Acute cerebral venous outflow obstruction during convexity meningioma resection.

BACKGROUND: Cerebral venous outflow obstruction involves idiopathic intracranial hypertension, and the most common related condition is dural venous sinus stenosis or, in other words, an obstruction of the dural venous sinuses. In these cases, the pathological process is often chronic, displays only mild symptoms, and rarely requires urgent surgical intervention. In this study, we present a unique case involving an acute cerebral venous outflow obstruction that occurred during meningioma resection that ultimately had catastrophic consequences. MATERIALS AND METHODS: The patient's preoperative imaging only revealed an unremarkable frontal convexity meningioma with an average diameter exceeding 8 cm. She was admitted for a scheduled right frontoparietal craniotomy for lesion resection. RESULTS: The patient's unique congenital dural venous sinus structure along with a non-surgical epidural hematoma both contributed to a catastrophic outcome, causing a progressive hemispheric encephalocele, significant blood loss, and wound closure difficulties. CONCLUSION: Neurosurgeons should place an additional focus on cerebral venous outflow patency during tumor resection, even if the tumor does not involve the transverse or sigmoid sinuses. It is well known that the tacking sutures play an essential role in preventing an epidural hematoma, but the procedure to mitigate hematomas occurring outside the surgical field of view is not fully recognized by neurosurgeons. If dural tacking sutures are placed after complete tumor resection, the prophylactic effect for preventing EDH in the non-surgical areas may not be guaranteed. Therefore, we strongly advocate for the tacking sutures to be accurately placed before dural incisions are made.

Trombose de seio sigmoide secundária a fístula liquórica espontânea para osso temporal: um relato de caso / Sigmoid sinus thrombosis secondary to spontaneous temporal bone cerebrospinal fluid fistula: a case report

A fístula liquórica para o osso temporal constitui um evento raro que decorre da comunicação anormal entre o espaço subaracnóideo e as células da mastoide, permitindo que o líquido cefalorraquidiano flua para as porções pneumatizadas do osso temporal. Tem como consequência a hipotensão intracraniana espontânea, caracterizada por perda de líquor e pela manifestação clínica de cefaleia ortostática. Acredita-se que a hipotensão intracraniana espontânea crie condições hemodinâmicas favoráveis à ocorrência de trombose venosa cerebral, uma desordem potencialmente fatal e de difícil diagnóstico, visto a inespecificidade de sinais clínicos e sintomas. Dessa forma, é pertinente atentar para a possibilidade de trombose venosa cerebral em pacientes com fístulas liquóricas, especialmente quando houver mudança do padrão da cefaleia, que passa de ortostática a intensa e contínua.

Temporal bone cerebrospinal fluid fistula is a rare event that results from abnormal communication between the subarachnoid space and the mastoid cells, allowing the cerebrospinal fluid to flow into the pneumatized portions of the temporal bone. It leads to spontaneous intracranial hypotension, characterized by loss of cerebrospinal fluid and orthostatic headache as a clinical manifestation. Spontaneous intracranial hypotension is believed to create favorable hemodynamic conditions to the occurrence of cerebral venous thrombosis, a potentially fatal disorder of difficult diagnosis given the nonspecific clinical signs and symptoms. Therefore, it is pertinent to consider the possibility of cerebral venous thrombosis in patients with cerebrospinal fluid fistulas, especially when there is a modification in the headache pattern from orthostatic to intense and continuous pain.

Dynamic Changes of Asymmetric Cortical Veins Relate to Neurologic Prognosis in Acute Ischemic Stroke.

