Comparison of therapeutic effects of steroid injection by benign vocal fold lesion type.

BACKGROUND: Benign vocal fold lesions (BVFLs) can cause voice changes, including reduced loudness and pitch range. In recent times, with progression in endoscopic technology, office-based vocal fold steroid injection (VFSI) has been used as an alternative therapy for BVFLs. AIMS/OBJECTIVES: In this study, we analyzed the efficacy and safety of VFSI to investigate the mechanism underlying its therapeutic effects and determine the conditions in which VFSI will be most effective. MATERIALS AND METHODS: In this retrospective cohort study, we included 40 condition-matched patients (8 patients per lesion) with chorditis, vocal nodules, vocal polyps, Reinke's edema (RE), or vocal scars who received similar regimens of steroid injection using a commercial preparation of triamcinolone acetonide. Their phonological outcomes were evaluated 2 or 3 months after the injection. RESULTS: Significant improvements were observed in Voice Handicap Index scores, results of laboratory voice evaluation, and voice quality measured using the Grade, Roughness, Breathiness, Asthenia, Strain scale in all participants. In subgroup analysis, VFSI was highly effective against chorditis and vocal nodules, but less effective against RE and vocal scars. CONCLUSIONS: Single-dose VFSI is valuable as an alternative to voice rehabilitation and laryngo-microsurgery, but higher concentrations or repeated injections are required for intractable lesions.

Validation of the Japanese Version of the Singing Voice Handicap Index.

PURPOSE: The aim of the present study was to translate the Singing Voice Handicap Index (SVHI) into Japanese and validate the Japanese version of the SVHI. METHODS: The SVHI was translated into Japanese from the validated original version, and the questionnaire was administered to 102 singers with voice problems and 88 healthy singers. Internal consistency and test-retest methods were implemented to evaluate the reliability of this index. The internal consistency method assessed validity via Cronbach's α, and test-retest reliability was analyzed by the intraclass correlation coefficient (ICC) and limits of agreement (LoA) according to the Bland Altman method. Construct validity was verified by confirming correlations between SVHI scores and visual analog scale (VAS) scores for disability in singing using Spearman correlation. Discriminant validity was evaluated by comparing SVHI scores between singers with voice problems and healthy singers using t tests. Using the Tukey's honestly significant difference (HSD) test, we also compared the Voice Handicap Index (VHI) and SVHI scores among three groups: healthy singers, singers with voice problems solely during singing, and singers with voice problems during both speaking and singing. RESULTS: The Japanese version of the SVHI showed excellent internal consistency (Cronbach's α = 0.981) and test-retest reliability (ICC: 0.93). The 95 percent LoA was calculated to be between -20.8 and 33.9. Construct validity was verified through correlated SVHI and VAS scores (r = 0.736, P < 0.001). Discriminant validity was verified as the SVHI scores of singers with voice problems were higher than those of healthy singers (77.8±37.5 vs. 30.0±26.5, P < 0.001). There were no statistically significant differences in VHI scores between singers with voice problems solely during singing and healthy singers; however, the SVHI scores of singers with voice problems solely during singing were significantly higher than those of healthy singers (63.4±36.8 vs. 30.0±26.5, P < 0.001). CONCLUSION: We confirmed that the Japanese version of the SVHI is a valid and reliable self-rated questionnaire for measuring the patient-perceived impact of singing voice problems among Japanese singers.

[A Case of Idiopathic Bridging Vocal Fold Adhesion that was Treated by Ambulatory Surgery under Local Anesthesia].

Patients with vocal fold adhesions usually undergo surgery under general anesthesia, because of the possibility of postoperative adhesions according to the severity and cause. However, it has been reported that patients with minor bridging adhesion can be treated by only discission without any postoperative adhesion. Herein, we report the case of a patient with idiopathic bridging vocal fold adhesions who was treated by ambulatory surgery at the ENT clinic and showed a benign course. A male former professional singer who was in his 70s presented with a history of cough followed by the development of bridging central vocal fold adhesion. On the 10th day after the initial visit, we performed discission of the adhesion under local anesthesia using a surgical knife for the vocal fold. Although a delicate surgical technique is desirable for phonosurgery, we were able to perform surgery under local anesthesia in this case, because the adhesion was minor. We consider that endoscopic laryngeal surgery under local anesthesia is useful for the treatment of patients with bridging adhesions.

Ca(2+) regulation of endocochlear potential in marginal cells.

