Small Intracerebral Hemorrhage Research Articles

Left atrial appendage closure in patients with atrial fibrillation and acute ischaemic stroke despite anticoagulation

BackgroundThe occurrence of acute ischaemic stroke (AIS) while using oral anticoagulants (OAC) is an increasingly recognised problem among nonvalvular atrial fibrillation (NVAF) patients. We aimed to elucidate the potential role...

Hemorrhagic Stroke and Blindness after Hyaluronic Acid/Polylactic Acid Filler Injection

The number of people receiving facial filler injections is increasing as it is relatively safe than the other cosmetic procedures. However, complications of facial filler injection range from mild redness and inflammation to cerebral infarction. We report the case of a patient who was diagnosed with cerebral infarction and intracranial hemorrhage after facial filler injection. A 61-year-old male presented to the emergency department with ocular pain and visual loss in the left eye after filler injection into the glabella. Neurological examination revealed monocular blindness. Initial brain magnetic resonance imaging (MRI) revealed small, acute multifocal infarctions in the left frontal, parietal, and temporal lobes. Follow-up MRI revealed subarachnoid hemorrhages in the left frontal and parietal lobe. Follow-up brain computed tomography showed small intracerebral hemorrhage in the left frontal lobe. Clinicians must be aware that not only cerebral infarction, but intracranial hemorrhage could also be a potential adverse effect of the cosmetic filler injection in the face.

Location-Specific Hematoma Volume Cutoff and Clinical Outcomes in Intracerebral Hemorrhage.

Major intracerebral hemorrhage (ICH) trials have largely been unable to demonstrate therapeutic benefit in improving functional outcomes. This may be partly due to the heterogeneity of ICH outcomes based on their location, where a small strategic ICH could be debilitating, thus confounding therapeutic effects. We aimed to determine the ideal hematoma volume cutoff for different ICH locations in predicting ICH outcomes. We retrospectively analyzed consecutive ICH patients enrolled in the University of Hong Kong prospective stroke registry from January 2011 to December 2018. Patients with premorbid modified Rankin Scale score >2 or who underwent neurosurgical intervention were excluded. ICH volume cutoff, sensitivity, and specificity in predicting respective 6-month neurological outcomes (good [modified Rankin Scale score 0-2], poor [modified Rankin Scale score 4-6], and mortality) for specific ICH locations were determined using receiver operating characteristic curves. Separate multivariate logistic regression models were also conducted for each location-specific volume cutoff to determine whether these cutoffs were independently associated with respective outcomes. Among 533 ICHs, the volume cutoff for good outcome according to ICH location was 40.5 mL for lobar, 32.5 mL for putamen/external capsule, 5.5 mL for internal capsule/globus pallidus, 6.5 mL for thalamus, 17 mL for cerebellum, and 3 mL for brainstem. ICH smaller than the cutoff for all supratentorial sites had higher odds of good outcomes (all P<0.05). Volumes exceeding 48 mL for lobar, 41 mL for putamen/external capsule, 6 mL for internal capsule/globus pallidus, 9.5 mL for thalamus, 22 mL for cerebellum, and 7.5 mL for brainstem were at greater risk of poor outcomes (all P<0.05). Mortality risks were significantly higher for volumes that exceeded 89.5 mL for lobar, 42 mL for putamen/external capsule, and 21 mL for internal capsule/globus pallidus (all P<0.001). All receiver operating characteristic models for location-specific cutoffs had good discriminant values (area under the curve >0.8), except in predicting good outcome for cerebellum. ICH outcomes differed with location-specific hematoma size. Location-specific volume cutoff should be considered in patient selection for ICH trials.

