Massive Cerebral Hemorrhage: Spontaneous and Experimentally Induced

Globus, Joseph H.; Epstein, Joseph A.

doi:10.1097/00005072-195304000-00001

Cited by 50 publications

(19 citation statements)

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“…5 The predisposing factor(s) responsible for HT are not well defined, although etiology (thrombotic versus embolic), [5][6][7] collateral circulation, 8,9 reperfusion, 10 hypertension, 6,8,[11][12][13] size of the ischemic lesion, 5,14 -20 and the use of anticoagulants, thrombolytics, [21][22][23][24] or both have been implicated. No precise predictors of HT have been determined, but caution is suggested when thrombolysis is considered in patients with early x-ray CT signs of major stroke such as sulcal effacement, mass effect, edema, or possible hemorrhage 25,26 or National Institutes of Health Stroke Scale score greater than 22.…”

Section: See Editorial Comment Page 151mentioning

confidence: 99%

Prediction of Impending Hemorrhagic Transformation in Ischemic Stroke Using Magnetic Resonance Imaging in Rats

Knight

Barker

Fagan

et al. 1998

Stroke

100

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Background and Purpose-Hemorrhagic transformation (HT) of ischemic brain tissue may occur in stroke patients either spontaneously or after thrombolysis. A method to assess the risk of HT in ischemic tissue after stroke would improve the safety of thrombolytic therapy. As a means of predicting HT, we investigated the role of contrast-enhanced MRI at acute time points in a rat middle cerebral artery occlusion model with reperfusion. Methods-Intraluminal suture occlusion of the middle cerebral artery was used to produce transient ischemia in male Wistar rats (nϭ11). Reperfusion was performed by withdrawal of the occluding filament after 2 (nϭ4), 3 (nϭ6), or 4 (nϭ1) hours. MRI studies were performed before and after reperfusion with the use of conventional T1-weighted imaging, with and without gadolinium (Gd-DTPA) contrast agent, and T2-weighted imaging. Follow-up MRI and histological studies were obtained at 24 hours. Results-Petechial hemorrhage occurred by 24 hours in 9 of 11 animals. All animals showed brain swelling and cellular death throughout the ischemic region at 24 hours. A hyperintense region in the preoptic area became visible after Gd-DTPA injection within minutes after reperfusion in animals with subsequent HT. All animals showing acute Gd-DTPA enhancement subsequently developed petechial hemorrhage (or died) by 24 hours. In these animals, statistically significant differences in signal intensity (Pϭ.0005) between the ipsilateral enhancing region and a homologous contralateral region were detected on post-Gd-DTPA T1-weighted imaging. There was also a statistically significant correlation (Pϭ.01) between the rate of Gd-DTPA uptake and the size of the enhancing area. Two animals did not enhance with Gd-DTPA and did not exhibit hemorrhage on histological examination or MRI at 24 hours. No abnormalities were seen on precontrast T1-weighted images before and shortly after reperfusion or postcontrast T1-weighted images before reperfusion. Conclusions-The primary finding of this study was the detection of early Gd-DTPA parenchymal enhancement in 82% of the animals after reperfusion. Enhancement was seen before any detectable hemorrhage, suggesting that early endothelial ischemic damage occurs before gross brain infarction and hemorrhage. Thus, we suggest that acute Gd-DTPA enhancement may provide an early prediction of petechial hemorrhage. (Stroke. 1998;29:144-151.)

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Section: See Editorial Comment Page 151mentioning

confidence: 99%

Prediction of Impending Hemorrhagic Transformation in Ischemic Stroke Using Magnetic Resonance Imaging in Rats

Knight

Barker

Fagan

et al. 1998

Stroke

100

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“…Thus, it is probably not the cause of ring enhancement because the newly formed capillaries that are closely related to ring enhancement are supposed to be im mature. 4) Electron microscopy showed that newly formed blood vessels had immature endo thelium containing many pinocytotic vesicles looking like tiny vacuoles. In the endothelium of normal cerebral capillaries, the junctions between endothelial cells overlap diagonally and are extremely tight, and very few pinocytotic vesicles are visible in the cytoplasm.')…”

Section: Discussionmentioning

confidence: 99%

“…In the first series of five dogs (No. [1][2][3][4][5], which were used in the early stage for preparation of hematomas, no intracerebral hematomas could be detected by CT as high density areas because of a technical failure. In the next series of 21 dogs (No.…”

Section: Methodsmentioning

confidence: 99%

Cause of Ring Enhancement in Computed Tomographic Image of Intracerebral Hematomas

