Multiple Intracranial Hemorrhages Research Articles

Application of zone classification in multiple intracranial aneurysmal subarachnoid hemorrhage treatment strategies

BackgroundThe options of surgical approach and treatment stage are two challenging treatment strategy issues with multiple intracranial aneurysmal subarachnoid hemorrhage (MIA-SAH). MethodsWe retrospectively analyzed data from patients with MIA-SAH who underwent surgery in our center between January 1, 2014 and September 1, 2022. To define “zone classification”, the cranial cavity was divided into four zones by the planes of cerebral falx and tentorium cerebelli. Aneurysms isolated to one zone were defined as zone classification I; those crossing two zones were defined as zone classification II; those crossing three zones were defined as zone classification III; and those crossing four zones were defined as zone classification IV. General and aneurysmal-related characteristics of patients with different zone classifications were collected and compared between two surgical approaches. Multivariate logistic regression analysis was used to identify factors independently associated with multistage treatment options. ResultsA total of 226 patients with 523 aneurysms were included. The proportion of patients undergoing endovascular treatment increased with higher zone classification (I: 85.4%; II: 94.0%; III: 100.0%; IV: 100.0%). The proportion of patients receiving one-stage treatment decreased with higher zone classification (I: 60.2%; II: 33.6%; III: 0.0%; IV: 0.0%). Compared with patients undergoing microsurgical clipping, more patients undergoing endovascular treatment had zone classification II–IV (56.9% vs. 31.8%, p = 0.025). Zone classification II–IV (odds ratio [OR] = 3.821, 95% confidence interval [CI]: 2.041–7.154, p < 0.001), endovascular treatment (OR = 8.756, 95% CI: 2.589–29.609, p < 0.001), and size of all unruptured aneurysms <3 mm (OR = 4.531, 95% CI: 2.315–8.871, p < 0.001) were each independently associated with multistage treatment. ConclusionsZone classification provides a new idea in MIA-SAH treatment strategies, especially regarding surgical approach and treatment stage options.

Cerebral Venous Thrombosis in Pediatric Age: Risk Factors and Prognosis.

Cerebral venous thrombosis (CVT) is a rare but potentially fatal disease in pediatric age with an important morbimortality. In adults several factors have been associated with worse outcomes, however there are still few studies in children. This study aims to identify risk factors associated with clinical manifestations and long-term sequelae in pediatric CVT. Retrospective analysis of pediatric inpatients admitted to a tertiary-care hospital due to CVT between 2008 and 2020. Fifty-four children were included, 56% male, median age of 6.5 years (9 months-17.3 years). Permanent risk factors were identified in 13 patients (malignancy, 8; hematologic condition, 5) and transient risk factors in 47, including head and neck infections (57%) and head trauma (15%). Multiple venous sinuses involvement was present in 65% and the deep venous system was affected in four patients. Seventeen percent had intracranial hemorrhage and 9% cerebral infarction. Sixty-four percent of patients with multiple venous sinuses involvement presented with severe clinical manifestations: impaired consciousness, intracranial hypertension, acute symptomatic seizures or focal deficits. Regarding long-term prognosis, six patients had major sequelae: epilepsy (n = 3), sensory motor deficits (n = 2), and cognitive impairment (n = 3). Permanent risk factors were associated with severe clinical manifestations (p = 0.043). Cerebral infarction and intracranial hemorrhage were associated with major sequelae (p = 0.006 and p = 0.03, respectively, adjusted for age and sex). Permanent risk factors, involvement of multiple venous sinuses, intracranial hemorrhage, and cerebral infarction, were related to worse prognosis. Detection and early management of risk factors may limit CVT extension and reduce its morbimortality.

Simultaneous Multifocal Intracranial Haemorrhages Associated with Staphylococcus Aureus Endocarditis: A Plausible Role for Diclofenac Administration.

