scholarly journals Monocyte depletion attenuates the development of posttraumatic hydrocephalus and preserves white matter integrity after traumatic brain injury

2018 ◽  
Author(s):  
Hadijat M. Makinde ◽  
Talia B. Just ◽  
Carla M. Cuda ◽  
Nicola Bertolino ◽  
Daniele Procissi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Fractional Anisotropy ◽  
Diffusion Mri ◽  
Lesion Size ◽  
White Matter Integrity ◽  
Regional Patterns ◽  
Software Program ◽  
Ventricle Volume

AbstractMonocytes are amongst the first cells recruited into the brain after traumatic brain injury (TBI). We have shown monocyte depletion 24 hours prior to TBI reduces brain edema, decreases neutrophil infiltration and improves behavioral outcomes. Additionally, both lesion and ventricle size correlate with poor neurologic outcome after TBI. Therefore, we aimed to determine the association between monocyte infiltration, lesion size, and ventricle volume. We hypothesized that monocyte depletion would attenuate lesion size, decrease ventricle enlargement, and preserve white matter in mice after TBI. C57BL/6 mice underwent pan monocyte depletion via intravenous injection of liposome-encapsulated clodronate. Control mice were injected with liposome-encapsulated PBS. TBI was induced via an open-head, controlled cortical impact. Mice were imaged using magnetic resonance imaging (MRI) at 1, 7, and 14 days post-injury to evaluate progression of lesion and to detect morphological changes associated with injury (3D T1- weighted MRI) including regional alterations in white matter patterns (multi-direction diffusion MRI). Lesion size and ventricle volume were measured using semi-automatic segmentation and active contour methods with the software program ITK-SNAP. Data was analyzed with the statistical software program PRISM. No significant effect of monocyte depletion on lesion size was detected using MRI following TBI (p=0.4). However, progressive ventricle enlargement following TBI was observed to be attenuated in the monocyte-depleted cohort (5.3 ± 0.9mm3) as compared to the sham-depleted cohort (13.2 ± 3.1mm3; p=0.02). Global white matter integrity and regional patterns were evaluated and quantified for each mouse after extracting fractional anisotropy maps from the multi-direction diffusion-MRI data using Siemens Syngo DTI analysis package. Fractional anisotropy values were preserved in the monocyte-depleted cohort (123.0 ± 4.4mm3) as compared to sham-depleted mice (94.9 ± 4.6mm3; p=0.025) by 14 days post-TBI. The MRI derived data suggests that monocyte depletion at the time of injury may be a novel therapeutic strategy in the treatment of TBI. Furthermore, non-invasive longitudinal imaging allows for the evaluation of both TBI progression as well as therapeutic response over the course of injury.

scholarly journals Diffuse axonal injury predicts neurodegeneration after moderate–severe traumatic brain injury

Brain ◽  
2020 ◽  
Author(s):  
Neil S N Graham ◽  
Amy Jolly ◽  
Karl Zimmerman ◽  
Niall J Bourke ◽  
Gregory Scott ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Fractional Anisotropy ◽  
Severe Traumatic Brain Injury ◽  
Brain Atrophy ◽  
Diffusion Mri ◽  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Post Traumatic

Abstract Traumatic brain injury is associated with elevated rates of neurodegenerative diseases such as Alzheimer’s disease and chronic traumatic encephalopathy. In experimental models, diffuse axonal injury triggers post-traumatic neurodegeneration, with axonal damage leading to Wallerian degeneration and toxic proteinopathies of amyloid and hyperphosphorylated tau. However, in humans the link between diffuse axonal injury and subsequent neurodegeneration has yet to be established. Here we test the hypothesis that the severity and location of diffuse axonal injury predicts the degree of progressive post-traumatic neurodegeneration. We investigated longitudinal changes in 55 patients in the chronic phase after moderate–severe traumatic brain injury and 19 healthy control subjects. Fractional anisotropy was calculated from diffusion tensor imaging as a measure of diffuse axonal injury. Jacobian determinant atrophy rates were calculated from serial volumetric T1 scans as a measure of measure post-traumatic neurodegeneration. We explored a range of potential predictors of longitudinal post-traumatic neurodegeneration and compared the variance in brain atrophy that they explained. Patients showed widespread evidence of diffuse axonal injury, with reductions of fractional anisotropy at baseline and follow-up in large parts of the white matter. No significant changes in fractional anisotropy over time were observed. In contrast, abnormally high rates of brain atrophy were seen in both the grey and white matter. The location and extent of diffuse axonal injury predicted the degree of brain atrophy: fractional anisotropy predicted progressive atrophy in both whole-brain and voxelwise analyses. The strongest relationships were seen in central white matter tracts, including the body of the corpus callosum, which are most commonly affected by diffuse axonal injury. Diffuse axonal injury predicted substantially more variability in white matter atrophy than other putative clinical or imaging measures, including baseline brain volume, age, clinical measures of injury severity and microbleeds (>50% for fractional anisotropy versus <5% for other measures). Grey matter atrophy was not predicted by diffuse axonal injury at baseline. In summary, diffusion MRI measures of diffuse axonal injury are a strong predictor of post-traumatic neurodegeneration. This supports a causal link between axonal injury and the progressive neurodegeneration that is commonly seen after moderate/severe traumatic brain injury but has been of uncertain aetiology. The assessment of diffuse axonal injury with diffusion MRI is likely to improve prognostic accuracy and help identify those at greatest neurodegenerative risk for inclusion in clinical treatment trials.

