T2* Magnetic Resonance Imaging Sequences Reflect Brain Tissue Iron Deposition Following Intracerebral Hemorrhage

Wu, Gang; Xi, Guohua; Hua, Ya; Sagher, Oren

doi:10.1007/s12975-009-0008-6

Cited by 45 publications

(31 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Degradation of heme by heme oxygenases (HO) after erythrocyte lysis results in the release of iron, carbon monoxide, and biliverdin, which is then converted to bilirubin (Maines, 1988). Iron overload in the brain starts within 24 hours to peak at 7 days after hemorrhage, and remains at least a month (Chaudhary et al, 2013; Wu et al, 2010; Wu et al, 2003). Iron toxicity may be based on the Fenton chemistry reaction that can produce highly reactive free radicals, and it can cause neurodegeneration via oxidative injury (Zecca et al, 2004).…”

Section: Primary and Secondary Brain Injury After Ichmentioning

confidence: 99%

Intercellular cross-talk in intracerebral hemorrhage

et al. 2015

Self Cite

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is a devastating cerebrovascular disorder with high mortality and morbidity. Currently, there are few treatment strategies for ICH-induced brain injury. A recent increase in interest in the pathophysiology of ICH, has led to elucidation of the pathways underlying ICH-induced brain injury, pathways where intercellular and hematoma to cell signaling play important roles. In this review, we summarize recent advances in ICH research focusing on intercellular and hematoma:cell cross-talk related to brain injury and recovery after ICH.

show abstract

Section: Primary and Secondary Brain Injury After Ichmentioning

confidence: 99%

Intercellular cross-talk in intracerebral hemorrhage

et al. 2015

Self Cite

View full text Add to dashboard Cite

show abstract

“…Ten-fold higher CSF iron levels are detected in subarachnoid hemorrhage (SAH) patients, and a high concentration is maintained for the first 2 weeks after ictus (16). The deposition of iron in brain can be determined by specific staining and magnetic resonance imaging (MRI (17-19)).…”

Section: Introductionmentioning

confidence: 99%

Deferoxamine Attenuates Acute Hydrocephalus After Traumatic Brain Injury in Rats

Zhao

Chen

et al. 2014

Transl. Stroke Res.

Self Cite

View full text Add to dashboard Cite

Acute post-traumatic ventricular dilation and hydrocephalus are relatively frequent consequences of traumatic brain injury (TBI). Several recent studies have indicated that high iron level in brain may relate to hydrocephalus development after intracranial hemorrhage. However, the role of iron in the development of post-traumatic hydrocephalus is still unclear. This study was to determine whether or not iron has a role in hydrocephalus development after TBI. TBI was induced by lateral fluid-percussion in male Sprague-Dawley rats. Some rats had intraventricular injection of iron. Acute hydrocephalus was measured by magnetic resonance T2-weighted imaging and brain hemorrhage was determined by T2* gradient-echo sequence imaging and brain hemoglobin levels. The effect of deferoxamine on TBI-induced hydrocephalus was examined. TBI resulted in acute hydrocephalus at 24 hours (lateral ventricle volume: 24.1±3.0 vs. 9.9±0.2 mm3 in sham group). Intraventricular injection of iron also caused hydrocephalus (25.7 ± 3.4 vs. 9.0 ± 0.6 mm3 in saline group). Deferoxamine treatment attenuated TBI-induced hydrocephalus and heme oxygenase-1 upregulation. In conclusion, iron may contribute to acute hydrocephalus after TBI.

show abstract

“…The T2* lesion was outlined along the border of the hyper-intense area and the lesion volume was obtained by combining the hyper-intense area over all slices and multiplied by sections thickness. In our previous study, we found that at day 1 and day 3 after ICH, T2* imaging can detect hematoma size 19 . In this study, therefore, T2* imaging was performed at day 1 and day 3 after ICH to determine the hematoma clearance.…”

Section: Methodsmentioning

confidence: 94%

Role of Erythrocyte CD47 in Intracerebral Hematoma Clearance

Mao

et al. 2016

Stroke

Self Cite

View full text Add to dashboard Cite

Background and Purpose Enhancing hematoma clearance through phagocytosis may reduce brain injury after intracerebral hemorrhage (ICH). In the current study, we investigated the role of CD47 in regulating erythrophagocytosis and brain injury after ICH in nude mice. Methods This study was in two parts. First, male adult nude mice had an intracaudate injection of 30-µl saline, blood from male adult wild type (WT) mice or blood from CD47 knockout (CD47 KO) mice. Second, mice had an intracaudate injection of 30-µl CD47 KO blood with clodronate or control liposomes. Clodronate liposomes were also tested in saline-injected mice. All mice then had magnetic resonance imaging to measure hematoma size and brain swelling. Brains were used for immunohistochemistry and Western blot. Results Erythrophagocytosis occurred in and around the hematoma. Injection of CD47 KO blood resulted in quicker clot resolution, less brain swelling, and less neurological deficits compared to WT blood. Higher brain heme oxygenase-1 levels and more microglial activation (mostly M2 polarized microglia) at day-3 were found after CD47 KO blood injection. Co-injection of clodronate liposomes, to deplete phagocytes, caused more severe brain swelling and less clot resolution. Conclusion These results indicated CD47 has a key role in hematoma clearance after ICH.

show abstract

T2* Magnetic Resonance Imaging Sequences Reflect Brain Tissue Iron Deposition Following Intracerebral Hemorrhage

Cited by 45 publications

References 10 publications

Intercellular cross-talk in intracerebral hemorrhage

Intercellular cross-talk in intracerebral hemorrhage

Deferoxamine Attenuates Acute Hydrocephalus After Traumatic Brain Injury in Rats

Role of Erythrocyte CD47 in Intracerebral Hematoma Clearance

Contact Info

Product

Resources

About