Brain stem ischemia

Recanalization remains the most important step in the treatment of ischemic stroke. In fact, without recanalization further treatment is very limited. However, recanalization alone does not restore all the function especially when ischemia has been allowed to last for several hours. Restoration of normal CBF to an ischemic brain region is beneficial only within the first 3-6 h. In very rare situations and mostly in the brain stem ischemias, recanaUzation procedures are undertaken beyond the 6-h limit. Recanalization into a severely ischanic tissue generates a cascade of untoward processes. Reperfusion injury leads to further deterioration of tissue that is already compromised. In general, shorter and less severe ischemia leads to fewer reperfusion injury consequences. In clinical practice the most significant and most visible complication of reperfusion into a severely injured brain parenchyma is hanonhage. It is mostly the increased risk of hemorrhagic transformation that limits the administration of thrombolytic therapy beyond 3 h. The key to success in thrombolysis remains a shorter duration of ischemia. 

III. Transplantation of Neural Stem Cells and Gene Therapy in the Brain Ischemia... 

Neural transplantation represents an attractive therapy to ameliorate neurological impairments after brain ischemia. Transplantation of bone marrow cells (Chen et al., 2001a), fetal neural stem/progenitor cells (NSPCs) (Ishibashi et al.,... 

Stem cell-based therapy for cerebral ischemia will be more complicated, because the extensive cell death and massive inflammatory response make these brains a more hostile environment for cell grafts. Various sources of cells have been tested for their ability to reconstruct the forebrain and improve function after transplantation in animal models of stroke (Lindvall and Kokaia, 2004). In most cases, only a few grafted cells could survive. Some recent exciting findings in rodents suggest that stroke can induce an increase in neurogenesis thus, a new therapeutic approach based on self-repair has been brought forth, as discussed in Sect. 13.11.1. 

Fig. 2 In vivo MRI of rabbit ischemic brain that received mesenchymal stem cells labeled with chitosan-SPION. Asterisk indicates ischemic area and open arrows indicate chitosan-SPION-labeled mesenchymal stem cells at the injection site, (a, b) T2WI and diffusion weighted image (DWI) of brain immediately after injection of mesenchymal stem cell at contralateral side of ischemic area (open arrows) on day 4 of ischemia, (c, d) T2WI and susceptibility weighted image (SWI) 16 days after stem cell transplantation. At the ischemic site, dark signal (white arrows) on SWI matches mesenchymal stem cells (black arrows) on Prussian staining (e, f)- (e. 0 Prussian blue staining detected iron-labeled stem cells at the liquefied infarct area in a section of 4% paraformaldehyde-fixed brain tissue tut day 16. Reprinted fiom [92] by permission fi om The Korean Academy of Medical Sciences, Journal of Korean Medical Science. Copyright 2010...

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