New Insights on Surgical Management of Pulsatile Tinnitus Secondary to Anomalies in the Sigmoid Sinus Wall: Location of the Sound Source and Adjustment of Extravascular Condition
- 1. Department of Otorhinolaryngology and Head and Neck Surgery, BenQ Medical Center, The affiliated BenQ Hospital of Nanjing Medical University, China
- 2. Department of Radiology, BenQ Medical Center, The affiliated BenQ Hospital of Nanjing Medical University, China
- 3. Department of Otorhinolaryngology and Head and Neck Surgery, Eye & ENT Hospital of Fudan University, China
Abstract
Objectives: To explore the principle and efficacy of surgical modification of extravascular conditions in the sigmoid sinus for the treatment of pulsatile tinnitus through the combination of physical modeling, biophysical field threshold theory acoustic analysis and Transmastoid Sigmoid Sinus Wall Reconstruction (TSSWR).
Methods: Mimics, Geomagic Studio, and Creo Parametric software was employed to simulate the modeling of sigmoid sinus and bony boundary conditions. To analyze the biophysical field associated with the sigmoid sinus by physical acoustic analysis. Search for the points responsible for the location of the sound source in the intraoperative exploration according to preoperative CT imaging, combined with postoperative effect analysis, used to make it clear.
Results: Five 3D finite element models with different bony boundary conditions of the sigmoid were established. Theoretical analysis suggests that the sound source originates from the vibration of blood vessels in the bone defect of the sigmoid sinus wall. The sound is transmitted by compressive bone conduction through a central-type bone septum in contact with the exposed vessel wall. The loudness of the sound is related to the peak pressure of the sigmoid sinus wall and the transmission efficiency of the bony septum. Nine patients underwent TSSWR treatment, including two patients with sigmoid sinus diverticulum. They were followed up in 5 to 50 months without recurrence of tinnitus. Sound sources were found at the high-risk site of tinnitus, the junction of transverse-sigmoid sinus in 8 cases, it was found at the low-risk site of the descending part of the sigmoid sinus only in 1 case.
Conclusions: The bone wall defect and the corresponding central-type bony septum may be the necessary condition for PT secondary to the SSWAs. It can be accurately positioned and dealt with safely and easily to achieve a better therapeutic effect.
Keywords
• Pulsatile Tinnitus
• Sigmoid Sinus Dehiscence
• Sigmoid Sinus Diverticulum
• Surgical Treatment
Citation
Huang J, Zhang Q, Wang Y, Wang W (2026) New Insights on Surgical Management of Pulsatile Tinnitus Secondary to Anomalies in the Sigmoid Sinus Wall: Location of the Sound Source and Adjustment of Extravascular Condition. Ann Otolaryngol Rhinol 13(2): 1387.
ABBREVIATIONS
PT: Pulsatile Tinnitus; SSWAs: Sigmoid Sinus Wall Abnormalities; SSW: Sigmoid Sinus Wall; TSSWR: Transmastoid Sigmoid Sinus Wall Reconstruction
INTRODUCTION
Tinnitus affects 10% of the population and of these, 4.4% described their tinnitus as pulse synchronous tinnitus [1]. Approximately 43% to 86% of patients with venous Pulsatile Tinnitus (PT) have abnormalities in the Sigmoid Sinus Wall (SSW), such as focal thinning of the calvarial cortex adjacent to the SSW or dehiscence of the sigmoid sinus wall dehiscence and sigmoid sinus wall diverticulum [2,3].The transverse sinus - sigmoid sinus and adjacent temporal bone are important sites for the generation and conduction of PT. Transmastoid Sigmoid Sinus Wall Reconstruction (TSSWR) has been proven to be an effective option to eliminate PT. However SSWAs were also found in some patients without tinnitus, and TSSWR treatment is not effective for all patients with PT with SSWAs, making diagnosis and treatment puzzling. This study included patients with PT secondary to SSWAs who underwent surgical treatment for TSSWR. Through the combination of biophysical field analysis and intraoperative findings, explore the location of the sound source and obtain useful details of the surgical operation to minimize the incidence of surgical failure.
PATIENTS AND METHODS
Patients
The ethics committee of our institution approved this study. Informed consent was obtained from all patients. PT patients received temporal bone CT, CT arteriography and venography, MR arteriography and venography examination. Patients undergoing TSSWR treatment were enrolled: Inclusion criteria: 1. Unilateral onset; Tinnitus can be relieved when the internal jugular vein on the same side is compressed [4]. 2. SSWAs were detected by CT. Exclusion criteria: Jugular spheroma, aneurysms, arteriovenous fistulas, otitis media, otitis externa, etc. were excluded.