Intracranial haemorrhage may complicate infective endocarditis, caused by ruptured mycotic aneurysms or haemorrhagic transformation of brain septic emboli. The risk of intracranial bleeding may increase with the use of non-steroidal anti-inflammatory agent (NSAIDs). We report on a 53-year-old male patient with a past history of intravenous drug abuse, who was treated with diclofenac (75 mg IM) for a few hours of preceding fever and arthralgia. Seven hours later he was hospitalised with impaired consciousness and hemiparesis. Evaluation revealed multiple intracranial haemorrhages, at least one originating from a mycotic aneurysm. Repeated blood cultures grew methicillin-resistant Staphylococcus aureus (MRSA), and echocardiography revealed a vegetation on the mitral valve, establishing the diagnosis of bacterial endocarditis. The abrupt simultaneous multifocal intracranial bleeds shortly following the administration of NSAIDs for a few hours of febrile disease, one clearly originating from a mycotic aneurism, are exceptional. This raises a possibility of a role for diclofenac the intracranial bleeding diathesis in this unique clinical presentation. Intracranial haemorrhage in the set-up of undiagnosed infective endocarditis (IE) might be added to the long list of potential adverse outcomes of NSAID administration, and the possibility of IE should be considered before their administration for febrile disease of undetermined cause. Intracranial haemorrhage in the set-up of undiagnosed infective endocarditis might be added to the long list of potential adverse outcomes of NSAID administration.The possibility of infective endocarditis should be considered before the administration of NSAIDs for febrile disease of an undetermined cause.

Broca’s Aphasia Caused by Hemorrhagic Stroke in a Young Patient: A Case Report

Broca aphasia is a non-fluent aphasia in which the output of spontaneous speech is markedly diminished and there is a loss of normal grammatical structure. We report a case of aphasia presenting different features of aphasia following cerebral hemorrhage in the left frontoparietal lobe, which includes Broca's area. A 25-year-old man presented to our emergency department with a headache, Broca aphasia, and difficulty in vision that started two days ago. Bilateral hemorrhagic areas were seen in dilated fundus examination. A CT scan was performed and showed multiple intracranial hemorrhages. Although stroke is considered a disease of the elderly, it can also be present among young people. An underlying malignancy may be the trigger for hemorrhagic ischemia. Injury to the frontal regions of the left hemisphere impacts how words are strung together to form complete sentences. This can lead to Broca's Aphasia.

Case Report of Cerebral Venous Sinus Thrombosis Complication after Microvascular Decompression Surgery in the Inactive Phase of Ulcerative Colitis

Background: The risk of thrombosis is high in patients with Ulcerative Colitis. The main location of thrombosis is in the extremity and pulmonary vein. Cerebral venous thrombosis is a rare location for thrombosis with high mortality. One of the risk factors for developing thrombosis is in association with surgery, especially during an active phase of Ulcerative Colitis (UC), and very few studies report cases occurring during the inactive phase. Hence, it is important for the surgeon to understand the risk of thrombosis, especially of cerebral sinus thrombosis in the Ulcerative Colitis patient. Case: We are presenting a fatal complication in a male patient of 62, who had sagittal sinus thrombosis and multiple intra-cranial hemorrhages in both frontal lobes 3 weeks after microvascular decompression surgery for hemifacial spasm. Conclusion: The risk of cerebral venous sinus thrombosis is higher in Ulcerative Colitis patients, especially in those who undergo surgery regardless of its type. Careful peri-operative assessment and treatment related to thromboembolism prevention are important to reduce complications in such cases.

Association Between Plasma Biomarkers of Amyloid, Tau, and Neurodegeneration with Cerebral Microbleeds.

Cerebral microbleeds (CMBs) are a common vascular pathology associated with future intracerebral hemorrhage. Plasma biomarkers of amyloid, tau, and neurodegeneration may provide a screening avenue to identify those with CMBs, but evidence is conflicting. To determine the association between plasma biomarkers (Aβ40, Aβ42, t-tau, p-tau181, p-tau217, neurofilament light chain (NfL)) and CMBs in a population-based study of aging and whether these biomarkers predict higher signal on Aβ-PET imaging in patients with multiple CMBs. 712 participants from the Mayo Clinic Study of Aging with T2* GRE MRI and plasma biomarkers were included. Biomarkers were analyzed utilizing Simoa (Aβ40, Aβ42, t-tau, NfL) or Meso Scale Discovery (p-tau181, p-tau217) platforms. Cross-sectional associations between CMBs, plasma biomarkers and Aβ-PET were evaluated using hurdle models and multivariable regression models. Among the 188 (26%) individuals with≥1 CMB, a lower plasma Aβ42/Aβ40 ratio was associated with more CMBs after adjusting for covariables (IRR 568.5 95% CI 2.8-116,127). No other biomarkers were associated with risk or number CMBs. In 81 individuals with≥2 CMBs, higher plasma t-tau, p-tau181, and p-tau217 all were associated with higher Aβ-PET signal, with plasma p-tau217 having the strongest predictive value (r2 0.603, AIC -53.0). Lower plasma Aβ42/Aβ40 ratio and higher plasma p-tau217 were associated with brain amyloidosis in individuals with CMBs from the general population. Our results suggest that in individuals with multiple CMBs and/or lobar intracranial hemorrhage that a lower plasma Aβ42/Aβ40 ratio or elevated p-tau217 may indicate underlying cerebral amyloid angiopathy.