Guillain-Barré Syndrome Mimicking Brainstem Death Following Traumatic Intracerebral Hemorrhage (P12-7.006)

<h3>Objective:</h3> NA <h3>Background:</h3> NA <h3>Design/Methods:</h3> NA <h3>Results:</h3> A 73-year-old man attended the ED following an assault where he sustained multiple traumatic blows to the head. He was alert, complained of headache but provided a detailed account. There were facial injuries but no clinical signs of cranial or skull base fractures. There was injury to the right eye, in which he had pre-existing visual impairment from previous injury. Vision was normal in the left. Right pupillary light reflex was absent but left was normal. The remainder of the neurological examination was unremarkable. CT-Head identified a small traumatic subarachnoid hemorrhage over the left cerebral convexity and a small contusion in the left temporo-parietal region. Vitreous hemorrhage was evident in the right eye. Clinically stable, follow-up CT on day 3 showed small intra-cerebral haemorrhage within the contusion, with minimal mass effect. However, on day 8, his GCS dropped and he was admitted to the ITU for airway management. Both pupils were non-responsive to light. Expansion of haemorrhage was suspected, however repeat CT was stable. EEG showed slowing over the left hemisphere without epileptiform activity. MRI excluded alternative causes for his neurological status such as brainstem ischaemia. With no clinical improvement, formal brainstem death testing was initiated. No potential confounders were recognised. The pupillary, corneal, oculocephalic, cough and gag reflexes were absent. Unexpectedly, deep tendon reflexes were absent in all limbs. A peripheral nerve stimulator using a train-of-four test protocol found no response. Post-traumatic Guillain-Barré syndrome (GBS) was suspected. Intravenous immunoglobulin was commenced. Nerve conduction studies found absent motor and sensory responses in all limbs. EMG showed fibrillation potentials and sharp waves. These findings were consistent with acute motor-sensory axonal neuropathy (AMSAN) variant of GBS. Serum Anti-GM1 antibodies were identified. After multiple rounds of plasmapheresis the patient was weaned from the ventilator. Nevertheless, severe neurological disability remained. <h3>Conclusions:</h3> NA <b>Disclosure:</b> Dr. Finegan has nothing to disclose. Dr. Ryan has nothing to disclose. Michael J. Hennessy has nothing to disclose. Kevin Murphy has nothing to disclose. Dr. Crowley has nothing to disclose. Dr. Elamin has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Roche .

Circulating macrophage colony-stimulating factor levels and stroke: A Mendelian randomization study

ObjectivesColony-stimulating factor 1 (CSF1), also known as macrophage colony-stimulating factor, has been shown to be associated with risk of ischemic stroke in conventional epidemiological study. We performed a Mendelian randomization analysis to evaluate the effects of genetically predicted circulating CSF1 levels on stroke and carotid intima-media thickness (cIMT). MethodsGenetic variants robustly associated with CSF1 levels, located in the vicinity of the CSF1 gene (cis), were used as instruments for CSF1 levels. Genetic association estimates for ischemic stroke and its subtypes, intra-cerebral hemorrhage (ICH), and cIMT were obtained from MEGASTROKE (60,341 cases and 454,450 controls), ISGC (1,545 cases and 1,481 controls), and UK Biobank (22,179 individuals), respectively. ResultsGenetically predicted higher CSF1 levels was significantly associated with a higher risk of any ischemic stroke, large artery stroke (LAS) and cardioembolic stroke (CES), but not with small vessel stroke (SVS) and ICH. The odds ratios (ORs) per genetically predicted one standard deviation (SD) increase in circulating CSF1 levels were 1.11 (95% CI 1.04–1.17) for any ischemic stroke, 1.23 (95% CI 1.07–1.42) for LAS, 1.18 (95% CI 1.05–1.33) for CES, 1.07 (95% CI 0.94–1.21) for SVS, and 1.15 (95% CI 0.73–1.83) for ICH. Similarly, we also found that genetically predicted higher CSF1 levels were associated with higher cIMT, as a measure of subclinical atherosclerosis (cIMT, β 0.016, 95% CI, 0.004-0.029). ConclusionsThis study provides evidence that genetically predicted higher CSF1 levels was associated with higher risk of any ischemic stroke, LAS, and CES. Whether targeting CSF1 or its receptors can reduce the risk of ischemic stroke needs further study.

Air bubble artifact: why postmortem brain MRI should always be combined with postmortem CT.

