Bérengère Aubert-Broche1, Katrin Weier2, Giulia Longoni2, Vladimir S Fonov2, Amit Bar-Or2, Ruth Ann Marrie2, E Ann Yeh2, Sridar Narayanan2, Douglas L Arnold2, Leonard H Verhey2, Brenda Banwell2, D Louis Collins2. 1. From the McConnell Brain Imaging Center (B.A.-B., K.W., V.S.F., S.N., D.L.A., D.L.C.) and Department of Neurology and Neurosurgery and Experimental Therapeutics Program (A.B.-O.), Montreal Neurological Institute, McGill University; The Hospital for Sick Children (G.L., E.A.Y., L.H.V.), University of Toronto; Departments of Internal Medicine and Community Health Sciences (R.A.M.), University of Manitoba, Winnipeg, Canada; and Children's Hospital of Philadelphia (B.B.), Perelman School of Medicine, University of Pennsylvania. broche@bic.mni.mcgill.ca. 2. From the McConnell Brain Imaging Center (B.A.-B., K.W., V.S.F., S.N., D.L.A., D.L.C.) and Department of Neurology and Neurosurgery and Experimental Therapeutics Program (A.B.-O.), Montreal Neurological Institute, McGill University; The Hospital for Sick Children (G.L., E.A.Y., L.H.V.), University of Toronto; Departments of Internal Medicine and Community Health Sciences (R.A.M.), University of Manitoba, Winnipeg, Canada; and Children's Hospital of Philadelphia (B.B.), Perelman School of Medicine, University of Pennsylvania.
Abstract
OBJECTIVE: To investigate how monophasic acquired demyelinating syndromes (ADS) affect age-expected brain growth over time. METHODS: We analyzed 83 pediatric patients imaged serially from initial demyelinating attack: 18 with acute disseminated encephalomyelitis (ADEM) and 65 with other monophasic ADS presentations (monoADS). We further subdivided the monoADS group by the presence (n = 33; monoADSlesion) or absence (n = 32; monoADSnolesion) of T2 lesions involving the brain at onset. We used normative data to compare brain volumes and calculate age- and sex-specific z scores, and used mixed-effect models to investigate their relationship with time from demyelinating illness. RESULTS: Children with monophasic demyelination (ADEM, non-ADEM with brain lesions, and those without brain involvement) demonstrated reduced age-expected brain growth on serial images, driven by reduced age-expected white matter growth. Cortical gray matter volumes were not reduced at onset but demonstrated reduced age-expected growth afterwards in all groups. Brain volumes differed from age- and sex-expected values to the greatest extent in children with ADEM. All patient groups failed to recover age-expected brain growth trajectories. CONCLUSIONS: Brain volume, and more importantly age-expected brain growth, is negatively affected by acquired demyelination, even in the absence of chronicity, implicating factors other than active inflammation as operative in this process.
OBJECTIVE: To investigate how monophasic acquired demyelinating syndromes (ADS) affect age-expected brain growth over time. METHODS: We analyzed 83 pediatric patients imaged serially from initial demyelinating attack: 18 with acute disseminated encephalomyelitis (ADEM) and 65 with other monophasic ADS presentations (monoADS). We further subdivided the monoADS group by the presence (n = 33; monoADSlesion) or absence (n = 32; monoADSnolesion) of T2 lesions involving the brain at onset. We used normative data to compare brain volumes and calculate age- and sex-specific z scores, and used mixed-effect models to investigate their relationship with time from demyelinating illness. RESULTS:Children with monophasic demyelination (ADEM, non-ADEM with brain lesions, and those without brain involvement) demonstrated reduced age-expected brain growth on serial images, driven by reduced age-expected white matter growth. Cortical gray matter volumes were not reduced at onset but demonstrated reduced age-expected growth afterwards in all groups. Brain volumes differed from age- and sex-expected values to the greatest extent in children with ADEM. All patient groups failed to recover age-expected brain growth trajectories. CONCLUSIONS: Brain volume, and more importantly age-expected brain growth, is negatively affected by acquired demyelination, even in the absence of chronicity, implicating factors other than active inflammation as operative in this process.
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