Spontaneous intracerebral hemorrhage in humans: hematoma enlargement, clot lysis, and brain edema

Wu, Gang; Xi, G.; Huang, Felix C.

doi:10.1007/3-211-30714-1_19

Cited by 39 publications

(34 citation statements)

References 14 publications

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“…55 The release of the intracellular contents of these cells induces brain edema, as studies have shown increases in edema volume following reductions in hematoma size due to clot lysis. 138 Studies in animals have shown delayed brain injury with intracerebral infusion of packed RBCs and dramatic edema formation within 24 hours following infusion of lysed RBCs. 53,133,140,145 Infusion of lysed RBCs also causes disruption of the BBB, DNA injury, and expression of heat shock proteins, indicating cell stress.…”

Section: Red Blood Cell Lysismentioning

confidence: 99%

Thrombin and hemin as central factors in the mechanisms of intracerebral hemorrhage–induced secondary brain injury and as potential targets for intervention

Babu¹,

Bagley²,

Di³

et al. 2012

FOC

164

138

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Intracerebral hemorrhage (ICH) is a subtype of stoke that may cause significant morbidity and mortality. Brain injury due to ICH initially occurs within the first few hours as a result of mass effect due to hematoma formation. However, there is increasing interest in the mechanisms of secondary brain injury as many patients continue to deteriorate clinically despite no signs of rehemorrhage or hematoma expansion. This continued insult after primary hemorrhage is believed to be mediated by the cytotoxic, excitotoxic, oxidative, and inflammatory effects of intraparenchymal blood. The main factors responsible for this injury are thrombin and erythrocyte contents such as hemoglobin. Therapies including thrombin inhibitors, N-methyl-D-aspartate antagonists, chelators to bind free iron, and antiinflammatory drugs are currently under investigation for reducing this secondary brain injury. This review will discuss the molecular mechanisms of brain injury as a result of intraparenchymal blood, potential targets for therapeutic intervention, and treatment strategies currently in development.

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Section: Red Blood Cell Lysismentioning

confidence: 99%

Thrombin and hemin as central factors in the mechanisms of intracerebral hemorrhage–induced secondary brain injury and as potential targets for intervention

Babu¹,

Bagley²,

Di³

et al. 2012

FOC

164

138

View full text Add to dashboard Cite

show abstract

“…For example, clot lysis is associated with perihematomal edema development. 5 Recent studies showed that high levels of serum ferritin, an iron storage protein, are independently associated with poor outcome and severe brain edema in ICH patients. 6,7 Lipocalin-2 (LCN2) is an acute phase protein that is upregulated in inflammation, infection, and a variety of injuries.…”

Section: Introductionmentioning

confidence: 99%

Role of Lipocalin-2 in Brain Injury after Intracerebral Hemorrhage

Zheng

et al. 2015

J Cereb Blood Flow Metab

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Lipocalin-2 (LCN2) is a siderophore-binding protein involved in cellular iron transport and neuroinflammation. Both iron and inflammation are involved in brain injury after intracerebral hemorrhage (ICH) and this study examined the role of LCN2 in such injury. Male adult C57BL/6 wild-type (WT) or LCN2-deficient (LCN2 − / − ) mice had an intracerebral injection of autologous blood or FeCl 2 . Control animals had a sham operation or saline injection. T2-weighted magnetic resonance imaging and behavioral tests were performed at days 1, 3, 7, 14, and 28 after injection. In WT mice, brain LCN2 levels were increased in the ipsilateral basal ganglia after ICH or iron injection. Lipocalin-2-positive cells were astrocytes, microglia, neurons, and endothelial cells. Intracerebral hemorrhage resulted in a significant increase in ferritin expression in the ipsilateral basal ganglia. Compared with WT mice, ICH caused less ferritin upregulation, microglia activation, brain swelling, brain atrophy, and neurologic deficits in LCN2− / − mice (P o0.05). The size of the lesion induced by FeCl 2 injection as well as the degree of brain swelling and blood-brain barrier disruption were also less in LCN2− / − mice (P o 0.05). These results suggest a role of LCN2 in enhancing brain injury and iron toxicity after ICH.

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“…The secondary pathophysiological processes have been implicated as causes of ongoing, injury including ischemia surrounding the hematoma, the development of cerebral edema [70], activation of apoptotic processes [71], toxic effects of components of the hematoma [72], and intraventricular extension of the primary hemorrhage [73]. The pathogenesis of symptoms and their subsequent recovery are also associated with hematoma size and location.…”

Section: Secondary Processesmentioning

confidence: 99%

“…Ultimately, it is the inflammation (phagocytosis) that leads to the restoration of tissue structure and function [96,97]. Although inflammation is triggered primarily to remove the blood and other debris left by the hemorrhage, the byproducts of this response are cytotoxic and lead to further tissue damage, blood brain barrier disruption, and edema [72,97,98].…”

Section: Pharmacologic Hematoma Clearancementioning

confidence: 99%

Treatment Targets in Intracerebral Hemorrhage

Sangha

Gonzales

2011

Neurotherapeutics

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Intracerebral hemorrhage (ICH) imparts a higher mortality and morbidity than ischemic stroke. The therapeutic interventions that are currently available focus mainly on supportive care and secondary prevention. There is a paucity of evidence to support any one acute intervention that improves functional outcome. This chapter highlights current treatment targets for ICH based on the pathophysiology of the disease.

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Spontaneous intracerebral hemorrhage in humans: hematoma enlargement, clot lysis, and brain edema

Cited by 39 publications

References 14 publications

Thrombin and hemin as central factors in the mechanisms of intracerebral hemorrhage–induced secondary brain injury and as potential targets for intervention

Thrombin and hemin as central factors in the mechanisms of intracerebral hemorrhage–induced secondary brain injury and as potential targets for intervention

Role of Lipocalin-2 in Brain Injury after Intracerebral Hemorrhage

Treatment Targets in Intracerebral Hemorrhage

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