Post-hemorrhagic hydrocephalus: Recent advances and new therapeutic insights

Chen, Qianwei; Feng, Zhanchun; Tan, Qiang; Guo, Jing; Tang, Jun; Tan, Liang; Feng, Hua; Chen, Zhi

doi:10.1016/j.jns.2017.01.072

Cited by 92 publications

(77 citation statements)

References 146 publications

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“…In a rodent model of subarachnoid hemorrhage (SAH), it has been shown that disrupted CSF/ISF drainage can be cleared using the perivascular pathway with an intraventricular tissue-type plasminogen activator treatment [149,156]. This approach has already been successfully applied in humans with hydrocephalus [157,158]. This strategy alleviated histological injury and improved behavioral function after SAH [149,157].…”

Section: Mendelsohn Andmentioning

confidence: 99%

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From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation

Goulay

Romo

Hol

et al. 2019

Transl. Stroke Res.

100

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Stroke and Alzheimer's disease (AD) are cerebral pathologies with high socioeconomic impact that can occur together and mutually interact. Vascular factors predisposing to cerebrovascular disease have also been specifically associated with development of AD, and acute stroke is known to increase the risk to develop dementia. Despite the apparent association, it remains unknown how acute cerebrovascular disease and development of AD are precisely linked and act on each other. It has been suggested that this interaction is strongly related to vascular deposition of amyloid-β (Aβ), i.e., cerebral amyloid angiopathy (CAA). Furthermore, the blood-brain barrier (BBB), perivascular space, and the glymphatic system, the latter proposedly responsible for the drainage of solutes from the brain parenchyma, may represent key pathophysiological pathways linking stroke, Aβ deposition, and dementia. In this review, we propose a hypothetic connection between CAA, stroke, perivascular space integrity, and dementia. Based on relevant pre-clinical research and a few clinical case reports, we speculate that impaired perivascular space integrity, inflammation, hypoxia, and BBB breakdown after stroke can lead to accelerated deposition of Aβ within brain parenchyma and cerebral vessel walls or exacerbation of CAA. The deposition of Aβ in the parenchyma would then be the initiating event leading to synaptic dysfunction, inducing cognitive decline and dementia. Maintaining the clearance of Aβ after stroke could offer a new therapeutic approach to prevent post-stroke cognitive impairment and development into dementia.

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Section: Mendelsohn Andmentioning

confidence: 99%

“…This approach has already been successfully applied in humans with hydrocephalus [157,158]. This strategy alleviated histological injury and improved behavioral function after SAH [149,157]. CSF drainage may also be applied to increase Aβ clearance in patients.…”

Section: Mendelsohn Andmentioning

confidence: 99%

From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation

Goulay

Romo

Hol

et al. 2019

Transl. Stroke Res.

100

View full text Add to dashboard Cite

show abstract

“…[11,12,13] There are often accumulations of CSF in the subgaleal space due to its slow absorption by the scalp's subcutaneous tissues. [14] There were no cases highlighted where there was no occurrence or resolution of scalp swelling. Scalp swelling can be distressing for the parents if not previously informed, and regular care and observation are required with the turning of the newborn's head every two hours, Kadri H, Mawla AA, Kazah J.…”

Section: Discussionmentioning

confidence: 99%

A Case Report of Neonatal posthemorrhagic hydrocephalus in a premature infant.

Niraula¹,

Niyaf²,

Razzag³

et al. 2024

Pak J Sur Med

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Background: Neurosurgical services in the Maldives began around five years ago, but the first neurosurgical center is responsible for various emergency and clinical neurosurgical services. Published literature on neurosurgery from the Maldives Islands is limited. It is imperative to report unique cases from isolated countries to promote diversity for readers across the globe. Case Presentation: We present a case of a ventriculo-subgaleal shunt placement in an extremely premature male baby with intra-ventricular hemorrhage, causing communicating hydrocephalus born at 22 weeks of gestation weighing 600 grams to a young primigravida. The shunt was performed in the first month of life (780 grams) for communicating hydrocephalus secondary to the germinal matrix bleed into the ventricles. Conclusion: Ventriculo-subgalel shunt under local anesthesia is a promising measure to treat hydrocephalus in pre-term very low birth weight infants secondary to germinal matrix hemorrhage.

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“…Post-hemorrhagic hydrocephalus (PHH) is a serious complication of intraventricular hemorrhage (IVH), subarachnoid hemorrhage (SAH), and traumatic brain injury (TBI). It has a high mortality and morbidity [1][2][3][4][5]. Failure to treat PHH immediately may lead to various complications, such as loss of consciousness, dementia, and persistent coma, seriously threatening the safety of patients [6].…”

Section: Introductionmentioning

confidence: 99%

Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

Zhan

Xiao

Zhang

et al. 2020

Translational Neuroscience

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AbstractBackgroundFibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-β1 (TGF-β1) may be involved in thrombin-induced arachnoid fibrosis.MethodsA rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed.ResultsDecreased expression of miR-30a and increased expression of TRAF3IP2, TGF-β1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3′UTR and inhibits the expression of TRAF3IP2, TGF-β1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2.ConclusionsThis study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.

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Post-hemorrhagic hydrocephalus: Recent advances and new therapeutic insights

Cited by 92 publications

References 146 publications

From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation

From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation

A Case Report of Neonatal posthemorrhagic hydrocephalus in a premature infant.

Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

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