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Тромбоз мозкових вен і венозний тромбоз мозкових синусів зустрічається рідко (до 1 % від усіх випадків інфарктів мозку). За даними ISCVT (International Study on Cerebral Vein and Dural Sinus Thrombosis, 2004), захворюваність щорічно становить 3–4 випадки на 1 млн у дорослих. Летальність при даному захворюванні становить від 5 до 30 %. Міжнародне дослідження тромбозу мозкових вен та венозних синусів (ISCVT) визначало частоту оклюзій за локалізацією так: поперечний синус — 86 %, верхній сагітальний синус — 62 %, прямий синус — 18 %, кортикальні вени — 17 %, внутрішні яремні вени — 12 %, вена Галена і внутрішні мозкові вени — 11 %. Основними факторами ризику розвитку тромбозу мозкових вен і венозного тромбозу мозкових синусів у популяції є інфекційні запальні процеси (отити, мастоїдити, синусити, септичні стани) і неінфекційні причини: черепно-мозкова травма, пухлини, хірургічні втручання в ділянці голови та шиї, а також імплантація кардіостимулятора чи постановка центрального венозного катетера. Захворювання, що сприяють даній патології: порушення гемодинаміки (застійна серцева недостатність, зневоднення організму), захворювання крові (поліцитемія, серпоподібноклітинна анемія, тромбоцитопенія) і коагулопатії (синдром дисемінованого внутрішньосудинного згортання крові, дефіцит антитромбіну, протеїну С і S), а також тромбофілітичні стани, пов’язані з вагітністю, родами та прийомом пероральних контрацептивів, антифосфоліпідний синдром, системні васкуліти. При цьому в 15 % випадків причина розвитку синус-тромбозу залишається невстановленою. Венозний тромбоз мозкових синусів характеризується дуже різноманітним клінічним перебігом, складною діагностикою, різноманітною етіологією і прогнозом. Одним з ускладнень тромбозу синусів є інсульт, що спостерігається приблизно в 30 % хворих та часто призводить до смерті хворого. У статті подано опис клінічного випадку церебрального венозного тромбозу, що ускладнився несумісним із життям двопівкульним субарахноїдально-паренхіматозним крововиливом.

BACKGROUND Studies on the acute management of extremely low birthweight (ELBW) infants reveal a high incidence of intraventricular hemorrhage (IVH) in infants with high-grade internal cerebral vein perfusion waveform fluctuations. In this prospective observational study we investigated the Doppler perfusion waveform fluctuations in the great cerebral vein, straight sinus, and internal cerebral veins of ELBW infants. METHODS We evaluated perfusion waveforms after birth every 12 h until 120 h in 73 ELBW infants (

There are many causes of bilateral thalamic lesions, but few cases of dural arteriovenous fistula (DAVF) associated with such lesions have been reported previously. Here, we describe an adult man with reversible rapid progressive dementia (RPD) in whom bilateral thalamic lesions were caused by a DAVF that had six supply arteries and drained into both the venous sinus and cortical veins. A 53-year-old man presented with memory decline and abnormal behavior. Head computed tomography (CT) revealed insignificant low density in the bilateral thalami and high density in the right occipital lobe. Brain magnetic resonance imaging showed hyperintensities in the thalami on T2-weighted images. Magnetic resonance venogram revealed no sign of the straight sinus, but multiple tortuous vessels in the cistern of the vein of Galen. Digital subtraction angiography revealed DAVFs near the tentorium cerebelli draining into the vein of Galen, which caused the vasogenic oedema of the thalami. The patient was then treated by transarterial embolization of the feeders. He gradually recovered after the surgery. RPD with bithalamic lesions caused by DAVF is rare but reversible. Therefore, the early recognition and intervention of DAVFs is crucial for the good prognosis of patients so that fistulas can be embolized in time.