A COL4A1 variant in a neonate with multiple intracranial hemorrhages and congenital cataracts

A 2-day-old neonate presented with seizures, multiple intracranial hemorrhages, and bilateral congenital cataracts. Targeted next-generation sequencing of the collagen type IV alpha 1 chain (COL4A1) gene revealed a heterozygous de novo missense variant (NM_001845.6:c.2291G>A/p.Gly764Asp). This missense variant adds to the compendium of COL4A1 variants and is associated with a COL4A1-related disorder.

Major hemorrhage and mortality in COVID-19 patients on therapeutic anticoagulation for venous thromboembolism.

We observed multiple fatal intracranial hemorrhages shortly after initiating therapeutic anticoagulation for treatment of venous thromboembolism (VTE) in COVID-19 patients suggesting increased anticoagulation risk associated with COVID-19. The objective of this study is to quantify risk of major hemorrhage in hospitalized COVID-19 patients on therapeutic anticoagulation for deep venous thrombosis (DVT) or pulmonary embolism (PE). Hospitalized patients with COVID-19 receiving therapeutic anticoagulation for DVT, PE or both at four New York City hospitals were evaluated for hemorrhagic complications. These were categorized as major (including fatal) or clinically relevant non-major according to the criteria of the International Society of Thrombosis and Haemostasis. Hemorrhagic complications were correlated with clinical and laboratory data, ICD-10 code diagnoses and type of anticoagulation treatment. Minor hemorrhages were excluded. Major/clinically relevant hemorrhages occurred in 36 of 170 (21%) hospitalized COVID-19 patients being treated with therapeutic anticoagulation for VTE including 4 (2.4%) fatal hemorrhages. Hemorrhage was 3.4 times more likely with unfractionated heparin 27/76 (36%) compared to 8/81 (10%) with low molecular weight heparin (p = 0.002). Multivariate analysis showed that major hemorrhage was associated with intubation (p = 0.04) and elevated serum LDH (p < 0.001) and low fibrinogen (p = 0.05). Increased risk of hemorrhagic complications in treating VTE in hospitalized COVID-19 patients should be considered especially when using unfractionated heparin, in intubated patients, with low fibrinogen and/or elevated LDH. Checking serum fibrinogen and LDH before initiating therapeutic anticoagulation and monitoring coagulation parameters frequently may reduce bleeding complications.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This chapter contains 213 references.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This review contains 12 figures, 6 tables, and 213 references.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This chapter contains 213 references.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This review contains 12 figures, 6 tables, and 213 references.

Risk factors and risk nomogram model of reoperation for hemorrhages after severe traumatic brain injury craniotomy.

This study aimed to explore the risk factors associated with reoperation for postoperative hemorrhages after severe traumatic brain injury (sTBI) craniotomy and establish a risk nomogram model. A retrospective case-control study was performed. Overall, 367 patients who were diagnosed with sTBI and fulfilled the inclusion criteria were enrolled from the Department of Neurosurgery of the Affiliated Hospital of Zunyi Medical University between January 2015 and December 2020. They were divided into a reoperation group and a non-reoperation group according to whether they underwent reoperation for hemorrhages. Using univariate binary logistic regression analysis, the possible risk factors were screened. Subsequently, the independent risk factors of reoperation for postoperative hemorrhages were screened using the forward step method of multivariate binary logistic regression analysis, and a corresponding nomogram model was constructed. The receiver operative characteristic (ROC) curve was used to evaluate the reliability of the model. Finally, 30% of the data were randomly selected for internal verification of the model. The reoperation rate for hemorrhage after sTBI emergency craniotomy was 14.71% (54/367); multivariate logistic regression analysis showed that multiple hemorrhages (odds ratio [OR] = 4.38, 95% confidence interval [CI]: 1.815-10.587, p = 0.001), day or night surgery (OR = 0.26, 95% CI: 0.119-0.547, p < 0.001), operation duration (OR = 0.74, 95% CI: 0.119-0.547, p < 0.025), and abnormal intraoperative blood pressure fluctuation (OR = 4.15, 95% CI: 2.090-8.245, p < 0.001) were statistically significant. The sensitivity and specificity of the nomogram model were 0.815 and 0.661, respectively, and the area under ROC curve was 0.76 (95% CI: 0.705-0.833). Internal verification showed that the area under the ROC curve was 0.783 (95% CI: 0.683-0.883). Taken together, the results of our study reveal that multiple preoperative intracranial hemorrhages, day and night operation, operation duration, and abnormal fluctuation of intraoperative blood pressure were independent risk factors for postoperative bleeding and reoperation for sTBI. Through the analysis of the influencing factors, a prediction model for the risk of bleeding and reoperation after craniocerebral trauma was developed. Compared with other relevant studies, this prediction model has good prediction efficiency and can be used to predict the occurrence of bleeding and reoperation after sTBI in patients.

