Glucose And Ischemic Brain Injury

Animal studies consistently show that hyperglycemia worsens ischemic brain injury and increases the risk of hemorrhagic transformation after cerebral infarction (30-32). Observational studies show that patients with hyperglycemia at the time of stroke onset have increased morbidity and mortality and that hyperglycemia is associated with more pronounced infarct growth (33-37). Patients with hyperglycemia are also at higher risk of hem-orrhagic transformation after stroke, which can occur spontaneously or following the use of anticoagulants and fibrinolytics (38,39). Independent of the occurrence of hemorrhagic transformation, hyperglycemia is also associated with an increased risk of clinical deterioration in the days after stroke onset (40). Experimental data suggest that hyperglycemia might contribute to ischemic brain injury by several mechanisms, including increases in lactic acidosis, in blood-brain barrier (BBB) breakdown (and hence, cerebral edema), and in the release of excitotoxic amino acids (41,42).

Whether strict maintenance of euglycemia with infusion of insulin can improve stroke outcome has not yet been proven. A seminal study showed that aggressive insulin therapy in the intensive care unit setting could improve mortality, but the study included very few patients with brain injury (43). Pilot studies that address the role of insulin therapy in patients with acute stroke are underway (44,45) . Furthermore, it is unclear whether normalization of glucose prior to administration of a thrombolytic will decrease the risk of hemorrhagic transformation. Appropriate clinical trial data are required before comprehensive recommendations about glucose management in stroke can be made, but it seems reasonable to target normoglycemia.

In experimental studies in which animals are pretreated with drugs that sensitize them to insulin [such as peroxisome proliferator-activated receptor (PPAR)-gamma agonists], outcome from stroke can be improved (46). The mechanism of action responsible for this neuroprotective effect is not yet fully understood. Trials of PPAR-gamma agonists for stroke prevention are underway, but it is too early to suggest that patients be started on PPAR-gamma agonists at stroke onset.

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