Forensic pathology increasingly uses postmortem magnetic resonance imaging (PMMRI), particularly in pediatric cases. It should be noted that each (sudden and unexpected) death of an infant or child should have a forensic approach as well. Current postmortem imaging protocols do not focus adequately on forensic queries. First, it is important to demonstrate or rule out bleeding, especially in the brain. Thus, when incorporating PMMRI, a blood sensitive sequence (T2* and/or susceptibility weighted imaging (SWI)) should always be included. Secondly, as intracranial air might mimic small focal intracerebral hemorrhages, PMMRI should be preceded by postmortem CT (PMCT) since air is easily recognizable on CT. This will be illustrated by a case of a deceased 3-week-old baby. Finally, note that postmortem scans will often be interpreted by clinical radiologists, sometimes with no specific training, which makes this case report relevant for a broader audience.

Abstract WP125: Relationships Of Hemoglobin With Ischemic Lesions After Intracerebral Hemorrhage

Introduction: Hemoglobin concentrations and diffusion weighted imaging (DWI) lesions are separately known to be associated with poor intracerebral hemorrhage (ICH) outcomes. Though hemoglobin concentrations are related to both hypoxia and thrombosis at their extremes, it is unknown whether hemoglobin concentrations relate to DWI lesions after ICH. Methods: Spontaneous, supratentorial ICH patients with available baseline hemoglobin and hospitalized MRI data enrolled into a multicenter cohort study between 2010-2016 were analyzed. Baseline hemoglobin was assessed as both a continuous variable (g/dL) and categorical variable (&lt;11, 11 to &lt;13, 13 to &lt;15, &gt;/=15 g/dL). Primary analyses assessed relationships of baseline hemoglobin with MRI DWI lesions. Secondary analyses assessed independent relationships of hemoglobin and DWI lesions with poor 3-month outcomes (modified Rankin Scale [mRS] 4-6). Separate multivariable regression models assessed these relationships after adjusting for relevant covariates. Results: Of 917 ICH patients analyzed, the mean baseline hemoglobin was 13.8 g/dL (+/-1.9), 60% were deep ICH, and DWI lesions were identified in 27% of the cohort. In our primary analyses, increased hemoglobin, defined as a continuous variable, was associated with DWI lesions (adjusted OR 1.21, 95% CI: 1.07-1.37) after adjusting for sex, race, ICH severity, time to MRI, and blood pressure treatment change. In secondary analyses, DWI lesions were associated with poor 3-month outcomes (adjusted OR 1.83, 95% CI: 1.24-2.69) adjusting for similar covariates. We identified associations of low hemoglobin categories, when referenced to hemoglobin 13 to &lt;15 g/dL, with poor outcomes (&lt;11 g/dL: adjusted OR 1.99, 95% CI: 1.05-3.79; 11 to &lt;13 g/dL: adjusted OR 1.62, 95% CI: 1.04-2.52). Effect estimates of high hemoglobin (&gt;/=15 g/dL) with poor outcomes were smaller and imprecise (adjusted OR 1.39, 95% CI: 0.89-2.17). Conclusions: We identified novel relationships between higher baseline hemoglobin concentrations and DWI lesions in ICH patients. Further studies are required to clarify the role of hemoglobin concentrations on both cerebral small vessel disease pathophysiology and ICH outcomes.

A Neurological Complication in Rheumatoid Arthritis - A Scenario of Catastrophic Proportions.

Rheumatoid Arthritis (RA) is a common systemic inflammatory disease that can present with a plethora of extraarticular manifestations. Many patients with RA from low- and middle-income countries do not get timely and adequate treatment with disease-modifying therapies. This results in the perpetuation of a chronic inflammatory state. Rheumatoid vasculitis (RV) is one of the most aggressive complications of RA resulting from a prolonged proinflammatory milieu. Usually, it has the involvement of multiple organ systems, with cutaneous manifestations being the most common. Neurological presentation is uncommon but severe when present. We present a case of severe RV presenting with an unexpected neurological complication consisting of cranial and peripheral neuropathy with small vessel disease and intracerebral haemorrhage. We intend to highlight the morbidity and long-term consequences of inadequately treated RA, the most common inflammatory disease of the connective system especially in light of the neurological presentation.