Background Cerebral oxygenation is closely related to neural function in acute ischemic stroke (AIS) and can be measured noninvasively from asymmetrically prominent cortical veins (APCVs) using quantitative susceptibility mapping (QSM). Purpose To quantify venous oxygen saturation (SvO2) using brain MRI with QSM in patients with AIS, to analyze its change at 2-week follow-up, and to assess the influence of SvO2 in clinical prognosis. Materials and Methods Between 2016 and 2020, consecutive patients with AIS who underwent brain MRI within 24 hours from symptom onset and 2 weeks after treatment were retrospectively enrolled. The SvO2 of APCVs was quantified using QSM. The independent sample t test was used to compare the SvO2 between patients with and patients without APCVs. The paired sample t test was used to assess the dynamic change in SvO2. Pearson and Spearman correlation analysis was used to explore the relationship among dynamic change in SvO2 and hypoperfusion, National Institutes of Health Stroke Scale (NIHSS) score change, and 90-day modified Rankin Scale (mRS) score. The independent sample t test was used to compare the dynamic change in SvO2 between different clinical prognoses and outcome subgroups. Results APCVs were detected in 39 of 73 patients (mean age, 70 years ± 10 [standard deviation]; 49 men) at admission and disappeared in 35 patients at 2-week follow-up MRI. The mean SvO2 increased from 35.0% ± 5.8 to 64.5% ± 10.0 (P < .001) in 39 patients. For the 35 patients with APCVs that disappeared, the dynamic change in SvO2 negatively correlated with change in NIHSS score (r = -0.37, R2 = 0.19, P = .03) and 90-day mRS score (r = -0.54, R2 = 0.27, P = .001), and the dynamic change in SvO2 in the subgroup with good 90-day outcomes (n = 19) was greater than that in the subgroup with poor 90-day outcomes (n = 16) (mean, 34.5% ± 5.8 vs 29.7% ± 6.3; 95% CI: 0.6, 8.9; P = .03). Conclusion Improved oxygen saturation of asymmetric cortical veins detected using brain MRI with quantitative susceptibility mapping corresponded with better acute ischemic stroke outcomes for patients with asymmetrically prominent cortical veins that disappeared at 2-week follow-up MRI. © RSNA, 2021 Online supplemental material is available for this article.

Dural Venous Sinus Variations in Idiopathic Subarachnoid Hemorrhage: A New Indicator of the Venous Origin with Diagnostic Usefulness?

OBJECTIVE: Venous hypertension associated with a primitive basal vein of Rosenthal (BVR) has been noted as the most likely cause of idiopathic subarachnoid hemorrhage (iSAH). Other types of venous drainage variations have been scarcely studied but may further explain the cases not associated with a BVR anomaly. Our aim was to investigate if dural venous sinus (DVS) anomalies are related with iSAH. METHODS: A total of 76 patients diagnosed with iSAH were identified from a prospectively maintained database and their angiographic findings compared with 76 patients diagnosed with aneurysmal subarachnoid hemorrhage. RESULTS: On top of the BVR variations, our data showed a higher prevalence of transverse sinus hypoplasia (47.4% vs. 28.9%; P = 0.019), superior petrosal sinus hypoplasia (32.9% vs. 13.2%; P = 0.003), and clival plexus hyperplasia (65.8% vs. 43.4%; P = 0.005) in patients with iSAH. Analyzing by total number of angiograms, the iSAH group showed also a higher prevalence of inferior petrosal sinus hyperplasia (36.2% vs. 25%; P = 0.003). Of the patients with iSAH without a primitive BVR, 84% harbored ≥1 perimesencephalic DVS variation and the overall number of venous drainage variations was significantly higher in patients with iSAH. CONCLUSIONS: In addition to the well-documented BVR anomalies, there seems to be a significant relationship of other DVS variations in patients with iSAH. Transverse sinus hypoplasia, superior petrosal sinus hypoplasia, inferior petrosal sinus hyperplasia, and clival plexus hyperplasia were significantly more frequent in patients with iSAH. The presence of ≥3 of those variations would increase the suspicion of a nonaneurysmatic subarachnoid hemorrhage and could help avoid a second angiogram.

De Novo Dural Arteriovenous Fistula on Draining Veins of Previously Treated Pial Arteriovenous Malformation: a Case Report.

A 71-year-old man, with a pial micro-arteriovenous malformation (pAVM) draining into the confluence of the vein of Trolard and the vein of Labbé was surgically removed, sparing these cortical veins. 4-months MR and angiographic controls showed a de novo dural arteriovenous fistula (dAVF) draining into the previously spared cortical veins. It was removed using intraoperative motor evoked potentials (MEP). This is the first case of iatrogenic dAVF developing on the same draining vein of a previously treated pAVM. De novo dAVFs are generally iatrogenic. This case suggests that the unresected venous drainage of an AVM might be the substratum for neo-angiogenetic processes; moreover inflammation related to surgery might be the trigger factor for the development of the dAVF.

