Deep White Matter Volume Loss and Social Reintegration After Traumatic Brain Injury in Children

Aims/Objectives/BackgroundMild traumatic brain injury (mTBI) accounts for one million emergency department attendances in the UK every year. Whilst 30–50% of patients suffer from persistent symptoms, unselected follow up would overwhelm the health care system. Magnetic resonance imaging (MRI), may help to stratify patients for clinical follow up and interventional trials. We therefore aimed to identify:Neuroanatomical features of concussion on MRI andthe optimal timing for magnetic resonance imaging (<72h or 2–3 weeks after injury).This is the largest study to date using serial scanning acutely in patients with mTBI.Methods/DesignData originated from two prospective cohorts: the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study (2014–2017) and a local cohort (2012–2013). Eligible patients presented to hospital within 24h of a mTBI (Glasgow Coma Score 13–15), satisfied local criteria for computed tomography scanning and received two MRIs: one within 72h (MR1) and one 2–3 weeks after injury (MR2). In addition, 104 controls were enrolled. Volumes and diffusion parameters for brain regions of interest were extracted via automated pipelines. Symptoms were measured using the Rivermead Post-Concussion Questionnaire acutely and the extended Glasgow Outcome Score at three months.Results/ConclusionsThe study included 81 patients (73 from CENTER-TBI, 8 local) with a median age of 44 years (range 14–85) and 57 (70%) men. Within patients, cerebral white matter volume decreased (MR1/MR2 0.98, p=0.001) and ventricular volume increased (MR1/MR2 1.06, p<0.001). Compared to controls, white matter volume was normal on MR1 (patient/control 1.00, p=0.277) but reduced on MR2 (patient/control 0.97, p<0.001). Diffusion changes followed one of three trajectories: progressive injury, minimal change, or pseudonormalisation. Concussion symptoms worsened, improved and were variable in the three groups respectively (delta [IQR] + 5.00 [+2.00-+5.00], -4.5 [-9.25-+1.75], 0.00 [-6.25 to +9.00], p=0.018). MR1 predicted three-month outcome better than MR2 (AUC [95% CI]: 0.93 [0.83–1.00] vs 0.72 [0.51–0.92]).

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Longitudinal Volumetric Changes following Traumatic Brain Injury: A Tensor-Based Morphometry Study

Journal of the International Neuropsychological Society ◽

10.1017/s1355617712000835 ◽

2012 ◽

Vol 18 (6) ◽

pp. 1006-1018 ◽

Cited By ~ 55

Author(s):

Kimberly D.M. Farbota ◽

Aparna Sodhi ◽

Barbara B. Bendlin ◽

Donald G. McLaren ◽

Guofan Xu ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

White Matter ◽

Degenerative Change ◽

Extended Period ◽

Spatiotemporal Pattern ◽

Volume Loss ◽

Post Injury ◽

Cognitive Changes ◽

Brain White Matter

AbstractAfter traumatic injury, the brain undergoes a prolonged period of degenerative change that is paradoxically accompanied by cognitive recovery. The spatiotemporal pattern of atrophy and the specific relationships of atrophy to cognitive changes are ill understood. The present study used tensor-based morphometry and neuropsychological testing to examine brain volume loss in 17 traumatic brain injury (TBI) patients and 13 controls over a 4-year period. Patients were scanned at 2 months, 1 year, and 4 years post-injury. High-dimensional warping procedures were used to create change maps of each subject's brain for each of the two intervals. TBI patients experienced volume loss in both cortical areas and white matter regions during the first interval. We also observed continuing volume loss in extensive regions of white matter during the second interval. Neuropsychological correlations indicated that cognitive tasks were associated with subsequent volume loss in task-relevant regions. The extensive volume loss in brain white matter observed well beyond the first year post-injury suggests that the injured brain remains malleable for an extended period, and the neuropsychological relationships suggest that this volume loss may be associated with subtle cognitive improvements. (JINS, 2012,18, 1–13)

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Endothelial progenitor cells are depleted in older adults with cognitive impairment and white matter volume loss

Alzheimer s & Dementia ◽

10.1002/alz.046352 ◽

2020 ◽

Vol 16 (S3) ◽

Author(s):

Anisa J. Marshall ◽

Aimee Gaubert ◽

Belinda Yew ◽

Jean K. Ho ◽

Jung Yun Jang ◽

...

