Cause Of Pulsatile Tinnitus Research Articles

Prevalence, Surgical Management, and Audiologic Impact of Sigmoid Sinus Dehiscence Causing Pulsatile Tinnitus.

To evaluate the prevalence, surgical management, and audiologic impact of pulsatile tinnitus caused by sigmoid sinus dehiscence. Retrospective chart review at a tertiary care hospital. Adults with unilateral pulsatile tinnitus attributable to sigmoid sinus dehiscence who underwent resurfacing between January 2010 and January 2020. Transmastoid sigmoid resurfacing. Resolution of pulsatile tinnitus; audiologic outcomes; complications; tinnitus etiologies. Nineteen patients (89.4% women) had surgery for suspected sigmoid sinus dehiscence. The mean dehiscence size was 6.1 mm (range, 1-10.7 mm). Eight patients had concurrent sigmoid sinus diverticulum and one patient also had jugular bulb dehiscence. Only two patients (10.5%) had the defect identified by radiology. Low-frequency pure-tone average, measured at frequencies of 250 and 500 Hz, showed a significant median improvement of 8.8 dB following resurfacing (18.8 dB versus 10.0 dB, p = 0.02). The majority of patients had complete resolution of pulsatile tinnitus (16/19, 84.2%). Of those without complete resolution, two patients had partial response and one patient had no improvement. There were no significant complications. Of 41 consecutively tracked patients with a pulsatile tinnitus chief complaint, sigmoid pathology represented 32% of cases. Sigmoid sinus dehiscence represents a common vascular cause of pulsatile tinnitus that, if properly assessed, may be amenable to surgical intervention. Sigmoid sinus resurfacing is safe, does not require decompression, and may improve low-frequency hearing. Radiographic findings of dehiscence are often overlooked without a high index of clinical suspicion. Its relationship with transverse sinus pathology and idiopathic intracranial hypertension remain unclear.

Longitudinal analysis of surgical outcome in subjects with pulsatile tinnitus originating from the sigmoid sinus

A dominant sigmoid sinus with either diverticulum or dehiscence (SS-Div/SS-Deh) is a common cause of pulsatile tinnitus (PT). For PT originating from SS-Div/SS-Deh, an etiology-specific and secure reconstruction using firm materials is vital for optimal outcomes. As a follow-up to our previous reports on transmastoid SS resurfacing or reshaping for SS-Div/SS-Deh, this study aimed to evaluate the long-term results of transmastoid resurfacing/reshaping. We retrospectively reviewed 20 PT patients who were diagnosed with SS-Div/SS-Deh, underwent transmastoid resurfacing/reshaping, and were followed up for more than 1 year postoperatively. For PT, immediate and long-term changes (> 1 year) in loudness and annoyance were analyzed using the visual analog scale (VAS). Additionally, pre and postoperative objective measurements of PT using transcanal sound recording and spectro-temporal analysis (TSR-STA), imaging results, and audiological findings were comprehensively analyzed. Significant improvements in PT were sustained or enhanced for > 1 year (median follow-up period: 37 months, range: 12–54 months). On TSR-STA, both peak and root mean square amplitudes decreased after surgery. Also, the average pure-tone threshold at 250 Hz improved after surgery. Thus, our long-term follow-up data confirmed that the surgical management of PT originating from SS-Div/SS-Deh is successful with regard to both objective and subjective measures.

Intraparotid Superficial Temporal Artery Arteriovenous Malformation Causing Persistent Pulsatile Tinnitus.

This article discusses the diagnosis, imaging workup, and management of a rare cause of pulsatile tinnitus: intraparotid arteriovenous malformation. A single patient with a superficial temporal arteriovenous malformation diagnosed by carotid duplex causing pulsatile tinnitus that failed initial surgical management. Repeat imaging failed to identify a cause for the persistent tinnitus. Reoperation with a parotid approach based on physical exam findings. Removal of a more proximal arteriovenous malformation in the parotid gland resulted in long-term resolution of the patient's pulsatile tinnitus. Physical examination is essential in the workup and management of pulsatile tinnitus. Imaging is a useful adjunct in the diagnosis of pulsatile tinnitus but should not be solely relied upon.

