Use of negative pressure wound therapy to treat a cochlear implant infection around the auricle: a case report.

Although negative pressure wound therapy (NPWT) is widely used, its application to the head and neck region remains challenging due to anatomical complexities. This report presents the case of a female patient presenting with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes, uncontrolled diabetes and severe bilateral sensorineural hearing loss. The patient had undergone cochlear implant surgery and five months later the wound was infected with methicillin-resistant Staphylococcus aureus (MRSA). NPWT was started shortly after removing the internal receiver and was stopped 11 days later. NPWT helped in controlling infection and led to a successful wound closure. In this case, NPWT was effective in treating infectious wounds around the auricle after cochlear implant surgery. Declaration of interest: The authors have no financial support for this article and no conflict of interest directly relevant to the content of this article.

Partial requirement of endothelin receptor B in spiral ganglion neurons for postnatal development of hearing.

Impairments of endothelin receptor B (Ednrb/EDNRB) cause the development of Waardenburg-Shah syndrome with congenital hearing loss, hypopigmentation, and megacolon disease in mice and humans. Hearing loss in Waardenburg-Shah syndrome has been thought to be caused by an Ednrb-mediated congenital defect of melanocytes in the stria vascularis (SV) of inner ears. Here we show that Ednrb expressed in spiral ganglion neurons (SGNs) in inner ears is required for postnatal development of hearing in mice. Ednrb protein was expressed in SGNs from WT mice on postnatal day 19 (P19), whereas it was undetectable in SGNs from WT mice on P3. Correspondingly, Ednrb homozygously deleted mice (Ednrb(-/-) mice) with congenital hearing loss showed degeneration of SGNs on P19 but not on P3. The congenital hearing loss involving neurodegeneration of SGNs as well as megacolon disease in Ednrb(-/-) mice were markedly improved by introducing an Ednrb transgene under control of the dopamine ß-hydroxylase promoter (Ednrb(-/-);DBH-Ednrb mice) on P19. Neither defects of melanocytes nor hypopigmentation in the SV and skin in Ednrb(-/-) mice was rescued in the Ednrb(-/-);DBH-Ednrb mice. Thus, the results of this study indicate a novel role of Ednrb expressed in SGNs distinct from that in melanocytes in the SV contributing partially to postnatal hearing development.

Mice lacking ganglioside GM3 synthase exhibit complete hearing loss due to selective degeneration of the organ of Corti.

The ganglioside GM3 synthase (SAT-I), encoded by a single-copy gene, is a primary glycosyltransferase for the synthesis of complex gangliosides. In SAT-I null mice, hearing ability, assessed by brainstem auditory-evoked potentials (BAEP), was impaired at the onset of hearing and had been completely lost by 17 days after birth (P17), showing a deformity in hair cells in the organ of Corti. By 2 months of age, the organ of Corti had selectively and completely disappeared without effect on balance or motor function or in the histology of vestibule. Interestingly, spatiotemporal changes in localization of individual gangliosides, including GM3 and GT1b, were observed during the postnatal development and maturation of the normal inner ear. GM3 expressed in almost all regions of cochlea at P3, but at the onset of hearing it distinctly localized in stria vascularis, spiral ganglion, and the organ of Corti. In addition, SAT-I null mice maintain the function of stria vascularis, because normal potassium concentration and endocochlear potential of endolymph were observed even when they lost the BAEP completely. Thus, the defect of hearing ability of SAT-I null mice could be attributed to the functional disorganization of the organ of Corti, and the expression of gangliosides, especially GM3, during the early part of the functional maturation of the cochlea could be essential for the acquisition and maintenance of hearing function.

Dihydrostreptomycin goes through the mechano-electric transduction channel in chick cochlear hair cells.

OBJECTIVE: This study evaluated the ability of dihydrostreptomycin (DHSM) to go through the mechano-electric transduction (MET) channels in hair cells under physiological conditions. MATERIALS AND METHODS: Tall hair cells were isolated from the chick basilar membrane (cochlea). Mechanical stimulation was applied by a glass rod attached to a piezoelectric bimorph, and MET currents were recorded with a whole-cell patch technique. The voltage-dependent block of DHSM to MET channel was estimated by calculating the relative conductances (the ratio of MET current in DHSM saline to DHSM-free saline) at various membrane potentials. RESULTS AND CONCLUSION: At membrane potentials between -100 and +50 mV, DHSM behaves as a voltage-dependent blocker according to a partial block model. At membrane potentials more negative than -100 mV, however, DHSM blocking decreased. This finding differed from the partial block model, but indicated that DHSM escaped through the channel pore into the cytoplasm by acting as a permeant channel blocker due to the large electrical driving force.

Inactivating potassium currents in apical and basal turn inner hair cells from guinea-pig cochlea.

Tetraethylammonium (TEA)-sensitive potassium currents in the cochlear inner hair cells (IHCs) possess the kinetics of fast inactivation. IHCs of guinea-pigs were separately isolated from the apical and basal turns and the tonotopic gradient of inactivation kinetics was investigated. TEA-sensitive potassium currents showed voltage-dependent time constant of the inactivation phase both in apical and basal IHCs, however, the degree of inactivation (compared to the ratio between the steady-state current and initial peak current) was voltage-independent. Inactivation time constant was faster in basal IHCs than in apical IHCs and the degree of inactivation was greater in basal IHCs than in apical IHCs, suggesting that inactivation was more predominant in basal IHCs than in apical IHCs.

Property of I(K,)(n) in inner hair cells isolated from guinea-pig cochlea.

One of the potassium currents, I(K,)(n), is already activated at the resting potential of the cell and thus determines the membrane potential. KCNQ4 channel has been identified as the molecular correlate of I(K,)(n). In the present study, we measured I(K,)(n) in acutely isolated IHCs of guinea-pig cochlea using the whole-cell voltage-clamp techniques, and investigated the properties of the currents. I(K,)(n) was 70% activated around the resting potential of -60 mV and deactivated on hyperpolarization. I(K,)(n) was blocked by the KCNQ-channel blockers, linopirdine (100 microM) and XE991 (10 microM), but was insensitive to both I(K,f) blocker, tetraethylammonium (TEA), and I(K,s) blocker, 4-aminopyridine (4-AP). There was no significant difference in the size of I(K,)(n) between the apical and basal turn IHCs.

Effect of hydrogen peroxide on potassium currents in inner hair cells isolated from guinea pig cochlea.

Hydrogen peroxide (H2O2) is a ubiquitous reactive oxygen species that can induce several inner ear disorders. In this study, we recorded the potassium (K) currents in acutely isolated inner hair cells of guinea pig cochlea, and investigated the effects of H2O2. We also observed the morphological changes in inner hair cells induced by H2O2. In the H2O2 solutions, the amplitude of outward K currents (I(K,f) and I(K,s)) clearly decreased after perfusion for approximately 15 min. Despite the decrease in outward currents, small inward currents (I(K,n)) did not show any reduction. H2O2 induced morphological changes in the inner hair cells. All the inner hair cells in the H2O2 solutions showed shrinkage and granularity of the cell body and led to loss of viability. These results showed the vulnerability of inner hair cells to reactive oxygen species-induced inner ear disorders.