Abstract TP406: Ipsilesional Myelination is Impaired in Children With Perinatal Arterial Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Sabrina Yu ◽  
Helen Carlson ◽  
Adam Kirton
Keyword(s):  
Brain Injury ◽  
Neurological Disorders ◽  
Repeated Measures ◽  
Population Based ◽  
T Test ◽  
Biological Processes ◽  
Typically Developing ◽  
Inclusion Criteria ◽  
Perinatal Brain Injury ◽  
Perinatal Stroke

Introduction: Stroke is a leading cause of perinatal brain injury and cerebral palsy. Current therapeutic efforts focus on optimizing developmental curves but the biological processes dictating these outcomes are poorly understood. Alterations in myelination are recognized as a major determinant of outcome in preterm brain injury but are unexplored in perinatal stroke (PS). Hypothesis: Ipsilesional delays in myelination occur in children with PS and are associated with poor developmental outcome. Methods: Participants were identified through the Alberta Perinatal Stroke Project, a population-based research cohort. Inclusion criteria were: 1) MRI-confirmed, unilateral arterial PS, 2) T1-weighted MRI >6mo, 3) absence of other neurological disorders, 4) neurological outcome (Pediatric Stroke Outcome Measure, PSOM), and 5) motor assessments (Assisting Hand Assessment, AHA; Melbourne Assessment). FreeSurfer software measured hemispheric asymmetry in myelination intensity. A second method using ImageJ validated the detection of myelination asymmetry. Overall PSOM scores were classified as poor (>1) or not. Repeated measures ANOVA compared perilesional, ipsilesional remote, and contralesional homologous regions. Myelination ratios for stroke cases were compared to typically developing controls (t-test), PSOM scores (t-test), and motor assessments (Pearson’s correlation). Results: Nineteen arterial stroke cases (mean age: 13.73±4.0yo) and 27 controls (mean age: 12.52±3.7yo) were studied. Stroke cases showed a greater degree of asymmetry with lower myelination in the lesioned hemisphere, compared to controls (p<0.001). Myelination in perilesional regions was decreased compared to ipsilesional remote (p<0.001) and contralesional homologous areas (p<0.001). Ipsilesional remote regions were decreased compared to homologous regions on the contralesional hemisphere (p=0.009). Contralesional myelination was also less than controls (p<0.001). Myelination ratios were not associated with PSOM, AHA, or Melbourne scores (p=0.144, 0.218, 0.366 respectively). Conclusion: Myelination of uninjured brain in the lesioned hemisphere is altered in children with PS. Further study is required to determine clinical significance.

Perilesional Gliosis Is Associated with Outcome after Perinatal Stroke

2021 ◽  
Author(s):  
Sabrina Yu ◽  
Charissa Lam ◽  
Siddharth Shinde ◽  
Andrea M. Kuczynski ◽  
Helen L. Carlson ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Motor Function ◽  
Developmental Plasticity ◽  
Infarct Volume ◽  
Population Based ◽  
Arterial Ischemic Stroke ◽  
Cross Sectional ◽  
Perinatal Stroke ◽  
Focal Brain Injury

AbstractPerinatal ischemic stroke results in focal brain injury and life-long disability. Hemiplegic cerebral palsy and additional sequelae are common. With no prevention strategies, improving outcomes depends on understanding brain development. Reactive astrogliosis is a hallmark of brain injury that has been associated with outcomes but is unstudied in perinatal stroke. We hypothesized that gliosis was quantifiable and its extent would inversely correlate with clinical motor function. This is a population-based, retrospective, and cross-sectional study. Children with perinatal arterial ischemic stroke (AIS) or periventricular venous infarction (PVI) with magnetic resonance (MR) imaging were included. An image thresholding technique based on image intensity was utilized to quantify the degree of chronic gliosis on T2-weighted sequences. Gliosis scores were corrected for infarct volume and compared with the Assisting Hand and Melbourne Assessments (AHA and MA), neuropsychological profiles, and robotic measures. In total, 42 children were included: 25 with AIS and 17 with PVI (median = 14.0 years, range: 6.3–19 years, 63% males). Gliosis was quantifiable in all scans and scores were highly reliable. Gliosis scores as percentage of brain volume ranged from 0.3 to 3.2% and were comparable between stroke types. Higher gliosis scores were associated with better motor function for all three outcomes in the AIS group, but no association was observed for PVI. Gliosis can be objectively quantified in children with perinatal stroke. Associations with motor outcome in arterial but not venous strokes suggest differing glial responses may play a role in tissue remodeling and developmental plasticity following early focal brain injury.