Takasugi

1980

Neurol. Med. Chir.(Tokyo)

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SummaryAs models of clinical hypertensive intracerebral hematomas, intracerebral hematomas were induced experimentally in 26 mongrel dogs. The CT images of the hematomas during healing were compared with histological findings to determine the cause of ring enhancement in contrast enhanced CT.The ring enhancement appeared at almost the same time in all dogs, 9 days after formation of the hematomas.Formation of many new capillaries in the peripheral region of the hematomas was seen from day 9 and the ring enhancement was found to be closely associated with these new capillaries. Electron microscopy showed that these newly formed capillary vessels had a similar ultrastructure to those of the muscle. These vessels seemed to have no blood brain barrier. Thus the ring enhance ment was attributed to the accumulation of contrast medium in these newly formed vessels and its leakage from the vessels owing to their increased permeability.

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“…2 However, we recently demonstrated in human autopsy cases that hemorrhagic transformation of an infarct in persons with cardioembolic stroke may occur without a reopening of the occluded artery and that restoration of blood flow to the infarcted area through Ieptomeningeal collaterals on the surface of the brain is likely to be responsible for the hemorrhagic transformation in cases with surges of arterial hypertension. 3 The pathogenesis of hemorrhagic infarction has been studied in experimental animals with 4 -6 and without 7 " 9 reopening of the occluded artery. In the latter, hemorrhagic transformation was attributed to underlying pathologic changes of the vasculature, such as hypertensive vascular changes preceding ischemia 8 or degenerative 7 or proliferative 9 vascular changes secondary to ischemia.…”

Section: S Ince Fisher and Adamsmentioning

confidence: 99%

“…3 The pathogenesis of hemorrhagic infarction has been studied in experimental animals with 4 -6 and without 7 " 9 reopening of the occluded artery. In the latter, hemorrhagic transformation was attributed to underlying pathologic changes of the vasculature, such as hypertensive vascular changes preceding ischemia 8 or degenerative 7 or proliferative 9 vascular changes secondary to ischemia. These factors operate in the presence of sufficient perfusion pressure of the infarcted area through Ieptomeningeal anastomoses.…”

Section: S Ince Fisher and Adamsmentioning

confidence: 99%

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

Saku

Choki

Waki

et al. 1990

Stroke

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The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 ±16.9 mm Hg (mean±SD) in the 11 cats with hemorrhagic infarcts and by 40.4 ±16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p<0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through Ieptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries. (Stroke 1990^1:589-595) S ince Fisher and Adams 1 first reported autopsy cases of cerebral embolism, hemorrhagic brain infarction has been thought of as a consequence of reperfusion of the damaged vascular bed by a reopening of the occluded artery.2 However, we recently demonstrated in human autopsy cases that hemorrhagic transformation of an infarct in persons with cardioembolic stroke may occur without a reopening of the occluded artery and that restoration of blood flow to the infarcted area through Ieptomeningeal collaterals on the surface of the brain is likely to be responsible for the hemorrhagic transformation in cases with surges of arterial hypertension. The pathogenesis of hemorrhagic infarction has been studied in experimental animals with 4 -6 and without 7 " 9 reopening of the occluded artery. In the latter, hemorrhagic transformation was attributed to underlying pathologic changes of the vasculature, such as hypertensive vascular changes preceding ischemia 8 or degenerative 7 or proliferative 9 vascular changes secondary to ischemia. These factors operate Received August 12, 1988; accepted October 31, 1989. in the presence of sufficient perfusion pressure of the infarcted area through Ieptomeningeal anastomoses. However, no previous study evaluated the mechanisms we proposed based on our observations of human autopsy cases. 3 Also, especially in early reports, 78 physiologic parameters were not adequately monitored. Thus, we designed this experiment to clarify whether a rapid rise in blood pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery and to assess the relation between the pathologic distribution of ischemic changes and hemorrhage and the regional cerebral blood flow (rCBF) in cats with induced hypertension after middle cerebral artery (MCA) occlusion. Materials and MethodsWe anesthetized 29 cats weighing 2.4-4.3 kg with 10 mg/kg i.m. ketamine hydro...

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Massive Cerebral Hemorrhage: Spontaneous and Experimentally Induced

Cited by 50 publications

References 0 publications

Prediction of Impending Hemorrhagic Transformation in Ischemic Stroke Using Magnetic Resonance Imaging in Rats

Prediction of Impending Hemorrhagic Transformation in Ischemic Stroke Using Magnetic Resonance Imaging in Rats

Cause of Ring Enhancement in Computed Tomographic Image of Intracerebral Hematomas

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

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