Abnormal development of cerebral arteries and veins in offspring of experimentally preeclamptic rats: Potential role in perinatal stroke.

Preeclampsia, a hypertensive disorder of pregnancy, complicates up to 10 % of all pregnancies and increases the risk for perinatal stroke in offspring. The mechanism of this increase is unknown, but may involve vascular dysfunction. The goal of this study was to evaluate the effect of experimental preeclampsia (ePE) on cerebrovascular function in offspring to eludciate a possible mechanism for this association. Dams were fed a high cholesterol diet beginning on day 7 of gestation to induce experimental preeclampsia. Middle cerebral arteries (MCA) and the Vein of Galen (VoG) were isolated from pups from ePE dams and compared to pups from normal pregnant (NP) dams at postnatal days 16, 23, and 30 and studied pressurized in an arteriograph chamber. Markers of inflammation and oxidative stress were measured in serum. Our results suggest altered structure and function in both MCA and VoG of ePE pups. We also found evidence of systemic inflammation and oxidative stress in ePE pups. These findings provide a potential link between preeclampsia and the occurrence or severity of perinatal stroke.

Changes in Angioarchitecture After Stereotactic Radiosurgery for Dural Arteriovenous Fistula.

INTRODUCTION: Dural arteriovenous fistulae (DAVF) are intracranial vascular abnormalities encountered in neurosurgery practice. Treatment options are microsurgical disconnection, endovascular embolization and/or radiosurgery. Past studies have reported the efficacy, safety, and predictors of success of radiosurgery. In this study, we investigated the angioarchitecture of fistulae at the time of radiosurgery and how the anatomy changed in the time after treatment based on angiogram follow-ups. METHODS: A retrospective analysis was performed on patients with angiographic diagnosis of DAVF treated with Gamma Knife radiosurgery (GKRS) between 2013 and 2018. Data collection included demographics, symptoms, grading scores, vascular anatomy, radiation data, treatment strategy, angiographic results, and length of patient follow-up. RESULTS: Our study reports data on 10 patients with a total of 14 fistulae. On follow-up angiography, 8 (57%) had complete occlusion of the fistula with a median time to follow up of 19.5 months. The remaining 6 (43%) were deemed as near-complete occlusion of fistula with a median time to follow up of 12.0 months. Time from radiosurgery to angiogram revealing incomplete vs. angiogram revealing complete obliteration was significantly different (p=0.045). Nearly all AVFs had decreased feeders over time after treatment with only one AVF developing an additional feeder post-treatment. Arterial feeders, drainage site, sex, Borden type, lesion volume and treatment volume had no predictive value of obliteration outcome. CONCLUSIONS: This study provides data on the angioarchitecture of fistulae treated with GKRS and also serves as an extension of previous studies reporting the safety and efficacy of GKRS treatment for DAVF in a specific patient population.

Predicting the need for retreatment in venous sinus stenting for idiopathic intracranial hypertension.

BACKGROUND: Idiopathic intracranial hypertension is a disease of raised intra-cranial pressure of unknown etiology. Lateral cerebral venous sinus stenosis (VSS) has been increasingly reported in these patients, and stenting has emerged as an alternative treatment for medically refractory symptoms. Treatment efficacy on meta-analysis appears promising, but identifying which patients are likely to benefit most, and which are likely to require repeat procedures, is currently unclear. METHODS: We retrospectively reviewed a prospectively collected database of 79 patients treated with venous sinus stenting at a single academic center with minimum follow-up of 18 months. We extracted baseline clinical data, as well as manometry at lumbar puncture and during angiography, and used logistic regression to identify parameters that could predict stent failure. RESULTS: Retreatment rate after successful VSS was 13.9%. Lumbar puncture opening pressure (OP) was shown to significantly predict treatment failure (ß=0.06; OR=1.064 (1.003-1.135); P=0.039). This effect remained significant when age, sex and body mass index were added to the model (ß=0.06; OR=1.066 (1.002-1.140); P=0.043). OP was correlated with venous sinus manometry readings in the superior sagittal and transverse sinus pre-stent placement, as well trans-stenotic gradient (P<0.001). CONCLUSIONS: Higher lumbar puncture OP was associated with an increased risk of stent failure in transverse sinus stenting for idiopathic intracranial hypertension, although the performance of this model as a linear discriminator was poor. Further studies are required to better assess which patients are at greatest risk of treatment failure.