Moderate–severe traumatic brain injury causes delayed loss of white matter integrity: Evidence of fornix deterioration in the chronic stage of injury

Brain Injury ◽  
2013 ◽  
Vol 27 (12) ◽  
pp. 1415-1422 ◽  
Author(s):  
Areeba Adnan ◽  
Adrian Crawley ◽  
David Mikulis ◽  
Morris Moscovitch ◽  
Brenda Colella ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Severe Traumatic Brain Injury ◽  
White Matter Integrity ◽  
Chronic Stage ◽  
Injury Causes

Whole brain white matter integrity measures on patients with moderate to severe traumatic brain injury (TBI). FA and entropy analysis

2016 ◽  
Vol 32 ◽  
pp. 250
Author(s):  
Charalambos Yiannakkaras ◽  
Nikos Konstantinou ◽  
Eva Pettemeridou ◽  
Fofi Constantinidou ◽  
Eleni Eracleous ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Severe Traumatic Brain Injury ◽  
White Matter Integrity ◽  
Entropy Analysis ◽  
Whole Brain ◽  
Brain White Matter

Apathetic symptoms and white matter integrity after traumatic brain injury

Brain Injury ◽  
2021 ◽  
pp. 1-11
Author(s):  
Blanca Navarro-Main ◽  
Ana Castaño-León ◽  
Amaya Hilario ◽  
Alfonso Lagares Gómez- Abascal ◽  
Jose Periañez ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
White Matter Integrity

White Matter Integrity Following Traumatic Brain Injury: The Association with Severity of Injury and Cognitive Functioning

2013 ◽  
Vol 26 (4) ◽  
pp. 648-660 ◽  
Author(s):  
Gershon Spitz ◽  
Jerome J. Maller ◽  
Richard O’Sullivan ◽  
Jennie L. Ponsford
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Cognitive Functioning ◽  
White Matter Integrity ◽  
Severity Of Injury

An investigation of white matter integrity and attention deficits following traumatic brain injury

Brain Injury ◽  
2018 ◽  
Vol 32 (6) ◽  
pp. 776-783 ◽  
Author(s):  
Jacqueline Anne Owens ◽  
Gershon Spitz ◽  
Jennie Louise Ponsford ◽  
Alicia Rhian Dymowski ◽  
Catherine Willmott
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Attention Deficits ◽  
White Matter Integrity

scholarly journals Frontostriatal White Matter Integrity Relations with “Cool” and “Hot” Self-Regulation after Pediatric Traumatic Brain Injury

2021 ◽  
Vol 38 (1) ◽  
pp. 122-132
Author(s):  
Jesse T. Fischer ◽  
Paul T. Cirino ◽  
Dana DeMaster ◽  
Candice Alfano ◽  
Johanna Bick ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Self Regulation ◽  
White Matter Integrity ◽  
Pediatric Traumatic Brain Injury

scholarly journals Diffuse disconnectivity in traumatic brain injury: a resting state fMRI and DTI study

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Cheuk Tang ◽  
Emily Eaves ◽  
Kristen Dams-O’Connor ◽  
Lap Ho ◽  
Eric Leung ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Default Mode Network ◽  
Resting State ◽  
Axonal Injury ◽  
White Matter Integrity ◽  
White Matter Tracts ◽  
Imaging Protocol ◽  
Default Mode

AbstractDiffuse axonal injury is a common pathological consequence of Traumatic Brain Injury (TBI). Diffusion Tensor Imaging is an ideal technique to study white matter integrity using the Fractional Anisotropy (FA) index which is a measure of axonal integrity and coherence. There have been several reports showing reduced FA in individuals with TBI, which suggest demyelination or reduced fiber density in white matter tracts secondary to injury. Individuals with TBI are usually diagnosed with cognitive deficits such as reduced attention span, memory and executive function. In this study we sought to investigate correlations between brain functional networks, white matter integrity, and TBI severity in individuals with TBI ranging from mild to severe. A resting state functional magnetic resonance imaging protocol was used to study the default mode network in subjects at rest. FA values were decreased throughout all white matter tracts in the mild to severe TBI subjects. FA values were also negatively correlated with TBI injury severity ratings. The default mode network showed several brain regions in which connectivity measures were higher among individuals with TBI relative to control subjects. These findings suggest that, subsequent to TBI, the brain may undergo adaptation responses at the cellular level to compensate for functional impairment due to axonal injury.

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