Evaluation of Delayed Neuronal and Axonal Damage Secondary to Moderate and Severe Traumatic Brain Injury Using Quantitative MR Imaging Techniques
ABSTRACT Traumatic brain injury (TBI) is a classic model of monophasic neuronal and axonal injury, in which tissue damage mainly occurs at the moment of trauma. There is some evidence of delayed progression of the neuronal and axonal loss. Our purpose was to test the hypothesis that quantitative MR imaging techniques can estimate the biologic changes secondary to delayed neuronal and axonal loss after TBI.
Nine patients (age, 11-28 years; 5 male) who sustained a moderate or severe TBI were evaluated at a mean of 3.1 years after trauma. We applied the following techniques: bicaudate (BCR) and bifrontal (BFR) ventricle-to-brain ratios; T2 relaxometry; magnetization transfer ratio (MTR); apparent diffusion coefficient (ADC); and proton spectroscopy, by using an N-acetylaspartate/creatine (NAA/Cr) ratio measured in normal-appearing white matter (NAWM) and the corpus callosum (CC). The results were compared with those of a control group.
BCR and BFR mean values were significantly increased (P < or = .05) in patients due to secondary subcortical atrophy; increased T2 relaxation time was observed in the NAWM and CC, reflecting an increase in water concentration secondary to axonal loss. Increased ADC mean values and reduced MTR mean values were found in the NAWM and CC, showing damage in the myelinated axonal fibers; and decreased NAA/Cr ratio mean values were found in the CC, indicating axonal loss.
These quantitative MR imaging techniques could noninvasively demonstrate the neuronal and axonal damage in the NAWM and CC of human brains, secondary to moderate or severe TBI.
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ABSTRACT: Our previous study has shown that ageing and hypertension may alter ADC and CBF and increase the ischemic susceptibility in non-ischemic rat brain. The present study wishes to further investigate whether ageing and hypertension may influence cerebral diffusion/perfusion and increase ischemic susceptibility in ischemic brain. Brain MR imaging was examined from 1 day before and 1 and 7 days after bilateral common carotid artery occlusion. Young and middle-aged normotensive Wistar-Kyoto (WKY) rat and young and middle-aged spontaneously hypertensive rat (SHR) were studied. Infarction occurred mainly in the parietal cortex and was larger in middle-aged SHR than the other three groups (P< 0.05). In pre-operation, ADC was higher and CBF was lower in middle-aged/hypertensive rats than young/normotensive rats (P< 0.05). The ADC was higher in the parietal cortex of the rats with infarction at 7 days when compared to the rats without infarction [ROC, P= 0.001; binary logistic regression (BLR), P= 0.006]. However, there was no difference in the hippocampus and thalamus. At day 1 post-operation, CBF reduced and ADC/CBF ratio elevated significantly in the parietal cortex of the rats with infarction when compared to the rats without infarction (CBF: ROC, P= 0.002; BLR, P= 0.017. ADC/CBF ratio: ROC, P= 0.001; BLR, P= 0.018). Our results demonstrated that pre-operation ADC and post-operation CBF and ADC/CBF ratio can be used as good MR markers in the prediction of ischemic susceptibility after cerebral hypoperfusion.Neuroscience 11/2013; 257. DOI:10.1016/j.neuroscience.2013.10.066 · 3.33 Impact Factor
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ABSTRACT: Whether persisting cognitive complaints and postconcussive symptoms (PCS) reported by Iraq and Afghanistan war Veterans with blast- and/or combined blast/impact-related mild traumatic brain injuries (mTBIs) are associated with enduring structural and/or functional brain abnormalities versus comorbid depression or posttraumatic stress disorder (PTSD) remains unclear. We sought to characterize relationships among these variables in a convenience sample of Iraq and Afghanistan-deployed Veterans with (n=34) and without (n=18) a history of one or more combined blast/impact-related mTBIs. Participants underwent magnetic resonance imaging of fractional anisotropy (FA) and macromolecular proton fraction (MPF) to assess brain white matter (WM) integrity; [18F]-fluorodeoxyglucose positron emission tomography imaging of cerebral glucose metabolism (CMRglu); structured clinical assessments of blast exposure, psychiatric diagnoses, and PTSD symptoms; neurologic evaluations; and self-report scales of PCS, combat exposure, depression, sleep quality, and alcohol use. Veterans with vs. without blast/impact-mTBIs exhibited reduced FA in the corpus callosum; reduced MPF values in subgyral, longitudinal, and cortical/subcortical WM tracts and gray matter/white matter border regions (with a possible threshold effect beginning at 20 blast-mTBIs); reduced CMRglu in parietal, somatosensory, and visual cortices; and higher scores on measures of PCS, PTSD, combat exposure, depression, sleep disturbance, and alcohol use. Neuroimaging metrics did not differ between participants with vs. without PTSD. Iraq and Afghanistan Veterans with a history of one or more blast-related mTBIs exhibit abnormalities of brain WM structural integrity and macromolecular organization and CMRglu which are not related to comorbid PTSD. These findings are congruent with recent neuropathologic evidence of chronic brain injury in this cohort of Veterans.Journal of neurotrauma 10/2013; DOI:10.1089/neu.2013.2952 · 3.97 Impact Factor
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ABSTRACT: To determine whether quantitative measure of magnetic resonance imaging data from patients with the inherited leukodystrophy, Pelizaeus-Merzbacher disease (PMD) correlates with clinical severity or progression. In our current work we have analyzed the clinical phenotypes and MRI scans of 51 male patients with PMD and 10 female carriers for whom the PLP1 genotype had been determined. In addition, we developed a 32-point functional disability scoring (FDS) system for PMD, and validated it for inter-rater reliability. Using conventional T1- and T2-weighted MRI images of the whole brain, we measured white matter and total brain volume (WMV and TBV), inter-caudate ratio (ICR), and corpus callosum area. There was a significant positive correlation of FDS with white matter fraction (WMV/TBV) and corpus callosum area. Also, when applying a median split based on FDS, patients with lower FDS showed reduced white matter fraction and corpus callosum area, and increased ICR compared to patients with relatively higher FDS, regardless of age. Although this patient population is heterogeneous, with multiple genetic and molecular mechanisms causing PMD, these data imply that white matter atrophy is a major pathological determinant of the clinical disability in most patients. Development of reliable non-invasive quantitative biomarkers of disease activity would be useful not only for following the natural history of the disease, but also raising the potential for evaluating future therapies.Journal of the neurological sciences 08/2013; 335(1-2). DOI:10.1016/j.jns.2013.08.030 · 2.26 Impact Factor