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Hemodynamic characteristics of sigmoid sinus wall dehiscence-pulsatile tinnitus patients with normal intracranial
Lanyue Chen1, Xiaobo Ma2, Xiancong Liu3
1Department of Radiology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Background:
Sigmoid sinus wall dehiscence (SSWD) is the most common etiology of venous pulsatile tinnitus (PT). However, the exact blood flow mechanisms of SSWD-PT remain unclear, and intracranial pressure is closely associated with its development. This study aimed to assess the hemodynamic characteristics of the sigmoid sinus in SSWD-PT patients with normal intracranial pressure using four-dimensional (4D)-flow magnetic resonance imaging (MRI) and explore potential noninvasive markers for identifying SSWD as the true etiology of PT.
Methods:
This is a case-control study. We enrolled 23 SSWD-PT patients with normal intracranial pressure and 35 age-, sex-matched healthy controls. Hemodynamics of the sigmoid sinus were evaluated by 4D-flow MRI, including average velocity (Vavg), maximum velocity (Vmax), average and maximum through-plane velocity (Vtp_avg, Vtp_max), forward and backward flow volumes (FFV, BFV), average blood flow (Flowavg), regurgitant fraction (RF), and average wall shear stress (WSSavg). Blood flow patterns were visually evaluated for vortex or turbulence. Interobserver agreement was assessed using interclass correlation coefficient (ICC). Hemodynamic parameters in the bilateral sigmoid sinuses of controls were compared using paired samples t-test or Wilcoxon signed-rank test. Group differences between SSWD-PT patients and controls were assessed using independent samples t-tests or Mann-Whitney U tests for continuous variables and Chi-squared tests for categorical variables. Logistic regression analysis was performed to identify independent predictors and build a diagnostic model. Receiver operating characteristic (ROC) curves were used to assess the diagnostic efficacy of the hemodynamic parameters. Internal validation of the model was conducted using bootstrapping with 1,000 iterations to assess model stability and robustness. The P<0.05 was considered statistically significant.
Results:
Compared with the corresponding side in controls, the symptomatic side of PT patients presented significantly higher Vavg (P<0.001), Vmax (P<0.001), BFV (P<0.001), RF (P<0.001), and WSSavg (P=0.002), and significantly lower Vtp_avg (P<0.001), FFV (P=0.006), and Flowavg (P<0.001). Vortex or turbulence were observed in 78.3% of symptomatic sigmoid sinuses (P<0.001). Interobserver agreement was excellent for all hemodynamic parameters (ICC =0.88-0.94). Logistic regression identified Vavg and WSSavg as independent predictors (both P<0.001). ROC analysis showed predictive value for Vavg [area under the curve (AUC) =0.880] and WSSavg (AUC =0.740), with the combination achieving superior performance (AUC =0.934; sensitivity 82.6%, specificity 94.3%, accuracy 87.9%, P<0.001). Bootstrapping validation confirmed the combined model's stability (AUC =0.932, sensitivity 85.2%, specificity 89.8%, accuracy 88.0%).
Conclusions:
SSWD-PT patients with normal intracranial pressure demonstrated increased blood flow complexity and hemodynamic changes in the symptomatic sigmoid sinus. The combination of Vavg and WSSavg may serve as a noninvasive marker to identify SSWD as the true etiology of PT.
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