Deep cerebral venous blood flow monitoring by transcranial doppler ultrasonography in the treatment of cerebral venous sinus thrombosis: A case report.

We report the case of a patient in whom we used deep cerebral venous blood flow monitoring by transcranial Doppler ultrasonography to monitor the effect of anticoagulation therapy on cerebral venous sinus thrombosis. The blood flow velocity of deep cerebral veins increased in the early stage of cerebral venous sinus thrombosis, then gradually decreased to the normal level as the disease improved. Moreover, the recovery of the blood flow velocity of deep cerebral veins occurred earlier than the morphological recovery demonstrated by magnetic resonance venography.

Mechanical and structural characterisation of the dural venous sinuses.

The dural venous sinuses play an integral role in draining venous blood from the cranial cavity. As a result of the sinuses anatomical location, they are of significant importance when evaluating the mechanopathology of traumatic brain injury (TBI). Despite the importance of the dural venous sinuses in normal neurophysiology, no mechanical analyses have been conducted on the tissues. In this study, we conduct mechanical and structural analysis on porcine dural venous sinus tissue to help elucidate the tissues' function in healthy and diseased conditions. With longitudinal elastic moduli values ranging from 33 to 58 MPa, we demonstrate that the sinuses exhibit higher mechanical stiffness than that of native dural tissue, which may be of interest to the field of TBI modelling. Furthermore, by employing histological staining and a colour deconvolution protocol, we show that the sinuses have a collagen-dominant extracellular matrix, with collagen area fractions ranging from 84 to 94%, which likely explains the tissue's large mechanical stiffness. In summary, we provide the first investigation of the dural venous sinus mechanical behaviour with accompanying structural analysis, which may aid in understanding TBI mechanopathology.

Participation of NO-Dependent Mechanisms in the Effects of Increased Systemic Level of Interleukin-1ß on Pial Microvessels under Conditions of Acute Hypoxia.

We studied the effect of increased systemic levels of the proinflammatory cytokine IL-1ß on the vasomotor reactions of pial microvessels in anesthetized rats under conditions of experimentally simulated progressively increasing acute normobaric hypoxia. Vital microscopy showed that more pronounced dilatation of pial vessels in response to IL-1ß under hypoxic conditions was almost completely prevented by pretreatment with non-specific NO synthase blocker L-NAME. These findings indicate the involvement of NO-dependent mechanisms in the vasodilator effect of proinflammatory cytokines under conditions of acute hypoxic exposure.

Isolated cortical vein thrombosis after nitrous oxide use in a young woman: a case report.

BACKGROUND: Nitrous oxide has become a popular inhalant as abused substance by young Chinese people in recent years. It has been mainly associated with medical conditions including megaloblastic anemia and myeloneuropathy. CASE PRESENTATION: We report a case of a 25-year-old high school graduate who had been abusing nitrous oxide for twenty months. She had a history of peripheral neuropathy and subacute combined degeneration in between. The young woman presented with headache, motor aphasia and right arm paralysis of eight hours after intermittently consuming nitrous oxide for one week. D-dimer was increased (1.1 mg/ml). Blood vitamin B12, folate, homocysteine and beta-HCG levels were normal. Head CT showed hemorrhagic infarction and subarachnoid hemorrhage. MR angiography and venography were normal. Head MRI identified left frontal isolated cortical vein thrombosis. Her muscle strength and verbal fluency significantly improved after initiation of Low Molecular Weight Heparin and serial head MRI showed continuous reduction in the size of thrombus. CONCLUSIONS: For the first time nitrous oxide use is found to be related to isolated cortical vein thrombosis. Public education regarding the potential consequences of abusing nitrous oxide especially in high-risk individuals is urgently needed.