Precipitating hydrophobic injecting liquid (PHIL) is a novel embolic agent used in the endovascular treatment of arteriovenous malformations (AVM) and arteriovenous fistulas. Complications can occur during embolization with migration of the liquid embolic material to normal vasculature. In these cases, use of a stent retriever is an option for removal of the plug. Herein, we present the case of a patient who presented with a right occipital hemorrhage due to a ruptured occipital AVM fed by the calcarine and parieto-occipital arteries with venous drainage to the straight sinus. Embolization via the anterior circulation through the right posterior communicating artery was attempted but PHIL migrated to right internal carotid artery and middle cerebral artery due to kinking and rupture of the microcatheter. The patient developed mild left hemiparesis. When this complication occurred, no stent retriever was available at our institution and 1 day later, the Solitaire AB stent was used to remove the plug of PHIL successfully, with good reperfusion of the proximal and distal vessels. The patient improved after the procedure and was discharged home without deficit. Mechanical stent retrievers can be used in cases of migration of liquid embolic agents to normal vasculature with good clinical and radiological results.

Few studies have explored arachnoid granulations (AGs) bulging into the cranial dural sinuses using contrast-enhanced magnetic resonance imaging (MRI). This study aimed to explore such AGs in the transverse (TS), sigmoid (SigS), and straight (StS) sinuses, and confluens sinuum (ConfS) using thin-sliced, contrast MRI. A total of 102 patients with intact dural sinuses underwent thin-sliced, contrast MRI in the axial, coronal, and sagittal planes. In 88.2%, more than one AG was identified in the TS and SigS, StS, and ConfS. In the TS, AGs were identified in 40.2% on the right side and 37.3% on the left and were frequently located in the middle and lateral thirds. In the SigS, AGs were identified on the right in 17.6% and on the left in 18.6% in the distal region. In the StS, AGs were identified in 35.3% of cases, most frequently located in the proximal third, followed by the distal third. In the ConfS, AGs were identified in 20.6% of cases. Furthermore, in 23.5%, a collection of multiple AGs of varying sizes was found in the TS. A statistical difference was not shown between the mean age of 90 patients with AGs and that of 12 patients without identifiable AGs. Bulging AGs may more frequently found in the TS. Thin-sliced, contrast MRI is useful for delineating AGs.

To date, no study has yet explored the bridging veins (BVs) of the cerebellum using neuroimaging modalities. Therefore, this study aimed to characterize them using magnetic resonance imaging (MRI). A total of 90 patients with intact cerebellar hemispheres and intracranial dural sinuses underwent thin-sliced, contrast-enhanced MRI. The BVs were classified into six routes based on the draining pattern into the dural sinuses. The superior vermian vein emptying into the straight sinus was delineated in 100% of the patients. The inferior vermian vein emptying into the confluence of the sinuses was identified in 66.7% of the patients. The inferior hemispheric and cerebellar cortical veins emptying into the transverse sinus were identified in 54.4% and 26.7% of the patients, respectively. The inferior vermian and cerebellar cortical veins emptying into the straight sinus were identified in 77.8% and 12.2% of the patients, respectively. The cerebellar cortical vein emptying into the tentorial sinus was identified in 83.3% of the patients; it was delineated on 54 sides with an average number per right hemisphere of 1.9 and 63 sides with an average number per left hemisphere of 2. The pontine-trigeminal and anterior hemispheric veins emptying into the superior petrosal sinus were identified in 42.2% of the patients. The BVs of the cerebellum can be classified into six distinct routes. Radiological classification may be useful for understanding the drainage pattern of the cerebellum.

Introduction: Pediatric gunshot wounds (GSWs) to the head are not well studied in the literature, especially in civilians. With a dearth of case-based and clinically relevant information, pediatric neurosurgeons may be challenged when considering the risks and benefits of removing retained bullet fragments in different intracranial locations. We explore the literature and highlight the key factors in the surgical decision-making case of a 16-year-old girl with GSW to the visual cortex. Case Report: A 16-year-old girl was shot in the head in a parieto-occipital trajectory with the bullet crossing midline, lodging in the occipital lobe into the straight sinus. Her initial Glasgow Coma Scale was 7, and she was urgently stabilized with intracranial pressure monitoring and external ventricular drainage. She underwent craniectomy, debridement, and irrigation and then a reoperation for further debridement and culture 2 weeks later for persistent fevers; cultures remained negative. The retained bullet was not removed. At 18 months post-injury, she had normal speech and motor function, moderate memory dysfunction, and 3-quadrant field loss with retained macular vision. Discussion/Conclusion: Pediatric penetrating GSWs to the head may be challenging to manage since literature is sparse. In this case, the primary focus of management was to maintain normal intracranial pressure, reduce risk of infection, and preserve potentially viable visual cortex. In the civilian context of available antibiotics and serial imaging, it may be possible to manage retained bullets conservatively without delayed complications.

