There are currently a large number of well-characterized, ischemic stroke animal models available for pre-clinical research. These models can be categorized into those two groups – those for the study of stroke-associated risk factors and those for the study of stroke pathophysiology. The latter can be further separated into models of focal verses global ischemia and are listed:
Focal Ischemia Models
The most commonly employed model is that of middle cerebral artery occlusion (MCAO) in rats. MCAO is generally achieved mechanically and may be either transient with variable duration or permanent. It is highly reproducible, requires minimal surgical intervention, and produces predictable infarcts similar to clinical observations. Rats offer the advantages of being small enough to allow sufficient numbers to be included in studies without increased costs and yet large enough to allow monitoring of physiological variables during experiments.  However, the main disadvantage is that the brains of rats are quite dissimilar to humans in many aspects including of size, gross anatomy, neuroanatomical connectivity, cognitive ability, and cerebral vasculature. Further, young and healthy rats are typically used, which do not adequately represent the demographic of humans who tend to experience acute ischemic stroke – those with risk factors that include advanced age, cardiovascular disease, diabetes, and others. This is perhaps one reason why promising, new neuroprotective strategies developed in the pre-clinical setting often fail in clinical trials, emphasizing the fact that care must be taken when interpreting data and translating findings to the clinical setting. [1, 2]
Despite these obstacles, our understanding of post-ischemic stroke neuroinflammation has advanced significantly with the help of in vitro systems and the MCAo, 4VO and other in vivo models and lessons taken from failed pre-clinical and clinical trials and autopsy results.