Asymmetry of medullary veins on multiphase CT-angiography in patients with acute ischemic stroke.

BACKGROUND: It was previously demonstrated that decreased cortical venous drainage is a predictive factor of poor clinical outcome in patients with an acute ischemic stroke. The aim of this investigation is to test the hypothesis that the decline in blood flow in medullary veins (MV) on CT angiogram (CTA) of patients with acute ischemic stroke (AIS) can also be predictive of clinical outcome. METHODS: We retrospectively reviewed a database of patients with AIS who were evaluated by multiphase CTA and enrolled individuals with AIS and evidence of occlusion of the intracranial internal carotid artery, the M1 or M2 segment of the middle cerebral artery, or combination of two occlusions. To characterize asymmetry of MV we used similar principle that was previously established for MV on SWI MR-images; asymmetry was defined was presence of 5 or more contrast opacified MV in one hemisphere as compared to the contralateral side. Clinical outcomes were evaluated by mRS in 90 days. The Fisher Exact test was used to examine the significance of the MV asymmetry. Odds ratio and interrater variability were calculated. RESULTS: 66 patients with AIS were included. The presence of asymmetry in MV was associated with the higher frequency of poor clinical outcomes (84.6% vs 50.9%); the OR was 5.3. Interrater agreement in assessment on MV was moderate in our study (κ=0.55). CONCLUSION: This study shows that (a) medullary veins can be reliably assessed on multiphase CTA, (b) in patients with AIS, asymmetric appearance of MV is associated with poor clinical outcome.

Trends in incidence and epidemiologic characteristics of cerebral venous thrombosis in the United States.

OBJECTIVE: To test the hypothesis that race-, age-, and sex-specific incidence of cerebral venous thrombosis (CVT) has increased in the United States over the last decade. METHODS: In this retrospective cohort study, validated ICD codes were used to identify all new cases of CVT (n = 5,567) in the State Inpatients Databases (SIDs) of New York and Florida (2006-2016). A new CVT case was defined as first hospitalization for CVT in the SID without prior CVT hospitalization. CVT counts were combined with annual Census data to compute incidence. Joinpoint regression was used to evaluate trends in incidence over time. RESULTS: From 2006 to 2016, annual age- and sex-standardized incidence of CVT in cases per 1 million population ranged from 13.9 to 20.2, but incidence varied significantly by sex (women 20.3-26.9, men 6.8-16.8) and by age/sex (women 18-44 years of age 24.0-32.6, men 18-44 years of age 5.3-12.8). Incidence also differed by race (Blacks: 18.6-27.2; Whites: 14.3-18.5; Asians: 5.1-13.8). On joinpoint regression, incidence increased across 2006 to 2016, but most of this increase was driven by an increase in all age groups of men (combined annualized percentage change [APC] 9.2%, p < 0.001), women 45 to 64 years of age (APC 7.8%, p < 0.001), and women ≥65 years of age (APC 7.4%, p < 0.001). Incidence in women 18 to 44 years of age remained unchanged over time. CONCLUSION: CVT incidence is disproportionately higher in Blacks compared to other races. New CVT hospitalizations increased significantly over the last decade mainly in men and older women. Further studies are needed to determine whether this increase represents a true increase from changing risk factors or an artifactual increase from improved detection.

Impact of Acute and Chronic Hypertension on Changes in Pial Collateral Tone In Vivo During Transient Ischemia.