Keyword(s):

Older Adults ◽

Cognitive Impairment ◽

White Matter ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Volume Loss ◽

White Matter Volume ◽

Endothelial Progenitor ◽

Matter Volume

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Gray matter and white matter volume loss in anorexia nervosa

Biological Psychiatry ◽

10.1016/0006-3223(96)84293-4 ◽

1996 ◽

Vol 39 (7) ◽

pp. 603

Author(s):

R.B. Zipursky ◽

E.K. Lambe ◽

D. Goldbloom ◽

J. Ridgley ◽

D.J. Mikulis ◽

...

Keyword(s):

Anorexia Nervosa ◽

White Matter ◽

Gray Matter ◽

Volume Loss ◽

White Matter Volume ◽

Matter Volume

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Causal effect of atrial fibrillation on brain white or grey matter volume: A Mendelian randomization study

10.1101/2020.12.17.20248314 ◽

2020 ◽

Author(s):

Sehoon Park ◽

Soojin Lee ◽

Yaerim Kim ◽

Semin Cho ◽

Kwangsoo Kim ◽

...

Keyword(s):

Atrial Fibrillation ◽

White Matter ◽

Grey Matter ◽

Mendelian Randomization ◽

Brain Volume ◽

Causal Effect ◽

Grey Matter Volume ◽

Volume Loss ◽

White Matter Volume ◽

Matter Volume

AbstractBackgroundAtrial fibrillation (AF) and brain volume loss are prevalent in older individuals. Further study investigating the causal effect of AF on brain volume is warranted.MethodsThis study was a Mendelian randomization (MR) analysis. The genetic instrument for AF was constructed from a previous genome-wide association study (GWAS) meta-analysis and included 537,409 individuals of European ancestry. The outcome summary statistics for quantile-normalized white or grey matter volume measured by magnetic resonance imaging were provided by the previous GWAS of 8426 white British UK Biobank participants. The main MR method was the inverse variance weighted method, supported by sensitivity MR analysis including MR-Egger regression and the weighted median method. The causal estimates from AF to white or grey matter volume were further adjusted for effects of any stroke or ischemic stroke by multivariable MR analysis.ResultsA higher genetic predisposition for AF (one standard deviation increase) was significantly associated with lower white matter volume [beta −0.128 (−0.208, −0.048)] but not grey matter volume [beta −0.041 (−0.101, 0.018)], supported by all utilized sensitivity MR analyses. The multivariable MR analysis indicated that AF is causally linked to lower white matter volume independent of the stroke effect.ConclusionsAF is a causative factor for white matter volume loss. The effect of AF on grey matter volume was inapparent in this study. A future trial is necessary to confirm whether appropriate AF management can be helpful in preventing cerebral white matter volume loss or related brain disorders in AF patients.

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The Neuropathology of MIRAGE Syndrome

Journal of Neuropathology & Experimental Neurology ◽

10.1093/jnen/nlaa009 ◽

2020 ◽

Vol 79 (4) ◽

pp. 458-462 ◽

Cited By ~ 2

Author(s):

Angela N Viaene ◽

Brian N Harding

Keyword(s):

