scholarly journals Diffuse Axonal Injury Grade on Early MRI is Associated with Worse Outcome in Children with Moderate-Severe Traumatic Brain Injury

Author(s):  
Anna M. Janas ◽  
FeiFei Qin ◽  
Scott Hamilton ◽  
Bin Jiang ◽  
Nicole Baier ◽  
...  
Author(s):  
Arief S. Hariyanto ◽  
Endang Retnowati ◽  
Agus Turchan

Glial Fibrillary Acidic Protein (GFAP) sangat khas untuk otak (highly brain specific protein), sebagai petunjuk kerusakan sel,merupakan protein yang berhubungan dengan peningkatan tekanan intrakranial dan sebagai petanda perjalanan penyakit di pasiencedera otak. Penelitian ini menganalisis profil kadar GFAP serum pasien cedera otak berat sebagai petanda perjalanan penyakit dankeluarannya. Desain penelitian deskriptif observasional. Kadar GFAP serum dari sampel darah vena, diperiksa dengan metode ELISApada hari pertama datang ke Instalasi Gawat Darurat dan hari ke-2,3,4 perawatan. Jumlah sampel 25 orang, laki-laki 20 orang (80%),perempuan 5 orang (20%). Umur terbanyak ≤ 25 tahun, 8 orang (32%), rerata umur 35,92 ± 13,80 tahun. Jejas berdasarkan hasilCT Scan kepala terbanyak Diffuse Axonal Injury (DAI) 7 (28%), tindakan operasi sebanyak 18 (72 %), non-operasi 7 (28%), penyebabcedera, kecelakaan lalu lintas 23 (92%), jatuh 2 (8%). Rerata kadar GFAP serum hari ke-1,2,3,4 berturut-turut 2,72±1,44 ng/mL,1,85±0,85 ng/mL, 1,67±1,26 ng/mL, 0,79±0,35 ng/mL. Keluaran pasien, hidup 19 (76%), meninggal 6 (24%). GFAP sangat khaspada otak berguna sebagai petanda di pasien cedera otak berat, yaitu peningkatan kadarnya dapat digunakan sebagai faktor perjalananpenyakit untuk kematian dan keluarannya. Peningkatan kadar GFAP serum dapat digunakan sebagai faktor perjalanan penyakit.Penelitian lanjutan diperlukan dengan sampel yang lebih besar


Brain ◽  
2020 ◽  
Author(s):  
Neil S N Graham ◽  
Amy Jolly ◽  
Karl Zimmerman ◽  
Niall J Bourke ◽  
Gregory Scott ◽  
...  

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.


2017 ◽  
Vol 24 (3) ◽  
pp. 237-246 ◽  
Author(s):  
Amanda R. Rabinowitz ◽  
Tessa Hart ◽  
John Whyte ◽  
Junghoon Kim

AbstractObjectives: The goal of the present study was to elucidate the influence of demographic and neuropathological moderators on the longitudinal trajectory neuropsychological functions during the first year after moderate to severe traumatic brain injury (TBI). In addition to examining demographic moderators such as age and education, we included a measure of whole-brain diffuse axonal injury (DAI), and examined measures of processing speed (PS), executive function (EF), and verbal learning (VL) separately. Methods: Forty-six adults with moderate to severe TBI were examined at 3, 6, and 12 months post-injury. Participants underwent neuropsychological evaluation and neuroimaging including diffusion tensor imaging. Using linear mixed effects modeling, we examined longitudinal trajectories and moderating factors of cognitive outcomes separately for three domains: PS, VL, and EF. Results: VL and EF showed linear improvements, whereas PS exhibited a curvilinear trend characterized by initial improvements that plateaued or declined, depending on age. Age moderated the recovery trajectories of EF and PS. Education and DAI did not influence trajectory but were related to initial level of functioning for PS and EF in the case of DAI, and all three cognitive domains in the case of education. Conclusions: We found disparate recovery trajectories across cognitive domains. Younger age was associated with more favorable recovery of EF and PS. These findings have both clinical and theoretical implications. Future research with a larger sample followed over a longer time period is needed to further elucidate the factors that may influence cognitive change over the acute to chronic period after TBI. (JINS, 2018, 24, 237–246)


2013 ◽  
Vol 18 (2) ◽  
pp. 56-61 ◽  
Author(s):  
Syed Tajuddin Syed Hassan ◽  
Husna Jamaludin ◽  
Rosna Abd Raman ◽  
Haliza Mohd Riji ◽  
Khaw Wan Fei

2011 ◽  
Vol 153 (8) ◽  
pp. 1687-1694 ◽  
Author(s):  
Hidetoshi Matsukawa ◽  
Masaki Shinoda ◽  
Motoharu Fujii ◽  
Osamu Takahashi ◽  
Daisuke Yamamoto ◽  
...  

2018 ◽  
Vol 89 (10) ◽  
pp. A42.1-A42
Author(s):  
Graham Neil SN ◽  
Jolly Amy E ◽  
Bourke Niall J ◽  
Scott Gregory ◽  
Cole James H ◽  
...  

BackgroundDementia rates are elevated after traumatic brain injury (TBI) and a subgroup develops chronic traumatic encephalopathy. Post-traumatic neurodegeneration can be measured by brain atrophy rates derived from neuroimaging, but it is unclear how atrophy relates to the initial pattern of injury.ObjectivesTo investigate the relationship between baseline TBI patterns and subsequent neurodegeneration measured by progressive brain atrophy.Methods55 patients after moderate-severe TBI (mean 3 years post-injury) and 20 controls underwent longitudinal MRI. Brain atrophy was quantified using the Jacobian determinant defined from volumetric T1 scans approximately one year apart. Diffuse axonal injury was measured using diffusion tensor imaging and focal injuries defined from T1 and FLAIR. Neuropsychological assessment was performed.ResultsAbnormal progressive brain atrophy was seen after TBI (~1.8%/year in white matter). This was accompanied by widespread reductions in fractional anisotropy, in keeping with the presence of diffuse axonal injury. There was a strong negative correlation between FA and brain atrophy, whereby areas of greater white matter damage showed greater atrophy over time.ConclusionsThe results show a strong relationship between the location of diffuse axonal injury and subsequent neurodegeneration. This suggests that TBI triggers progressive neurodegeneration through the long-lasting effects of diffuse axonal injury.


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