RESUMEN

OBJECTIVE: Epilepsy develops in one third of the patients after perinatal stroke. It is still unclear which vascular syndrome of ischemic stroke carries higher risk of epilepsy. The aim of the current study was to evaluate the risk of epilepsy according to the vascular syndrome of perinatal stroke. METHODS: The study included 39 children with perinatal arterial ischemic stroke (13 with anterior or posterior trunk of the distal middle cerebral artery occlusion, 23 with proximal or distal M1 middle cerebral artery occlusion and three with lenticulostriate arteria infarction), and 44 children with presumed perinatal venous infarction. Magnetic resonance imaging obtained at the chronic stage was used to evaluate the vascular syndrome of stroke. RESULTS: The median follow-up time was 15.1 years (95% CI: 12.4-16.5 years), epilepsy developed in 19/83 (22.9%) patients. The cumulative probability to be without epilepsy at 15 years was 75.4% (95% CI: 65.8-86.4). The probability of having epilepsy was higher in the group of proximal or distal M1 artery occlusion compared to patients with periventricular venous infarction (HR 7.2, 95% CI: 2.5-26, p = .0007). Patients with periventricular venous infarction had significantly more often status epilepticus or spike-wave activation in sleep ≥85% of it compared to patients with anterior or posterior trunk of the distal middle cerebral artery occlusion (OR = 81; 95% CI: 1.3-5046, p = .029). SIGNIFICANCE: The emphasis of this study is placed on classifying the vascular syndrome of perinatal stroke and on the targeted follow-up of patients for epilepsy until young adulthood. The risk for having epilepsy after perinatal stroke is the highest in children with proximal or distal M1 middle cerebral artery occlusion. Patients with periventricular venous infarction have a more severe course of epilepsy.

Asunto(s)

RESUMEN

Development of cerebral venous sinus thrombosis (CVST) is a rare manifestation of heparin-induced thrombocytopenia (HIT). Herein, we present a case in which heparin administration for primary CVST caused paradoxical worsening of CVST secondary to HIT. A 53-year-old woman diagnosed with CVST was provided with intravenous unfractionated heparin therapy. After 12 days, the patient presented tonic convulsive seizures (TCS). Subsequent magnetic resonance image (MRI) scans revealed an exacerbation of cerebral edema with a subcortical hemorrhage on the left parietal lobe. Laboratory test results revealed a significant decline in platelet count. Heparin was immediately discontinued and replaced with argatroban. The definitive diagnosis of HIT was made through the presence of HIT antibodies. The present case, in which HIT caused the secondary CVST exacerbation, is distinctly rare. Our case provides an instructive example by highlighting the potential of TCS as the first sign of HIT development during CVST treatment.

RESUMEN

The natural history and epidemiological aspects of traumatic cerebral venous thrombosis (CVT) are not fully understood. Due to the concomitant occurrence with intracranial hemorrhages, guidelines for medical treatment have been highly controversial. In this study, our objective was to carry out an analysis description of the population and to conduct a literature review. A prospectively gathered radiology registry data of patients hospitalized at the tertiary hospital of Centro Hospitalar Universitário do São João, Porto, Portugal, between 2016 and 2021 was carried out. All patients with traumatic brain injury (TBI) and concomitant CVT were identified. CVT was confirmed by CT venogram. Demographic, clinical, and radiological data and their medical management were reported. In-hospital complications and treatment outcomes were compared between patients measured by the Glasgow Outcome Score Extended (GOSE) at discharge and GOSE at three months. There were 41 patients with traumatic CVT admitted to this study. The majority (45.2%) had a hyperdense signal near the lateral sinus at admission, and only 26.2% presented with skull fractures. Of this cohort, 95% had experienced lateral sinus thrombosis. Twenty-five patients (60%) had occlusive venous thrombosis. Venous infarct was the main complication following CVT. Thirty-two patients (78%) were anticoagulated after CVT and four developed complications. At the three-month follow-up after discharge, 28.2% had good recovery (GOSE > 6). This study revealed a higher incidence of CVT in severe TBI and a mild association with skull fractures. There is a higher incidence of CVT in the lateral sinus. Management was inconsistent, with no difference in outcome without or with anticoagulation. Larger, prospective cohort studies are required to better comprehend this condition and determine evidence-based guidelines.