Expanded dengue syndrome presenting with acute liver failure, acute kidney injury, pancreatic involvement, coagulopathy, and multiple intracranial hemorrhages in a young child: a case report

BackgroundDengue is a mosquito-borne viral infection that typically occurs in tropical and subtropical countries. The clinical manifestations of dengue infection range from an asymptomatic subclinical course to severe dengue shock syndrome. Besides, dengue can affect any organ in the body and can present with atypical manifestations.Case presentationWe report a 6-year-old previously healthy Tamil child who had dengue complicated with multiorgan involvement. She initially presented with high fever, headache, body aches for 5 days, blood and mucus diarrhea, hematuria, and right knee joint swelling for 2 days. Dengue NS1 antigen was positive on day 2 of febrile illness. She was managed symptomatically in the local hospital for 3 days and transferred to the tertiary care hospital for further management. She was eventually diagnosed as having dengue hemorrhagic fever complicated with multiorgan involvement including acute liver failure, pancreatic involvement, coagulopathy, arthritis, acute kidney injury, and multiple intracranial hemorrhages. The constellation of disease manifestations was identified as expanded dengue syndrome. She was managed with fresh blood, platelet, and cryoprecipitate transfusions and intravenous antibiotics in addition to renal and liver support in the intensive care unit. On day 14 of illness, she deteriorated while on the ventilator and died due to multiple intracranial hemorrhages.ConclusionThe reported child with dengue hemorrhagic fever developed several unusual presentations such as acute liver and renal failure, disseminated intravascular coagulopathy, pancreatic involvement, and multiple intracranial hemorrhages, which form part of expanded dengue syndrome. In the seriously unwell child, it is important to look for unusual complications actively to improve outcomes.

Multiple embolic infarctions and intracranial hemorrhage in a patient with gestational trophoblastic disease

Multiple embolic infarctions and intracranial hemorrhage in a patient with gestational trophoblastic disease

POSTPARTUM CEREBRAL VENOUS THROMBOSIS ASSOCIATED WITH PROTEIN S DEFICIENCY: A CASE REPORT

There is a decline in the levels of protein S during pregnancy due to an increase in its binding protein. Thus, protein S deficiency increases the risk of thrombosis and may lead to poor pregnancy outcomes. In the setting of a hypercoagulable state during pregnancy, it is difficult to interpret protein S levels when measured with other tests of thrombophilia in pregnancy. The rate of developing thrombotic events is higher in those pregnant females with a deficiency of any natural anticoagulant like protein S. We report the case of a recently delivered female with multiple intracranial hemorrhages and cerebral venous thrombosis associated with protein S deficiency. This case highlights the need to extensively identify all risk factors of thrombosis in newly delivered females for the early and effective management of postpartum thrombosis.

Intracranial hemorrhage type and same-admission mortality in patients with left ventricular assist devices