ГЕМОРРАГИЧЕСКИЕ ИНСУЛЬТЫ У ДЕТЕЙ РАННЕГО ВОЗРАСТА

To date, cerebrovascular diseases of childhood are poorly understood. The need to study hemorrhagic strokes in children is due to the high prevalence in early childhood, the difficulty in identifying the causes and the non-specificity of the first signs of pathology. At different stages of child development, the etiological significance of various pathogenic factors is not the same. The purpose of this study - to analyze the results of diagnosis and treatment of intracranial complications in late hemorrhagic disease of the newborn. Methods. 158 cases of treatment of patients with intracranial hemorrhages against the background of vitamin-K dependent hemorrhagic syndrome were chosen as the objects of the study. Among the sick boys prevailed and amounted to 76 percent. At the age of 40 days ± 2, the disease began in 129 (86.6%) patients. The results of treatment were monitored in 158 patients within the period from one to 3 months. Indicators reflecting the results of treatment were subjected to statistical analysis. Results. According to the type of hematoma, the patients were distributed as follows - 64 (41.1%) intracerebral hematoma, 31 (20.2%) were diagnosed with subdural hemorrhage, intraventricular hemorrhage was detected in 6 (3.8%) cases, mixed subduralintracerebral hemorrhage was detected in 15 (9.5%) patients. 43 (26.6%) patients were not operated on: with subarachnoid hemorrhages - 34 (21.4%) and 9 patients (5.7%) - with small intracerebral and suberal hemorrhages. Lethal outcome occurred in 29 children (18.4%), mortality after surgery in 8 (5.1%) cases. In 43% of cases, a follow-up study did not reveal a neurological deficit. Conclusions. Full-term infants with a combination of the following factors are susceptible to the occurrence of hemorrhagic disease of the newborn: lack of prophylactic administration of vitamin K preparations, breastfeeding, and transient cholestasis. Timely surgical treatment in most patients gives positive results, despite the operation in a very difficult general condition of the patient and unstable hemostasis. Residual neurological deficit was noted during the follow-up study mainly in patients with primary gross damage to the brain parenchyma and with late diagnosis of the disease.

Updated Stroke Gene Panels: Rapid evolution of knowledge on monogenic causes of stroke

This article updates our previous Stroke Gene Panels (SGP) from 2017. Online Mendelian Inheritance in Man and PubMed were searched. We divided detected genes into two SGP groups, SGP1: genes reported in at least one person with stroke and associated with one or more clinical subgroups: large artery atherosclerotic, large artery non-atherosclerotic (tortuosity, dolichoectasia, aneurysm, non-atherosclerotic dissection or occlusion), cerebral small vessel diseases, cardio-embolic (arrhythmia, heart defect, cardiomyopathy), coagulation dysfunctions (venous thrombosis, arterial thrombosis, bleeding tendency), intracerebral hemorrhage, vascular malformations (cavernoma, arteriovenous malformations) and metabolism disorders; and SGP2: genes related to diseases that may predispose to stroke. We identified 168 SGP1 genes, 70 of these were validated for clinical practice. We also detected 72 SGP2 genes. Nine genes were removed because of conflicting evidence. The number of genes increased from 168 to 240 during 4.5-years, reflecting a dynamic evolution and the need for regular updates for research and clinical use.

A Comparative Study on the Clinical Efficacy of Stereotaxic Catheter Drainage and Conservative Treatment for Small and Medium Amount Intracerebral Hemorrhage in the Basal Ganglia.

The incidence rate and fatal disability rate of cerebral hemorrhage increase year by year. At present, most patients with a hematoma volume of ≤20 mL are treated conservatively by internal medicine. With the development of the stereotactic technique, it has been widely used for the treatment of cerebral hemorrhage in clinics. This study compared the clinical differences between stereotactic surgery and conservative treatment for small- and medium-sized cerebral hemorrhages. The results show that stereotactic hematoma evacuation is more effective than conservative treatment in the treatment of medium and small intracerebral hemorrhages in the basal ganglia. It can accelerate the resolution of hematoma and improve the neurological function and quality of life of patients, which is worthy of clinical promotion and application.

