Changes in the cerebral vascular bed in experimental hydrocephalus: An angio-architectural and histological study

Nakada, Jun-ichi; Oka, Naoki; Nagahori, Takeshi; Endo, Shunro; Takaku, Akira

doi:10.1007/bf01401113

Cited by 27 publications

(14 citation statements)

References 11 publications

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“…In an animal study of experimental hydrocephalus, Rosenberg et al [36] have shown that increased intraventricular pressure leads to a significant reduction in cerebral blood flow, predominantly in periventricular tissue. Furthermore, a reduction in the number of capillaries has been observed following the induction of experimental hydrocephalus [37,38]. An additional mechanism has been suggested by the findings of Shapiro et al [31], who investigated a series of patients with severe fourth ventricular hemorrhage.…”

Section: Discussionmentioning

confidence: 93%

Influence of intraventricular hemorrhage on outcome after rupture of intracranial aneurysm

et al. 2001

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This study was performed to analyze the effect of intraventricular hemorrhage (IVH) on 14-day mortality, outcome at 6 months, and the occurrence of chronic hydrocephalus in patients with aneurysmal subarachnoid hemorrhage. Clinical grade of subarachnoid hemorrhage and the distribution of extravasated blood were evaluated in 219 patients with ruptured aneurysms. Computed tomographic scans performed within 72 h of hemorrhage were analyzed to determine the severity of intraventricular and subarachnoid hemorrhage and the volume of intracerebral hematomas. Outcome at 6 months was assessed using the Glasgow Outcome Scale. Intraventricular hemorrhage extension occurred in 109 of the 219 patients studied. Fourteen-day mortality increased from 7.3% in patients without IVH to 14.1% in those with moderate IVH (IVH score 1-6) and to 41.7% in those with more severe IVH (IVH score> 6). The corresponding figures for unfavorable outcome at 6 months are 19.8%, 30.5%, and 66.7%, respectively. According to logistic regression analyses, the severity of IVH was an independent predictor of mortality and functional outcome. The clinical outcome after aneurysm rupture is at least in part determined by the severity of IVH. Knowledge of the effect of IVH may help guide physicians in the care of patients with aneurysmal bleeding.

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Section: Discussionmentioning

confidence: 93%

Influence of intraventricular hemorrhage on outcome after rupture of intracranial aneurysm

et al. 2001

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“…Despite their distance from the dilated ventricles, those vessels coming from the cortical surface will become distorted in an effort to supply the corresponding cerebral tissue [106]. Damage may compromise both peripheral and deep vessels.…”

Section: Cerebral Blood Vessels and Cerebral Blood Flowmentioning

confidence: 99%

Pathophysiology of Hydrocephalus

Silva

2005

Pediatric Hydrocephalus

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Hydrocephalus is a pathological entity that has been known since Hippocrates and Galen [33]. It is one of the most common disorders treated by neurosurgeons. The overall incidence and prevalence of the disease can be difficult to estimate, as it can occur as an isolated entity or in association with other neurological disorders. Congenital hydrocephalus is present in 3 of 1000 live births [97]. Aside from the congenital etiology, hydrocephalus can result from a series of neurological conditions such as head trauma, intracranial hemorrhage, tumor, or infection of the central nervous system at any time during life.Whatever its cause, the symptomatology of hydrocephalus is remarkably similar among patients. The radiological appearance is also deceptively alike for most age groups. However, age is an important factor in determining the clinical picture. Hydrocephalus due to a congenital infection of the central nervous system in a neonate is a different disorder from the normal-pressure hydrocephalus of the adult, despite the fact that both are morphologically represented by ventriculomegaly. Like the etiology, the specific damage caused by hydrocephalus is also strongly influenced by the age at onset of the disease.The pathophysiology of hydrocephalus is much more complex than its clinical or radiological presentation, going beyond the ventricular dilatation and mantle thinning obvious at first inspection. Together with gross macroscopic changes, hydrocephalus leads to alterations of the normal physiology, biochemistry, and ultrastructure of the brain. Three factors are basic for the determination of the severity of the injuries caused by hydrocephalus and the ultimate outcome. They are: age at onset, etiology, and the duration of the disease.The stage of maturation of the brain afflicted by hydrocephalus must be taken into account when discussing pathophysiology. Development is a fundamental aspect of the physiology of the brain in young immature animals and humans: metabolic pathways are maturing, neuronal activity is greatly increased, biosynthetic activity is intense, and myelination proceeds at a

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“…We also showed decreased vascularity and CBF in frontal cortex after induced CH and have suggested that these changes may be related to increased ICP, decreased cardiac output, or mechanical compression[6, 7]. However, the blood vessel density changes in chronic hydrocephalus have been observed to be in both directions and hence cannot be explained by simple spatial compression[4, 6, 20]. In the current study, we further explored the underlying mechanisms and demonstrated decreased VEGFR-2 levels, correlating with decreased CBF in frontal cortex after CH induction.…”

Section: Discussionmentioning

confidence: 97%

VEGF/VEGFR-2 changes in frontal cortex, choroid plexus, and CSF after chronic obstructive hydrocephalus

Yang

Dombrowski

Deshpande

et al. 2010

Journal of the Neurological Sciences

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Chronic Hydrocephalus (CH) is often associated with decreased cerebral blood flow (CBF) and oxygen levels. While the exact pathophysiology is not clear, vascular endothelial growth factor (VEGF) and its receptor-2 (VEGFR-2) may be involved. Because the choroid plexus (CP) is involved in cerebrospinal fluid (CSF) production and secretes numerous growth factors including VEGF, it is important to understand VEGF/VEGFR-2 levels in the CP-CSF circulatory system. Our results showed significant decreases in CBF and VEGFR-2 levels in frontal cortex (FC) in CH compared with SC; there were no significant changes in VEGF levels. CBF change in FC was positively correlated with VEGFR-2 levels (P=0.024). Immunohistochemistry (IHC) showed robust expression of VEGF/VEGFR-2 in CP. After CH induction, ventricular CSF volume and VEGF levels significantly increased. These results suggest that the decreased VEGFR-2 levels in FC may be contributed to decreased CBF and increased ventricular CSF-VEGF levels possibly reflected a hypoxic response and/or accumulation of VEGF from CP secretion after blockage of CSF outlet. Further investigation into CSF-VEGF levels in different sites may provide a better understanding of VEGF/VEGFR-2 modulation in the normal and hydrocephalic brain, and may represent a feasible approach to potential therapeutic options for hydrocephalus.

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Changes in the cerebral vascular bed in experimental hydrocephalus: An angio-architectural and histological study

Cited by 27 publications

References 11 publications

Influence of intraventricular hemorrhage on outcome after rupture of intracranial aneurysm

Influence of intraventricular hemorrhage on outcome after rupture of intracranial aneurysm

Pathophysiology of Hydrocephalus

VEGF/VEGFR-2 changes in frontal cortex, choroid plexus, and CSF after chronic obstructive hydrocephalus

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