We investigated vasoconstrictive responses of pial collaterals in vivo at baseline and during transient middle cerebral artery occlusion during chronic hypertension. A cranial window was used to measure diameter of leptomeningeal anastomoses (pial collaterals) in male Wistar (n=8) and spontaneously hypertensive rats (SHRs; n=8) using video dimensional analysis. Middle cerebral artery occlusion was induced by remote filament for 2 hours with 2 hours reperfusion. Phenylephrine was infused during ischemia as a pressor therapy. Active diameters of pial collaterals were significantly smaller in SHRs versus Wistar (14.1±1.5 versus 21.6±2.8 µm; P<0.01); however, passive diameters were similar (25.0±2.9 versus 25.0±2.6 µm; P>0.05). Basal tone of pial collaterals before occlusion was 42±5% in SHRs versus 15±4% in Wistar (P<0.01). Tone decreased in both Wistar and SHRs during occlusion but remained higher in SHRs (9±2% versus 29±4%; P<0.05). Phenylephrine increased blood pressure in both groups but had little effect on leptomeningeal anastomoses diameters. Reperfusion caused vasoconstriction of pial collaterals, increasing tone from 8±1% to 20±5% in Wistar and 29±5% to 44±5% in SHRs (P<0.01). Higher tone in pial collaterals from SHRs basally and during occlusion/reperfusion could limit flow to the penumbra and promote evolution of infarction. Sustained elevated tone of pial collaterals from SHRs with phenylephrine suggests pressor therapy may not be appropriate during chronic hypertension.

Cerebral hemodynamics in the non-alcoholic fatty liver.

INTRODUCTION AND OBJECTIVES: The association between non-alcoholic fatty liver disease and cerebral hemodynamics arises from cardiovascular damage mechanisms such as endothelial dysfunction, arterial wall increased stiffness, high thickness of the intimate index of the internal carotid artery, left ventricular hypertrophy, left diastolic dysfunction, calcification coronary arteries and increased epicardial fat. The multidirectional relationship between systemic inflammation and lipid metabolism constitutes a common and simultaneous mechanism that causes vascular damage. This study aims to provide insight into the relationship between non-alcoholic fatty liver disease and the function of systemic circulation and cerebral circulation using Doppler ultrasound. PATIENTS AND METHODS: Is an observational, cross-sectional, prospective, comparative study conducted at Medica Sur Hospital. Thirty-five patients were selected consecutively. The patients consulted neurological service for various symptoms without severity criteria, such as vertigo, primary headache and balance disturbances. RESULTS: There is a difference in the variables mean of the right MCA PI (p = 0.023), left MCA PI" (p = 0.004), and left VA PI (p = 0.036) between the control and NAFLD groups. The correlation analysis between these variables and the CAP showed a positive correlation of the three variables with the CAP, "right MCA PI" (r = 0.384), left MCA PI "(r = 0.509) and" left VA PI " (r = 0.551). CONCLUSIONS: This study demonstrates a subclinical process of the middle cerebral artery in subjects with NAFLD, which suggests it may be involved in the disease development and points the need to make decisions for this liver manifestation prevention and treatment.

Early venous filling after reperfusion therapy in acute ischemic stroke.

BACKGROUND AND PURPOSE: Early venous filling after endovascular mechanical thrombectomy in acute ischemic stroke (AIS) is a specific finding that may serve as a biomarker for intracranial hemorrhage. However, the pathophysiology of early venous filling and postoperative hemorrhage remains unclear. The aim of this study was to investigate correlation between early venous filling and various factors involving patient demographics and perioperative imaging. METHODS: We prospectively analyzed 35 patients with AIS due to cardioembolism (CE) who underwent successful acute revascularization (TICI ≥2). Ischemic lesions were scored by magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI). Outcomes were assessed using the modified Rankin Scale (mRS) 90 days after stroke onset. Blood flow analysis was evaluated by MRI with arterial spin labeling (ASL). Early venous filling was assessed by digital subtraction angiography (DSA). Univariate analysis was performed to investigate correlations between early venous filling and patient demographics and imaging findings. RESULTS: Early venous filling was observed in 22 of 35 (66%) patients after reperfusion therapy. There was a significant correlation between early venous filling and DWI-ASPECTS (6.2 vs 8.8, p=0.0003), outcome (5 vs 9, p=0.006), hyperperfusion (17 vs 1, p< 0.0001), and hemorrhagic transformation (17 vs 1, p=0.005). CONCLUSIONS: This comprehensive study revealed that early venous filling after reperfusion therapy is associated with postoperative hyperperfusion. Early venous filling may be a marker of the process of hyperperfusion, leading to hemorrhage and an unfavorable outcome. Detection of early venous filling may be an important finding on DSA for subsequent intensive perioperative management.