Higher Cerebral Small Vessel Disease Burden in Patients With Small Intracerebral Hemorrhage.

ObjectiveTo investigate the association between cerebral small vessel disease (SVD) and hematoma volume in primary intracerebral hemorrhage (ICH).MethodsPatients from a prospective ICH cohort were enrolled. Admission and follow-up CT scan within 72 h after onset were reviewed to calculate the final hematoma volume. We evaluated cortical superficial siderosis and the global SVD score, including white matter hyperintensities, lacunes, enlarged perivascular space, and cerebral microbleeds on MRI. We conducted the multivariate logistic regression analyses to explore the association between SVD markers and small ICH, as well as hematoma volume. Hematoma location was stratified into lobar and non-lobar for subgroup analysis.ResultsA total of 187 patients with primary ICH (mean age 62.4 ± 13.4 years, 67.9% male) were enrolled. 94 (50.2%) patients had small ICH. The multivariate logistic regression analysis showed an association between global SVD score and small ICH [adjusted odds ratio (aOR) 1.27, 95% CI 1.03–1.57, p = 0.027] and a trend of higher global SVD score towards non-lobar small ICH (aOR 1.23, 95% CI 0.95–1.58, p = 0.122). In the multivariate linear regression analysis, global SVD score was inversely related to hematoma volume of all ICH (β = −0.084, 95% CI −0.142 to −0.025, p = 0.005) and non-lobar ICH (β = −0.112, 95% CI −0.186 to −0.037, p = 0.004). Lacune (β = −0.245, 95% CI −0.487 to −0.004, p = 0.046) was associated with lower non-lobar ICH volume.ConclusionGlobal SVD score is associated with small ICH and inversely correlated with hematoma volume. This finding predominantly exists in non-lobar ICH.

ICA1L Is Associated with Small Vessel Disease: A Proteome-Wide Association Study in Small Vessel Stroke and Intracerebral Haemorrhage.

Small vessel strokes (SVS) and intracerebral haemorrhages (ICH) are acute outcomes of cerebral small vessel disease (SVD). Genetic studies combining both phenotypes have identified three loci associated with both traits. However, the genetic cis-regulation at the protein level associated with SVD has not been studied before. We performed a proteome-wide association study (PWAS) using FUSION to integrate a genome-wide association study (GWAS) and brain proteomic data to discover the common mechanisms regulating both SVS and ICH. Dorsolateral prefrontal cortex (dPFC) brain proteomes from the ROS/MAP study (N = 376 subjects and 1443 proteins) and the summary statistics for the SVS GWAS from the MEGASTROKE study (N = 237,511) and multi-trait analysis of GWAS (MTAG)-ICH–SVS from Chung et al. (N = 240,269) were selected. We performed PWAS and then a co-localization analysis with COLOC. The significant and nominal results were validated using a replication dPFC proteome (N = 152). The replicated results (q-value < 0.05) were further investigated for the causality relationship using summary data-based Mendelian randomization (SMR). One protein (ICA1L) was significantly associated with SVS (z-score = −4.42 and p-value = 9.6 × 10−6) and non-lobar ICH (z-score = −4.8 and p-value = 1.58 × 10−6) in the discovery PWAS, with a high co-localization posterior probability of 4. In the validation PWAS, ICA1L remained significantly associated with both traits. The SMR results for ICA1L indicated a causal association of protein expression levels in the brain with SVS (p-value = 3.66 × 10−5) and non-lobar ICH (p-value = 1.81 × 10−5). Our results show that the association of ICA1L with SVS and non-lobar ICH is conditioned by the cis-regulation of its protein levels in the brain.

