Hydrocephalus in ICH: What Do We Really Know?

Zazulia, Allyson R.

doi:10.1007/s12028-008-9055-1

Cited by 11 publications

(9 citation statements)

References 13 publications

(16 reference statements)

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“…ICH is a common and devastating cerebral disease with a higher morbidity and mortality than ischemic stroke [ 22 – 24 ]. ICH-induced brain injury involves multiple mechanisms.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage

Yuan¹,

Shen²,

Li³

et al. 2015

J Neuroinflammation

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BackgroundIntracerebral hemorrhage (ICH) induces microglial activation and the release of inflammatory cytokines, leading to inflammation in the brain. IRAK4, an essential component of the MyD88-dependent pathway, activates subsets of divergent signaling pathways in inflammation.MethodsIn the experiment, microglia were stimulated with erythrocyte lysates, and then miR-367, IRAK4, NF-ĸB activation and downstream proinflammatory mediator production were analyzed. In addition, inflammation, brain edema, and neurological functions in ICH mice were also assessed.ResultsHere, we report that ICH downregulated miR-367 expression but upregulated IRAK4 expression in primary microglia. We also demonstrate that miR-367 suppressed IRAK4 expression by directly binding its 3′-untranslated region. MiR-367 inhibited NF-ĸB activation and downstream proinflammatory mediator production. Knocking down IRAK4 in microglia significantly decreased the IRAK4 expression and inhibited the NF-ĸB activation and the downstream production of proinflammatory mediators. In addition, our results indicate that miR-367 could inhibit expression of proinflammatory cytokines, reduce brain edema, and improve neurological functions in ICH mice.ConclusionsIn conclusion, our study demonstrates that miR-367/IRAK4 pathway plays an important role in microglial activation and neuroinflammation in ICH. Our finding also suggests that miR-367 might represent a potential therapeutic target for ICH.

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“…ICH is a common and devastating cerebral disease with a higher morbidity and mortality than ischemic stroke [ 22 – 24 ]. ICH-induced brain injury involves multiple mechanisms.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage

Yuan¹,

Shen²,

Li³

et al. 2015

J Neuroinflammation

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“…This is typically not done while vasospasm is a clinical concern after SAH, and weaning of the drain may be delayed until the patient is otherwise stable. Clinical studies to assess which patients will require ventricular drainage or a permanent shunt have not yielded clear answers, and protocols for removal of ventricular drains are variable [36]. While most clinicians agree that a ventricular drain should be placed in a patient with brain hemorrhage and a depressed level of consciousness, hydrocephalus remains a predominantly clinical diagnosis, and the lack of standardized diagnostic criteria and protocols for drain removal make it difficult to determine a consistent effect on LOS.…”

Section: Discussionmentioning

confidence: 99%

Medical Complications Drive Length of Stay After Brain Hemorrhage: A Cohort Study

et al. 2008

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“…7 reported that patients who subsequently had chronic hydrocephalus requiring CSF shunting possessed higher CSF ferritin levels during the acute stage of subarachnoid hemorrhage (SAH). Moreover, in clinical studies demonstrating that some of patients would develop into hydrocephalus after hemorrhagic stroke, 1,8 iron contributes to the pathogenic mechanisms leading to hydrocephalus.…”

Section: Biomarkers Of Phhmentioning

confidence: 99%

“…Disease management is challenging due to limited understanding of the underlying pathogenesis of PHH and because 40–50% of patients with intraventricular hemorrhage (IVH) will develop hydrocephalus. 1 Hydrocephalus is described as either early, acute (developing during the first three days), subacute (days 4–13), or chronic (persisting after 14 days). 2 While the precise molecular mechanisms leading to PHH pathology was remain elusive.…”

Section: Introductionmentioning

confidence: 99%

Biomarkers in adult posthemorrhagic hydrocephalus

Cong

Zhao

2017

International Journal of Stroke

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Posthemorrhagic hydrocephalus is a severe complication following intracranial hemorrhage. Posthemorrhagic hydrocephalus is often associated with high morbidity and mortality and serves as an important clinical predictor of adverse outcomes after intracranial hemorrhage. Currently, no effective medical intervention exists to improve functional outcomes in posthemorrhagic hydrocephalus patients because little is still known about the mechanisms of posthemorrhagic hydrocephalus pathogenesis. Because a better understanding of the posthemorrhagic hydrocephalus pathogenesis would facilitate development of clinical treatments, this is an active research area. The purpose of this review is to describe recent progress in elucidation of molecular mechanisms that cause posthemorrhagic hydrocephalus. What we are certain of is that the entry of blood into the ventricular system and subarachnoid space results in release of lytic blood products which cause a series of physiological and pathological changes in the brain. Blood components that can be linked to pathology would serve as disease biomarkers. From studies of posthemorrhagic hydrocephalus, such biomarkers are known to mutually synergize to initiate and promote posthemorrhagic hydrocephalus progression. These findings suggest that modulation of biomarker expression or function may benefit posthemorrhagic hydrocephalus patients.

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Hydrocephalus in ICH: What Do We Really Know?

Cited by 11 publications

References 13 publications

MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage

MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage

Medical Complications Drive Length of Stay After Brain Hemorrhage: A Cohort Study

Biomarkers in adult posthemorrhagic hydrocephalus

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