We examined the effect of the cytosolic Ca(2+) concentration ([Ca(2+)](c)) in marginal cells on the asphyxia- or furosemide-induced decrease in the endocochlear potential (EP) by perfusing the endolymph with or without a Ca(2+) chelator or inhibitors of Ca(2+)-permeable channels or Ca(2+)-pump during transient asphyxia or intravenous administration of furosemide. We obtained the following results. (1) Endolymphatic administration of SKF96365 (an inhibitor of TRPC and L-type Ca(2+) channels) or EGTA-acetoxymethyl ester (EGTA-AM) significantly inhibited both the transient asphyxia-induced decrease in EP (TAID) and the furosemide-induced decrease in EP (FUID). (2) Endolymphatic perfusion with nifedipine significantly inhibited the TAID but not the FUID. (3) The recovery from the FUID was significantly suppressed by perfusing the endolymph with EGTA-AM, nifedipine, or SKF96365. (4) Endolymphatic administration of thapsigargin inhibited both the FUID and TAID. (5) The recovery rate from the FUID was much slower than that from the TAID, indicating that furosemide may inhibit the Ca(2+)-pump. (6) A strong reaction in immunohistochemical staining for TRPC channels was observed in the luminal and basolateral membranes of marginal cells. (7) A positive staining reaction for the gamma subunit of epithelial Na(+) channels was observed in the luminal and basolateral membranes of marginal cells. (8) Positive EP was diminished toward 0 mV by the endolymphatic perfusion with 10 muM amiloride or 10 muM phenamil. Taken together, these findings suggest that [Ca(2+)](c) regulated by endoplasmic Ca(2+)-pump and Ca(2+)-permeable channels in marginal cells may regulate the positive EP, which is partly produced by the diffusion potential of Na(+) across the basolateral membrane in marginal cells.

Effects of CO2/HCO3- in perilymph on the endocochlear potential in guinea pigs.

The effect of CO(2)/HCO(3)(-) on the endocochlear potential (EP) was examined by using both ion-selective and conventional microelectrodes and the endolymphatic or perilymphatic perfusion technique. The main findings were as follows: (i) A decrease in the EP from approximately +75 to approximately +35 mV was produced by perilymphatic perfusion with CO(2)/HCO(3)(-)-free solution, which decrease was accompanied by an increase in the endolymphatic pH (DeltapH(e), approximately 0.4). (ii) Perilymphatic perfusion with a solution containing 20 mM NH(4)Cl produced a decrease in the EP (DeltaEP, approximately 20 mV) with an increase in the pH(e) (DeltapH(e), approximately 0.2), whereas switching the perfusion solution from the NH(4)Cl solution to a 5% CO(2)/25 mM HCO(3)(-) solution produced a gradual increase in the EP to the control level with the concomitant recovery of the pH(e). (iii) The perfusion with a solution of high or low HCO(3)(-) with a constant CO(2) level within 10 min produced no significant changes in the EP. (iv) Perfusion of the perilymph with 10 microg/ml nifedipine suppressed the transient asphyxia-induced decrease in EP slightly, but not significantly. (v) By contrast, the administration of 1 microg/ml nifedipine via the endolymph inhibited significantly the reduction in the EP induced by transient asphyxia or perilymphatic perfusion with CO(2)/HCO(3)(-)-free or 20 mM NH(4)Cl solution. These findings suggest that the effect of CO(2) removal from perilymphatic perfusion solution on the EP may be mediated by an increase in cytosolic Ca(2+) concentration induced by an elevation of cytosolic pH in endolymphatic surface cells.

Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs.

We examined the effect of the Ca(2+) concentration in the endolymph ([Ca](e)) or in the endolymphatic surface cells ([Ca](i)) on the endocochlear potential (EP) by using an endolymphatic or perilymphatic perfusion technique, respectively. (i) A large increase in [Ca](e) up to approximately 10(-3) M with a fall in the EP was induced by transient asphyxia ( approximately 2 min) or by the intravenous administration of furosemide (60 mg/kg), and a significant correlation was obtained between the EP and p[Ca](e) (= -log [Ca](e), r = 0.998). (ii) Perfusion of the endolymph with 10 mM EGTA for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP (DeltaEP(asp)), suggesting that neither [Ca](e) nor the Ca(2+) concentration gradient across the stria vascularis contributed directly to the generation of the EP in the condition of low [Ca](e). In contrast, endolymphatic perfusion with high Ca(2+) (more than 10 mM) produced a decrease in EP and a significant correlation was obtained between the EP and the Ca(2+) concentration of perfusion solution (r = 0.982), suggesting that Ca(2+) permeability may exist across the stria vascularis. (iii) The administration of a Ca(2+) chelator, EGTA-acetoxymethyl ester (AM, 0.3 mM), to the endolymph, which produced a gradual increase in EP, suppressed significantly, by 60-80%, DeltaEP(asp) or furosemide-induced changes in EP. In contrast, perilymphatic administration of 0.5 mM EGTA-AM caused no significant suppression of the DeltaEP(asp). These findings suggest that [Ca](i) plays an important role in generating/maintaining a large positive EP.