BACKGROUND: Identification of factors that predispose to bleeding into ischemic brain could lead to safer use of thrombolytic agents in the setting of ischemic stroke. Recently de Courten-Meyers and colleagues reported that occluding the middle cerebral artery of markedly hyperglycemic cats was associated with 5-fold more frequent and 25-fold more extensive hemorrhage into infarcts than in normoglycemic animals. Hemorrhage associated with hyperglycemia in cats was much more pronounced with reperfusion than with permanent middle cerebral artery occlusion. CASE DESCRIPTION: We describe two patients with a unique presentation of diffuse hemorrhagic infarction of the caudate and lentiform nuclei associated with initially marked hyperglycemia and the subsequent development of hemichorea. CONCLUSIONS: We hypothesize that the marked hyperglycemia due to poor control of diabetes contributed to the hemorrhagic change of the caudate and lenticular nuclei. Because the hemorrhage in hyperglycemic cats was more pronounced in the setting of reperfusion, hemorrhagic risk associated with hyperglycemia should be investigated, particularly in ongoing thrombolytic treatment trials for acute ischemic stroke. We encourage other acute stroke investigators to prospectively look at the risk of brain hemorrhage in stroke patients with marked hyperglycemia.
BACKGROUND: Identification of factors that predispose to bleeding into ischemic brain could lead to safer use of thrombolytic agents in the setting of ischemic stroke. Recently de Courten-Meyers and colleagues reported that occluding the middle cerebral artery of markedly hyperglycemiccats was associated with 5-fold more frequent and 25-fold more extensive hemorrhage into infarcts than in normoglycemic animals. Hemorrhage associated with hyperglycemia in cats was much more pronounced with reperfusion than with permanent middle cerebral artery occlusion. CASE DESCRIPTION: We describe two patients with a unique presentation of diffuse hemorrhagic infarction of the caudate and lentiform nuclei associated with initially marked hyperglycemia and the subsequent development of hemichorea. CONCLUSIONS: We hypothesize that the marked hyperglycemia due to poor control of diabetes contributed to the hemorrhagic change of the caudate and lenticular nuclei. Because the hemorrhage in hyperglycemiccats was more pronounced in the setting of reperfusion, hemorrhagic risk associated with hyperglycemia should be investigated, particularly in ongoing thrombolytic treatment trials for acute ischemic stroke. We encourage other acute stroke investigators to prospectively look at the risk of brain hemorrhage in strokepatients with marked hyperglycemia.
Authors: William J Meurer; Phillip A Scott; Angela F Caveney; Jennifer J Majersik; Shirley M Frederiksen; Annette Sandretto; Ann B Holden; Robert Silbergleit Journal: Int J Stroke Date: 2010-06 Impact factor: 5.266
Authors: A R Jain; M Jain; A R Kanthala; D Damania; L G Stead; H Z Wang; B S Jahromi Journal: AJNR Am J Neuroradiol Date: 2013-04-18 Impact factor: 3.825
Authors: Katie D Vo; Fernando Santiago; Weili Lin; Chung Y Hsu; Yueh Lee; Jin-Moo Lee Journal: AJNR Am J Neuroradiol Date: 2003-04 Impact factor: 3.825