Hemodynamic study on the different therapeutic effects of SSWD resurfacing surgery on patients with pulsatile tinnitus

Sigmoid sinus wall anomalies (SSWA) are a common pathophysiology of pulsatile tinnitus (PT) and usually treated by sigmoid sinus wall dehiscence (SSWD) resurfacing surgery. However, symptoms of tinnitus remain unrelieved after surgery in some patients with PT, and even new tinnitus appears. The cause of the difference in therapeutic effects is unclear. In this study, eight patient-specific SSWA geometric models were reconstructed on the basis of computed tomography angiography, including four cases of postoperative rehabilitation (group 1, 1–4 cases) and four cases of non-rehabilitation (group 2, 5–8 cases). Transient-state computational fluid dynamics (CFD) was performed to clarify the SS blood flow pattern and hemodynamic states. The wall pressure distribution on SSWA area, pressure difference, and flow pattern in SS were calculated to evaluate the hemodynamic changes of rehabilitation and non-rehabilitation patients before and after surgery. The difference of hemodynamics between these patients was statistically analyzed. The accuracy of CFD simulation was evaluated by cross validating the numerical and particle image velocimetry experimental results. Results showed that the SSWA area in patients with PT was loaded with high pressure. No difference was found in the hemodynamic characteristics between the two groups pre- and postoperation. When the average pressure (Pavg) and time-average Pavg (TAPavg) on the SSWA area were studied, the TAPavg difference pre- and postoperation between the two groups was found significant (p = 0.0021). The TAPavg difference had a negative change in postoperative rehabilitation patients (case 1, -44.49 Pa vs. case 2, -15.85 Pa vs. case 3, -25.88 Pa vs. case 4, -16.58 Pa). The postoperative TAPavg of non-rehabilitation patients was higher than the preoperative one (case 5, 24.70 Pa vs. case 6, 28.56 Pa vs. case 7, 5.81 Pa vs. case 8, 13.04 Pa). The velocity streamlines in the SS with rehabilitation became smoother and more regular than that without rehabilitation. By contrast, the velocity streamlines in SS without rehabilitation showed increased twisting and curling. No difference was found in time-average volume-averaged vorticity (TAVavgV) between the two groups. Therefore, the high pressure of the vessel wall on SSWA area was one of the causes of PT. The variation of SSWA wall pressure difference before and after PT was the cause of the difference in therapeutic effects after SSWD resurfacing surgery. In patients with SSWA, disordered blood flow in SS was another cause of PT. SSWD repair may relieve tinnitus to some extent, but blood flow disorders may still arise.

The styloid process and the formation of sigmoid sinus diverticulum: is there a link?

IntroductionSigmoid sinus diverticulum has been considered the most common cause of pulsatile tinnitus; the mechanism underlying sigmoid sinus diverticulum formation is unclear. To the best of our knowledge, no previous studies have assessed whether the formation of sigmoid sinus diverticulum is related to compression of the internal jugular vein by the styloid process. ObjectiveTo discuss the relationship between the styloid process and the formation of sigmoid sinus diverticulum. MethodsThe medical records of nine patients diagnosed with venous pulsatile tinnitus caused by sigmoid sinus diverticulum were reviewed between April 2009 and May 2019. All patients underwent high-resolution computed tomography of the temporal bones, computed tomography venogram of the head and neck, magnetic resonance venography, and brain magnetic resonance imaging. The length and medial angulation of the styloid process were measured, and compression of the internal jugular vein was recorded. ResultsThe study population consisted of nine female right-sided pulsatile tinnitus patients with a mean age of 53.8±4.6 years. The mean lengths of the styloid process were 3.9±0.6cm on the right side and 4.1±0.7cm on the left side. The mean medial angulation of the styloid process was significantly smaller on the right side than the left side (65.3°±1.2° vs. 67.8°±1.7°, p<0.05). In addition, computed tomography venogram of the head and neck demonstrated the left internal jugular vein was compressed by the styloid process in eight of the nine patients. ConclusionThe formation of sigmoid sinus diverticulum with venous pulsatile tinnitus may be related to compression of the contralateral internal jugular vein by the styloid process. However, accumulation of data in additional cases is required to verify this suggestion.

A novel water occlusion test for disorders causing pulsatile tinnitus: Our experience in 32 patients.

Pulsatile tinnitus (PT) originates mainly from the vascular structures near the cochlea and the vascular sound is believed to be transmitted to the cochlea by bony or vascular structures. Digital pressure test over the internal jugular vein ipsilateral to PT side is a simple test for differentiating venous from arterial PT by lessening venous flow. Pulsation of dehiscent venous sinus wall itself can be a cause of PT and diagnosed when PT disappears during water occlusion test (WOT), filling the external auditory canal with water. Turbulence by arteriovenous fistula increased the subjective intensity of PT when the external auditory canal was filled with water. WOT results provide insights into the new pathophysiology of PT and help to optimize diagnostic and treatment options.

