Subtotal facial nerve decompression in preventing further recurrence and promoting facial nerve recovery of severe idiopathic recurrent facial palsy.

The objective of the study is to document the role of subtotal facial nerve decompression in preventing further recurrence and promoting facial nerve recovery of severe idiopathic recurrent facial palsy. Twenty-two cases with idiopathic recurrent facial palsy, which had over 95% degeneration of facial nerve on electroneurography, were included in the study, among which 12 accepting subtotal facial nerve decompression were involved in surgery group, and 10 who refused surgery and received prednisolone were classified into control group. The recurrence of facial palsy and facial nerve recovery was compared. The patients were followed up for 5.3 years (range 3-8 years) and 5.2 years (range 3-7 years) in surgery group and control group, respectively. Further recurrence of facial palsy occurred in none of 12 patients (0%) in surgery group in contrast to 4 of 10 cases (40%) in control group, with statistical difference (p < 0.05). 11 of 12 cases (91.7%) in surgery group recovered to Grade I or Grade II compared to 3 of 10 cases (30.0%) in control group, with significant difference (p < 0.05). Subtotal facial nerve decompression is effective to prevent further recurrence of facial palsy and promote facial nerve recovery of severe idiopathic recurrent facial palsy.

Decreased calcium-activated potassium channels by hypoxia causes abnormal firing in the spontaneous firing medial vestibular nuclei neurons.

Vertebrobasilar insufficiency (VBI) presents complex varied clinical symptoms, including vertigo and hearing loss. Little is known, however, about how Ca(2+)-activated K(+) channel attributes to the medial vestibular nucleus (MVN) neural activity in VBI. To address this issue, we performed whole-cell patch clamp and quantitative polymerase chain reaction (qPCR) to examine the effects of hypoxia on neural activity and the changes of the large conductance Ca(2+) activated K(+) channels (BKCa channels) in the MVN neurons in brain slices of male C57BL/6 mice. Brief hypoxic stimuli of the brain slices containing MVN were administrated by switching the normoxic artificial cerebrospinal fluid (ACSF) equilibrated with 21% O2/5% CO2 to hypoxic ACSF equilibrated with 5% O2/5% CO2 (balance N2). 3-min hypoxia caused a depolarization in the resting membrane potential (RM) in 8/11 non-spontaneous firing MVN neurons. 60/72 spontaneous firing MVN neurons showed a dramatic increase in firing frequency and a depolarization in the RM following brief hypoxia. The amplitude of the afterhyperpolarization (AHPA) was significantly decreased in both type A and type B spontaneous firing MVN neurons. Hypoxia-induced firing response was alleviated by pretreatment with NS1619, a selective BKCa activator. Furthermore, brief hypoxia caused a decrease in the amplitude of iberiotoxin-sensitive outward currents and mRNA level of BKCa in MVN neurons. These results suggest that BKCa channels protect against abnormal MVN neuronal activity induced by hypoxia, and might be a key target for treatment of vertigo and hearing loss in VBI.