RESUMEN

Objective: Cerebral venous infarction (CVI) after vein injury during intraoperative lesion resection is associated with intracranial hemorrhage. We conducted this study to identify the incidence, clinical and imaging features, and prognosis of hemorrhage CVI. Methods: We performed a retrospective analysis of patients with confirmed CVI after vein injury who underwent craniotomy in our hospital. Postoperative clinical symptoms were observed, and imaging features were compared between patients with and without intracranial hemorrhages through CT examination. Variables were analyzed using univariate and multivariate regression analyses. Results: Among 2,767 patients who underwent craniotomy, 93 cases of injured veins were identified intraoperatively. Hemorrhagic CVI was found in 38% (35/93). Multivariate analysis revealed that midline approach, meningioma, postoperative seizures, disorders of consciousness and interval in hours < 72 h were identified as predictors of hemorrhagic CVI. After 3 months of follow-up, the prognosis was poor in 15 cases (16%, 15/93), including death (two cases), vegetative survival (four cases), and severe disability (nine cases). Conclusions: Hemorrhagic CVI, as a critical complication after venous injury, can have disastrous consequences. Do not injure known veins intraoperatively. In case of injury, requisite remedial measures should be adopted during and after surgery.

Asunto(s)

RESUMEN

PURPOSE: Cerebrospinal fluid (CSF) leakage is a frequent complication after spinal surgery. The lumbar drainage procedure (LDP) is the preferred method for early closure of a dural tear. This study was conducted to assess the safety and effectiveness of LDP after spinal surgery. MATERIALS AND METHODS: We retrospectively reviewed 122 patients (55 male and 67 female) who underwent LDP after spinal surgery between January 2010 and June 2021. LDP was performed on patients with suspected CSF leakage due to a dural tear during spinal surgery or in whom mixed-color CSF was observed in the hemo-drain after surgery. LDP was performed aseptically by a resident according to our institution's protocol, and the amount drained was from 200cc to 300cc per day. Absolute bed rest was maintained during the lumbar drainage period. The hemo-drain was opened to confirm that CSF was no longer mixed or oozing, at which time the lumbar drain was removed. Culture was performed at the drain tip when the lumbar drain was removed. RESULTS: The spinal surgery level was cervical in 23 patients, thoracic in 27 patients, and lumbar in 72 patients. The mean duration of the indwelling lumbar drain was 7.2 days (2 days-18 days), and the mean amount of drainage was 1198.2cc (100cc-2542cc). Among the 122 patients, the CSF leakage in 101 patients was resolved with the initial procedure, but 21 patients required re-insertion. Of those 21 patients, improper insertion due to a technical problem occurred in 15 patients, poor line fixation occurred in 2 patients, and CSF leakage was again observed after removal of the lumbar drain in 4 patients. In only 1 case was open surgery done after LDP because follow-up magnetic resonance imaging showed a suspected infection. During lumbar drainage, 76 patients used antibiotics, and 46 patients did not. Four patients showed bacterial growth in the tip culture, and 3 of them had been using antibiotics. All 4 of those patients were treated without complications and discharged. Among the 122 patients, 1 patient was discharged with left hemiparesis due to cerebral venous infarction (CVI) and hemorrhage after LDP, and 1 patient underwent re-operation because the CSF collection was not resolved. CONCLUSIONS: No major complications such as systemic infection, deep vein thrombosis, or aspiration pneumonia occurred during the lumbar drainage, except for 1 patient (0.8%) with CVI caused by over-drainage. One patient (0.8%) required open surgery after LDP, but no cases of systemic infection occurred while maintaining lumbar drainage, irrespective of antibiotic use. In conclusion, LDP is a safe and effective treatment for CSF leakage after spinal surgery.