Extraluminal Sigmoid Sinus Angioplasty: A Pertinent Reconstructive Surgical Method Targeting Dural Sinus Hemodynamics to Resolve Pulsatile Tinnitus.

1) To provide information on the treatment of pulsatile tinnitus (PT) with transtemporal extraluminal sigmoid sinus angioplasty (ESSA); and 2) to discuss the current clinical management of PT. This was a retrospective study. Multi-institutional tertiary university medical centers. Fifty-four PT patients with transverse-sigmoid sinus enlargement and prominent transverse-sigmoid junction with or without sigmoid sinus wall anomalies or transverse sinus anomalies. All patients underwent ESSA under local anesthesia. Intraoperative discoveries and surgical resolution of PT, morphology, and computational fluid dynamics. Fifty-three of the 54 (98%) patients experienced a significant reduction in, or complete resolution of, PT after ESSA. No major surgical complications occurred, except for one case where we observed a full collapse of the sinus wall. On average, this surgery reduced the cross-sectional area at the transverse-sigmoid junction by 61.5%. Our intraoperative discoveries suggest that sigmoid sinus wall anomalies may not be a definitive cause of PT. The transverse-sigmoid sinus system was significantly larger (in term of both cross-sectional area and volume) on the ipsilesional side compared with the contralesional side. Following ESSA, the vascular wall pressure and vortex flow at the transverse-sigmoid junction decreased considerably, and the flow velocity and wall shear stress increased significantly. ESSA is a highly effective surgical technique for PT patients with transverse-sigmoid sinus enlargement and prominent transverse-sigmoid junction, regardless of whether they also have sigmoid sinus wall or transverse sinus anomalies. A large transverse-sigmoid system with prominent transverse-sigmoid junction is a predisposing factor for PT, and only by improving patients' intrasinus hemodynamics could PT be resolved efficiently. In cases without complete obstruction of venous return, ESSA is safe. No postoperative complications related to neurological disorders were observed.

Reduced Jet Velocity in Venous Flow after CSF Drainage: Assessing Hemodynamic Causes of Pulsatile Tinnitus.

Idiopathic intracranial hypertension is commonly associated with transverse sinus stenosis, a venous cause of pulsatile tinnitus. In patients with idiopathic intracranial hypertension, CSF drainage via lumbar puncture decreases intracranial pressure, which relieves the stenosis, and may provide at least temporary cessation of pulsatile tinnitus. The objective of this study was to evaluate changes in venous blood flow caused by lowered intracranial pressure in patients with pulsatile tinnitus to help identify the cause of pulsatile tinnitus. Ten patients with suspected transverse sinus stenosis as a venous etiology for pulsatile tinnitus symptoms underwent MR imaging before and after lumbar puncture in the same session. The protocol included flow assessment and rating of pulsatile tinnitus intensity before and after lumbar puncture and MR venography before lumbar puncture. Post-lumbar puncture MR venography was performed in 1 subject. There was a lumbar puncture-induced reduction in venous peak velocity that correlated with the opening pressure (r = -0.72, P = .019) without a concomitant reduction in flow rate. Patients with flow jets had their peak velocity reduced by 0.30 ± 0.18 m/s (P = .002), correlating with a reduction in CSF pressure (r = 0.82, P = .024) and the reduction in subjectively scored pulsatile tinnitus intensity (r = 0.78, P = .023). The post-lumbar puncture MR venography demonstrated alleviation of the stenosis. Our results show a lumbar puncture-induced reduction in venous peak velocity without a concomitant reduction in flow rate. We hypothesize that the reduction is caused by the expansion of the stenosis after lumbar puncture. Our results further show a correlation between the peak velocity and pulsatile tinnitus intensity, suggesting the flow jet to be instrumental in the development of sound.

Sigmoid sinus diverticulum and dehiscence: Diagnosis and management

Introduction: Sigmoid sinus diverticulum (SSD) is a relatively rare vascular disorder characterized by a dilated sac in the sinus wall protruding into the mastoid cells. It may be associated with SSDe-Sigmoid sinus plate dehiscence (SSDe); however, SSDe can occur in isolation too. SSD may be associated with prediverticular venous sinus stenosis (SS) and commonly presents as pulsatile tinnitus (PT). Aim: This study aims to present a series of patients who were diagnosed and managed for SSD and SSDe and discuss their treatment options. Methods: A retrospective chart review was carried out between January 2016 and August 2018, and all patients presenting with PT and diagnosed with SSD and or SSDe were included in this study. Results: We had six patients who were diagnosed with SSD and SSDe during this time frame. High-resolution computed tomography and magnetic resonance venogram were used for the diagnosis. In addition, cerebral angiogram was done for 2 patients who had prediverticular stenosis of the sinus. Transmastoid decompression and repair of SSD gave excellent relief from tinnitus in one patient. Conclusion: SSD and SSDe are treatable causes of PT. SSD may be associated with a prediverticular venous SS. A prediverticular high-pressure gradient stenosis should be managed before decompression and repair of SSD.

