Uncovering a New Cause of Obstructive Hydrocephalus Following Subarachnoid Hemorrhage: Choroidal Artery Vasospasm–Related Ependymal Cell Degeneration and Aqueductal Stenosis—First Experimental Study

Yolaş, Coşkun; Özdemir, Nuriye Güzin; Kanat, Ayhan; Aydın, Mehmet Dumlu; Keleş, Papatya; Kepoğlu, Ümit; Aydın, Nazan; Gündoğdu, Cemal

doi:10.1016/j.wneu.2016.03.049

Cited by 48 publications

(30 citation statements)

References 32 publications

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“…It seems that degeneration of CP cells increases in severity depending on the volume of blood in the subarachnoid space [199]. Nevertheless, hydrocephalus may also occur in the absence of CSF hypersecretion probably due to desquamation of the ependymal and CP epithelial cells leading to reduction of cerebral aqueduct volume [200].…”

Section: Transporters Othersmentioning

confidence: 99%

Choroid plexus and the blood–cerebrospinal fluid barrier in disease

Solar

Zamani

Kubíčková

et al. 2020

Fluids Barriers CNS

210

142

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The choroid plexus (CP) forming the blood-cerebrospinal fluid (B-CSF) barrier is among the least studied structures of the central nervous system (CNS) despite its clinical importance. The CP is an epithelio-endothelial convolute comprising a highly vascularized stroma with fenestrated capillaries and a continuous lining of epithelial cells joined by apical tight junctions (TJs) that are crucial in forming the B-CSF barrier. Integrity of the CP is critical for maintaining brain homeostasis and B-CSF barrier permeability. Recent experimental and clinical research has uncovered the significance of the CP in the pathophysiology of various diseases affecting the CNS. The CP is involved in penetration of various pathogens into the CNS, as well as the development of neurodegenerative (e.g., Alzheimer´s disease) and autoimmune diseases (e.g., multiple sclerosis). Moreover, the CP was shown to be important for restoring brain homeostasis following stroke and trauma. In addition, new diagnostic methods and treatment of CP papilloma and carcinoma have recently been developed. This review describes and summarizes the current state of knowledge with regard to the roles of the CP and B-CSF barrier in the pathophysiology of various types of CNS diseases and sets up the foundation for further avenues of research. Publisher's NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Section: Transporters Othersmentioning

confidence: 99%

Choroid plexus and the blood–cerebrospinal fluid barrier in disease

Solar

Zamani

Kubíčková

et al. 2020

Fluids Barriers CNS

210

142

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“…Vasospasm of choroidal artery probably originates HCP through stenosing the aqueduct and impairing ependymal cells after SAH [8]. Devascularization of brain parenchyma likely results from sequential vasospasm of SAH and is confirmed to induce the proliferation of neural stem cells directed by glia cells [9].…”

Section: Etiologymentioning

confidence: 99%

Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Chen

Luo

Reis

et al. 2017

BioMed Research International

125

131

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Hydrocephalus (HCP) is a common complication in patients with subarachnoid hemorrhage. In this review, we summarize the advanced research on HCP and discuss the understanding of the molecular originators of HCP and the development of diagnoses and remedies of HCP after SAH. It has been reported that inflammation, apoptosis, autophagy, and oxidative stress are the important causes of HCP, and well-known molecules including transforming growth factor, matrix metalloproteinases, and iron terminally lead to fibrosis and blockage of HCP. Potential medicines for HCP are still in preclinical status, and surgery is the most prevalent and efficient therapy, despite respective risks of different surgical methods, including lamina terminalis fenestration, ventricle-peritoneal shunting, and lumbar-peritoneal shunting. HCP remains an ailment that cannot be ignored and even with various solutions the medical community is still trying to understand and settle why and how it develops and accordingly improve the prognosis of these patients with HCP.

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“…showed an important link between petrous ganglion cells and water vesicles of CP were decreased in the late phase of SAH due to ischemic insult of the petrous ganglion network . Acute hydrocephalus is due to vasospasm of choroidal arteries, ependymal cell desquamation and also CSF acidosis …”

Section: Discussionmentioning

confidence: 99%

First definition of burned choroid plexus in acidic cerebrospinal fluid‐filled brain ventricles during subarachnoid hemorrhage: Experimental study

et al. 2020

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Blood and cerebrospinal fluid (CSF) acidosis is the most troubling complication in subarachnoid hemorrhage (SAH) if carotid body (CB) networks are disrupted. However, histopathological examination of the choroid plexus (CP) in acidic CSF has not been evaluated so far. In this study, we aimed to investigate the CP in acidic CSF following SAH. Twenty‐eight rabbits were used. Five rabbits were used to analyze CB network (control group; n = 5); seven rabbits were injected 1 mL of saline (Sham group; n = 7); and the rest 16 rabbits were given 1 mL of autologous arterial blood inject into the cisterna magna to create SAH (SAH group; n = 16). Blood and CSF pH values were recorded before/during/after the experimental procedures. Nuclear darkening, cellular shrinkage and pyknosis suggested the presence of apoptosis of epithelial cells of CP. The densities of normal and degenerated epithelial cells of CPs were estimated using stereological methods. The relationship between the pH values and degenerated epithelial cell densities of CPs were statistically compared by Mann–Whitney U‐test. The pH values of blood were estimated as 7.359 ± 0.039 in the control group, 7.318 ± 0.062 in the Sham group, 7.23 ± 0.013 in the SAH group. CSF pH values were 7.313 ± 0.028 in the control group, 7.296 ± 0.045 in the Sham group, and 7.224 ± 0.012 in the SAH group. Degenerated epithelial cell density of CP was 25 ± 7 in the control group, 226 ± 64 in the Sham group, and 2115 ± 635 in the SAH group. There was a considerable link between CSF pH values and degenerated epithelial cells of CP (P < 0.0001). This study shows that CB insult causes acidosis of CSF as well as cellular degeneration of CP during SAH. This is the first description of this in the literature.

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Uncovering a New Cause of Obstructive Hydrocephalus Following Subarachnoid Hemorrhage: Choroidal Artery Vasospasm–Related Ependymal Cell Degeneration and Aqueductal Stenosis—First Experimental Study

Cited by 48 publications

References 32 publications

Choroid plexus and the blood–cerebrospinal fluid barrier in disease

Choroid plexus and the blood–cerebrospinal fluid barrier in disease

Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

First definition of burned choroid plexus in acidic cerebrospinal fluid‐filled brain ventricles during subarachnoid hemorrhage: Experimental study

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