Asunto(s)

RESUMEN

BACKGROUND: The transpetrosal approach is a complex skull base procedure with a high risk of complications, particularly caused by injury of the venous system. It is in part related to variability of blood outflow pathways and their distinctive patterns in each individual patient. OBJECTIVE: To evaluate outcomes and complications after skull base surgery with use of the petrosal approach modifications, which selection was based on the detailed preoperative assessment of venous drainage patterns. METHODS: Overall, 74 patients, who underwent surgery via the transpetrosal approach at our institution between 2000 and 2017, were included in this study. In all cases, the venous drainage pattern was assessed preoperatively and categorized according to the predominant blood outflow pathway into four types as previously suggested by Hacker: (1) sphenoparietal sinus (SpPrt), (2) sphenobasal vein (SpB), (3) sphenopetrosal sinus (SpPS), and (4) cortical. The blood outflow through the bridging petrosal vein and the vein of Labbé was also taken into consideration. In patients with SpPrt- and a cortical-type venous drainage, the transpetrosal approach was used in a standard way. In patients with SpB-type venous drainage, limited extradural anterior petrosectomy was combined with intradural anterior petrosectomy after dural opening, superior petrosal sinus transection, tentorial cutting, Meckel's cave opening, and trigeminal nerve mobilization. In patients with SpPS-type venous drainage, after standard petrosectomy, dural opening, and tentorial cutting, SpPS ligation was done followed by 2-week interval before staged definitive tumor resection. RESULTS: Gross total, near-total, and subtotal resection of the lesion (meningioma, 48 cases; retrochiasmatic craniopharyngioma, 11 cases; brain stem cavernoma, 7 cases; other tumors, 8 cases) was achieved in 30 (40.5%), 24 (32.4%), and 20 (27.0%) patients, respectively. Postoperative complications that were possibly related to venous compromise were noted in 18 patients (24.3%), but neither one was major. Of these 18 patients, 9 were symptomatic, but all symptoms-aphasia (4 cases), seizures (2 cases), and confusion (3 cases)-fully resolved after conservative treatment. Overall, 13 patients, including 4 symptomatic, had signal changes on T2-weighted brain MRI, which were permanent only in 3 cases (all asymptomatic). CONCLUSION: Our suggested surgical strategy can be applied to any type of the venous drainage pattern. Preoperative evaluation and intraoperative preservation of the blood outflow pathways are crucial means for safe and effective application of the transpetrosal approach.

Asunto(s)

RESUMEN

A 52-year-old man was admitted to our hospital with symptoms of raised intracranial pressure and cerebellar dysfunction caused by a medium-sized (4 cm in diameter) tentorial meningioma with an infratentorial extension. Preoperative magnetic resonance imaging showed that the tumor indented and possibly partially invaded the adjacent junction of the nondominant transverse and sigmoid sinuses. The contralateral dominant transverse sinus was fully patent. Total surgical removal of the lesion was done through the left retrosigmoid approach. During dissection of the meningioma, some bleeding from the venous sinus was noted, which was easily controlled by packing with hemostatic materials. The initial postoperative period was unremarkable, but approximately 48 h after surgery, acute clinical deterioration caused by hemorrhagic venous infarction of the left cerebellar hemisphere and brain stem developed and necessitated urgent reoperation for the evacuation of hematoma and brain decompression. Thereafter, the patient remained in a prolonged coma with a severe neurological deficit. After several years of extensive neurorehabilitation, he was able to walk with support but had a tracheostomy, required a feeding tube, and voided with a urinary catheter. Such a catastrophic outcome after an apparently trivial nondominant transverse sinus injury during resection of a tentorial meningioma raises the question whether reconstruction of the sinus wall with preservation of its patency might have prevented this complication in our patient.

Asunto(s)

RESUMEN

A right-handed woman in her 80s was admitted to the emergency department 1 h after sudden-onset global aphasia and right-sided hemiparesis. Medical history included arterial hypertension, dyslipidemia, hyperuricemia, aortic stenosis, osteoporosis, and recent pulmonary embolism. Medication consisted of apixaban, bisoprolol, hydrochlorothiazide, allopurinol, fenofibrate, and vitamin D. Vital parameters (blood pressure, heart rate, body temperature, oxygen saturation) and glycemia were all within normal range. Electrocardiogram showed a first-degree atrioventricular block. The patient was promptly transported to the emergency computed tomography (CT) scanner. Non-contrast brain CT revealed a unilateral hyperdensity in the left caudate and lentiform nuclei. No other intracranial lesion was visualized. Laboratory studies were not yet available at the time of imaging. What is your diagnosis?

