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Background: Although the imaging features of sigmoid sinus diverticulum induced pulsatile tinnitus (PT) have been presented in some extent, detailed imaging findings still have not been systematically evaluated and precise diagnostic radiographic criteria has not been established. Purpose: To examine the computed tomography (CT) characteristics of sigmoid sinus diverticulum accompanied with PT. Material and Methods: Fifteen PT patients with sigmoid sinus diverticula proven by surgery were recruited after consenting. CT images of 15 patients were obtained and analyzed, including features of diverticula, brain venous systems, integrity of the sigmoid plate, and the degree of temporal bone pneumatization. Results: Sigmoid sinus diverticulum was located on the same side of PT in 15 patients. Diverticula originated at the superior curve of the sigmoid sinus in 11 patients and the descending segment of the sigmoid sinus in four patients. Sigmoid sinus diverticula focally eroded into the adjacent mastoid air cells in 12 patients and mastoid cortex in three patients. Among eight patients with unilateral dominant brain venous systems, the diverticula were seen on the dominant side in seven patients and non-dominant side in one patient. In contrast, the other seven patients showed co-dominant brain venous systems, with three presenting diverticula on the right side and four on the left. More notably, dehiscent sigmoid plate on the PT side was demonstrated in all patients. In addition, temporal bone hyper-pneumatization was found in nine patients, good and moderate pneumatization in three patients, respectively. Conclusion: Dehiscent sigmoid plate and extensive temporal bone pneumatization are two important imaging characteristics of the PT induced by sigmoid sinus diverticulum. [ABSTRACT FROM AUTHOR]

Abstract Pulsatile tinnitus (PT), characterized as pulse-synchronous, is generally objective. Sigmoid sinus (SS) venous sound is widely suggested to be a possible sound source of PT. The dehiscence and thinness of SS cortical plate (CP) was commonly reported as PT pathology in previous studies, but lack quantitative or biomechanical analysis. In this study, it was aimed to quantify the relationship between venous sound and CP dehiscence/thinness using in vitro experiment. The in vitro models of SS and CP were established based on 3D-printing, with the developed pulsatile venous flow in the SS model. The generated sound signal and the vibration response at the dehiscent/thinned area were analyzed. The sound signal generated in the normal-sized dehiscence model was pulse-synchronous within 100-–400 Hz, which had similar acoustic characteristics as the clinical PT sounds. It was concluded that the pulsatile venous sound is produced at TS-SS junction in case of CP dehiscence. The CP, even a thinned one can effectively diminish the venous sound and sound-generating pulsatile vibration at TS-SS junction. The CP dehiscence would induce pulse-synchronous and high pressure venous sound, as well as pulse-synchronous vibration above 20 Hz, regardless of the dehiscence size. On the contrary, the CP thinness would not induce obvious venous sound or pulsatile vibration above 20 Hz. [ABSTRACT FROM AUTHOR]

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 56.9 dB in SSCPD case and −45.2 dB 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. [ABSTRACT FROM AUTHOR]