Research on the anatomy of cerebral deep veins (CDVs) around the vein of Galen (VG) is very important and has fundamental clinical significance. Large-scale anatomical studies of CDVs using computed tomography angiography (CTA) are rarely reported. A retrospective study of the CDVs around the VG was conducted in Chinese patients of Han nationality. One hundred cases were included in the final analysis. The patients were aged from 17 to 78 years (mean: 42.3 years). Also, 46% of the patients were female. The diameter of the internal cerebral vein (ICV) at its beginning and termination points ranged from 0.4 to 2.8 mm (1.49 ± 0.39 mm) and 0.4 to 3.5 mm (2.05 ± 0.47 mm), respectively. There was statistical significance regarding the diameter of the ICV at its beginning and termination points (P

Traumatic brain injury frequently causes an elevation of intracranial pressure (ICP) that could lead to reduction of cerebral perfusion pressure and cause brain ischemia. Invasive ICP monitoring is recommended by international guidelines, in order to reduce the incidence of secondary brain injury; although rare, the complications related to ICP probes could be dependent on the duration of monitoring. The aim of this manuscript is to clarify the appropriate timing for removal and management of invasive ICP monitoring, in order to reduce the risk of related complications and guarantee adequate cerebral autoregulatory control. There is no universal consensus concerning the duration of invasive ICP monitoring and its related complications, although the pertinent literature seems to show that the longer is the monitoring maintenance, the higher is the risk of technical issues. Besides, upon 72 h of normal ICP values or less than 72 h if the first computed tomography scan is normal (none or minimal signs of injury) and the neurological exam is available (allowing to observe variations and possible occurrence of new-onset pathological response), the removal of invasive ICP monitoring can be justified. The availability of non-invasive monitoring systems should be considered to follow up patients’ clinical course after invasive ICP probe removal or for substituting the invasive monitoring in case of contraindication to its placement. Recently, optic nerve sheath diameter and straight sinus systolic flow velocity evaluation through ultrasound methods showed a good correlation with ICP values, demonstrating their potential role in place of invasive monitoring or in the early weaning phase from the invasive ICP monitoring.

Introduction Transcranial color-coded duplex sonography (TCCS) with and without ultrasound contrast agent has been used to diagnose cerebral venous thrombosis, however, no experience in the diagnosis of patients with cerebral venous thrombosis and with dural arteriovenous fistula (dAVF) by contrast-enhanced TCCS has been reported yet. Case report The authors reported a 49-year-old male patient with straight sinus (StS) thrombosis and dAVF. Plain TCCS and contrast-enhanced TCCS demonstrated the direct presentation of the selected feeder and drainage veins of the dAVFs, arterialized venous flow waveform, and an enlarged optic nerve sheath diameter, indicating an increased intracranial pressure, and a filling defect in the StS even after administration of an ultrasound contrast agent. After intravascular thrombolysis and blockage of 2 feeders of the dAVF, TCCS still showed retrograde flow direction in the left basal vein and significantly elevated flow velocity in the StS, reflecting a high venous pressure caused by a high volume of arteriovenous shunt and severe stenosis in the StS. The patient's clinical manifestation did not substantially improve until 3 stents were implanted in the StS, and TCCS unveiled that the stents were well filled with flow signal, and the flow velocity in the StS dramatically decreased. Conclusions TCCS could provide reliable data about the feeder and drainage veins of dAVF in our case. The extent of an increase in venous flow velocity may be closely associated with clinical manifestations, which may influence therapy. Moreover, TCCS possesses a unique advantage in terms of evaluating the patency of the stents compared with other neuroimaging techniques.

