Oxygen metabolism changes in patients with idiopathic normal pressure hydrocephalus before and after shunting operation

Miyamoto, Junichi; Tatsuzawa, Kazunori; Inoue, Yasuaki; Imahori, Yoshio; Mineura, Katsuyoshi

doi:10.1111/j.1600-0404.2007.00798.x

Cited by 25 publications

(12 citation statements)

References 17 publications

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“…The gadobutrol propagated at the brain surface along large leptomeningeal arteries. The cerebral blood perfusion is reduced in iNPH as is the cerebral metabolism (Calcagni et al, ; Eide & Stanisic, ; Miyamoto, Tatsuzawa, Inoue, Imahori, & Mineura, ; Ziegelitz et al, ). Surgical diversion of CSF reduces the pulsatile and static ICP, likely facilitating the fluid and nutrient transfer at the capillary level as reflected by a long‐lasting clinical improvement (Eide & Sorteberg, ).…”

Section: Discussionmentioning

confidence: 99%

Loss of perivascular aquaporin‐4 in idiopathic normal pressure hydrocephalus

Hasan‐Olive

Enger

Hansson

et al. 2018

Glia

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Idiopathic normal pressure hydrocephalus (iNPH) is a subtype of dementia that may be successfully treated with cerebrospinal fluid (CSF) diversion. Recently, magnetic resonance imaging (MRI) using a MRI contrast agent as a CSF tracer revealed impaired clearance of the CSF tracer from various brain regions such as the entorhinal cortex of iNPH patients. Hampered clearance of waste solutes, for example, soluble amyloid‐β, may underlie neurodegeneration and dementia in iNPH. The goal of the present study was to explore whether iNPH is associated with altered subcellular distribution of aquaporin‐4 (AQP4) water channels, which is reported to facilitate CSF circulation and paravascular glymphatic drainage of metabolites from the brain parenchyma. Cortical brain biopsies of 30 iNPH patients and 12 reference individuals were subjected to AQP4 immunogold cytochemistry. Electron microscopy revealed significantly reduced density of AQP4 water channels in astrocytic endfoot membranes along cortical microvessels in patients with iNPH versus reference subjects. There was a significant positive correlation between density of AQP4 toward endothelial cells (perivascular) and toward parenchyma, but the reduced density of AQP4 toward parenchyma was not significant in iNPH. We conclude that perivascular AQP4 expression is attenuated in iNPH, potentially contributing to impaired glymphatic circulation, and waste clearance, and subsequent neurodegeneration. Hence, restoring normal perivascular AQP4 distribution may emerge as a novel treatment strategy for iNPH.

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Section: Discussionmentioning

confidence: 99%

Loss of perivascular aquaporin‐4 in idiopathic normal pressure hydrocephalus

Hasan‐Olive

Enger

Hansson

et al. 2018

Glia

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“…Of note, similar abnormalities and processes are implicated in hydrocephalus, stroke and traumatic brain injury, which may relate to shared pathogenic factors. Lastly, specific to hydrocephalus, shunting results in normalization of local CBF that has been linked to improved outcomes [200-202]; however, others have suggested that this may not account for clinical improvement seen in the long-term [193]. …”

Section: Cerebrovasculaturementioning

confidence: 99%

Neonatal Brain Hemorrhage (NBH) of Prematurity: Translational Mechanisms of the Vascular-Neural Network

Lekic¹,

Klebe²,

Poblete³

et al. 2015

CMC

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Neonatal brain hemorrhage (NBH) of prematurity is an unfortunate consequence of preterm birth. Complications result in shunt dependence and long-term structural changes such as post-hemorrhagic hydrocephalus, periventricular leukomalacia, gliosis, and neurological dysfunction. Several animal models are available to study this condition, and many basic mechanisms, etiological factors, and outcome consequences, are becoming understood. NBH is an important clinical condition, of which treatment may potentially circumvent shunt complication, and improve functional recovery (cerebral palsy, and cognitive impairments). This review highlights key pathophysiological findings of the neonatal vascular-neural network in the context of molecular mechanisms targeting the post-hemorrhagic hydrocephalus affecting this vulnerable infant population.

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“…CBF and related parameters have been measured in human hydrocephalus using a variety of techniques including positron emission tomography, transcranial Doppler, and radionuclide angiography; most have demonstrated CBF reductions especially in white matter Shirane et al, 1992;Chang et al, 2009]. Improvement of blood flow after shunting may correlate with clinical improvement [Brooks et al, 1986;Nishimaki et al, 2004;Miyamoto et al, 2007]. Decreased blood flow is associated with local increases in glucose utilization in cats [Chumas et al, 1994], oxidative stress including lipid peroxidation and protein nitrosylation in H-Tx rats [Socci et al, 1999], and activation of calcium-dependent proteolytic enzymes that destroy axons in rats with kaolin-induced hydrocephalus [Del Bigio, 2000].…”

Section: Pathogenesis Of Brain Damage In Hydrocephalusmentioning

confidence: 99%

Neuropathology and structural changes in hydrocephalus

Bigio¹

2010

Dev Disabil Res Revs

200

161

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In the context of spina bifida, hydrocephalus is usually caused by crowding of the posterior fossa with obstruction to cerebrospinal fluid flow from the forth ventricle, and less often by malformation of the cerebral aqueduct. Enlargement of the cerebral ventricles causes gradual destruction of periventricular white matter axons. Motor, sensory, visual, and memory systems may be disturbed through involvement of the long projection axons, periventricular structures including the corpus callosum, and the fimbria-fornix pathway. Secondary changes occur in neuronal cell bodies and synapses, but there is minimal death of neurons. The clinical syndrome of hydrocephalic brain dysfunction is thus due to subcortical disconnection. Some of the brain dysfunction is reversible by shunting, probably through restoration of cerebral blood flow and normalization of the extracellular environment. However, destroyed axons cannot be restored.

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Oxygen metabolism changes in patients with idiopathic normal pressure hydrocephalus before and after shunting operation

Abstract: The improvement of rCMRO(2) correlated with the response to VPS. Significant changes in rOEF might predict poor response to VPS.

Cited by 25 publications

References 17 publications

Loss of perivascular aquaporin‐4 in idiopathic normal pressure hydrocephalus

Loss of perivascular aquaporin‐4 in idiopathic normal pressure hydrocephalus

Neonatal Brain Hemorrhage (NBH) of Prematurity: Translational Mechanisms of the Vascular-Neural Network

Neuropathology and structural changes in hydrocephalus

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