Neonatal seizures and white matter injury: Role of rotavirus infection and probiotics

2019 ◽  
Vol 41 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Jung Sook Yeom ◽  
Ji Sook Park ◽  
Young-Soo Kim ◽  
Rock Bum Kim ◽  
Dae-Sup Choi ◽  
...  
Keyword(s):  
White Matter ◽  
White Matter Injury ◽  
Neonatal Seizures ◽  
Rotavirus Infection

scholarly journals Important Role of Reverse Na+-Ca2+Exchange in Spinal Cord White Matter Injury at Physiological Temperature

2000 ◽  
Vol 84 (2) ◽  
pp. 1116-1119 ◽  
Author(s):  
Shuxin Li ◽  
Qiubo Jiang ◽  
Peter K. Stys
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Traumatic Injury ◽  
White Matter Injury ◽  
Mechanical Trauma ◽  
White Matter Tracts ◽  
Physiological Temperature ◽  
Cord Injury ◽  
Cellular Ca

Spinal cord injury is a devastating condition in which most of the clinical disability results from dysfunction of white matter tracts. Excessive cellular Ca2+ accumulation is a common phenomenon after anoxia/ischemia or mechanical trauma to white matter, leading to irreversible injury because of overactivation of multiple Ca2+-dependent biochemical pathways. In the present study, we examined the role of Na+-Ca2+ exchange, a ubiquitous Ca2+ transport mechanism, in anoxic and traumatic injury to rat spinal dorsal columns in vitro. Excised tissue was maintained in a recording chamber at 37°C and injured by exposure to an anoxic atmosphere for 60 min or locally compressed with a force of 2 g for 15 s. Mean compound action potential amplitude recovered to ≈25% of control after anoxia and to ≈30% after trauma. Inhibitors of Na+-Ca2+ exchange (50 μM bepridil or 10 μM KB-R7943) improved functional recovery to ≈60% after anoxia and ≈70% after traumatic compression. These inhibitors also prevented the increase in calpain-mediated spectrin breakdown products induced by anoxia. We conclude that, at physiological temperature, reverse Na+-Ca2+exchange plays an important role in cellular Ca2+ overload and irreversible damage after anoxic and traumatic injury to dorsal column white matter tracts.

scholarly journals A Systematic Review of WNT Signaling in Endothelial Cell Oligodendrocyte Interactions: Potential Relevance to Cerebral Small Vessel Disease

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1545
Author(s):  
Narek Manukjan ◽  
Zubair Ahmed ◽  
Daniel Fulton ◽  
W. Matthijs Blankesteijn ◽  
Sébastien Foulquier
Keyword(s):  
White Matter ◽  
Small Vessel Disease ◽  
Clinical Manifestations ◽  
Cell Types ◽  
Cerebral Small Vessel Disease ◽  
White Matter Injury ◽  
Small Vessel ◽  
Limited Attention ◽  
Vessel Disease

Key pathological features of cerebral small vessel disease (cSVD) include impairment of the blood brain barrier (BBB) and the progression of white matter lesions (WMLs) amongst other structural lesions, leading to the clinical manifestations of cSVD. The function of endothelial cells (ECs) is of major importance to maintain a proper BBB. ECs interact with several cell types to provide structural and functional support to the brain. Oligodendrocytes (OLs) myelinate axons in the central nervous system and are crucial in sustaining the integrity of white matter. The interplay between ECs and OLs and their precursor cells (OPCs) has received limited attention yet seems of relevance for the study of BBB dysfunction and white matter injury in cSVD. Emerging evidence shows a crosstalk between ECs and OPCs/OLs, mediated by signaling through the Wingless and Int-1 (WNT)/β-catenin pathway. As the latter is involved in EC function (e.g., angiogenesis) and oligodendrogenesis, we reviewed the role of WNT/β-catenin signaling for both cell types and performed a systematic search to identify studies describing a WNT-mediated interplay between ECs and OPCs/OLs. Dysregulation of this interaction may limit remyelination of WMLs and render the BBB leaky, thereby initiating a vicious neuroinflammatory cycle. A better understanding of the role of this signaling pathway in EC–OL crosstalk is essential in understanding cSVD development.