Cranial dural arteriovenous fistula (cDAVF) may rarely lead to parkinsonism and rapid cognitive decline. Dysfunction of the extrapyramidal system and the thalamus, due to venous congestion of the Galenic system with subsequent parenchymal edema, is likely to represent an important pathophysiological mechanism. Here, we report a case of a 57-year-old man with a cDAVF of the straight sinus (Borden type III; DES-Zurich bridging vein shunt [BVS] type with direct, exclusive, and strained leptomeningeal venous drainage [LVD]) and subsequent edema of both thalami, the internal capsule, the hippocampi, the pallidum, and the mesencephalon. Several attempts at venous embolization were unsuccessful, and the neurological condition of the patient further deteriorated with progressive parkinsonism and intermittent episodes of loss of consciousness (KPS 30). A suboccipital mini-craniotomy was performed and the culminal vein was disconnected from the medial tentorial sinus, achieving an immediate fistula occlusion. Three-month follow-up MRI revealed complete regression of the edema. Clinically, parkinsonism remitted completely, allowing for tapering of dopaminergic medication. His cognition markedly improved in further course. The purpose of this report is to highlight the importance of rapid and complete cDAVF occlusion to reverse venous hypertension and prevent progressive clinical impairment. The review of the literature underlines the high morbidity and mortality of these patients. Microsurgical disconnection of the fistula plays an important role in the management of these patients and, surprisingly, has not been reported so far.

Background Dural arteriovenous fistulas (dAVFs) can often be successfully treated with endovascular embolization; however, surgery is occasionally still required. Case Description Herein, we discuss a 65-year-old male patient who presented with a Hunt-Hess IV subarachnoid hemorrhage, intraventricular hemorrhage, and cerebellar intracranial hemorrhage secondary to a ruptured Borden type III tentorial (straight sinus) dAVF. Angiography revealed supply from the left occipital and posterior meningeal arteries and direct drainage into the cerebellar cortical veins with venous aneurysms in both cerebellar hemispheres. Both transarterial and transvenous embolization were attempted, without success. Therefore, the patient was taken to the operating room for clip ligation of the dAVF. The operative video demonstrates a bilateral suboccipital craniotomy and supracerebellar infratentorial approach for surgical clipping of the dAVF. Conclusions The case and operative video provide a valuable addition to surgical literature in an era where surgical management of dAVFs has become relatively rare.

Background Children referred to a tertiary hospital for the indication, “rule out idiopathic intracranial hypertension (IIH)” may have an increased risk of raised venous sinus pressure. An increase in sinus pressure could be due to obesity, venous outflow stenosis or cerebral hyperemia. The purpose of this paper is to define the incidence of each of these variables in these children. Methods Following a data base review, 42 children between the ages of 3 and 15 years were found to have been referred over a 10 year period. The body mass index was assessed. The cross sectional areas and circumferences of the venous sinuses were measured at 4 levels to calculate the hydraulic and effective diameters. The arterial inflow, sagittal and straight sinus outflows were measured. Automatic cerebral volumetry allowed the brain volume and cerebral blood flow (CBF) to be calculated. The optic nerve sheath diameter was used as a surrogate marker of raised intracranial pressure (ICP). The sagittal sinus percentage venous return was used as a surrogate marker of elevated venous pressure. Age and sex matched control groups were used for comparison. Results Compared to controls, the obesity rates were not significantly different in this cohort. Compared to controls, those at risk for IIH had a 17% reduction in transverse sinus and 14% reduction in sigmoid sinus effective cross sectional area (p = 0.005 and 0.0009). Compared to controls, the patients at risk for IIH had an arterial inflow increased by 34% (p Conclusion In children with the chronic headache/ IIH spectrum, the highest associations were with cerebral hyperemia and mild venous sinus stenosis. Obesity was not significantly different in this cohort. There is evidence to suggest hyperemia increases the venous sinus pressure and ICP.