Lysophosphatidic Acid Reduces Microregional Oxygen Supply/Consumption Balance after Cerebral Ischemia-Reperfusion.

BACKGROUND: Lysophosphatidic acid (LPA) is a small phospholipid-signaling molecule, which can alter responses to stress in the central nervous system. OBJECTIVE: We hypothesized that exogenous LPA would increase the size of infarct and reduce microregional O2 supply/consumption balance after cerebral ischemia-reperfusion. METHODS: This was tested in isoflurane-anesthetized rats with middle cerebral artery blockade for 1 h and reperfusion for 2 h with or without LPA (1 mg/kg, at 30, 60, and 90 min after reperfusion). Regional cerebral blood flow was determined using a C14-iodoantipyrine autoradiographic technique. Regional small-vessel (20-60 µm in diameter) arterial and venous oxygen saturations were determined microspectrophotometrically. RESULTS: There were no significant hemodynamic or arterial blood gas differences between groups. The control ischemic-reperfused cortex had a similar O2 consumption to the contralateral cortex. However, microregional O2 supply/consumption balance was significantly reduced in the ischemic-reperfused cortex with many areas of low O2 saturation (43 of 80 veins with O2 saturation below 50%). LPA did not significantly alter cerebral blood flow, but it did significantly increase O2 extraction and consumption of the ischemic-reperfused region. It also significantly increased the number of small veins with low O2 saturations in the reperfused region (76 of 80 veins with O2 saturation below 50%). This was associated with a significantly increased cortical infarct size after LPA administration (11.4 ± 0.5% control vs. 16.4 ± 0.6% LPA). CONCLUSION: This suggests that LPA reduces cell survival and that it is associated with an increase in the number of small microregions with reduced local oxygen balance after cerebral ischemia-reperfusion.

The characteristics of brain injury following cerebral venous infarction induced by surgical interruption of the cortical bridging vein in mice.

Cerebral venous infarction (CVI) caused by the injury of cortical bridging veins (CBVs), is one of the most serious complications following neurosurgical craniotomy. Different from cerebral artery infarction, this CVI pathological process is more complicated, accompanied by acute venous hypertension, brain edema, cerebral ischemia and hemorrhage in the veins bridged brain area. Therefore, a reliable and stable small animal model is particularly important for the pathological study of CVI induced by surgical CBV interruption (CBVi). A mouse model established by cutting off the right CBVs from bregma to lambda with microsurgical technique is used for the assessment of the pathological process. Adult male mice underwent craniotomy after transection of the parietal skin under anesthesia. The right CBVs were exposed by removing the right skull along the right lateral edge of the sagittal sinus (forming a 4 mm × 3 mm bone window from bregma to lambda) with a drill under the operating microscope. Following the final inspection of the cerebral veins, the CBVs (30% one, 60% two, 10% none) were sacrificed using bipolar coagulation technique. Intracranial pressure (ICP) monitoring, motor function examination, brain edema assessment and brain histopathological observation after perfusion were performed at different time points (6 h, 12 h, 24 h, and 48 h) in the postoperative mice. Cerebral hemisphere swelling, midline shift and subcortical petechial hemorrhage were found on histological sections 6 h after CBVs dissection. The change of ICP was consistent with cerebral edema and peaked at 12 h after surgery, as well as the disruption of the blood-brain barrier assessed by Evans Blue staining. Tissue necrosis, nerve cell loss and monocytes infiltration were also dynamically increased in the postoperative hemispheric cortex. Behavioral tests showed obvious somato- and forelimb-motor dysfunction, and severe somatosensory disorder on the operative mice at 12 h, which were substantially recovered at 48 h. Our study provided a novel mouse model of CVI caused by surgical CBVi that was close to clinical practice, and preliminarily confirmed its pathological process. This model might become an important tool to study the clinical pathology and the molecular mechanism of nerve injury following CVI.