Tian Shan, Wang Lizhen, Yang Jiemeng, Mao Rui, Liu Zhaohui, Fan Yubo
Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, 37# Xueyuan Road, Haidian District, Beijing 100191, China.
National Research Center for Rehabilitation Technical Aids, Beijing 100176, China.
J Biomech. 2017 Feb 8;52:68-73. doi: 10.1016/j.jbiomech.2016.12.012. Epub 2016 Dec 16.
Sigmoid sinus cortical plate dehiscence (SSCPD) is common in pulsatile tinnitus (PT) patients, and is treated through SSCPD resurfacing surgery in clinic, but the bio-mechanism is not clear as so far. This study aimed to clarify the bio-mechanism of PT sensation induced by SSCPD, and quantify the relationship of cortical plate (CP) thickness and PT sensation intensity. It was hypothesized that SSCPD would induce PT through significantly amplifying sigmoid sinus (SS) venous sound in this study. Finite element (FE) analysis based on radiology data of typical patient was used to verify this hypothesis, and was validated with clinical reports. In cases with different CP thickness, FE simulations of SS venous sound generation and propagation procedure were performed, involving SS venous flow field, vibration response of tissue overlying dehiscence area (including SS vessel wall and CP) and sound propagation in temporal bone air cells. It was shown in results that SS venous sound at tympanic membrane was 56.9dB in SSCPD case and -45.2dB in intact CP case, and was inaudible in all thin CP cases. It was concluded that SSCPD would directly induce PT through significantly amplifying SS venous sound, and thin CP would not be the only pathophysiology of PT. This conclusion would provide a theoretical basis for the design of SSCPD resurfacing surgery for PT patients with SSCPD or thin CP.
乙状窦皮质板裂开（SSCPD）在搏动性耳鸣（PT）患者中很常见，临床上通过乙状窦皮质板裂开修复手术进行治疗，但迄今为止其生物机制尚不清楚。本研究旨在阐明SSCPD诱发PT感觉的生物机制，并量化皮质板（CP）厚度与PT感觉强度之间的关系。本研究假设SSCPD会通过显著放大乙状窦（SS）静脉声音来诱发PT。基于典型患者的放射学数据进行有限元（FE）分析以验证该假设，并通过临床报告进行验证。在具有不同CP厚度的病例中，对SS静脉声音产生和传播过程进行了有限元模拟，包括SS静脉流场、裂开区域上方组织（包括SS血管壁和CP）的振动响应以及颞骨气室中的声音传播。结果显示，在SSCPD病例中，鼓膜处的SS静脉声音为56.9dB，在完整CP病例中为-45.2dB，在所有薄CP病例中均听不到。得出的结论是，SSCPD会通过显著放大SS静脉声音直接诱发PT，薄CP不是PT的唯一病理生理学因素。这一结论将为患有SSCPD或薄CP的PT患者的SSCPD修复手术设计提供理论依据。