Abstract TP131: Association Of Hemoglobin Over The First Week With Clinical Outcomes And Neuroimaging Characteristics In Patients With Spontaneous Intracerebral Hemorrhage

Introduction: Studies have shown independent associations of lower admission hemoglobin (HB) levels with larger spontaneous intracerebral hemorrhage (ICH) volumes and poor outcomes, possibly mediated by hematoma expansion (HE). Objective: We retrospectively investigated the association of HB levels over the first week post ICH with functional outcomes (FO) and neuroimaging findings in patients with spontaneous ICH (&gt;30 mL). We explored whether comorbidities modify the effects of HB. Methods: We analyzed HB levels from subjects enrolled in the Minimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation phase 3 trial (MISTIE III). The exposure was admission HB and the HB nadir in the first week. The primary outcome was good FO at 180 days, defined as modified Rankin Scale of 0-3. Secondary outcomes were good FO at 365 days, 30-day mortality, admission ICH volume, and HE (&gt;6 mL). Linear and logistic regression models were used to test the association of HB with clinical outcomes and neuroimaging findings. All models were adjusted for age, sex, race, treatment (medical Vs. MISTIE), Glasgow Coma Scale, ICH volume, presence of intraventricular hemorrhage, and ICH location (deep Vs. lobar). We investigated effect modification of comorbidities on association of HB with FO. Results: A total of 493 of 499 enrolled patients (61% males, mean age 61(SD=12) years, median ICH volume 41.8 (IQR=30.8-51.5) mL) were included. Patients with good FO at 180 days had a higher admission HB (13.2 Vs. 12.6 g/dl, p=0.001) and a higher nadir HB (11.7 Vs. 10.9 g/dl, p&lt;0.001). In adjusted analyses, each additional g/dl in nadir HB (but not admission HB) was associated with higher odds of good FO at 180 (OR 1.29, p=0.005) and 365 (OR 1.18, P=0.048) days. Baseline (B= -1.16, p=0.02) and nadir HB (B= -1.71, p=0.001) were inversely associated with hematoma volumes, but not with HE. There was evidence of heterogeneity in the effects of diabetes on the association of nadir HB with day 180 FO (OR 0.67; p interaction = 0.045). Conclusions: In patients with ICH &gt; 30 mL, higher nadir HB in the first week was associated with better long-term FO and smaller ICH volumes, but not with HE. Early hemoglobin changes may serve as a prognostic biomarker and a potentially modifiable factor to improve FO.

The influence of cerebrovascular disease in dementia with Lewy bodies and Parkinson's disease dementia.

Lewy body dementia (LBD), including dementia with Lewy bodies (DLB) and Parkinson's disease dementia, is a common form of neurodegenerative dementia. The frequency and influence of comorbid cerebrovascular disease is not understood but has potentially important clinical management implications. A systematic literature search was conducted (MEDLINE and Embase) for studies including participants with DLB and/or Parkinson's disease dementia assessing cerebrovascular lesions (imaging and pathological studies). They included white matter changes, cerebral amyloid angiopathy, cerebral microbleeds (CMB), macroscopic infarcts, microinfarcts and intracerebral haemorrhage. Of 4411 articles, 63 studies were included. Cerebrovascular lesions commonly studied included white matter changes (41 studies) and CMB (18 studies). There was an increased severity of white matter changes on magnetic resonance imaging (visualized as white matter hyperintensities), but not neuropathology, in LBD compared to Parkinson's disease without dementia and age-matched controls. CMB prevalence in DLB was highly variable but broadly similar to Alzheimer's disease (0%-48%), with a lobar predominance. No relationship was found between large cortical or small subcortical infarcts or intracerebral haemorrhage and the presence of LBD. The underlying mechanisms of white matter hyperintensities in LBD require further exploration, as their increased severity in LBD was not supported by neuropathological examination of white matter. CMB in LBD had a similar prevalence to Alzheimer's disease. There is a need for larger studies assessing the influence of cerebrovascular lesions on clinical symptoms, disease progression and outcomes.

Cerebral venous congestion exacerbates cerebral microhemorrhages in mice.