Establishment of the Sigmoid Sinus Model and the Boundary of the Vessel and Physical Acoustic Analysis.
The 3D finite-element models of sigmoid-sigmoid plate and bony boundary was established using Mimics, Geomagic Studio, and Creo Parametric software. The narrowest part before the transverse sinus transitions to the sigmoid sinus is defined as point A (fluid inlet), the outermost point and anterolateral point of the expansed curved tube of the transverse sinus transitions to the sigmoid sinus is defined as points B and C. The narroattest point before the sigmoid sinus becomes the jugular bulb is defined as point D (fluid outlet). Different thicknesses of the semi-enclosed skull wall of the sigmoid sinus, the area of defect, and conditions of the bony septum were designed at points A, B, C, and D, which helped to analyze the generation, propagation of sound, and the formation of tinnitus from the perspective of biophysical fields and physical acoustics.
Temporal Bone Ct Analysis of the Sound Source Site
CT images should be reconstructed for a high-resolution algorithm with a section thickness of 0.67 mm, a small field of view, and axial and coronal reformats provided for analysis. Bone windows must be carefully examined to evaluate the integrity of the sigmoid sinus plate. Two experienced radiologists observed the number, location and extent of SSWAs of the sigmoid sinus plate, including sigmoid sinus diverticulum on the symptomatic side. The central-type bony septum was defined as the one located on the central-part of the exposed SSW, and rank it the Roman number according to the order of the occurrence from top to bottom. The marginal-type bony septum was defined as the one located in the margin of the bony defect. The bone septum located at the largest vibration displacement of the vessel wall was defined as the main responsible bone septum, and the smaller bone septum was defined as the secondary responsible bone septum. The maximum diameter of defective bone wall on axial CT images was a diameter, the slice thickness was the other diameter, to calculate the area of the bone defect as a plane ellipse. The thickness of the central-type bone septum facing the surface of the sigmoid sinus is measured as the responsible bony septum, and we measure the angle of the septum from the curved tube section.
Transmastoid Sinus Wall Reconstruction
Based on the results of the physical acoustic analysis of the localization of the sound source, locate the bone defect of the sigmoid plate or diverticulum and the corresponding bony septum on the CT image. Give priority to searching the high-risk point at point B and point C, and check the other site if necessary. Through the retroauricular approach, the mastoid cortex was opened with a 5mm otological drill under the microscope and the bone powder was left for reconstruction. The bony septum was removed at the defect facing the exposed walls of the blood vessels, and the fascia pocket filled with bone powder was added back to reinforce the bone wall.
Statistical Analysis
Statistical analyzes were performed using SPSS for Windows. Descriptive statistical data are expressed in terms of mean, standard deviation, and median.
RESULTS
Five 3D finite element models of the sigmoid sinus with different boundary conditions
Five models of sigmoid sinus with different boundary conditions were prepared, among them 2 models have 0.2mm or 0.5mm thick bony semi-enclosed structures with no bone defect, respectively (Figure 1, 1-2). Points A, B, C, and D were selected to establish circular bone defects in the three models with small defects (d = 1mm Figure 1, 3), and large defects (d = 3.4mm Figure 1, 2 & 3). The bone cylinders were placed on the surface of the sigmoid sinus vascular wall at angles of 90 °, 60 ° and 30 ° respectively in the tangent plane to form the bony boundary conditions.
Figure 1 Models of the sigmoid sinus and bone wall boundary. Point A: The narrowest point before the transverse sinus turning into the sigmoid sinus. Point B: The outermost point of the curved tube (transverse sinus turning into the sigmoid sinus), Point C: The most anterior lateral point of the curved tube (transverse sinus turning into the sigmoid sinus), Point D: The most narrow point before the sigmoid sinus turning into the the jugular bulb Small red cylinder: vertical pipe wall tangent line; Small green column: at an Angle of 30° from the red column; Small yellow column: an Angle of 60° from the red column; The thickness of the gray bone shell was 0.2mm and the green bone shell was 0.5mm; a-b: No bone wall defect; c: Bone wall defect diameter 1mm; d,e: Bone wall defect diameter 3.4mm; a-d: Small cylinder diameter 0.1mm; e: Small cylinder diameter 1mm.