RESUMEN

INTRODUCTION: The aim of this study was to evaluate genetic risk factors in term-born children with antenatal periventricular hemorrhagic infarction (PVHI), presumed antenatal periventricular venous infarction and periventricular hemorrhagic infarction in preterm neonates. METHODS: Genetic analysis and magnetic resonance imaging were performed in 85 children: term-born children (≥36 gestational weeks) with antenatal periventricular hemorrhagic infarction (n = 6) or presumed antenatal (n = 40) periventricular venous infarction and preterm children (<36 gestational weeks) with periventricular hemorrhagic infarction (n = 39). Genetic testing was performed using exome or large gene panel (n = 6700 genes) sequencing. RESULTS: Pathogenic variants associated with stroke were found in 11 of 85 (12.9%) children with periventricular hemorrhagic infarction/periventricular venous infarction. Among the pathogenic variants, COL4A1/A2 and COL5A1 variants were found in 7 of 11 (63%) children. Additionally, 2 children had pathogenic variants associated with coagulopathy, whereas 2 other children had other variants associated with stroke. Children with collagenopathies had significantly more often bilateral multifocal stroke with severe white matter loss and diffuse hyperintensities in the white matter, moderate to severe hydrocephalus, moderate to severe decrease in size of the ipsilesional basal ganglia and thalamus compared to children with periventricular hemorrhagic infarction/periventricular venous infarction without genetic changes in the studied genes (P ≤ .01). Severe motor deficit and epilepsy developed more often in children with collagenopathies compared to children without genetic variants (P = .0013, odds ratio [OR] = 233, 95% confidence interval [CI]: 2.8-531; and P = .025, OR = 7.3, 95% CI: 1.3-41, respectively). CONCLUSIONS: Children with periventricular hemorrhagic infarction/periventricular venous infarction have high prevalence of pathogenic variants in collagene genes (COL4A1/A2 and COL5A1). Genetic testing should be considered for all children with periventricular hemorrhagic infarction/periventricular venous infarction; COL4A1/A2 and COL5A1/A2 genes should be investigated first.

Asunto(s)

RESUMEN

BACKGROUND: Spontaneous thrombosis of a developmental venous abnormality (DVA) is a rare complication associated with hypercoagulability. The objective of this case report is to describe an association between DVA thrombosis and mild coronavirus disease 2019 (COVID-19) infection in a vaccinated patient. OBSERVATIONS: A 28-year-old male with hypertension presented with severe headache and left-sided hemiparesis. Five weeks prior to presentation, the patient experienced mild respiratory symptoms and tested positive for COVID-19. Admission brain computed tomography (CT) showed a large right parieto-occipital intracerebral hemorrhage with surrounding edema. CT venography and catheter angiography showed a thrombosed DVA with associated venous infarction as the hemorrhage etiology. He was treated with decompressive hemicraniectomy, external ventricular drain placement, and systemic anticoagulation. The patient was functionally independent (modified Rankin Scale score, 2) at 4-month follow-up. Hypercoagulability work-up was unremarkable. LESSONS: Delayed DVA thrombosis after the COVID-19 infectious period may represent an association between the infection and a protracted systemic viral-induced hypercoagulable state. The severity of COVID-19 symptomatology does not appear to correlate with risk of DVA thrombosis. Young patients with a recent history of COVID-19 infection who present with venous infarction should be evaluated for an underlying thrombosed DVA.

RESUMEN

We present a 35-year-old male with ulcerative colitis initially admitted for a flare-up who then presented with altered mental status and was found to have extensive cerebral venous sinus thrombosis on computed tomography imaging. The patient underwent successful partial recanalization of the superior sagittal sinus and bilateral transverse sinuses using the Penumbra Indigo® Aspiration System with improved outcomes. To our knowledge, this is the first reported use of this device in the treatment of cerebral venous sinus thrombosis.