Pulsatile Tinnitus Due to a Sigmoid Sinus Diverticulum and/or Dehiscence

In 2009, a 52-year-old man presented with a two year history of intermittent right-sided pulse-synchronous tinnitus. He noted that the tinnitus worsened when his blood pressure was elevated. Otologic exam was unremarkable, with no obvious middle ear fluid or mass. There was no neck bruit, and the tinnitus diminished on manual compression of the ipsilateral internal jugular vein. In keeping with the recommendations for clinical imaging at that time, a non-contrast CT of the temporal bone was performed. This was to evaluate for conditions such as : a middle ear glomus, an aberrant internal carotid artery, a jugular bulb variant (e.g. a high-riding jugular bulb), otosclerosis, superior semicircular canal dehiscence syndrome, a persistent stapedial artery, or a hemangioma of the temporal bone.1 No evidence of these conditions was found. An MRI of the brain, with MR angiography and venography of the intracranial vasculature also performed to evaluate for conditions such as: idiopathic intracranial hypertension, a dural arteriovenous fistula, an arteriovenous malformation, vascular loop syndrome, and dural sinus stenosis or thrombosis.2 All of these conditions were excluded. As no definite pathology was identified, no firm treatment reommendations were initiallly made.&#x0D; In 2011, Eisenman reported on a series of 13 patients with pulsatile tinnitus due to a sigmoid sinus diverticulum and/or dehiscence who were successfully treated surgically via an extraluminal transmastoid approach.3 This was the first relatively large series published in the otologic literature. This publication likewise reported on the subtle radiologic signs that signify the presence of a sigmoid sinus diverticulum and/or dehiscence, such as an irregularity of the normal semicircular contour of the bony sinus wall, focal thinning of the calvarial cortex overlying the adjacent sinus wall, absence of the normal thin layer of cortical bone overlying the sinus, and the "air-on-sinus" sign, where mastoid air cells directly contact the sinus wall, without overlying bone.3&#x0D; In light of this new information, the patient's imaging studies were re-evaluated, and evidence of a right-sided sigmoid sinus diverticulum and/or dehiscence was identified. The images below show the findings on an axial slice of the patient's temporal bone CT study.&#x0D; How significant is this condition ? Sigmoid sinus diverticulum and/or dehiscence is being increasingly recognized as a common cause of pulsatile tinnitus. In fact, a recent study by Schoeff et al. found its prevalence to be 23% in patients with pulsatile tinnitus.4 As such, the identification of this condition is highly relevant, particularly because effective surgical management is available for its alleviation.

The assessment of pulsatile tinnitus—a systematic review of underlying pathologies and modern diagnostic approaches

Background: Pulsatile tinnitus (PT) is an auditory phenomenon that occurs in the absence of an external stimulus and presents as a humming or whooshing sound synchronous with the subject’s heartbeat. PT has many causes, ranging from the benign to the life threatening. In the following report, we focus on defining the most common causes of PT and explore changing approaches to diagnostic radiology used in the assessment of PT patients, with the goal of providing an updated and practical set of guidelines for the assessment of this complicated condition. Methods: A collection of case studies, retrospective reviews and technical reports were sourced from PubMed’s online database. The initial cohort was filtered by language and content, and then sorted according to patient demographics, presenting symptoms, imaging protocols and relative success of radiological investigations. Results: The most common causes of PT include vascular anomalies, benign or idiopathic intracranial hypertension (BIH/IIH), and certain middle ear masses. We recommend using magnetic resonance imaging (MRI) as the primary imaging modality for investigating most cases of PT, due to an increase in sensitivity and decrease in medical risk for the patient compared to computed tomography (CT) and traditional angiography. We detail protocols for both basic and comprehensive MRI studies to be used in the assessment of PT and provide descriptions of common radiological findings with representative images for reference. Finally, we make an argument in favour of foregoing extensive imaging studies in cases of subjective idiopathic PT, where no risk factors can be identified in the patient’s medical history or physical examination. Conclusions: The diagnosis of pulsatile tinnitus should be guided by comprehensive clinical data and dominated by the conservative use of MRI. In subjective PT where no risk factors are present, we recommend foregoing extensive imaging.