White Matter ◽

Granule Neurons ◽

Cerebellar Hypoplasia ◽

Volume Loss ◽

White Matter Volume ◽

Multisystem Disorder ◽

Sterile Alpha Motif Domain ◽

Common Features ◽

Matter Volume ◽

Adrenal Hypoplasia

Abstract MIRAGE syndrome is a multisystem disorder characterized by myelodysplasia, infections, restriction of growth, adrenal hypoplasia, genital phenotypes, and enteropathy. Mutations in the sterile alpha motif domain containing 9 (SAMD9) gene which encodes a protein involved in growth factor signal transduction are thought to cause MIRAGE syndrome. SAMD9 mutations lead to an antiproliferative effect resulting in a multisystem growth restriction disorder. Though rare, a few patients with SAMD9 mutations were reported to have hydrocephalus and/or cerebellar hypoplasia on imaging. The neuropathologic features of MIRAGE syndrome have not been previously described. Here, we describe the postmortem neuropathologic examinations of 2 patients with a clinical diagnosis of MIRAGE syndrome and confirmed SAMD9 mutations. Common features included microcephaly, hydrocephalus, white matter abnormalities, and perivascular calcifications. One of the 2 cases showed marked cerebellar hypoplasia with loss of Purkinje and granule neurons as well as multifocal polymicrogyria and severe white matter volume loss; similar findings were not observed in the second patient. These cases demonstrate the variation in neuropathologic findings in patients with MIRAGE syndrome. Interestingly, the findings are similar to those reported in ataxia-pancytopenia syndrome caused by mutations in SAMD9L, a paralogue of SAMD9.

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Spinal Cord Atrophy in Multiple Sclerosis Caused by White Matter Volume Loss

Archives of Neurology ◽

10.1001/archneur.62.12.1859 ◽

2005 ◽

Vol 62 (12) ◽

pp. 1859 ◽

Cited By ~ 37

Author(s):

Christopher P. Gilmore ◽

Gabriele C. DeLuca ◽

Lars Bö ◽

Trudy Owens ◽

James Lowe ◽

...

Keyword(s):

Multiple Sclerosis ◽

Spinal Cord ◽

White Matter ◽

Volume Loss ◽

White Matter Volume ◽

Spinal Cord Atrophy ◽

Matter Volume

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Brain volume reductions in medication-naive patients with schizophrenia in relation to intelligence quotient

Psychological Medicine ◽

10.1017/s0033291712000098 ◽

2012 ◽

Vol 42 (9) ◽

pp. 1847-1856 ◽

Cited By ~ 20

Author(s):

M. Rais ◽

W. Cahn ◽

H. G. Schnack ◽

H. E. Hulshoff Pol ◽

R. S. Kahn ◽

...

Keyword(s):

White Matter ◽

Healthy Subjects ◽

Intelligence Quotient ◽

Brain Volume ◽

First Episode ◽

Volume Loss ◽

White Matter Volume ◽

Matter Volume ◽

Brain Volume Loss ◽

First Episode Schizophrenia

BackgroundGlobal brain abnormalities such as brain volume loss and grey- and white-matter deficits are consistently reported in first-episode schizophrenia patients and may already be detectable in the very early stages of the illness. Whether these changes are dependent on medication use or related to intelligence quotient (IQ) is still debated.MethodMagnetic resonance imaging scans were obtained for 20 medication-naive patients with first-episode schizophrenia and 26 matched healthy subjects. Volume measures of total brain grey and white matter, third and lateral ventricles and cortical thickness/surface were obtained. Differences between the groups were investigated, taking into account the effect of intelligence.ResultsMedication-naive patients showed statistically significant reductions in whole-brain volume and cerebral grey- and white-matter volume together with lateral ventricle enlargement compared to healthy subjects. IQ was significantly lower in patients compared to controls and was positively associated with brain and white-matter volume in the whole group. No significant differences in cortical thickness were found between the groups but medication-naive patients had a significantly smaller surface in the left superior temporal pole, Heschl's gyrus and insula compared to controls.ConclusionsOur findings suggest that brain volume loss is present at illness onset, and can be explained by the reduced surface of the temporal and insular cortex. These abnormalities are not related to medication, but IQ.

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