Asunto(s)

RESUMEN

Neurogenesis in the subventricular zone (SVZ), subgranular zone (SGZ), and cerebral cortex is now a familiar event to confirm by cerebral arterial ischemia in rat models. However, it remains unclear whether cerebral venous ischemia (CVI) alone causes neurogenesis, and where that neurogenesis occurs. After creating CVI rat models via a two-vein occlusion (2-VO) method, neurogenesis was immunohistochemically evaluated by double-labeling 5-bromo-2'-deoxyuridine (BrdU)-positive cells with neuronal nuclei (NeuN) or doublecortin (DCX) antibody. Fifty Wistar rats were divided into two major groups (BrdU-NeuN and BrdU-DCX) and then separated into two subgroups (2-VO or sham). The total number of double-positive cells expressed inside a predefined region of interest (ROI) covering the ischemic area was compared between the two subgroups. Then, we divided the ROI into six sections to evaluate and compare the distribution of double-positive cells generated in each section between the two subgroups. The 2-VO subgroup presented more double-positive cells than the sham group in both BrdU-NeuN and BrdU-DCX groups, while the BrdU-DCX+2-VO group showed a characteristic distribution of double-positive cells in ROI 2 and ROI 3, suggesting areas of the ischemic core and penumbra, with a significant difference compared to the BrdU-DCX+sham group. This study demonstrates that CVI has the potential to induce endogenous neurogenesis, with significant numbers of both newly generated neurons and precursors observed in the ischemic area. The distribution of these cells suggests that the cortex could be the main origin of neurogenesis after cortical CVI.

RESUMEN

Ulcerative colitis is an idiopathic inflammatory bowel condition that may be worsened by thromboembolic events such deep vein thrombosis, cerebral venous thrombosis, and pulmonary embolism. Cerebral venous thrombosis is a rare but critical consequence of ulcerative colitis characterized by high mortality and morbidity rate. It is thought to be caused by the hypercoagulable state that occurs during ulcerative colitis relapse. Cerebral venous thrombosis is a reversible condition with good outcomes when detected early and treated properly. In this study, we describe the case of a young woman who presented with cerebral venous thrombosis secondary to ulcerative colitis complicated by venous infarction with petechial cerebral hemorrhage.

RESUMEN

BACKGROUND AND PURPOSE: Cerebral venous sinus thrombosis (CVST) is a rare cerebrovascular disease with a wide spectrum of clinical manifestations. The aim of this study is to assess the presence of subarachnoid hemorrhage (SAH) in the context of CVST and to present its epidemiological, clinical and radiological/laboratory aspects. METHODS: Between October 2012 and October 2019, 43 patients with CVST were reviewed. Eleven (25.58%) cases presented SAH. RESULTS: A quarter of the patients evaluated with CVST had SAH. There were 9 women (81.82%) and 2 men, with a mean age at presentation of 37.7 years (range 28-49). The most common risk factor was the use of oral contraceptives and the most prevalent symptom was headache. Both sinuses, the superior sagittal sinus and the transverse sinus, were the most affected. There was no isolated involvement of the cortical vein. The SAH was limited to some sulci of cerebral convexity in 8 cases (72.73%). In one case, the location of SAH was in the cerebellum and in two cases in the Sylvian fissure. In two cases, there was an evolution to venous infarction; and in three cases, intraparenchymal hemorrhage was present. Seven patients (63.64%) improved considerably with anticoagulation after 6 months of treatment. CONCLUSIONS: This series found that 25.58% of patients with CVST had SAH. It is the highest incidence described in the literature so far. Findings of SAH located in the cerebral convexities, without affecting the base cisterns, should always lead to the suspicion of CVST.

Asunto(s)