Stent Placement for Disabling Pulsatile Tinnitus Caused by a Lateral Sinus Stenosis: A Retrospective Study.

Lateral sinus stenosis is a little-known cause for pulsatile tinnitus (PT). In several small series, stenting has been described as an effective treatment for disabling PT linked with this type of stenosis. To describe the clinical, radiological, and manometric characteristics of patients treated for disabling PT by lateral sinus stenosis. Assessment of the efficacy of stenting for this indication. Retrospective study of patients treated for isolated PT by stenting of a lateral sinus stenosis in our institution, between 2009 and 2015. Fourteen patients were included in our study. All of them were women. The median age at the onset of symptoms was 39.0 (21.0) years. The median body mass index was 28.5 (7.0) kg/m 2 . Stenting of the lateral sinus led to the disappearance of PT without recurrence in 13 patients. In one patient, stenting did not modify the noise. In this case, another cause of PT was diagnosed after stent placement. Lateral sinus stenosis is a curable cause of venous PT. Other causes of PT must be ruled out before an endovascular treatment is undertaken, due to the frequent asymptomatic nature of Pacchioni granulations in the lateral sinus. Treatment by stenting is effective in all cases, provided that stenosis underlies the PT.

Research progress of vascular pulsatile tinnitus

Pulsatile tinnitus (PT) is relatively rare, which accounts for approximately 4% of patients with tinnitus. It originates from mostly vascular structures within the cranial cavity, head and neck region or thoracic cavity, and is transmitted to the cochlear by bony or vascular structures and the blood flow, stimulating patient's hearing. It can be the patient's subjective feelings, there can be objective performance.Vascular PT is more common than non-vascular PT. Vascular PT can be further classified by vessel of origin as arterial and venous ones, and the latter is more commonly seen clinically.It's rhythm is synchronous with patients' pulse, and its tinnitus frequency is less than 600 Hz. The cause of pulsatile tinnitus is complex and diverse, and 56 cases are reported in the literature. Objective tinnitus or somatosensory, associated with tympanic membrane myoclonus, ear blood flow changes adjacent to blood vessels and other in vivo factors. While subjective tinnitus lacks a clear source of the body. PT's pathogenesis has not been fully understood yet, so intensive study targeting PT is of great importance. This review focuses on the pathophysiological mechanisms,etiology,clinical manifestation, diagnosis and progress of treatment of vascular PT.

Dehiscent High Jugular Bulb

A dehiscent jugular bulb is defined as a normal venous variant with superior and lateral extension of the jugular bulb into the middle-ear cavity through a dehiscent sigmoid plate. Despite its rare frequency, dehiscent jugular bulb is one of the common cause of pulsatile tinnitus. In a study, high resolution CT scans of 700 temporal bones of 350 patients were retrospectively examined for the incidence of vascular variations showed that dehiscent jugular bulb was seen in 27 (3.9%) temporal bones. Patients with dehiscent jugular bulb can be completely asymptomatic or may suffer from dizziness, pulsatile tinnitus and hear loss.

Granulation Tissue mimicking a Glomus Tumor in a Patient with Chronic Middle Ear Infection

Objective: To present an unusual cause of pulsatile tinnitus, presenting in a young adult suffering from chronic recurrent foul-smelling discharge from the same ear.&#x0D; Methods:&#x0D; Study Design: Case report&#x0D; Setting: Tertiary National University Hospital&#x0D; Patient: One&#x0D; &#x0D; Results: A 24-year old woman presented with pulsatile tinnitus on a background of chronic recurrent foul-smelling discharge. Clinico-radiologic findings seemed consistent with a glomus tympanicum coexisting with chronic suppurative otitis media with cholesteatoma. She underwent tympanomastoidectomy with excision of the mass. Histopathologic evaluation revealed the mass to be granulation tissue.&#x0D; Conclusion: Pulsatile tinnitus is rarely associated with chronic middle ear infection. Granulation tissue arising at the promontory may mimic glomus tumors when accompanied with this symptom. Despite this revelation, it would still be prudent to prepare for a possible glomus tumor intraoperatively, so that profuse bleeding and complications may be avoided.&#x0D; Keywords: tinnitus, pulsatile; otitis media, suppurative; glomus tympanicum