Figure 2 CT images show the sigmoid sinus plate and bony border conditions. a,b: Axial CT showing two small central type bony septums in PT side and the marginal type bony septum in healthy side of one patient. c,d: CT showing severalcentral type bony septum in one patient with sigmoid sinus diverticulum. Note the inferior medial side of the root of finger-like process diverticulum. e-h: Two consecutive CT axial slices showing preoperative and postoperative sigmoid sinus bone wall of one patient. White arrow: Bony defect in the anterolateral wall of the sigmoid sinus; Blue arrow: Responsible bony septum; Red arrow: The reconstructed sigmoid sinus plate.
Figure 3 The exposed sigmoid sinus wall and the bony septum were found under CT guidance.
These models represent the extravascular variables of the sigroid sinus that may cause vascular PT in a concise manner.
The Results of the Theoretical Analysis of the Physical Acoustic in the Sigmoid Sinus Field
The Frequency of Pt: The vibration frequency of an object is determined mainly by its own structure and material. The texture, elasticity, size, shape, and size of the rating object are different, and its vibration will produce different tones. We first excluded the possibility of turbulent in the sigmoid sinusis by characteristics analysis. The basic characteristics of turbulence include: vortical motion, irregularity, randomness, the dissipability of energy, coherent structures.There is a difference between irregularity, randomness sound, and rhythmic PT. Rhythmic blood flows pulse at a frequency of 1 to 1.67 Hz (60-100 beats/min), the vibration frequency is less than 20Hz, which is an infrasonic wave and cannot be sensed by the inner ear. Other alterations that affect hemodynamics, such as the formation of a jet stream through the transverse sinus stenotic and the increase in intracranial pressure, remain at the same frequency as the pulse. It can change the amplitude rather than the frequency of the wall by changing the wall pressure. The sinus wall at the site of sigmoid plate rupture has room for inward displacement under the impact of blood flow. The frequency of vibration is related to the mass, elasticity, density and stiffness, the length, size, and the external influence of the vessel wall below the SSW defect.
Transmission of Sound: When sound waves propagate in a gas, the gas molecules vibrate back and forth near their original position and transmit the vibrations to neighboring gas molecules in turn. In a mastoid air cell, the gas is in a relatively independent space, and it is difficult to transmit sound to another cell. The flow pipe often has vibration displacement in the curved part, but the sigmoid sinus plate is in a relatively fixed state in the skull, and it needs higher frequency to cause the displacement of the skull. In the high-frequency sound conduction process, it is also more prone to energy scattering and absorption loss, so the penetration depth is small. Even if a high-frequency sound is formed, it is difficult to transmit through the mobile bone-conduction method. In terms of physical acoustics, the sound below 800 Hz is mainly transmitted by compressive bone conduction, such as water pumps and transformers, which are often transmitted by structural sound transmission through the girders of the basic structure of the residential building.
The Loudness of the Sound: In physics, the pressure of the sound wave refers to the physical intensity of sound and is related to the amplitude. Sound intensity is the sound energy passed per unit area. The loudness of sound is the subjective perception of the intensity of sound by the ear. The sound amplitude is associated with the peak pressure of the bared SSW, and the more perpendicular the angle between the bone septum and the canal wall, the greater the pressure distributed to the bone septum and the sound pressure. The intensity of the sound is associated with the cross section of the bony septum and the sound pressure. The finer the bony septum, the greater the intensity of the sound.
Clinical Characteristics
A total of nine patients underwent TSSWR surgery. Among them, 4 patients were men and 5 patients were women at the age of 33.22±7.83 years. Five left ears and four right ears were affected. Only 4 patients had no emotional disorders and 3 patients had no sleep disorders. The frequency of tinnitus was in the low-frequency range, ranging from 125 to 630 Hz, and the loudness was 49.7±7.49 dBHL. The Specific PT disappeared immediately after the operation in 6 patients without dizziness and hearing loss. Three patients immediately felt a reduction in tinnitus and intermittent dizziness after the operation, and the tinnitus completely disappeared three days later. There was no recurrence of tinnitus in the follow-up time from 5 to 50 months (Table 1). One month after surgery, the hearing thresholds at 250 Hz and 500 Hz increased from 35.00±12.02 dBHL and 25.56±14.99 dBHL to 23.89±6.98 dBHL and 15.18±8.75 dBHL respectively.
