Serology in facial paralysis caused by clinically presumed herpes zoster infection

Njoo, F. L.; Dillen, Pauline Wertheim-van; Devriese, P. P.

doi:10.1007/bf00463933

Cited by 16 publications

(3 citation statements)

References 15 publications

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“…Interestingly, besides the small number of case reports describing the development of peripheral facial paralysis in patients with mumps sialadenitis, the association of trigeminal herpes zoster and mumps parotitis has also been reported [11], as well as an increasing titer of mumps IgM in clinically diagnosed cases of Ramsay Hunt syndrome (without clinical sialadenitis) [12]. With the addition of our case, further speculation may be possible that these cases may represent the incomplete clinical presentation of mumps virus infection and subsequent VZV reactivation.…”

Section: Discussionmentioning

confidence: 99%

Mumps, Cervical Zoster, and Facial Paralysis: Coincidence or Association?

Kondo

Kanaya

Baba

et al. 2014

Case Reports in Otolaryngology

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The association of mumps with peripheral facial paralysis has been suggested, but its pathogenesis remains unclear. An 8-year-old girl simultaneously developed left peripheral facial paralysis, ipsilateral cervical herpes zoster, and bilateral mumps sialadenitis. Elevated anti-mumps and anti-varicella zoster virus IgM antibodies in serological testing indicated recent infection of mumps and reactivation of VZV. Molecular studies have provided mounting evidence that the mumps virus dysregulates the host's immune system and enables the virus to proliferate in the infected host cells. This dysregulation of the immune system by mumps virus may have occurred in our patient, enabling the latent VZV infection to reactivate.

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Section: Discussionmentioning

confidence: 99%

Mumps, Cervical Zoster, and Facial Paralysis: Coincidence or Association?

Kondo

Kanaya

Baba

et al. 2014

Case Reports in Otolaryngology

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“…Additionally, VZV is expected to be the cause of Bell's palsy in a subset of patients who show serological data of asymptomatic VZV reactivation but no cutaneous deformities [25,26]. Mumps, Epstein-Barr virus (EBV), cytomegalovirus, rubella, and, in recent years, human immunodeficiency virus have also emerged as potential agents, which can be occasionally linked to Bell's palsy [27][28][29][30][31]. Different studies found different rates of full recovery rates depending on the kind of steroid linked to acyclovir [32,33].…”

Section: Facial Nerve Paralysismentioning

confidence: 99%

Clinical Features and Prognosis of Facial Palsy and Hearing Loss in Patients With Ramsay Hunt Syndrome

Malhotra¹,

Mudey²,

Agrawal³

2022

Cureus

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Ramsay Hunt syndrome, a late manifestation of varicella-zoster virus infection, occurs when the virus reactivates, infects, and produces an inflammatory reaction in the seventh cranial nerve geniculate ganglion. The detection is made clinically on the basis of the following three features: facial nerve palsy, the presence of characteristic herpetic vesicles around the mouth, and pain in the ear. However, it is often diagnosed quite late and sometimes even missed, increasing the chances of complications that have long-term effects. The two significant complications following the development of Ramsay Hunt syndrome are facial nerve palsy and hearing impairment. Ramsay Hunt syndrome is among the principal causes of facial nerve palsy, implicated in around 2-10% of all cases. While hearing loss though prevalent, is a less common complication than facial palsy. This review aimed to analyze the clinical presentation and prognostic features of the complications of Ramsay Hunt syndrome mentioned above, that is, hearing loss and facial nerve palsy. It was seen that while the association of Ramsay Hunt syndrome with facial nerve palsy has been studied quite extensively, the literature on hearing loss as a sequela is quite lacking. The course and outcome of facial nerve palsy is determined by the early clinical picture, while the otological symptoms rely on the extent of nerve involvement. Early diagnosis and treatment go a long way in preventing these complications and increasing the chances of complete recovery. Treatment options most commonly studied included antiviral drugs such as acyclovir, steroids, and anti-inflammatory agents.

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“…The aetiology of this condition remains hypothetical. Several studies have created a long catalogue of possible underlying pathogens, such as varicella zoster, herpes simplex, mumps, rubella, human immunodeficiency or Epstein-Barr virus (EBV) and Borrelia burgdorferi [1][2][3][4][5][6][7]. The clinical manifestation of facial nerve palsy has commonly been associated with endogenous reactivations of latent microorganisms rather than first infections with the respective pathogens.…”

Section: Introductionmentioning

confidence: 99%

Increased seroprevalence of Toxoplasma gondii in a population of patients with Bell’s palsy: a sceptical interpretation of the results regarding the pathogenesis of facial nerve palsy

Riga

Kefalidis

Chatzimoschou

et al. 2011

Eur Arch Otorhinolaryngol

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Facial nerve oedema and anatomical predisposition to compression within the fallopian tube seem to be the only generally accepted facts in the pathophysiology of Bell's palsy. Several infectious causes have been suggested as possible triggers of this oedema. Most of the suggested pathogens have been associated with facial nerve lesions during latent infections, reinfections or endogenous reactivations. The aim of this study was to investigate the seroprevalence of three such pathogens Toxoplasma gondii, Epstein-Barr virus (EBV) and cytomegalovirus (CMV) in a population of patients with facial nerve palsy. Fifty-six patients with Bell's palsy were included in the study. A group of 25 individuals with similar age and gender distribution was used as control. Seropositivity for T. gondii, EBV viral capsid antigen (VCA) and CMV-specific IgM and IgG antibodies was investigated 2-5 days after the onset of the palsy. Comparisons for both IgM and IgG antibodies against T. gondii attributed significantly higher seroprevalence in the patients' group than in the control group (p = 0.024 and 0.013, respectively). The respective examinations for EBV and CMV attributed no significant results. The roles of EBV and CMV in the pathogenesis of Bell's palsy were not confirmed by this study. However, a significantly higher seroprevalence of IgM- and IgG-specific T. gondii antibodies was detected in patients with Bell's palsy when compared to healthy controls. The possibility that facial nerve palsy might be a late complication of acquired toxoplasmosis may need to be addressed in further studies.

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Serology in facial paralysis caused by clinically presumed herpes zoster infection

Cited by 16 publications

References 15 publications

Mumps, Cervical Zoster, and Facial Paralysis: Coincidence or Association?

Mumps, Cervical Zoster, and Facial Paralysis: Coincidence or Association?

Clinical Features and Prognosis of Facial Palsy and Hearing Loss in Patients With Ramsay Hunt Syndrome

Increased seroprevalence of Toxoplasma gondii in a population of patients with Bell’s palsy: a sceptical interpretation of the results regarding the pathogenesis of facial nerve palsy

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