ObjectivesLeft ventricular assist devices (LVAD) provide mechanical circulatory support for patients with advanced heart failure. Intracranial hemorrhage in this population represent a significant management challenge. The objective of this study is to report our initial experience on same-admission outcomes with LVAD patients that presented with various types of intracranial hemorrhage (ICH). Patients and MethodsA retrospective review of a large volume center over a two-year period was performed. LVAD patients with ICH requiring a neurosurgical consultation were identified. Hemorrhage type, interventions, discharge disposition and cause of death were recorded. Results27 LVAD patients with ICH received a neurosurgical consultation. The average INR at the time of ICH was 2.7 (1.0–8.8). Hemorrhage types seen were lobar (10/27, 37 %), SAH (5/27, 19 %), SDH (4/27, 15 %), cerebellar ICH (3/27, 11 %), multiple ICH (3/27, 11 %), and hemorrhagic conversion (2/27, 7 %). The overall mortality rate was 48.2 % (13/27), with the highest mortality being in those patients who had multiple ICH at the time of presentation (3/3, 100 %). The majority of patients with ICH (85.2 %) were non-operative. Lobar IPH was <3 cm in 80 % (8/10) of these, and 6/8 (75 %) ultimately died. 11 %(3/27) received surgical intervention. Of these, 67 % ultimately withdrew care. 77 % (10/13) of patients died as a result of the ICH. 80 % of patients with SAH were ultimately discharged home. ConclusionsPatients with a LVAD and ICH have a high rate of same-admission mortality (48 %). Hemorrhage location, intra-axial or extra-axial, resulted in patients being a risk for death secondary to either the hemorrhage itself or pump thrombosis, respectively.

Correlation between the skull base fracture and the incidence of intracranial hemorrhage in patients with traumatic brain injury

PurposeA head injury (HI) may cause a skull fracture, which may or may not be associated with injury to the brain. In essence, a skull base fracture (SBF) is a linear fracture at the base of the skull. Loss of consciousness and Glasgow coma score (GCS) may vary depending on an associated intracranial pathology. The pathomechanism is believed to be caused by high energy impact directly to the mastoid and supraorbital bone or indirectly from the cranial vault. Aim of this study is to define the correlation between SBF and intracranial hemorrhage (ICH) in patients with HI. MethodsAnalysis of data obtained from a retrospective review of medical records and from a systematized database pertaining to diagnostic criteria of SBF patients based only on clinical symptoms associated with ICH caused by HI treated in the Department of Neurosurgery at Dr. Hasan Sadikin Hospital, Bandung, Indonesia from January 1, 2012 to December 31, 2017. The exclusion criteria included age less than 15 years and no head computed tomography (CT) scan examination provided. ResultsA total of 9006 patients were included into this study in which they were divided into 3 groups: group 1, HI with no ICH; group 2, HI with single ICH and group 3, HI with multiple ICH. In all the SBF cases, SBF at anterior fossa accounted for 69.40% of them, which were mostly accompanied with mild HI (64.70%). Severity of HI and site of SBF correlated with the existence of traumatic brain lesions on CT scan, thus these factors were able to predict whether there were traumatic brain lesions or not. Most of the patients with epidural hemorrhage (EDH) has single traumatic lesion on CT scan, whereas most of the patients with cerebral contusion (CC) has multiple traumatic lesions on CT scan. On patients with both traumatic brain injury and SBF, most of the patients with anterior fossa SBF has EDH; whereas most of the patients with middle fossa SBF were accompanied with CC. Surgery was not required for most of the patients with SBF. ConclusionSBFs were strongly correlated with traumatic ICH lesions patients with anterior fossa SBF were more likely to suffer EDH whereas with middle fossa SBF were more likely to suffer CC.

Dural Arteriovenous Fistulae in the Tentorium Manifesting as Dementia

Tentorial dural arteriovenous fistula(dAVF)is a relatively rare disease which accounts for about 4.8% of all types of dAVF reported in Japan. Approximately 12.5% of intracranial dAVFs manifest with dementia-like symptoms. However, a tentorial dAVF typically presents more aggressively and rarely manifests as dementia. Here, we report the case of a patient with a tentorial dAVF manifesting as dementia, who was successfully treated with surgical interruption of the draining vein using indocyanine green video angiography(ICG-VA). A case of a 69-year-old man with a history of colon cancer, hypertension, and previous stroke presenting with cognitive impairment. CT showed multiple intracranial hemorrhages in the left parietal and occipital lobes, and MRI demonstrated flow void in the left cerebellopontine angle. DSA revealed left tentorial dAVF with venous reflux. We performed surgical interruption of the draining vein. The patient's mental status immediately returned to baseline. Serial MRIs showed decreasing edema in the left occipital lobe and thalamus. Cognitive impairment is an uncommon but curable symptom of tentorial dAVF. Surgical interruption of the draining vein using ICG-VA is a relatively simple and safe procedure to perform in such a case.

One case of multiple intracranial hemorrhage caused by acute severe methanol poisoning

One case of multiple intracranial hemorrhage caused by acute severe methanol poisoning