Table 1: Clinical characteristics of patients with pulsatile tinnitus and surgical outcomes
|
Patient |
Gender (M/F) |
Age (Y) |
Affected Side (L/R) |
Preoperative |
Postoperative |
|||||||||
|
Emotional Disorder |
Sleep Disorder |
PTA |
PTA (1month) |
PT Disappeared |
Follow-up Time (Months) |
Tinnitus Recurs |
||||||||
|
PT Frequency (Hz) |
PT Loudness (dBHL) |
Affected Side (250HZ) |
Affected Side (500HZ) |
Affected Side (250HZ) |
Affected Side (500HZ) |
|||||||||
|
No.1 |
M |
24 |
L |
Severe |
Severe |
250 |
50 |
20 |
5 |
15 |
5 |
D1 |
22 |
No |
|
No.2 |
F |
29 |
L |
Mild |
Mild |
315 |
45 |
40 |
20 |
25 |
20 |
D1 |
19 |
No |
|
No.3 |
F |
26 |
R |
Mild |
Without |
125 |
41 |
35 |
20 |
15 |
15 |
D1 |
50 |
No |
|
No.4 |
M |
33 |
R |
Without |
Without |
320 |
60 |
55 |
45 |
30 |
20 |
D3 |
14 |
No |
|
No.5 |
M |
32 |
L |
Moderate |
Mild |
250 |
59 |
40 |
20 |
25 |
20 |
D1 |
29 |
No |
|
No.6 |
F |
50 |
R |
Without |
Mild |
300 |
45 |
40 |
30 |
30 |
30 |
D1 |
30 |
No |
|
No.7 |
M |
27 |
R |
Without |
Without |
180 |
55 |
45 |
55 |
35 |
35 |
D1 |
29 |
No |
|
No.8 |
F |
41 |
L |
Without |
Mild |
275 |
55 |
15 |
10 |
15 |
10 |
D3 |
5 |
No |
|
No.9 |
F |
37 |
L |
Mild |
Mild |
630 |
38 |
25 |
25 |
25 |
15 |
D3 |
10 |
No |
|
x±s |
M/F (4/5) |
33.22± 7.83 |
L/R (5/4) |
W/Mo/ Mi/S 4/1/3/1 |
W/Mi/S 3/5/1 |
293.8± 133.27 |
49.78± 7.49 |
35.00± 12.02 |
25.56± 14.99 |
23.89± 6.98 (t 3.885 p0.005**) |
18.89± 8.75 (t 2.066 p0.073) |
|
23.11± 12.65 |
|
Note: **denotes P<0.01.
Location of the sound source (CT combined with intraoperative and postoperative findings) Among the 9 patients who underwent TSSWR, bone defects were found in the curved part of the transverse sigmoid sinus in 8 cases in the anterior lateral wall or lateral wall, including 2 cases of diverticulum. Only one case has poor mastoid pneumatization (Figure 3 e1), the bone wall defect was located in the anterior wall of the sigmoid sinus. Under the guidance of CT images, the exposed SSW and the corresponding central-type bony septum can be found in all 9 patients (Figure 3). The area of bone defect ranged from 5.50 to 63.78 mm2, with a median of 30.62 mm2, and might contain 1or 2 central bony bony septums. The angle between the bony septum and the surface of the vascular defect was 71.67±14.7° (Table 2). Patients with sigmoid sinus diverticulum have secondary bone defects and corresponding bony septums (Figure 2cd). One patient has bone defects in both ears, central-type bony septums were found on the affected side (Figure 2 a) and a marginal-type bony septum was found on the healthy side (Figure 2b). The central-type bony septum may be one or more in number; all of them may be the responsible skeletal septum. Postoperative imaging showed a good reconstruction of the shape of the contour of the bone wall (Figure 2 f, h).
