| Autor: |
Hu S; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Exner C; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Sienel RI; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., When AC; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Seker FB; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Boldoczki FM; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Guo Y; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Duering M; Medical Image Analysis Center (MIAC) and Department of Biomedical Engineering, University of Basel, Basel, Switzerland., Pasternak O; Neuroscience Image Computing, Harvard Medical School, Boston, Massachusetts, USA., Plesnila N; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Schwarzmaier SM; Institute for Stroke and Dementia Research (ISD)and Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.; Department of Anesthesiology, Ludwig-Maximilians University (LMU), Munich, Germany. |
| Abstrakt: |
Brain edema formation is a key factor for secondary tissue damage after traumatic brain injury (TBI), however, the type of brain edema and the temporal profile of edema formation are still unclear. We performed free water imaging, a bi-tensor model based diffusion MRI analysis, to characterize vasogenic brain edema (VBE) and cytotoxic edema (CBE) formation up to 7 days after experimental TBI. Male C57/Bl6 mice were subjected to controlled cortical impact (CCI) or sham surgery and investigated by MRI 4h, 1, 2, 3, 5, and 7 days thereafter ( n = 8/group). We determined mean diffusivity (MD) and free water (FW) in contusion, pericontusional area, ipsi- and contralateral brain tissue. Free (i.e., non-restricted) water was interpreted as VBE, restricted water as CBE. To verify the results, VBE formation was investigated by in-vivo 2-Photon Microscopy (2-PM) 48h after surgery. We found that MD and FW values decreased for 48h within the contusion, indicating the occurrence of CBE. In pericontusional tissue, MD and FW indices were increased at all time points, suggesting the formation of VBE. This was consistent with our results obtained by 2-PM. Taken together, CBE formation occurs for 48h after trauma and is restricted to the contusion, while VBE forms in pericontusional tissue up to 7 days after TBI. Our results indicate that free water magnetic resonance imaging may represent a promising tool to investigate vasogenic and cytotoxic brain edema in the laboratory and in patients. |
