Cerebral Venous Sinus Occlusion Research Articles

Optic nerve sheath fenestration for visual impairment in cerebral venous diseases.

Visual impairment is the most common clinical feature of cerebral venous sinus occlusion or cerebral venous thrombosis-induced intracranial hypertension, which can result in optic atrophy, leading to irreversible vision loss, visual field defections, and finally, permanent blindness. Papilledema is a typical early pathophysiological alteration in visual impairment. Optic nerve sheath fenestration (ONSF) has become increasingly accepted as an option to prevent or halt progressive visual loss owing to its low risk and complications. The objective of this study is to review the latest research progress on ONSF for the treatment of visual impairment related to cerebral venous diseases. Study were searched following PRISMA guidelines based on three electronic databases (Pubmed, Embase and Medline-Ovid). We used the following keywords and variations as keywords to identify studies: "optic nerve sheath fenestration, papilledema, cerebral venous diseases, cerebral venous stenosis, cerebral venous thrombosis, idiopathic intracranial hypertension". The publication date of studies was restricted between 1,872.1.1 and 2,021.12.31. The application of ONSF in papilledema due to cerebral venous diseases is reviewed. Additionally, the common surgical approaches as well as advantages and disadvantages are also described graphically. With the improvement of specific details of the ONSF procedure and surgical instruments, complications of ONSF have reduced and its safety has been significantly improved, although the number of clinically investigated cases in the literature remains low. We recommend that ONSF should be considered as an imperative alternative to reduce or delay the visual morbidity of cerebral venous diseases, although there is yet no consensus on the optimal surgical timing.

Otogenic Cerebral Venous Sinus Thrombosis: A Case Report and Literature Review

Cerebral venous sinus occlusion is an exceptional presentation in the emergency department. Otitis and mastoiditis are rarely associated with cerebral venous sinus occlusion. It is considered as a redoubtable complication with potentially severe outcomes. Symptoms that may indicate this thrombosis are variable and include progressive headache, intracranial hypertension, seizures, focal neurological deficits, and ophthalmologic symptoms. In this article, we report a case of a young female patient presenting with otitis and mastoiditis complicated with intracranial thrombosis. She was successfully treated with antibiotics, anticoagulants, and analgesics. Furthermore, we provide a brief review on cerebral venous sinus thrombosis with a focus on its risk factors and its management. Finally, we emphasize the need for better awareness about this potential intracranial complication.

Effect of HMGB1 and RAGE on brain injury and the protective mechanism of glycyrrhizin in intracranial‑sinus occlusion followed by mechanical thrombectomy recanalization

The key to successful treatment of cerebral venous-sinus occlusion (CVO) is the rapid recanalization of the sinus following venous-sinus occlusion; however, rapid recanalization of the sinus may also cause secondary cerebral injury. The present study examined mechanical thrombectomy-related brain injury and the possible molecular mechanisms following CVO recanalization, and investigated the protective effect of glycyrrhizin (GL) in CVO recanalization. The cerebral venous sinus thrombosis (CVST) model was induced in rats using 40% FeCl3. Mechanical thrombectomy was performed at 6 h post-thrombosis. GL was administered to rats following thromboembolism. Neurological function and brain water content were measured prior to sacrifice of the rats. Serum malondialdehyde, superoxide dismutase and nitric-oxide synthase concentrations were measured. The expression levels of high-mobility group box 1 (HMGB1) and receptor of advanced glycation end products (RAGE) and its downstream inflammatory mediators were measured in serum and brain tissues. Rapid CVO recanalization caused brain injury, and the brain parenchymal damage and neurological deficits caused by CVO were not completely restored following recanalization. Similarly, following rapid recanalization in the venous sinus, the expression levels of HMGB1 and RAGE were lower than those in the CVST group, but remained significantly higher than those of the sham group. The combination of mechanical thrombectomy and GL improved cerebral infarction and cerebral edema in rats, and inhibited the extracellular transport of HMGB1, and the expression of downstream inflammatory factors and oxidative-stress products. The administration of exogenous recombinant HMGB1 reversed the neural protective effects of GL. In conclusion, mechanical thrombectomy subsequent to CVO in rats can cause brain injury following recanalization. HMGB1 and RAGE promote inflammation in the process of brain injury following recanalization. GL has a relatively reliable neuroprotective effect on brain injury by inhibiting HMGB1 and its downstream inflammatory factors, and decreasing oxidative stress.

