4 results match your criteria: "University of Pennsylvania. banwellb@email.chop.edu.[Affiliation]"

Dramatic Response to Anti-IL-6 Receptor Therapy in Children With Life-Threatening Myelin Oligodendrocyte Glycoprotein-Associated Disease.

Neurol Neuroimmunol Neuroinflamm

November 2023

From the Division of Neurology (L.A.M., C.G., M.R.S., B.B.), Department of Pediatrics, Children's Hospital of Philadelphia; Department of Neurology, Perelman School of Medicine, University of Pennsylvania; Department of Pathology (A.V.), Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania; Division of Critical Care Medicine (N.A.F., E.I.L., J.H., M.F.K.), Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania; and Division of Neurosurgery (A.M.T., P.J.M., J.D.A.), Children's Hospital of Philadelphia; Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania.

Objectives: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an immune-mediated neuroinflammatory disorder leading to demyelination of the CNS. Interleukin (IL)-6 receptor blockade is under study in relapsing MOGAD as a preventative strategy, but little is known about the role of such treatment for acute MOGAD attacks.

Methods: We discuss the cases of a 7-year-old boy and a 15-year-old adolescent boy with severe acute CNS demyelination and malignant cerebral edema with early brain herniation associated with clearly positive serum titers of MOG-IgG, whose symptoms were incompletely responsive to standard acute therapies (high-dose steroids, IV immunoglobulins (IVIGs), and therapeutic plasma exchange).

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Deviation From Normative Whole Brain and Deep Gray Matter Growth in Children With MOGAD, MS, and Monophasic Seronegative Demyelination.

Neurology

July 2023

From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania.

Article Synopsis
  • The study investigates how pediatric MOG antibody-associated disease (MOGAD) affects brain growth in children compared to healthy peers and those with MS or monophasic demyelination, highlighting the possible impact on brain maturation.* -
  • Researchers included children diagnosed with MOGAD, MS, or monophasic demyelination from a longitudinal study and used brain MRI scans to analyze regional brain volumes against normative data from healthy children.* -
  • Findings revealed that children with MOGAD show significant delays in expected brain growth, particularly in areas like the thalamus and caudate, indicating a deviation from typical brain development patterns.*
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Onset of multiple sclerosis before adulthood leads to failure of age-expected brain growth.

Neurology

December 2014

From the McConnell Brain Imaging Center (B.A.-B., V.F., S.N., D.L.A., D.A., D.F., D.L.C.), Montreal Neurological Institute, McGill University; The Hospital for Sick Children (C.T., J.G.S., B.B.), University of Toronto; York University (C.T.), Toronto, Canada; and Children's Hospital of Philadelphia (B.B.), University of Pennsylvania.

Objective: To determine the impact of pediatric-onset multiple sclerosis (MS) on age-expected brain growth.

Methods: Whole brain and regional volumes of 36 patients with relapsing-remitting MS onset prior to 18 years of age were segmented in 185 longitudinal MRI scans (2-11 scans per participant, 3-month to 2-year scan intervals). MRI scans of 25 age- and sex-matched healthy normal controls (NC) were also acquired at baseline and 2 years later on the same scanner as the MS group.

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