Background Pial arterial feeders in an intracranial dural arteriovenous fistula (dAVF) are risk factors for both ischemic and hemorrhagic complications during endovascular embolization. Microsurgery in dAVF with pial arterial feeders has rarely been reported. Objective To assess our original experience with microsurgery for dAVF with pial arterial feeders by investigating surgical findings and outcomes. Methods In 40 patients with intracranial dAVF who underwent microsurgery, we found 8 patients who had pial arterial feeders. A retrospective review was conducted. Results The locations of the dAVFs were as follows: tentorium, 2 patients; Galenic system, 1; straight sinus, 1; torcula, 1; transverse sinus, 1; ethmoid, 1; and convexity, 1. Preoperative angiography revealed that the pial arterial feeders originated from the middle cerebral artery in 2 patients, the anterior cerebral artery in 1, the posterior cerebral artery in 2, and the posterior medial choroidal artery in 1. Of note, in 2 patients (6.7%), feeders from the superior cerebellar artery were determined to be angiographically occult during preoperative examination and were detected through careful intraoperative observation and arachnoid dissection. In 5 cases, the additional obliteration of the pial arterial feeders and/or more distal cortical venous drainers after the simple disconnection of proximal cortical drainers was necessary to cure the dAVF. Finally, all shunts were cured with only 1 minor complication. Conclusion Although microsurgical results were acceptable, the surgeon should be aware of the presence of pial arterial feeders even after the simple disconnection of cortical venous drainage. Angiographically occult feeders may also exist.

Rarely is hypoplasia of the tentorium seen without serious clinical impact. Usually, these developmental defects are associated with serious central nervous system (CNS) malformations such as Chiari and Dandy-Walker malformations. Only six prior cases of tentorium hypoplasia including one pediatric case are published. Herein, we discuss the first reported case showing bilateral occipital hemispheric involvement with central precocious puberty. This report illustrates more benign clinical outcomes may be expected as well.

Background Foetal vein of Galen aneurysmal malformation (VGAM) is a very rare congenital malformation of the cerebral blood vessels. We sought to evaluate the diagnostic value of ultrasound in combination with magnetic resonance imaging (MRI) in foetal VGAM. Case presentation Prenatal ultrasound combined with MRI diagnosed five cases of VGAM. Two dimensional ultrasound images were used to find the echo-free cystic structure below the thalamus and above the cerebellum with five cases. Colour blood flow showed dilated VGAM in five cases, while the arteriovenous spectrum was explored in two cases and foetal heart failure was found in other three cases. MRI was manifested as a dilated VGAM found at the midline of the brain, demonstrating widening or dilation of the straight sinus in four cases, ventricular dilatation in one case, brain parenchyma bleeding in two cases, and grey matter softening in one case. One infant died on the day of its birth, while the other four infants died within one month to six months after birth. Conclusions Ultrasound combined with MRI can more accurately and comprehensively observe the pathological characteristics of VGAM, diagnose related complications early and determine its prognosis.

BACKGROUND: Cerebral venous sinus thrombosis (CVST) is a scarce disease with poor prognosis and its diagnosis often challenges physicians due to nonspecific symptoms and widespread clinical manifestations. AIM: To investigate the findings of magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) of patients with CVST diagnosis in Ali Ebne Abitaleb Hospital in Zahedan during 2013–2016 and to evaluate imaging pitfalls involving in late diagnosis, complications, and even death. METHODS: This retrospective descriptive study was done on 57 patients with confirmed CVST during 2013–2016 in Ali Ebne Abitaleb Hospital in Southeast of Iran (Zahedan). The MRI and MRV findings and related diagnostic pitfalls were evaluated. Twenty-one patients are pediatrics and 33 patients are adults. RESULTS: Of 57 patients, evidences of cerebral edema were found in 33 patients, among whom 2 patients showed parenchymal edema (cerebral edema) without infarction, and 31 patients exhibited parenchymal edema with infarction. The frequency of involvement in descending order was as followed; transverse sinus (96.49%), sigmoid sinus (49.12%), superior sagittal sinus (29.82%), jugular vein (19.29%), internal cerebral veins (7.01%), straight sinus (5.2%), and cortical veins (5.2%). Diagnostic pitfalls were also found in 8 patients. Seven patients exhibited acute and subacute thrombosis mimicked normal sinus flow void in T2-weighted images. No filling defect was seen on gadolinium-enhanced T1-weighted image in the other patient due to the sub-acute phase of thrombosis. CONCLUSION: The delayed diagnosis of CVST originating from nonspecific clinical features and diagnostic imaging pitfalls can result in poor outcomes in patients. To prevent the diagnostic pitfalls, the clinician should give a brief history and clinical data and radiologist(s) should interpret the findings in addition to the use of advanced MR sequences.