Cases of visual impairment caused by cerebral venous sinus occlusion-induced intracranial hypertension in the absence of headache

BackgroundCerebral venous sinus thrombosis or stenosis (here collectively referred to as cerebral venous sinus occlusion, CVSO) can cause chronically-elevated intracranial pressure (ICP). Patients may have no neurological symptoms other than visual impairment, secondary to bilateral papilledema. Correctly recognizing these conditions, through proper ophthalmological examination and brain imaging, is very important to avoid delayed diagnosis and treatment.Case presentationWe report a case series of 3 patients with chronic CVSO, who were admitted to an ophthalmological department in Chongqing, China, from 2015 March to 2017 February. All patients presented with decreased vision and bilateral papilledema, but had no headache or other neurological symptoms. The visual fields of all patients were impaired. Flash visual evoked potentials (VEPs) in two patients showed essentially normal peak time of P2 wave, and pattern VEPs in one patient displayed decreased P100 amplitude in one eye, while a normal P100 wave in the other eye. In all patients, lumbar puncture (LP) revealed significantly elevated ICP. And magnetic resonance venography (MRV) demonstrated cerebral venous sinus abnormalities in every patient: one right sigmoid sinus thrombosis, one superior sagittal sinus thrombosis, and one right transverse sinus stenosis.ConclusionsCVSO can cause chronically-elevated ICP, leading to bilateral papilledema and visual impairment. A considerable amount of patients have no apparent neurological symptoms other than visual loss. Unlike other optic nerve lesions, such as neuritis or ischemic optic neuropathy, the optic disc edema in CVSO is usually bilateral, the flash or pattern VEP is often normal or only mildly affected, and patients are often not sensitive to steroid therapy. CVSO should be suspected in such patients when unenhanced brain imaging is normal. Further investigations, such as LP and contrast-enhanced imaging (MRV and digital subtraction angiography), should be performed to diagnose or exclude CVSO.

Update on the application of optic nerve sheath fenestration.

With the ongoing development of surgical procedures and instruments, the safety of optic nerve sheath fenestration (ONSF) has been improved. Through the past three decades, progress has been made in preventing visual loss from chronic optic nerve swelling in idiopathic intracranial hypertension (IIH), secondary intracranial hypertension and local optic nerve diseases. We now review the updated application of ONSF in those diseases. The application of ONSF in papilledema due to IIH, secondary intracranial hypertension to cerebral venous sinus occlusion, Cryptococcal meningitis, and intracranial mass or tumors is reviewed. Additionally, the potential benefits of ONSF in local optic neuropathy from optic nerve sheath meningioma, optic nerve drusen, traumatic optic neuropathy and optic nerve/sheath biopsy are also described. Although ONSF has little or no effect on intracranial pressure, it is a safe, relative easy and effective surgical procedure to prevent or reverse visual loss in IIH. When other treatment modalities fail to timely protect vision, ONSF can be useful in protecting visual function or delay visual loss in secondary intracranial hypertension. We recommend that ONSF should be considered as a meaningful alternative or an adjunct therapy to reduce or delay the visual morbidity of these diseases, although the use of ONSF for some of them remains controversial.

Risk factors and early diagnosis of cerebral venous sinus occlusion secondary to traumatic brain injury.

This study was designed to investigate the risk factors of, and the strategy for early diagnosis of cerebral venous sinus occlusion (CVSO) secondary to traumatic brain injury. The clinical data of 240 consecutive patients were analyzed retrospectively. The clinical symptoms were observed and imaging was carried out. The risk factors of CVSO were evaluated with logistic regression analysis. Early diagnosis of CVSO was established based on the clinical and imaging features. Forty patients were diagnosed to be having CVSO according to the findings of computerized tomographic venogram (CTV) and magnetic resonance venogram (MRV). They were classified into three sub-types (thrombosis occlusion type, compression type, and mixed type). A skull fracture crossing the sinus (odds ratio [OR] =8.026; 95% confidence interval [CI]: 3.107-20.734) and an epidural hematoma crossing the sinus (OR = 3.062; 95% CI: 1.355-6.921) were risk factors associated with CVSO, and the former played a more significant role. The female gender (OR = 0.306; 95% CI: 1.715-61.943) was the risk factor for the thrombosis occlusion type of CVSO. An epidural hematoma crossing the sinus (OR = 5.653; 95% CI: 1.767-18.084) was the risk factor of the compression type of CVSO. The past medical history of deep vein thrombosis (DVT) (OR = 11.276; 95% CI: 1.315-96.664) combined with a skull fracture and epidural hematoma crossing the sinus were risk factors for the mixed type of CVSO. Paying close attention to the past medical history of DVT, skull fracture, and the imaging finding of an epidural hematoma that crosses the sinus are necessary for the early diagnosis of CVSO. CTV and MRV help in making an early diagnosis of CVSO.

Iatrogenic cerebral venous sinus occlusion with flowable topical hemostatic matrix

The use of commercially available topical hemostatic adjuncts has increased the safety profile of surgery as a whole. Cranial surgery has also benefited from the development of numerous agents designed to permit more rapid achievement of hemostasis. Flowable topical hemostatic agents applied via syringe injection are now commonly employed in many neurosurgical procedures, including cranial surgery. Intravascular use of these strongly thrombogenic agents is contraindicated, but in certain settings, inadvertent intravascular administration can occur, resulting in vascular occlusion, thrombosis, and potential dissemination. To date, there have no reports detailing the presence and incidence of this complication. The authors conducted a retrospective review of all cranial surgeries performed at Presbyterian University Hospital by members of the University of Pittsburgh Medical Center's Department of Neurological Surgery between 2007 and 2009. Cases complicated by vascular occlusion due to inadvertent intravascular administration of flowable topical hemostatic matrix (FTHM) were identified and analyzed. Iatrogenic vascular occlusion induced by FTHM was identified in 5 (0.1%) of 3969 cranial surgery cases. None of these events occurred in 3318 supratentorial cases, whereas 5 cases of cerebral venous sinus occlusion occurred in 651 infratentorial cases (0.8%). The risk of accidental vessel occlusion was significantly associated with infratentorial surgery, and all events occurred in the transverse and/or sigmoid sinus. No episodes of inadvertent vascular occlusion occurred during endoscopic surgery. No cases of arterial occlusion were identified. Of the 5 patients with FTHM-related cerebral venous sinus occlusion, none developed long-term neurological sequelae referable to the event. Inadvertent intravascular administration of FTHM is a rare complication associated with cranial surgery that occurs most commonly during infratentorial procedures around the transverse and/or sigmoid sinuses. Modifications in the choice of when to use an FTHM and the method of application may help prevent accidental venous sinus administration.

