased levels of total protein (30 cases) and occasional pleocytosis (9 cases) in 91 patients with Bell's palsy.…”

Section: Discussionmentioning

confidence: 99%

“…Even the site along the facial nerve of the lesion is still uncertain. Since cases of Bell's palsy are often preceded by a mild infection (4) and patients may have an accompaning cerebrospinal fluid (CSF) pleocytosis (5,6), some studies have attempted to correlate facial paralysis with viral infection. Viruses, including herpes simplex (7,8), rubella (9), mumps (10) and Epstein-Barr virus (ll), have been associated with Bell's palsy.…”

Section: Introductionmentioning

confidence: 99%

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Virus-Associated Demyelination in the Pathogenesis of Bell's Palsy.

Honda

Takahashi

1992

Intern. Med.

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We examined the cerebrospinal fluid findings, including the activity of the myelin-associated enzyme 2' ,3'-cyclic nucleotide 3'-phosphohydrolase (CNP), and virus serology in patients with Bell's palsy. Eighty-nine of 164 patients showed hematological and/or serological evidence of an inflammatory reaction. Examinations of the CSF disclosed an elevated total protein level and pleocytosis in 33% and 10% of the 91 patients, respectively. The activity of CNP was significantly elevated in the patient group (15.5 ± 3.8 nmol/h/ml) as compared with the control (13.2 ± 1.3 nmol/h/ml) (p < 0.01), suggesting the presence of intrathecal myelin breakdown. Furthermore, there was an association between antibodies against herpes simplex virus (HSV) and elevated CNP activity. The inflammatory alterations and accompanying spinal fluid abnormalities, together with the high frequency of HSV antibodies suggest that HSV-associated demyelination may play a pathogenetic role in Bell's palsy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Virus-Associated Demyelination in the Pathogenesis of Bell's Palsy.

Honda

Takahashi

1992

Intern. Med.

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“…If the reactivation of HSV-1 in the geniculate or trigeminal ganglia causes acute facial palsy, HSV-1 is shed into the saliva via either the chorda tympani nerve or the trigeminal nerve, and should be detectable at the onset of palsy. Only a few investigators have reported on the isolation of HSV-1 from the oropharynx in patients with Bell's palsy [Djupesland et al, 1976;Vahlne et al, 1981], and no study has compared the frequency of HSV-1 isolation between patients with Bell's palsy and control subjects. To gain further insight into the relationship between Bell's palsy and reactivation of HSV-1, the prevalence of shed HSV-1 into saliva in patients with Bell's palsy or Ramsay Hunt syndrome, and in healthy HSV-seropositive volunteers was tested by using a sensitive nested-polymerase chain reaction (PCR) method.…”

Section: Introductionmentioning

confidence: 99%

Reactivation of herpes simplex virus type 1 in patients with Bell's palsy

et al. 1998

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Reactivation of herpes simplex virus type 1 (HSV-1) has been implicated in the pathogenesis of idiopathic peripheral facial palsy (Bell's palsy). The present study used the polymerase chain reaction (PCR) to analyze the saliva of patients with Bell's palsy for the presence of shed HSV-1. The study involved 47 patients with Bell's palsy, 24 patients with Ramsay Hunt syndrome, and 16 healthy HSV-seropositive volunteers. HSV-1 DNA was not detected in the saliva samples from HSV-seronegative patients. The prevalence of shed HSV-1 in patients with Bell's palsy (50%) was significantly higher than that in healthy volunteers (19%, p<0.05). When saliva samples were tested within 7 days after the onset of palsy, the prevalence of shed HSV-1 in patients with Bell's palsy (40%) was significantly higher than that in patients with Ramsay Hunt syndrome (7%, p<0.05). Furthermore, HSV-1 usually became undetectable by the second week after the onset of Bell's palsy when HSV-1 was detected during the acute phase of the disease. These findings strongly suggest that reactivation of HSV-1 is involved in the pathogenesis Bell's palsy, and indicate that PCR is a useful tool for early diagnosis of HSV-1 reactivation in patients with Bell's palsy.

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“…However, there have been reports associating Epstein-Barr [31,32], mumps [33] and cytomegalic inclusion virus [34] with IFP. These neurotropic viruses gain access to cell bodies of sensory neurons by entering nerve endings at an epithelial surface followed by retrograde transport to the cell body.…”

Section: Discussionmentioning

confidence: 99%

Meatal Ganglionitis: Clinical Pathologic Correlation in Idiopathic Facial Paralysis (Bell’s Palsy)

Gacek¹,

Gacek²

1999

Otorhinolaryngol Nova

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Hypothesis: Present evidence which supports the concept that inflammation of the facial nerve (FN) meatal ganglion (MG) is the site of virus accumulation in idiopathic facial paralysis (IFP). Materials and Methods: Four bodies of evidence are used to support the hypothesis. (1) A case report of a 51-year-old female with left IFP is representative of a series with 5 patients who were monitored with MRI. Sequential MRI of the FN at 1, 8 and 15 weeks after onset of IFP monitored the inflammatory process in the FN. (2) A human temporal bone (TB) taken from an 81-year-old female who recovered from IFP 3 years before death was examined in the light microscope. (3) Eleven reports of MRI in patients with IFP were reviewed. (4) The data from 2 human TB studies describing the MG in normal and abnormal FN are summarized. Results: (1) The MRI of the FN in the majority of imaging reports of patients with IFP demonstrated enhancement of the meatal segment of the FN as the earliest focus in IFP. (2) The meatal FN segment was the earliest site of enhancement in our series of 5 patients with IFP. (3) The TB from the patient who recovered from IFP demonstrated degenerated cells in the MG and degeneration of vestibular neurons innervating cristae. (4) TB studies describe the occurrence of the MG in human FN. In the majority of FN (80%), the MG is represented by a smaller ganglion than the geniculate one. However, the MG equals or exceeds in size the geniculate ganglion in 20% of TB. A second TB study demonstrated ganglion cell lesions consistent with virally induced pathology in the MG and vestibular nerve (and ganglion) in a high percentage of TB. Conclusions: Clinical, radiologic and anatomical evidence supports meatal ganglionitis as a pathologic correlate in IFP.

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Viral Infection as a Cause of Acute Peripheral Facial Palsy

Cited by 83 publications

References 25 publications

Virus-Associated Demyelination in the Pathogenesis of Bell's Palsy.

Virus-Associated Demyelination in the Pathogenesis of Bell's Palsy.

Reactivation of herpes simplex virus type 1 in patients with Bell's palsy

Meatal Ganglionitis: Clinical Pathologic Correlation in Idiopathic Facial Paralysis (Bell’s Palsy)

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