Seoul National University College of Medicine;
Soree Ear Clinic;
J Neurosurg. 2016 Aug;125(2):441-9. doi: 10.3171/2015.6.JNS15961. Epub 2016 Jan 8.
OBJECTIVE A dominant sigmoid sinus with focal dehiscence or thinning (DSSD/T) of the overlying bony wall is a commonly encountered, but frequently overlooked, cause of vascular pulsatile tinnitus (VPT). Also, the pathophysiological mechanism of sound perception in patients with VPT remains poorly understood. In the present study, a novel surgical method, termed transmastoid SS-reshaping surgery, was introduced to ameliorate VPT in patients with DSSD/T. The authors reviewed a case series, analyzed the surgical outcomes, and suggested the pathophysiological mechanism of sound perception. The theoretical background underlying VPT improvement after transmastoid SS-reshaping surgery was also explored. METHODS Eight patients with VPT that was considered attributable to DSSD/T underwent transmastoid SS-reshaping surgery between February 2010 and February 2015. The mean postoperative follow-up period was 9.5 months (range 4-13 months). Transmastoid SS-reshaping surgery featured simple mastoidectomy, partial compression of the SS using harvested cortical bone chips, and reinforcement of the bony SS wall with bone cement. Perioperative medical records, imaging results, and audiological findings were comprehensively reviewed. RESULTS In 7 of the 8 patients (87.5%), the VPT abated immediately after surgery. Statistically significant improvements in tinnitus loudness and distress were evident on numeric rating scales. Three patients with preoperative ipsilesional low-frequency hearing loss exhibited postoperative improvements in their low-frequency hearing thresholds. No major postoperative complications were encountered except in the first subject, who experienced increased intracranial pressure postoperatively. This subsided after a revision operation for partial decompression of the SS. CONCLUSIONS Transmastoid SS-reshaping surgery may be a good surgical option in patients with DSSD/T, a previously unrecognized cause of VPT. Redistribution of severely asymmetrical blood flow, reinforcement of the bony SS wall with bone cement to reconstruct a soundproof barrier, and disconnection of a problematic sound conduction route via simple mastoidectomy silence VPT.
优势型乙状窦伴局部骨质缺损或薄弱(DSSD/T)是引起血管性搏动性耳鸣(VPT)的常见原因,但常被忽视。此外,VPT 患者的声音感知病理生理机制仍知之甚少。本研究提出了一种新的手术方法,称为经乳突乙状窦重塑术,以改善 DSSD/T 患者的 VPT。作者回顾了一系列病例,分析了手术结果,并提出了声音感知的病理生理机制。还探讨了经乳突乙状窦重塑术改善 VPT 的理论基础。
2010 年 2 月至 2015 年 2 月,8 例 VPT 患者(均归因于 DSSD/T)接受了经乳突乙状窦重塑术。平均术后随访时间为 9.5 个月(4-13 个月)。经乳突乙状窦重塑术的特点是单纯乳突切除术、使用皮质骨碎片对乙状窦进行部分压迫、使用骨水泥加固乙状窦骨壁。全面回顾围手术期病历、影像学结果和听力结果。
8 例患者中有 7 例(87.5%)VPT 在术后即刻减轻。数字评分量表显示耳鸣响度和苦恼程度均有显著改善。3 例术前同侧低频听力损失患者术后低频听力阈值改善。除 1 例患者术后出现颅内压增高外,无其他重大术后并发症。该患者接受了乙状窦部分减压的翻修手术,颅内压增高缓解。
经乳突乙状窦重塑术可能是 DSSD/T 患者的一种较好的手术选择,DSSD/T 是一种以前未被认识的 VPT 原因。通过单纯乳突切除术切断有问题的声音传导途径,使用骨水泥重新构建隔音屏障以加强乙状窦骨壁,重新分配严重不对称的血流,可能会使 VPT 静音。