Table 2: Bone defects and status of the bony septum of the sigmoid sinus wall in patients undergoing surgery
|
Patient |
Combined with diverticulum |
Bone defects in Intraoperative found |
Bony defects and bony septums on CT image |
|||||||||||||
|
Point B |
Point C |
Point between C and D |
Area (mm2) |
Angle ( °) |
||||||||||||
|
Area (mm2) |
Bone septum |
Area (mm2) |
Bone septum |
Area (mm2) |
Bone septum |
|||||||||||
|
Type |
Thickness (mm) |
Angle ( °) |
Type |
thickness (mm) |
Angle ( °) |
Type |
thickness(mm) |
Angle ( °) |
||||||||
|
No.1 |
No |
Yes |
63.78 |
central |
0.2 |
86 |
|
|
|
|
|
|
|
|
28.61± 19.53 |
71.67± 14.78 |
|
No.2 |
No |
Yes |
13.54 |
central |
0.2 |
45 |
|
|
|
|
|
|
|
|
||
|
No.3 |
No |
Yes |
12.56 |
central |
<0.1 |
|
|
|
|
|
|
|
|
|||
|
No.4 |
No |
Yes |
|
|
|
|
30.62 |
central |
0.1 |
78 |
|
|
|
|
||
|
No.5 |
No |
Yes |
54.95 |
central |
0.2 |
60 |
|
|
|
|
|
|
|
|
||
|
No.6 |
No |
Yes |
|
|
|
|
|
|
|
|
5.50 |
central |
<0.1 |
|||
|
No.7 |
No |
Yes |
8.25 |
central |
0.2 |
57 |
|
|
|
|
|
|
|
|
||
|
No.8 |
Yes |
Yes |
32.97 |
central |
0.5 |
63 |
|
|
|
|
|
|
|
|
||
|
central |
0.7 |
89 |
|
|
|
|
|
|
|
|
||||||
|
No.9 |
Yes |
Yes |
35.33 |
central |
0.4 |
83 |
|
|
|
|
|
|
|
|
||
|
central |
0.3 |
84 |
|
|
|
|
|
|
|
|
||||||
DISCUSSION
Aberrant perception of rhythmic endogenous sound, a pulse-like sound that is synchronized with cardiac rhythm, is known as PT or pulse synchronous tinnitus. Studies have shown that cerebrovascular thrombosis is associated with PT [5], and thrombolytic therapy can eliminate the symptoms of tinnitus [6]. The giant arachnoid particles in the transverse sinus can narrow the sinus cavity, and high-speed blood flow forms a jet that impinges on the transverse-sigmoid sinus junction. The closer the stenosis is to the sigmoid sinus, the faster the blood flow velocity, the greater the impact on the SSW, and the more likely it is to cause vascular tinnitus [7]. Placing a transverse sinus stent to and slowing the blood flow rate, or using coils to fill the sigmoid sinus diverticulum [8], can all effectively relieve vascular tinnitus by improving the hemodynamic state in the sigmoid sinus .However, Doppler ultrasound examination revealed that the eddy currents in the sigmoid sinus diverticula had extremely low pulse synchronization with tinnitus, and when the ipsilateral internal jugular vein was compressed to make the tinnitus disappeared, the eddy currents in the sigmoid sinus still existed [4]. The transtenotic pressure gradient of the transverse sinus has been reported as a key factor in PT, which plays a role in generating jet-like flow and a strong impact force toward the SSW [9].
From the perspective of etiology, PT is related to SSWAs and hyperdynamic changes in blood, which can be triggered by changes in blood components, transverse sinus stenosis, blood pressure, intracranial pressure and heart rhythm. In 2000, Emmanuel Houdart first reported the treatment of vascular tinnitus by coil occlusion of the sinus diverticulum [10]. In 2006, Kristen J Otto treated PT caused by sigmoid sinus diverticulum through TSSWR, and later confirmed that TSSWR is also effective in sigmoid plate dehiscence [11]. Some otologists discussed whether surgical efficacy was related to reduced gas volume in gas mastoid air cells or the repair materials [12]. The others hold that PT can be eradicated only by addressing hemodynamic abnormalities [13]. In fact, all vascular factors, intravascular factors, and extravascular factors can affect surgical outcomes. It is possible to eliminate PT by eliminating only one of three causes of the sound source, transmission and perception.
The sigmoid sinus is a paired S-shaped dural venous sinus located at the base of the skull. It is an extension of the transverse sinus and drains venous blood from the brain into the internal jugular vein through the jugular foramen. There is a possible physiological stenosis before the conversion of the transverse sinus to the sigmoid sinus. Blood flow needs a higher flow rate at the narrow point to pass through the curved tube smoothly. The velocity of blood flow in the curved tube decreases (Fourier formula, ratio of flow rate to diameter), but the pressure on the wall facing the impact in the direction of blood flow increases. Outward, forward, and downward flow of blood in the sigmoid sinus causes maximum wall pressure in the lateral and anterolateral wall around the superior curvature of sigmoid sinus [14].