Association between the extent of sigmoid sinus dehiscence and an occurrence of pulsatile tinnitus: a retrospective imaging study

To assess the extent of sigmoid sinus dehiscence (SSD) on high-resolution computed tomography venography (HRCTV) or high-resolution computed tomography (HRCT) images in pulsatile tinnitus (PT) and non-PT groups to determine whether there is an association between the extent of SSD and occurrence of PT. Twenty-eight SSD patients with ipsilateral PT and 28 age- and gender-matched SSD patients without PT who underwent HRCTV or HRCT were enrolled in this study and categorised into two groups: "PT group" and "non-PT group". The extent of SSD in each group was calculated and compared. The largest transverse diameter and largest vertical diameter of SSD in the PT group were 6.21±1.7 and 6.15±2.19mm, respectively. The largest transverse diameter and largest vertical diameter of SSD in the non-PT group were 3.06±1.38 and 2.51±1.03mm, respectively. The extent of SSD was statistically different between the two groups (p<0.001; p<0.001). As a cause of PT, SSD can also occur in individuals without PT symptoms. Preliminary findings suggest that there may be a potential correlation between the extent of SSD and an occurrence of PT.

Atypical Feeding and Drainage of Dural AV Fistula.

Dural arteriovenous fistulas (DAVF) are frequent causes of pulsatile tinnitus. Color Doppler sonography may play a useful, complementary role to CTA/MRA and digital subtraction angiography (DSA) in the assessment of these anomalies’ characteristics, such as an ipsilateral increased flow volume and a low resistive index. In this article, we report a case of DAVF first detected with Color Doppler sonography that displayed an uncharacteristic venous drainage pattern.

Arterial Abnormalities Leading to Tinnitus.

Tinnitus is a common symptom that usually originates in the middle ear. Vascular causes of pulsatile tinnitus are categorized by the location of the source of the noise within the cerebral-cervical vasculature: arterial, arteriovenous, and venous. Arterial stenosis secondary to atherosclerotic disease or dissection, arterial anatomic variants at the skull base, and vascular skull base tumors are some of the more common causes of arterial and arteriovenous pulsatile tinnitus. Noninvasive imaging is indicated to evaluate for possible causes of pulsatile tinnitus, and should be followed by catheter angiography if there is a strong clinical suspicion for a dural arteriovenous fistula.

Dural Arteriovenous Fistulae: Imaging and Management.

Intracranial dural arteriovenous fistulae (DAVF) are pathologic arteriovenous shunts between meningeal arteries and dural venous sinuses or veins. They account for approximately 10% to 15% of all intracranial vascular malformations and are most common in middle-aged patients. DAVF are the most common vascular cause of pulsatile tinnitus. Digital subtraction angiography remains the gold standard for diagnosing these lesions. The pattern of venous drainage determines the type of DAVF and their risk for hemorrhage. Endovascular treatment has become a first-line option for their management. This article describes the natural history, clinical presentation, classification, imaging features, and management options of intracranial DAVF.

Surgical treatment of pulsatile tinnitus caused by the sigmoid sinus diverticulum: a preliminary study.

The sigmoid sinus diverticulum (SSD) is an increasingly recognized cause of pulsatile tinnitus (PT). Surgical reconstruction of the sigmoid sinus wall has been found to be highly effective for SSD; however, surgical techniques still need to be refined to reduce the incidence of serious postoperative complications. Moreover, scrutinizing more cases of SSD is desirable for establishing the diagnostic criteria and standardizing the surgical technique. This study was retrospectively undertaken in 28 patients who were diagnosed with SSD upon computed tomography angiography (CTA) and digital subtraction angiography findings at Beijing Tongren Hospital in China. A majority of patients (20/28) presented with SSD and accompanying sigmoid sinus wall dehiscence (SSWD). Twenty-five patients opted to undergo sigmoid sinus wall reconstruction, and 3 patients refused surgery. Following surgery, 17 patients experienced complete resolution of PT, 3 patients experienced partial resolution, and 5 patients experienced no change in PT. No serious complications were found postoperatively. A comparative analysis of the preoperative and postoperative CTA findings suggested that completely resolving SSD and the accompanying SSWD resulted in the elimination of PT. In conclusion, SSD is generally accompanied by SSWD. Sigmoid sinus wall reconstruction is a safe and effective approach for the treatment of SSD. During surgery, completely resolving both SSD and SSWD is advisable, and maintaining the normal diameter of the sigmoid sinus is imperative.