Shen Y, Kou Z, Kreipke CW, Petrov T, Hu J, Haacke EMIn vivo measurement of tissue damage, oxygen saturation changes and blood flow changes after experimental traumatic brain injury in rats using susceptibility weighted imaging. Magn Reson Imaging 25:219-227
Traumatic brain injury (TBI) is a prevalent disease, and many TBI patients experience disturbed cerebral blood flow (CBF) after injury. Moreover, TBI is difficult to quantify with conventional imaging modalities. In this paper, we utilized susceptibility weighted imaging (SWI) as a means to monitor functional blood oxygenation changes and to quantify CBF changes in animals after trauma. In this study using six rats, brain trauma was induced by a weight drop model and the brain was scanned over four time points: pre trauma, and 4 h, 24 h and 48 h post trauma. Five rats survived and one died after trauma. A blood phase analysis using filtered SWI phase images suggested that three rats recovered after 48 h and two rats deteriorated. SWI also suggested that CBF decreased by up to 26%. The CBF change is in agreement with the results of arterial spin labeling methods conducted in this study and with previously published results. Furthermore, SWI revealed an enlargement of the major venous vasculature in deep brain structures, in accordance with the location of diffuse axonal injury. Compared with the traditional, invasive, clinical monitoring of cerebral vascular damage and reduction in blood flow, this method offers a novel, safe and noninvasive approach to quantify changes in oxygen saturation and CBF and to visualize structural changes in blood vasculature after TBI.
"SWI calculates the oxygen saturation based on the differences in the magnetic sensitivities of oxyhemoglobin and deoxyhemoglobin . The SWI images of venous structures depend on the T2* time, which may be shortened by deoxyhemoglobin-induced non-uniformity of the magnetic field, and phase differences between the surrounding tissue and blood vessels ; therefore, changes in CBF can also cause changes in the SWI signals . The R2* parameter of BOLD may be affected by blood volume, the red blood cell volume ratio, oxygen consumption, and small arteries , as well as by other factors such as subject age . "
[Show abstract][Hide abstract] ABSTRACT: Background
The aim of this study was to investigate susceptibility-weighted imaging (SWI) signal changes in different brain regions in a rabbit model of acute hemorrhagic anemia.
Ten New Zealand white rabbits were used for construction of the model of acute hemorrhagic anemia. Signal intensities of SWI images of the bilateral frontal cortex, frontal white matter, temporal lobe, and thalamic nuclei were measured. In addition, the cerebral gray-white contrast and venous structures of the SWI images were evaluated by an experienced physician.
Repeated bloodletting was associated with significant reductions in red blood cell count, hemoglobin concentration, hematocrit, pH, and PaCO2, and elevations of blood lactate and PaO2. In normal status, the SWI signal intensity was significantly higher in the frontal cortex than in the frontal white matter (63.10±22.82 vs. 52.50±20.29; P<0.05). Repeated bloodletting (5 occasions) caused significant (P<0.05) decreases in the SWI signals of the frontal cortex (from 63.10±22.82 to 37.70±4.32), temporal lobe (from 52.50±20.29 to 42.60±5.54), and thalamus (from 60.40±20.29 to 39.40±3.47), but was without effect in the frontal white matter. The cerebral white-gray contrast and venous structures were clearer after bloodletting than before bloodletting.
The effect of hemorrhage on the brain is reflected by SWI signal changes in the cerebral cortex and gray matter nuclei.
Medical science monitor: international medical journal of experimental and clinical research 07/2014; 20:1291-7. DOI:10.12659/MSM.890641 · 1.43 Impact Factor
"Susceptibility weighted imaging (SWI) is used to detect microhemorrhages, the intact structure of the venous system, and oxygen saturation following neurotrauma (Shen et al., 2007). Microhemorrhages, venous thrombosis, and ischemia are common secondary injuries following mTBI (Aiken and Gean, 2010). "
[Show abstract][Hide abstract] ABSTRACT: The diagnosis of chronic traumatic encephalopathy (CTE) upon autopsy in a growing number of athletes and soldiers alike has resulted in increased awareness, by both the scientific/medical and lay communities, of the potential for lasting effects of repetitive traumatic brain injury. While the scientific community has come to better understand the clinical presentation and underlying pathophysiology of CTE, the diagnosis of CTE remains autopsy-based, which prevents adequate monitoring and tracking of the disease. The lack of established biomarkers or imaging modalities for diagnostic and prognostic purposes also prevents the development and implementation of therapeutic protocols. In this work the clinical history and pathologic findings associated with CTE are reviewed, as well as imaging modalities that have demonstrated some promise for future use in the diagnosis and/or tracking of CTE or repetitive brain injury. Biomarkers under investigation are also discussed with particular attention to the timing of release and potential utility in situations of repetitive traumatic brain injury. Further investigation into imaging modalities and biomarker elucidation for the diagnosis of CTE is clearly both needed and warranted.
Frontiers in Neurology 01/2012; 3:186. DOI:10.3389/fneur.2012.00186
"The rat was placed in a prone position and restrained on a cradle with a custom-built palate holder equipped with an adjustable nose cone and stereotaxic ear bars to inhibit movement during MRI scans. Its head was positioned at the isocenter of a magnet (Shen et al., 2007). All of the MRI data acquisition was performed on a 4.7- Tesla horizontal-bore magnetic resonance spectrometer (Bruker AVANCE) with an 11.6-cm bore actively shielded gradient coil set capable of producing a magnetic field gradient of up to 250 mT/m. "
[Show abstract][Hide abstract] ABSTRACT: Abstract The current study used a rat model to investigate the underlying mechanisms of blast-induced tinnitus, hearing loss, and associated traumatic brain injury (TBI). Seven rats were used to evaluate behavioral evidence of tinnitus and hearing loss, and TBI using magnetic resonance imaging following a single 10-msec blast at 14 psi or 194 dB sound pressure level (SPL). The results demonstrated that the blast exposure induced early onset of tinnitus and central hearing impairment at a broad frequency range. The induced tinnitus and central hearing impairment tended to shift towards high frequencies over time. Hearing threshold measured with auditory brainstem responses also showed an immediate elevation followed by recovery on day 14, coinciding with behaviorally-measured results. Diffusion tensor magnetic resonance imaging results demonstrated significant damage and compensatory plastic changes to certain auditory brain regions, with the majority of changes occurring in the inferior colliculus and medial geniculate body. No significant microstructural changes found in the corpus callosum indicates that the currently adopted blast exposure mainly exerts effects through the auditory pathways rather than through direct impact onto the brain parenchyma. The results showed that this animal model is appropriate for investigation of the mechanisms underlying blast-induced tinnitus, hearing loss, and related TBI. Continued investigation along these lines will help identify pathology with injury/recovery patterns, aiding development of effective treatment strategies.
Journal of neurotrauma 09/2011; 29(2):430-44. DOI:10.1089/neu.2011.1934 · 3.71 Impact Factor
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