Facial nerve palsy after reactivation of herpes simplex virus type 1 in diabetic mice

Esaki, Shinichi; Yamano, Koji; Katsumi, Sachiyo; Minakata, Toshiya; Murakami, Shingo

doi:10.1002/lary.24994

Cited by 16 publications

(9 citation statements)

References 24 publications

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“…One cause may be an inflammation process of the nerve or the surrounding tissue [22,23] after wound healing. But also direct pressure on the nerve [15,24] caused for instance by the cochlear implant electrode, an infection or reactivation of herpes viruses [25] or other factors [26][27][28] may be a reason. However, surgical edema is unlikely to be an etiological factor in delayed onset FN palsy [29].…”

Section: Results Divided According To Time Of Onsetmentioning

confidence: 99%

Facial palsy following cochlear implantation

Alzhrani

Lenarz

Teschner

2016

Eur Arch Otorhinolaryngol

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Owing to its anatomical location, the facial nerve (FN) is at risk of damage during cochlear implantation, especially during posterior tympanotomy. The aim of this study was, therefore, to evaluate the risk of FN palsy following cochlear implantation surgery via mastoidectomy and posterior tympanotomy approach (facial recess). This is a retrospective study. The data bank of patients who received a cochlear implant between 2000 and 2012 was analyzed. 3403 surgeries were done during this period. Records of the patients who had suffered from FN palsy were evaluated and the type of FN palsy, the severity, time of onset, and need for revision surgery were recorded. 0.76 % (26/3403) of the patients had FN palsy and were, therefore, included in the study. 76.9 % (20/26) subjects were 18 years or older. 0.15 % (5 subjects) suffered from immediate FN palsy and 0.62 % (21 subjects) from delayed FN palsy. Intraoperative FN injury was documented in only three subjects of the immediate FN palsy group. In two subjects with immediate FN palsy, the FN was intraoperatively exposed but not injured, despite these individuals' experiencing FN palsy. In 100 % of the immediate onset FN palsy group a part of the FN was exposed during surgery, whereas it was exposed only in 9.5 % of the delay onset FN palsy group. Although the FN was bone protected in 19 subjects, they had FN palsy. Most of the subjects presented House-Brackmann grade III or IV (69.2 %). All of the subjects were treated initially with a conservative therapy, only 42.3 % (11 subjects) underwent revision surgery. The recovery rate was 80.8 % (in immediate onset palsy 40 %, in delayed onset palsy 90.5 %). Cochlear implantation entails only a minimal risk of FN palsy and that FN palsy is chiefly a transient problem.

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Section: Results Divided According To Time Of Onsetmentioning

confidence: 99%

Facial palsy following cochlear implantation

Alzhrani

Lenarz

Teschner

2016

Eur Arch Otorhinolaryngol

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“…Bell's palsy seems to usually coincide with the narrower fallopian tube of the patient [13,14] The mean width was significantly smaller at the labyrinthine section of the facial canal in the influenced temporal bone than the equivalent in the uninfluenced (p = 0.00) [14] Significant relationship was found between the HB grade and the facial canal diameter at the level of second genu (p = 0.02) [9] In patients with higher primary HB-scores, their 6-month later HB-scores were also higher. In patients with higher 6-month HB score; their IAC inlet and mid-canal values were lower Table 2 Summary of key evidence for the etiological theory about virus infection Key references Summary of evidence [21][22][23][24] The α-HV which target peripheral neurons (e.g., HSV-1, HSV-2, and VZV) can establish lifelong infections and infectivity potential in the host including in the autonomic and sensory ganglia of the head, neck and cranial [25] Reactivation of HSV-1 centered around the geniculate ganglion was first outlined by McCormick in 1972 [26] The presence of HSV-1 deoxyribonucleic acid (DNA) was detected in clinical specimens, i.e., intra-temporal facial nerve endoneural fluid in Bell's palsy patients [27][28][29] Animal models have the capability to cause facial paralysis through initial infection and virus reactivation incited by immune modulation [36,37] Earlier work examining cellular electrophysiology in the setting of herpes infection demonstrated a pathway for the quick and dynamic control of excitability in sensory neurons by internalization of sodium channels. The processes of intra-axonal degeneration would drive the abrupt onset of Bell's palsy [38] The aquaporin 1 water channel protein (AQP1) in Schwann cells of intratemporal facial nerve is involved in the evolution of facial palsy caused by HSV-1 and may play an important role in the pathogenesis of this disease [39] Decreasing LAT levels in neurons reduced the ability of the virus to reactivate.…”

Section: Anatomical Structurementioning

confidence: 99%

“…The reactivation of HSV-1 centered around the geniculate ganglion, and thus potentially linked to BP, was first outlined by McCormick [25]. An association with HSV-1 is supported by the presence of HSV-1 DNA in clinical specimens (i.e., intra-temporal facial nerve endo-neural fluid) [26] in BP patients, as well as its capability to cause facial paralysis in animal models after initial infection [27] and reactivation incited by immune modulation [28,29]. A possible cause of HSV-1-mediated neural dysfunction is the activation of apoptotic pathways and intra-axonal degradation, which are driven by the axon's local indirect and direct responses to the viruses themselves in susceptible phenotypes.…”

Section: Viral Infectionmentioning

confidence: 99%

The etiology of Bell’s palsy: a review

et al. 2019

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Bell's palsy is the most common condition involving a rapid and unilateral onset of peripheral paresis/paralysis of the seventh cranial nerve. It affects 11.5-53.3 per 100,000 individuals a year across different populations. Bell's palsy is a health issue causing concern and has an extremely negative effect on both patients and their families. Therefore, diagnosis and prompt cause determination are key for early treatment. However, the etiology of Bell's palsy is unclear, and this affects its treatment. Thus, it is critical to determine the causes of Bell's palsy so that targeted treatment approaches can be developed and employed. This article reviews the literature on the diagnosis of Bell's palsy and examines possible etiologies of the disorder. It also suggests that the diagnosis of idiopathic facial palsy is based on exclusion and is most often made based on five factors including anatomical structure, viral infection, ischemia, inflammation, and cold stimulation responsivity.

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“…One possible cause that has been suggested is that of a reactivated herpes simplex virus (HSV-1) infection centred around the geniculate ganglion, a theory first outlined by McCormick 5. The association with HSV-1 is supported by the presence of HSV-1 in intratemporal facial nerve endoneural fluid13 harvested during nerve decompression, and the ability to incite facial palsy in an animal model through primary infection14 and reactivation induced by immune modulation 15. Despite this evidence, the behaviour of Bell's palsy is unusual compared with other diseases more commonly caused by HSV, such as herpes labialis (cold sores) and genital herpes 4.…”

Section: Aetiologymentioning

confidence: 99%