Cerebral Fluid Dynamics and Brain Regional Blood Flow in Experimental Hydrocephalus

Ransohoff, Joseph; DiMattio, Joseph; Hochwald, G. M.; Epstein, Fred J.

doi:10.1159/000119593

Cited by 7 publications

(10 citation statements)

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“…Both clinical 2,24,61 and experimental 23,27,34,35,47,5z studies have established that hydrocephalus is associated with a reduction in cerebral blood flow (CBF), although not to levels considered low enough to cause cerebral ischemia. 7~ Previous work from this laboratory using a neonatal kitten model of hydrocephalus has confirmed the presence of cerebral hypoperfusion and has shown changes on magnetic resonance (MR) spectroscopy consistent with mild cerebral ischemia and delayed myelination (unpublished data).…”

mentioning

confidence: 99%

Anaerobic glycolysis preceding white-matter destruction in experimental neonatal hydrocephalus

Chumas¹,

Drake²,

Bigio³

et al. 1994

Journal of Neurosurgery

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The metabolic changes in neonatal hydrocephalus that lead to permanent brain injury are not clearly defined, nor is the extent to which these changes can be prevented by a cerebrospinal fluid shunt. To clarify these processes, cerebral glucose utilization was examined using [14C]2-deoxyglucose autoradiography in 1-month-old kittens, kaolin-induced hydrocephalic littermates, and hydrocephalic kittens in which a ventriculoperitoneal shunt had been inserted 10 days after kaolin injection. The hydrocephalic kittens showed thinning of the cerebral mantle and an anterior-to-posterior gradient of enlargement of the ventricular system, with a ventricle:brain ratio of 24% for the frontal and 35% for the occipital horns compared with control (< 0.5%) and shunted (< 5%) animals. White matter in hydrocephalic animals was edematous. Myelination was delayed in the periventricular region and in the cores of the cerebral gyri. Glucose utilization in hydrocephalic and shunted animals was unchanged from control animals in all gray-matter regions examined. However, in hydrocephalic animals, the frontal white matter exhibited a significant increase in glucose utilization (25 mumol.100 gm-1.min-1) in the cores of gyri compared with normal surrounding white-matter values (14.8 mumol.100 gm-1.min-1). Very low values (mean 4 mumol.100 gm-1.min-1) were found in areas corresponding to severe white-matter edema, and these areas were surrounded by a halo of increased activity (24 mumol.100 gm-1.min-1). In contrast, cytochrome oxidase activity in white matter was homogeneous. Shunting resulted in restoration of the cerebral mantle thickness, a return to normal levels of glucose utilization in the white matter, and an improvement in myelination. It is suggested that the areas of increased glucose utilization seen in the white matter represent anaerobic glycolysis which, if untreated, progresses to infarction. The pattern of this increased glucose utilization matches that of expected myelination and, during this period of high energy demand, white matter may be susceptible to the hypoperfusion associated with hydrocephalus.

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mentioning

confidence: 99%

Anaerobic glycolysis preceding white-matter destruction in experimental neonatal hydrocephalus

Chumas¹,

Drake²,

Bigio³

et al. 1994

Journal of Neurosurgery

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“…Although most studies have described cerebrovascular compression in CH (Del Bigio and Bruni, 1988), a few studies have observed increased vascular density in certain brain regions and at various time points in CH (Dombrowski et al, 2008;Luciano et al, 2001;Ransohoff et al, 1975). Previously, we have shown an initial decrease in vascularity followed by a return above baseline in cortical gray and periventricular white matter in CH .…”

Section: Introductionmentioning

confidence: 76%

Dissociation between Vascular Endothelial Growth Factor Receptor-2 and Blood Vessel Density in the Caudate Nucleus after Chronic Hydrocephalus

Deshpande

Dombrowski

Leichliter

et al. 2009

J Cereb Blood Flow Metab

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Chronic hydrocephalus (CH) is characterized by the presence of ventricular enlargement, decreased cerebral blood flow (CBF), and brain tissue oxygen delivery. Although the underlying pathophysiological role of vascular endothelial growth factor (VEGF) is not clear, ischemic-hypoxic events in CH are known to trigger its release. Previously, we have shown increased VEGF receptor-2 (VEGFR-2) and blood vessel density (BVd) in the hippocampus after CH. We investigated changes in neuronal and glial VEGFR-2 density and BVd in the caudate nucleus in an experimental model of CH. Animals with CH were divided into short term (ST, 2 to 4 weeks) and long term (LT, 12 to 16 weeks) and were compared with surgical controls (SCs, 12 to 16 weeks). The cellular and BVds were estimated using immunohistochemical and stereological counting methods. Overall, percentage (%)VEGFR-2 neurons were approximately two times greater in CH (ST, LT) than in SC. By comparison, glial cell %VEGFR-2 was greater by 10% to 17% in ST and 4% to 11% lower in LT compared with that in SC. Blood vessel density was significantly lower in CH than in SC in the superficial caudate. Changes in cerebrospinal fluid ventricular volume and pressure, as well as in CBF did not correlate with either VEGFR-2 or BVd. These observed findings suggest that destructive forces may outweigh angiogenic forces and possibly show a disassociation between VEGFR-2 and BV expressions.