Benign fibrous histiocytoma of the skull with increased intracranial pressure caused by cerebral venous sinus occlusion

The authors present a very rare case of benign fibrous histiocytoma of the skull with increased intracranial pressure caused by sinus occlusion. A 33-year-old woman was referred for investigation of a right occipital protrusion with tenderness and double vision. She had only mild divergence insufficiency and bilateral papilledema neurologically. Imaging findings showed that the skull tumor was located at the right occipital bone with bone disruption and a compressed right sigmoid sinus. When planning the resection, caution was required to spare the collateral flow so as to manage the intracranial pressure. Immunohistochemical analysis showed that the tumor was positive for CD68, alpha1-antichymotrypsin, and alpha1-antitrypsin. From these findings, the tumor was diagnosed as a primary benign fibrous histiocytoma of the skull.

Evaluation of Posttraumatic Venous Sinus Occlusion With CT Venography

Although cerebral venous sinus occlusion (CVSO) is reported to be associated with intracranial hypertension, its incidence or significance in head trauma is not clear. This study investigated with CT venography the incidence of posttraumatic CVSO, its clinical course, and relation to intracranial hypertension. This study comprised 97 consecutive patients admitted to our Trauma Center from 2002 through 2008 with skull fracture of the petrous portion of the temporal bone or that crossed the dural sinus. Patients with CVSO were examined with CT venography and followed up with CT venography or magnetic resonance imaging. The relation of CVSO to patient outcome and incidence of "talk and deteriorate" was also investigated. CVSO was observed in 22 of 97 patients (22.4%). Mortality was significantly higher in the CVSO group versus no-CVSO group (50.0% vs. 9.3%, p < 0.001). Incidence of lethal intracranial hypertension was higher in the CVSO versus no-CVSO group (40.9% vs. 5.3%, p < 0.001), although there was no difference in Glasgow Coma Scale score at admission between the two groups (CVSO group, 8 +/- 5 vs. no-CVSO group, 10 +/- 4). Recanalization without treatment for CVSO occurred by 6 months in 9 of the 11 survivors (81.8%) who could be followed up. CVSO incidence after head injury was much higher than ever thought. It was associated with mortality and lethal intracranial hypertension, indicating that CVSO may induce acute increase in intracranial pressure in some cases. Early recognition of CVSO may be important to predict deterioration after admission and for starting immediate treatment.

The preservation and reconstruction of cerebral veins and sinuses

Although cerebral veins and venous sinuses are very important to the neurosurgeon, they have received adequate attention only recently. The consequences of cerebral venous occlusion are well known. When the venous outflow is compromised due to a lack of adequate collateral circulation, venous infarction follows, with swelling, haemorrhage and neuronal death. The clinical consequences will depend upon the region of involvement of the brain and the site of the infarcted tissue. The symptoms may include seizures, hemiplegia, aphasia, coma and death. Similarly, the consequences of cerebral venous sinus occlusion depend upon the availability of collateral circulation. When such collaterals are not available, papilledema and visual loss and a pseudotumour cerebri syndrome are observed in milder cases, whereas, severe diffuse brain swelling, coma and death may be observed in severe cases.Acute venous or venous sinus occlusion is potentially very dangerous, whereas slow and chronic venous or venous sinus occlusion is better tolerated. Even in such patients, some neurological manifestations may follow, when the collaterals are poor.

Pseudotumor syndrome associated with cerebral venous sinus occlusion and antiphospholipid antibodies.

Antiphospholipid antibodies are known to be associated with increased risk of venous and arterial thrombotic events, including cerebral venous thromboses. Pseudotumor syndrome can be produced by cerebral venous thrombosis. A patient with cerebral venous thrombosis associated with antiphospholipid antibodies who exhibited pseudotumor syndrome is reported. A 49-year-old man who noted visual blurring and persistent vertical wavy lines in his fields of vision was found to have papilledema. Cerebrospinal fluid values were normal except for an opening pressure increase to 510 mm of fluid. His visual symptoms improved with lumbar puncture and the use of acetazolamide. Imaging studies showed that the transverse sinus was occluded completely on the left and partially on the right and that there was a small left cerebellar cortical venous infarction. Antiphospholipid syndrome should be considered in the differential diagnosis of pseudotumor syndrome related to cerebral venous thrombosis.