Cerebral microhemorrhages (CMHs; microbleeds), which are small focal intracerebral hemorrhages, importantly contribute to the pathogenesis of cognitive decline and dementia in older adults. Although recently it has been increasingly recognized that the venous side of the cerebral circulation likely plays a fundamental role in the pathogenesis of a wide spectrum of cerebrovascular and brain disorders, its role in the pathogenesis of CMHs has never been studied. The present study was designed to experimentally test the hypothesis that venous congestion can exacerbate the genesis of CMHs. Increased cerebral venous pressure was induced by internal and external jugular vein ligation (JVL) in C57BL/6 mice in which systemic hypertension was induced by treatment with angiotensin II plus L-NAME. Histological analysis (diaminobenzidine staining) showed that mice with JVL developed multiple CMHs. CMHs in mice with JVL were often localized adjacent to veins and venules and their morphology was consistent with venous origin of the bleeds. In brains of mice with JVL, a higher total count of CMHs was observed compared to control mice. CMHs were distributed widely in the brain of mice with JVL, including the cortical gray matter, brain stem, the basal ganglia, subcortical white matter, cerebellum, and the hippocampi. In mice with JVL, there were more CMHs predominantly in cerebral cortex, brain stem, and cerebellum than in control mice. CMH burden, defined as total CMH volume, also significantly increased in mice with JVL. Thus, cerebral venous congestion can exacerbate CMHs. These observations have relevance to the pathogenesis of cognitive impairment associated with right heart failure as well as elevated cerebral venous pressure due to jugular venous reflux in older adults.

Diagnostic Value of Susceptibility-Weighted Imaging Combined with Diffusion-Weighted Imaging in Early Intracerebral Hemorrhage.

Objective The incidence of early intracerebral hemorrhage (ICH) is gradually increasing and has been shown to affect an increasing number of younger people. Conventional imaging modalities might have a low detection rate of early and small ICH lesions. This study aimed to investigate the diagnostic value of susceptibility-weighted imaging (SWI) combined with diffusion-weighted imaging (DWI) in early ICH. Materials and Methods The data of 61 patients with early ICH diagnosed by computed tomography (CT) scan between January 2019 and February 2020 were assessed. Using CT as the gold standard, we compared the diagnostic sensitivity, accuracy, and imaging characteristics of SWI + DWI versus SWI or DWI alone. Results A total of 78 lesions were detected by CT in 61 patients with early ICH. The diagnostic sensitivity and accuracy of SWI + DWI were significantly higher than those of SWI or DWI alone. In terms of imaging characteristics, DWI demonstrated very low signal intensity in the hematoma center at different stages of early ICH with high signal intensity in the surrounding tissue, and the signal range gradually increased over time. By contrast, SWI displayed very low signal intensity at different stages, and the signal intensity also gradually increased over time. Conclusion Compared with SWI or DWI alone, SWI combined with DWI could improve the detection rate of hematoma lesions in patients with early ICH.

Genetically Predicted Cardiac Troponin I Concentrations and Risk of Stroke and Atrial Fibrillation

ObjectivesObservational studies have shown that elevated circulating cardiac troponin I (cTnI) concentrations were linked to higher risk of stroke and atrial fibrillation, but the causality remains unclear. Therefore, we used mendelian randomization to assess the potential causal effects of cTnI concentrations on the risk of stroke, its subtypes and atrial fibrillation. Materials and methodsThe instrumental variables for circulating cTnI concentrations were selected from a genome-wide association study meta-analysis of 48,115 European individuals. We examined the associations of circulating cTnI concentrations with stroke, ischemic stroke, ischemic stroke subtypes (cardioembolic, large artery, small vessel stroke), intracerebral hemorrhage and atrial fibrillation. ResultsGenetically predicted elevated circulating cTnI concentrations were associated with higher risk of cardioembolic stroke (odds ratio [OR], 1.80; 95% confidence interval [CI], 1.20–2.68; P = 0.004), but not associated with large artery stroke, small vessel stroke, total stroke, ischemic stroke and intracerebral hemorrhage. Additionally, we also found that elevated cTnI concentrations were causally linked to higher risk of atrial fibrillation (OR, 1.30; 95% CI, 1.10–1.53; P = 0.003). ConclusionsThis study provides evidence that genetically predicted circulating cTnI concentrations are causally linked to higher risk of cardioembolic stroke and atrial fibrillation.