Vascular tinnitus is often low-frequency, with site matching ranging from 125 to 700HZ, and the loudness is usually greater than 40dBHL. When venous blood flows at a rate of 60 to 100 beats per minute (1 to 1.67 Hertz per second), the resulting vibration is less than 20HZ, which belongs to infrasound and cannot be perceived by the inner ear. Therefore, pulsation of blood flow is not the source of tinnitus. In industrial oil pipelines, especially curved pipes, they can generate vibration, displacement, and noise, and their intensities are related to the flow velocity. The wall of the sigmoid sinus is limited by the semi-enclosed bone structure and is difficult to shift outward [15]. However, when there are bone defects around the sigmoid sinus, changes in vascular wall pressure can cause the vascular wall to vibrate. The displacement of the vascular wall underneath the dehiscent area was 9.6 times greater than that of the outermost sigmoid plate, while it was 3,617 times smaller than that across the vascular wall away from the surfacing osseous structures [16]. After bone defect, the vibration amplitude of the vascular wall in the sigmoid sinus increases by 9.6 times [17], which can generate vibration noise ranging from 48.75 to 116.57dB [8-15]. A larger amplitude of the flow sound can be detected at the location where the blood flow velocity of the transverse sigmoate sinus is fast and the pressure gradient of the vessel wall differs greatly [8]. In all cases, we observed that all patients had bone defects in the vertical vascular wall section, which could be the sound source site of tinnitus.
After sound is produced, it still needs a conduction path to reach the inner ear. The traditional view holds that the oscillation of gas in the mastoid air cell conducts sound. In fact, the degree of impedance matching between air and soft tissue is low and the attenuation ability of sound waves is strong [18,19]. The air-containing mastoid structure can shield sound to some extent. There are mainly three ways of bone conduction of sound: mobile bone conduction, compressive bone conduction, and bone drum pathway. Sounds below 800 HZ are mainly conducted through mobile bone conduction. For example, water pumps and transformers often transmit sound through the main beams of the foundation structure of residential buildings in the form of structural sound transmission. Fluid dynamics studies show that the main frequency of the wall vibration sound caused by venous blood flow is below 400Hz [16]. The acoustic impedance of bone is relatively high and has good conductivity for low-frequency sounds. The bony septum around the curved tube shunt of the sigmoid sinus may be the main path of sound transmission.
The cross-sectional area, shape of the bony spacer, and the angle it forms with the tangent of the pipe wall may be related to the sound conduction efficiency. The existence of bone wall defects in the sigmoid sinus and the responsible bony septum may be necessary conditions for the appearance of vascular tinnitus, which can explain why there are bone wall defects in the sigmoid sinus in the population, while asymptomatic cases [20], abnormal bone walls of the sigmoid sinus in both ears, unilateral onset, etc. [21]. Vascular tinnitus is often accompanied by well-vaporized mastoids because it is easier to meet both conditions simultaneously. Patients with poor mastoid vaporization may also have vascular tinnitus (such as case e). During the operation, we found that multiple responsible bony septa might exist simultaneously. After the sound transmission septum is removed during the operation, it is often necessary to repair the exposed vascular wall to avoid the formation of diverticula in the later stage [22], because the protruding diverticula can lead to the generation of a new bony septum. According to Bernoulli’s principle, vessel wall pressure is relatively low in nonhigh-risk areas, but it may also produce tinnitus intensity perceived by the human ear. Therefore, extravascular conditions at low points need to be treated according to tinnitus frequency analysis during operation.
Bhatnagar found that patients with PT often have occult low-frequency sensorineural hearing impairment, and contralateral bone conduction is not involved [23]. Some scholars have proposed that pseudo-low-frequency hearing loss and its improvement after treatment may be objective signs of vascular lesions in patients with PT [24,25]. The present data show that PT due to SSWAs can cause an average interaural difference of 6 dBHL in low frequency hearing, up to 30 dBHL in individual patients, due to elevations of the BC threshold elevations from the masking noise [23]. In our cases, the postoperative low frequency hearing improved in 7 cases and was consistent with preoperative hearing in 2 cases, which could be a pseudo hearing loss caused by masking the frequency threshold of tinnitus.
The morphology of the sigmoid sinus and fluid movement make the transverse-sigmoid sinus junction a high-risk site for the sound source of PT. We can effectively treat vascular tinnitus by grinding out the bone wall defect and the corresponding central-type bony septum at these locations. In our study, the sigmoid sinus diverticulum was not considered separately and the surgical approach does not emphasize reducing the diverticulum and narrowing the sigmoid sinus cavity to avoid secondary cerebral edema and intracranial hypertension. During the operation, the defective bone is repaired to prevent fatigue herniation of the vascular wall, formation of diverticula, and formation of secondary sound source sites.
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