Congenital Anomalies in Children With Cerebral Palsy: A Systematic Review

2019 ◽  
Vol 34 (12) ◽  
pp. 720-727 ◽  
Author(s):  
Shona Goldsmith ◽  
Sarah McIntyre ◽  
Michele Hansen ◽  
Nadia Badawi
Keyword(s):  
Systematic Review ◽  
Cerebral Palsy ◽  
Brain Injury ◽  
Congenital Anomalies ◽  
Circulatory System ◽  
Population Based ◽  
Included Study ◽  
Quality Data ◽  
Study Cohort ◽  
Perinatal Brain Injury

Congenital anomalies are a strong risk factor for cerebral palsy, particularly for children born at term. This systematic review aimed to address gaps in our understanding of the association between congenital anomalies and cerebral palsy. Eight population-based studies (n = 10 081) were identified. Congenital anomalies were reported in 12% to 32% of children with pre/perinatal brain injury and 20% of children with postneonatal brain injury. Variation between studies included study cohort inclusion criteria and the definitions and classification of included anomalies. The most common cerebral anomalies were microcephaly and hydrocephaly, whereas circulatory system anomalies were the most common noncerebral anomalies. The proportion of congenital anomalies was higher in children born at term than preterm. Synthesizing the highest quality data published, this review identified that congenital anomalies are common in cerebral palsy. New collaborative research, addressing sources of variation, is vital to identify pathways to cerebral palsy that include specific congenital anomalies, and explore opportunities for prevention.

Divergence in the epidemiological estimates of traumatic brain injury in the United States: comparison of two national databases

2020 ◽  
pp. 1-10
Author(s):  
Brittany M. Stopa ◽  
Maya Harary ◽  
Ray Jhun ◽  
Arun Job ◽  
Saef Izzy ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Emergency Department ◽  
Brain Injury ◽  
Data Bank ◽  
The United States ◽  
National Sample ◽  
Population Based ◽  
Weighted Estimates ◽  
True Incidence ◽  
Ed Visits

OBJECTIVETraumatic brain injury (TBI) is a leading cause of morbidity and mortality in the US, but the true incidence of TBI is unknown.METHODSThe National Trauma Data Bank National Sample Program (NTDB NSP) was queried for 2007 and 2013, and population-based weighted estimates of TBI-related emergency department (ED) visits, hospitalizations, and deaths were calculated. These data were compared to the 2017 Centers for Disease Control and Prevention (CDC) report on TBI, which used the Healthcare Cost and Utilization Project’s National (“Nationwide” before 2012) Inpatient Sample and National Emergency Department Sample.RESULTSIn the NTDB NSP the incidence of TBI-related ED visits was 59/100,000 in 2007 and 62/100,000 in 2013. However, in the CDC report there were 534/100,000 in 2007 and 787/100,000 in 2013. The CDC estimate for ED visits was 805% higher in 2007 and 1169% higher in 2013. In the NTDB NSP, the incidence of TBI-related deaths was 5/100,000 in 2007 and 4/100,000 in 2013. In the CDC report, the incidence was 18/100,000 in both years. The CDC estimate for deaths was 260% higher in 2007 and 325% higher in 2013.CONCLUSIONSThe databases disagreed widely in their weighted estimates of TBI incidence: CDC estimates were consistently higher than NTDB NSP estimates, by an average of 448%. Although such a discrepancy may be intuitive, this is the first study to quantify the magnitude of disagreement between these databases. Given that research, funding, and policy decisions are made based on these estimates, there is a need for a more accurate estimate of the true national incidence of TBI.