Size-Related Differences in Computed Tomography Markers of Hematoma Expansion in Acute Intracerebral Hemorrhage.

Noncontrast computed tomography (NCCT) markers for hematoma expansion (HE) in intracerebral hemorrhage (ICH) are difficult to be found in small ICHs, of which can also expand. We aimed to investigate whether there were size-related differences in the prevalence of NCCT markers and their association with HE. This retrospective analysis of prospectively collected stroke registry included 267 consecutive patients with ICH who underwent baseline NCCT within 12h of onset. Qualitative NCCT markers, including heterogeneous density and irregular shape, were assessed. Hematoma density, defined as mean Hounsfield unit of hematoma, and hematoma volume were measured by semiautomated planimetry. Hematoma volume was categorized as small (≤ 10ml) and large (> 10ml). Associations of NCCT markers with HE were analyzed using multivariable logistic regression analyses. The model performances of NCCT markers and hematoma density were compared using receiver operating characteristic curves. Hematoma expansion occurred in 29.9% of small ICHs and 35.5% of large ICHs. Qualitative NCCT markers were less frequently observed in small ICHs. Heterogeneous density, irregular shape, and hematoma density were associated with HE in small ICH (adjusted odds ratios [95% confidence interval] 3.94 [1.50-10.81], 4.23 [1.73-10.81], and 0.72 [0.60-0.84], respectively), and hematoma density was also related to HE in large ICH (0.84 [0.73-0.97). The model performance was significantly improved in small ICHs when hematoma density was added to the baseline model (DeLong's test, p = 0.02). The prevalence of NCCT markers and their association with HE differed according to hematoma volume. Quantitative hematoma density was associated with HE, regardless of hematoma size.

Prevalence, Characteristics, and Outcomes of Undetermined Intracerebral Hemorrhage: A Systematic Review and Meta-Analysis.

There are scarce data regarding the prevalence, characteristics and outcomes of intracerebral hemorrhage (ICH) of undetermined (unknown or cryptogenic) etiology. We sought to determine the prevalence, radiological characteristics, and clinical outcomes of undetermined ICH. Systematic review and meta-analysis of studies involving patients with spontaneous ICH was conducted to primarily assess the prevalence and clinical-radiological characteristics of undetermined ICH. Additionally, we assessed the rates for ICH secondary to hypertensive arteriopathy and cerebral amyloid angiopathy. Subgroup analyses were performed based on the use of (1) etiology-oriented ICH classification, (2) detailed neuroimaging, and (3) Boston criteria among patients with cerebral amyloid angiopathy related ICH. We pooled the prevalence rates using random-effects models, and assessed the heterogeneity using Cochran Q and I2 statistics. We identified 24 studies comprising 15 828 spontaneous ICH patients (mean age, 64.8 years; men, 60.8%). The pooled prevalences of hypertensive arteriopathy ICH, undetermined ICH, and cerebral amyloid angiopathy ICH were 50% (95% CI, 43%–58%), 18% (95% CI, 13%–23%), and 12% (95% CI, 7%–17% [P<0.001 between subgroups]). The volume of ICH was the largest in cerebral amyloid angiopathy ICH (24.7 [95% CI, 19.7–29.8] mL), followed by hypertensive arteriopathy ICH (16.2 [95% CI, 10.9–21.5] mL) and undetermined ICH (15.4 [95% CI, 6.2–24.5] mL). Among patients with undetermined ICH, the rates of short-term mortality (within 3 months) and concomitant intraventricular hemorrhage were 33% (95% CI, 25%–42%) and 38% (95% CI, 28%–48%), respectively. Subgroup analysis demonstrated a higher rate of undetermined ICH among studies that did not use an etiology-oriented classification (22% [95% CI, 15%–29%]). No difference was observed between studies based on the completion of detailed neuroimaging to assess the rates of undetermined ICH (P=0.62). The etiology of spontaneous ICH remains unknown or cryptogenic among 1 in 7 patients in studies using etiology-oriented classification and among 1 in 4 patients in studies that avoid using etiology-oriented classification. The short-term mortality in undetermined ICH is high despite the relatively small ICH volume.