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“…Compression of capillaries, also called cerebrovascular compression, plays a significant role in the acute stage. Various research studies have confirmed collapse of cerebral capillaries in the periventricular white matter and cortical and subcortical gray matter [154][155][156][157][158]. Changes of cerebral circulation, which are adaptive in their nature, also known as cerebrovascular adaptation, occur in the chronic stage of hydrocephalus.…”

Section: Vascular Changes In Hydrocephalusmentioning

confidence: 99%

The Role of Transcranial Doppler Sonography in the Management of Pediatric Hydrocephalus

Kolarovszki¹

2019

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IV 5. Etiology of hydrocephalus 5.1 Congenital hydrocephalus 5.2 Acquired postnatal hydrocephalus 6. Pathophysiology of hydrocephalus 6.1 Pathophysiological mechanisms of onset and development of hydrocephalus 6.2 Pathologic changes in hydrocephalus 6.3 Vascular changes in hydrocephalus 6.4 Biochemical changes in hydrocephalus 6.5 Changes of cerebral metabolism in hydrocephalus 7. Clinical manifestations of pediatric hydrocephalus 8. Basic properties of ultrasound 9. Biological effects of ultrasound 9.1 Thermal effects 9.2 Cavitation 9.3 Other mechanic effects 10. Doppler sonography 10.1 The role of Doppler principle in ultrasonography 10.2 The Doppler systems with continuous wave (CW) 10.3 The pulsatility Doppler systems (the pulsed waves, PW) 10.4 The color flow Doppler tomography (CFD, real-time two-dimensional Doppler) 10.5 The technique of the color Doppler power mapping (color Doppler energy, CDE; color power angio, CPA; Doppler power mode; power mapping) 11. The transcranial color-coded Doppler ultrasonography 11.1 The transcranial color-coded Doppler ultrasonographic examination 12. The Doppler curve, measured and calculated parameters 12.1 The Doppler curve 12.2 Measured and assessed parameters of the Doppler curve 12.3 Development of Doppler parameters of cerebral circulation: physiological values 12.3.1 Neonates 12.3.2 Infancy V 12.4 The factors influencing the value of qualitative indices of the Doppler curve 12.4.1 The factors increasing the resistance index of cerebral arteries 12.4.2 Factors decreasing the resistance index of cerebral arteries 13. Morphology of the cerebral ventricles in pediatric hydrocephalus 14. Assessment of Doppler parameters of the cerebral arteries in children with hydrocephalus 15. Case reports 15.1 Assessment of intracranial dynamics in the preterm neonate with hydrocephalus before and after insertion of external ventricular drainage 15.2 Observation of intraindividual dynamics in the preterm neonate with asphyxia and development of progressive hydrocephalus regarding indication of drainage procedure 15.3 Impact of tachycardia on Doppler parameters of blood flow in ACA in the infant with active hydrocephalus 15.4 Assessment of intracranial dynamics of the infant with schizencephaly 15.5 Assessment of intracranial dynamics in the term neonate with congenital hydrocephalus, Arnold-Chiari malformation type II and lumbosacral myelomeningocele 15.6 Assessment of intracranial dynamics in the preterm neonate with posthemorrhagic hydrocephalus 15.7 Assessment of intracranial dynamics in the neonate with occipital encephalocele and congenital hydrocephalus 15.8 Assessment of intracranial dynamics in the term neonate with birth trauma, intracerebral hemorrhage and hemocephalus 15.9 Assessment of intracranial dynamics in the neonate with congenital hydrocephalus and VP shunt revision 15.10 Assessment of intracranial dynamics of congenital hydrocephalus in prenatal and postnatal period

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Cerebral Fluid Dynamics and Brain Regional Blood Flow in Experimental Hydrocephalus

Cited by 7 publications

References 0 publications

Anaerobic glycolysis preceding white-matter destruction in experimental neonatal hydrocephalus

Anaerobic glycolysis preceding white-matter destruction in experimental neonatal hydrocephalus

Dissociation between Vascular Endothelial Growth Factor Receptor-2 and Blood Vessel Density in the Caudate Nucleus after Chronic Hydrocephalus

The Role of Transcranial Doppler Sonography in the Management of Pediatric Hydrocephalus

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