We describe a patient with multiple cranial dural arteriovenous fistulas (DAVFs) presenting with thalamic dementia. A 52-year-old man experienced progressive dementia and behavioral change for 1 month. Cranial computed tomography scan and magnetic resonance imaging (MRI) showed bilateral thalamic edema with subsequent hemorrhagic transformation. Cerebral angiography demonstrated multiple cranial DAVFs at the straight sinus and posterior part of the superior sagittal sinus. The symptomatic fistula was the straight sinus DAVF, Cognard Type II a + b, supplied by meningeal branches of the left superior cerebellar artery, the left ascending pharyngeal artery originating from the left occipital artery, and multiple tiny branches of the left occipital artery with retrograde venous drainage into the straight sinus and vein of Galen. In addition, there was probable thrombosis at the middle part of the straight sinus associated with anatomical variation of the dural venous sinuses at the torcular herophili. The patient underwent successfully endovascular treatments in a two-staged embolization using liquid embolic materials. The patient has gradually recovered and could get back to the activities of daily living at home within 2 months. Follow-up MRI of the brain at 6 months revealed nearly complete resolution of the bilateral thalamic congestion. Cerebral angiography, obtained 1 year after endovascular treatment, confirmed complete obliteration of both DAVFs. We also reviewed the literature of thalamic dementia caused by intracranial DAVFs.

OBJECTIVEIntracranial hypertension is a major concern in children with syndromic craniosynostosis (sCS). Cerebral venous hypertension caused by cerebral venous outflow obstruction is believed to contribute to intracranial hypertension. The authors therefore hypothesized that cerebral venous volume would be increased in those children with sCS and intracranial hypertension.METHODSIn a case series of 105 children with sCS, of whom 32 had intracranial hypertension, cerebral MRI techniques were used to quantify the volume of the superior sagittal sinus, straight sinus (StrS), and both transverse sinuses.RESULTSLinear regression showed that total cerebral venous volume increased by 580.8 mm3 per cm increase in occipitofrontal head circumference (p < 0.001). No significant difference was found between the intracranial hypertension group and the nonintracranial hypertension group (p = 0.470). Multivariate ANOVA showed increased StrS volume (as a proportion of total volume) in the intracranial hypertension group (8.5% vs 5.1% in the nonintracranial hypertension group, p < 0.001). Multivariate logistic regression showed that a 100-mm3 increase in StrS volume is associated with increased odds of having intracranial hypertension by 60% (OR 1.60, 95% CI 1.24–2.08).CONCLUSIONSAlthough intracranial hypertension was not associated with total cerebral venous volume increase, it was associated with an isolated increase in StrS volume. Hence, it is unlikely that general cerebral venous outflow obstruction is the mechanism of intracranial hypertension in sCS. Rather, these findings indicate either a central cerebral vulnerability to intracranial hypertension or a mechanism involving venous blood redistribution.

Background Although the clinical course of spontaneous intracranial hypotension (SIH) is generally benign, in unusual cases it can result in deterioration of consciousness. The exact mechanisms involved have not always been described in previously reported cases. Case Description Herein we describe the case of a 36-year-old man who presented complaining of orthostatic headache. Brain magnetic resonance imaging depicted typical findings associated with SIH. He initially underwent conservative treatments, but he subsequently began to exhibit deterioration of consciousness. Magnetic resonance imaging revealed progressive brain sagging, swelling of the brainstem, and focal hyperintensity in the left side of the thalamus on diffusion-weighted imaging. The vein of Galen was stretched downwards, creating a narrow angle between it and the straight sinus. We concluded that deep venous hypertension had occurred due to functional venous stenosis. He underwent epidural blood patch twice and ultimately recovered without any neurologic deficits. Conclusions SIH should be recognized as a possible cause of coma as a result of deep cerebral vein stagnation due to severe brain sagging. A change in the vein of Galen/straight sinus angle may be an anatomic marker associated with functional venous stenosis.