RESUMEN

Objective:To summarize the clinical characteristics and efficacy of hemorrhage resulted from cortical venous infarction with seizure as the first symptom after craniotomy.Methods:Eleven patients with hemorrhage resulted from cortical venous infarction with seizure as the first symptom after craniotomy admitted to Neurosurgical Center, 988 th Hospital of PLA Joint Logistic Support Force from June 2011 to September 2019 were chosen in our study; primary diseases included meningioma in 7 patients, contusion and laceration of frontal lobe in 2, hypertensive cerebral hemorrhage in 1, and obsessive-compulsive disorder in 1 patient. Epilepsy was the first symptom after craniotomy. Clinical characteristics and efficacy of these patients were analyzed retrospectively; seizure control efficacy was evaluated by Engel grading. Results:First seizure occurred 4 h-7 d after craniotomy in these 11 patients, including 2 with focal sensory retention seizure, 3 with focal bilateral tonic-clonic seizure, and 6 with general tonic-clonic seizure. Follow-up cranial CT revealed hematoma in surgical region, adjacent cortex or subcortex in 9 patients (hematoma volume: 15-50 mL); emergency craniotomy (hematoma clearance) and decompressive craniectomy was performed in 5 patients; only emergency craniotomy (hematoma clearance) was performed in 3 patients; conservative treatment was performed in 1 patient. A small amount of diffuse bleeding with severe cerebral edema in the surgical region appeared in 2 patients, and the transient limb paralysis gradually recovered after 2 months of conservative treatment. Follow-up was performed for (4.5±1.7) years ([2.3-7.0] years). During the last follow-up, 4 patients were normal, 5 patients had mild to moderate hemiplegia, 1 had mild decreased vision in the right eye, and 1 had long-term coma. Epileptic control efficacy analysis indicated that 8 had Engel grading I and 3 grading II.Conclusion:Complete removal of hematoma and inactivated brain tissues can effectively control seizures and rebleeding in patients with hemorrhage resulted from cortical venous infarction.

RESUMEN

Perinatal ischemic stroke is a common cause of lifelong disability.

Asunto(s)

RESUMEN

Cerebral venous thrombosis (CVT) is a rare type of venous thromboembolism (VTE). It is an important cause of stroke in young adults and children. Severe CVT, which is characterized by cerebral venous infarction or hemorrhage, seizures, or disturbance of consciousness, has more severe clinical manifestations and a worse prognosis. It is commonly believed that the onset of severe CVT gave credit to venous return disorder, with the underlying pathogenesis remaining unclear. There is increasing evidence suggesting that an inflammatory response is closely associated with the pathophysiology of severe CVT. Preclinical studies have identified the components of neuroinflammation, including microglia, astrocytes, and neutrophils. After CVT occurrence, microglia are activated and secrete cytokines (e.g., interleukin-1ß and tumor necrosis factor-α), which result in a series of brain injuries, including blood-brain barrier disruption, brain edema, and cerebral venous infarction. Additionally, astrocytes are activated at the initial CVT stage and may interact with microglia to exacerbate the inflammatory response. The extent of cerebral edema and neutrophil recruitment increases temporally in the acute phase. Further, there are also changes in the morphology of inflammatory cells, expression of inflammatory mediators, and inflammatory pathway molecules with CVT progression. Lately, some clinical research suggested that some inflammation-related biomarkers are of great value in assessing the course, severity, and prognosis of severe CVT. Moreover, basic and clinical research suggested that anti-inflammatory therapy might hold promise in severe CVT. This study reviews the current literature regarding the involvement of inflammation in the pathophysiology and anti-inflammatory interventions of severe CVT, which would contribute to informing the pathophysiology mechanism and laying a foundation for exploring novel severe CVT therapeutic strategies.

RESUMEN

BACKGROUND: Cerebral venous infarction (CVI) is a serious complication after meningioma resection. The risk factors of postoperative cerebral venous infarction after surgical resection of meningioma can be determined through large samples and this study can add evidence to the literature. METHODS: The clinical and imaging data of 1127 patients with intracranial meningiomas who underwent resection in our hospital were retrospectively collected and analyzed. CVI was evaluated by postoperative imaging and clinical manifestations. Univariate and multivariate analyses were performed to identify risk factors associated with CVI. RESULTS: Overall, 4.7% (53/1127) of patients experienced CVI after meningioma resection. Multivariate analysis revealed superficial meningioma, moderate to severe peritumoral edema, peritumoral critical vein and WHO grade II-III as independent predictors of a postoperative CVI. After timely intervention, the symptoms were clearly alleviated in one month, and the prognosis was good, but injury to key veins could cause irreversible neurological disorders. CONCLUSIONS: Intraoperative protection of veins is the primary way to prevent CVI. The present study identified several significant and independent risk factors for postoperative venous infarction, thereby enabling the identification of high-risk patients who require special attention during clinical and surgical management.

Asunto(s)