Rotavirus-Induced Neonatal Epileptic Encephalopathy—A Disease Spectrum Illustrated by Monochorionic Twins

2019 ◽  
Vol 51 (01) ◽  
pp. 062-067 ◽  
Author(s):  
Esther M. Hopmans ◽  
Astrid van der Heide ◽  
Pui Khi Chung ◽  
Daniëlle Brinkman ◽  
Mariet C.W. Feltkamp ◽  
...  
Keyword(s):  
White Matter ◽  
Epileptic Encephalopathy ◽  
Neonatal Seizures ◽  
Monochorionic Twins ◽  
Rotavirus Infection ◽  
Disease Spectrum ◽  
Pattern Characteristic ◽  
Magnetic Resonance Imaging Mri ◽  
Electroencephalogram Eeg ◽  
Eeg Pattern

AbstractRotavirus has been associated with neonatal seizures and specific white matter magnetic resonance imaging (MRI) abnormalities. We describe monochorionic twins who not only tested positive for rotavirus with these white matter MRI abnormalities but who also showed an electroencephalogram (EEG) pattern characteristic of early infantile epileptic encephalopathy (EIEE), which has so far solely been described in epileptic encephalopathies with a poor prognosis. This report suggests that rotavirus infection must be added to the list of causes of EIEE EEG, and that the outcome then is likely more favorable. As MRI and EEG signs of rotavirus encephalopathy were present in one twin with only subtle neurologic symptoms, rotavirus may well cause insidious central nervous system complications more often. We suggest considering rotavirus infection in neonates presenting with seizures, and to add rotavirus infection to the differential diagnosis of EIEE.

White Matter Injury in the Preterm Neonate: The Role of Perfusion

2001 ◽  
Vol 23 (3) ◽  
pp. 209-212 ◽  
Author(s):  
Gorm Greisen ◽  
Klaus Børch
Keyword(s):  
White Matter ◽  
Preterm Neonate ◽  
White Matter Injury

scholarly journals 6-Gingerol Alleviates Neonatal Hypoxic-Ischemic Cerebral and White Matter Injury and Contributes to Functional Recovery

2021 ◽  
Vol 12 ◽  
Author(s):  
Man Zhao ◽  
Yuan Yao ◽  
Jingyi Du ◽  
Liang Kong ◽  
Tiantian Zhao ◽  
...  
Keyword(s):  
Cell Death ◽  
White Matter ◽  
Inflammatory Responses ◽  
Epigenetic Modification ◽  
Pathological Process ◽  
White Matter Injury ◽  
Inflammatory Factor ◽  
Ginger Extract ◽  
Motor Disability

Hypoxic-ischemic encephalopathy (HIE) is one main cause of neonatal death and disability, causing substantial injury to white and gray matter, which can lead to severe neurobehavioral dysfunction, including intellectual disability and dyskinesia. Inflammation, nerve cell death, and white matter injury are important factors in the pathological process of HIE. 6-Gingerol is a ginger extract, which reduces inflammatory response and cell death. However, the role of 6-Gingerol in neonatal hypoxic-ischemic brain injury (HIBI) remains unknown. In this study, we constructed a mouse HIBI model and analyzed the protective effect of 6-Gingerol on HIBI by using behavioral tests, histological staining, qPCR and western blot. Here, we found that 6-Gingerol treatment could alleviate HIBI and improve short-term reflex performance, which is closely related to cell death and neuroinflammation. Additionally, 6-Gingerol reduced neuronal apoptosis, pro-inflammatory factor release, as well as microglial activation. Furthermore, 6-Gingerol significantly improved motor disability, which is associated with white matter damage. Thus, our results showed that 6-Gingerol could reduce the loss of myelin sheaths, alleviate cell death of oligodendrocytes, and stimulate the maturation of oligodendrocytes. In terms of mechanism, we found that 6-Gingerol decreased histone H3K27me3 levels, activated AKT pathway and inhibited the activation of ERK and NF-κB pathway at 3 days post-HIBI. Taken together, our data clearly indicate that 6-Gingerol plays a neuroprotective role against HIBI by epigenetic modification and regulation of AKT, ERK, and NF-κB pathways, inhibiting inflammatory responses and reducing cell death.

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