Outcome at Age Five Years or Older for Children with Perinatal Brain Injury Treated with Neurohabilitation or Neurodevelopmental Therapy

2019 ◽  
Author(s):  
Nicol&aacute;s Gar&oacute;falo-G&oacute;mez ◽  
Jes&uacute;s Barrera-Res&eacute;ndiz ◽  
Mar&iacute;a Elena Ju&aacute;rez-Col&iacute;n ◽  
Mar&iacute;a del Consuelo Pedraza-Aguilar ◽  
Cristina Carrillo-Prado ◽  
...  
Keyword(s):  
Brain Injury ◽  
Perinatal Brain Injury

scholarly journals Psychotropic and pain medication use in individuals with traumatic brain injury—a Swedish total population cohort study of 240 000 persons

2021 ◽  
Vol 92 (5) ◽  
pp. 519-527
Author(s):  
Yasmina Molero ◽  
David James Sharp ◽  
Brian Matthew D'Onofrio ◽  
Henrik Larsson ◽  
Seena Fazel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Total Population ◽  
Medication Use ◽  
Population Based ◽  
Pain Medication ◽  
Short Term ◽  
Pain Medications ◽  
Before And After

ObjectiveTo examine psychotropic and pain medication use in a population-based cohort of individuals with traumatic brain injury (TBI), and compare them with controls from similar backgrounds.MethodsWe assessed Swedish nationwide registers to include all individuals diagnosed with incident TBI between 2006 and 2012 in hospitals or specialist outpatient care. Full siblings never diagnosed with TBI acted as controls. We examined dispensed prescriptions for psychotropic and pain medications for the 12 months before and after the TBI.ResultsWe identified 239 425 individuals with incident TBI, and 199 658 unaffected sibling controls. In the TBI cohort, 36.6% had collected at least one prescription for a psychotropic or pain medication in the 12 months before the TBI. In the 12 months after, medication use increased to 45.0%, an absolute rate increase of 8.4% (p<0.001). The largest post-TBI increases were found for opioids (from 16.3% to 21.6%, p<0.001), and non-opioid pain medications (from 20.3% to 26.6%, p<0.001). The majority of prescriptions were short-term; 20.6% of those prescribed opioids and 37.3% of those with benzodiazepines collected prescriptions for more than 6 months. Increased odds of any psychotropic or pain medication were associated with individuals before (OR: 1.62, 95% CI: 1.59 to 1.65), and after the TBI (OR: 2.30, 95% CI: 2.26 to 2.34) as compared with sibling controls, and ORs were consistently increased for all medication classes.ConclusionHigh rates of psychotropic and pain medications after a TBI suggest that medical follow-up should be routine and review medication use.

Repeated measures of FIB-4 improve prediction of severe liver disease: population-based cohort study of 40,729 individuals

2020 ◽  
Vol 73 ◽  
pp. S70-S71
Author(s):  
Hannes Hagström ◽  
Mats Talbäck ◽  
Anna Andreasson ◽  
Göran Walldius ◽  
Niklas Hammar
Keyword(s):  
Cohort Study ◽  
Liver Disease ◽  
Repeated Measures ◽  
Population Based ◽  
Severe Liver ◽  
Severe Liver Disease

scholarly journals Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

2010 ◽  
Vol 31 (1) ◽  
pp. 17-35 ◽  
Author(s):  
Martin Lauritzen ◽  
Jens Peter Dreier ◽  
Martin Fabricius ◽  
Jed A Hartings ◽  
Rudolf Graf ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Disorders ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Ion Homeostasis ◽  
Large Body ◽  
Treatment Strategies ◽  
Pathophysiological Mechanism

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

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