Glucose Levels And Lesion Volume

If hyperglycemia is indeed casually related to poor outcome after stroke, one would expect a relation between higher levels of blood glucose and an increased lesion volume. In hemorrhagic stroke, only little is known about the association between glucose levels and the size of the hemorrhage or its evolution during the clinical course. The evidence is limited to experimental settings where it has been shown that hyperglycemia exacerbates brain edema and peri-hematomal cell death after hemorrhagic stroke (56). In patients with ischemic stroke treated with rt-PA, hyperglycemia has been associated with an increased risk of hemorrhagic complications (57-59). In contrast to hemorrhagic stroke, research concerning hyperglycemia and lesion volume after ischemic stroke is much more extensive. Central in the pathophysiology of ischemic stroke is the concept of the ischemic penumbra (Fig. 1C). The penumbra is a rim of tissue surrounding the infarct core that consists of potentially salvageable hypoperfused tissue that is clinically not functional and at risk of infarction. For survival of the penumbra, restoration of the blood flow due to spontaneous or rt-PA-induced recanalization with adequate reperfusion is of paramount importance. In longitudinal imaging studies it has been shown that without reperfusion, the infarct core increases at the cost of penumbral tissue, a process that seems to be most important in the initial phase of stroke but has been shown to last up till 3-8 days post-ictus (60-62). In this context it is important to realize that it is not clear whether the concept of the penumbra applies to all types of stroke. For example, usually a penumbra does not exist after hemorrhagic stroke (63) and in most patients with subcortical or lacunar infarction there is no penumbra (64). As mentioned earlier, extensive research has been done on the association between hyperglycemia and (expansion of) infarct volume. Although there are inconsistencies (65-67), most studies did indeed report such an association (66, 68-72), and this association is more pronounced with persistent hyperglycemia (50).

In experimental studies an increased infarct volume associated with hyperglycemia is predominantly seen in animal models with medial cerebral artery occlusion, mimicking human cortical infarction. In contrast, in end-artery models, mimicking subcortical infarcts, this is not seen (66, 67). Also, clinical studies that report such an association only included patients with cortical infarcts. These findings are therefore in line with the observation that in contrast to cortical infarction, hyperglycemia is not associated with worse clinical outcome after lacunar infarction. From a pathophysio-logical point of view, this may be explained by the presence or the absence of a penumbra in patients with cortical or subcortical stroke, respectively. The hypothesis that in cortical stroke hyperglycemia exerts its deleterious effects on the penumbra has been confirmed by a study which demonstrated that high levels of glucose were associated directly with decreased penum-bral salvage and poor outcome (71) (Fig. 3).

Stroke Hyperglycemia
Fig. 3. Penumbral salvage vs. blood glucose. (From Parsons et al. (71). Copyright 2002 American Neurological Association. Reprinted with permission of John Wiley & Sons, Inc.)
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