Hydrocephalus associated with childhood nonaccidental head trauma

Vadivelu, Sudhakar; Rekate, Harold L.; Esernio-Jenssen, Debra; Mittler, Mark A.; Schneider, Steven J.

doi:10.3171/2016.8.focus16266

Cited by 9 publications

(6 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hydrocephalus is a disease in which excessive secretion, circulation and absorption of cerebrospinal fluid (CSF) are impaired by craniocerebral diseases, resulting in increased intracranial CSF levels, expansion of the ventricular system and progressive expansion of the subarachnoid space 1 . Hydrocephalus can be primary or secondary to trauma, spontaneous bleeding, infection and tumours and can also be comorbid with neurological diseases such as dementia, Alzheimer's disease and Parkinson's disease 2‐4 . Hydrocephalus is a great challenge in neurosurgery because of its complicated aetiology, unclear mechanism, difficult treatment and many complications.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of neuronal necroptosis mediated by RIP1/RIP3/MLKL provides neuroprotective effects on kaolin‐induced hydrocephalus in mice

et al. 2021

View full text Add to dashboard Cite

Objectives Necroptosis is widespread in neurodegenerative diseases. Here, we examined necroptosis in the hippocampus and cortex after hydrocephalus and found that a necroptosis pathway inhibitor alleviates necroptosis and provides neuroprotective effects. Materials and methods Hydrocephalus was induced in C57BL/6 mice by kaolin. Haematoxylin and eosin (HE), Nissl, PI and Fluoro‐Jade B (FJB) staining were used for general observations. Phosphorylated receptor‐interacting protein kinase 3 (p‐RIP3) and phosphorylated mixed lineage kinase domain‐like (p‐MLKL) were measured by Western blotting and immunohistochemistry. Scanning electron microscopy (SEM) was used to observe ependymal cilia. Magnetic resonance imaging (MRI) and the Morris water maze (MWM) test were used to assess neurobehavioral changes. Immunofluorescence was used to detect microglial and astrocyte activation. Inflammatory cytokines were measured by Western blotting and RT‐PCR. Results Obvious pathological changes appeared in the hippocampus and cortex after hydrocephalus, and expression of the necroptosis markers p‐RIP3, p‐MLKL and inflammatory cytokines increased. Necrostatin‐1 (Nec‐1) and GSK872 reduced necrotic cell death, attenuated p‐RIP3 and p‐MLKL levels, slightly improved neurobehaviours and inhibited microglial and astrocyte activation and inflammation. Conclusions RIP1/RIP3/MLKL mediates necroptosis in the cortex and hippocampus in a hydrocephalus mouse model, and Nec‐1 and GSK872 have some neuroprotective effects.

show abstract

Section: Introductionmentioning

confidence: 99%

Inhibition of neuronal necroptosis mediated by RIP1/RIP3/MLKL provides neuroprotective effects on kaolin‐induced hydrocephalus in mice

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Neurological and neurodegenerative conditions in the brain can result in an increase in the release of inflammatory mediators into the injured areas. These conditions can include head trauma, intracranial hemorrhage, infection, brain tumor, genetic defect, or neurodegenerative disease (11,13,16,18,20,21,27,29,45,46). In many of these cases, the development of transient or chronic enlargement of the brain ventricles and an increase in pressure due to the accumulation of cerebrospinal fluid (CSF) occurs.…”

Section: Introductionmentioning

confidence: 99%

“…Microglia, the macrophage-like cells of the central nervous system (CNS), can be triggered to release proinflammatory cytokines in response to abnormal protein accumulation or neuronal injury from chemical or physical means (7,50). It is possible that such inflammation is associated with increases in CSF production associated with neurological disease (4,17,18,35,46). Summarized in Table 1, proinflammatory cytokines found upregulated in neurodegenerative states include interleukin (IL)-1␤ and tumor necrosis factor-␣ (TNF-␣).…”

Section: Introductionmentioning

confidence: 99%

Cytokine and inflammatory mediator effects on TRPV4 function in choroid plexus epithelial cells

Simpson

Preston

Schwerk

et al. 2019

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

The choroid plexus (CP), composed of capillaries surrounded by a barrier epithelium, is the main producer of cerebrospinal fluid (CSF). The CP epithelium regulates the transport of ions and water between the blood and the ventricles, contributing to CSF production and composition. Several studies suggest a connection between the cation channel transient receptor potential vanilloid-4 (TRPV4) and transepithelial ion movement. TRPV4 is a nonselective, calcium-permeable cation channel present in CP epithelia reported to be activated by cytokines and inflammatory mediators. Utilizing the PCP-R (porcine choroid plexus-Riems) cell line, we investigated the effects of various cytokines and inflammatory mediators on TRPV4-mediated activity. Select proinflammatory cytokines (TNF-α, IL-1β, TGF-β1) had inhibitory effects on TRPV4-stimulated transepithelial ion flux and permeability changes, whereas anti-inflammatory cytokines (IL-10, IL-4, and IL-6) had none. Quantitative mRNA analysis showed that these cytokines had no effect on TRPV4 transcription levels. Inhibition of the transcription factor NF-κB, involved in the production and regulation of several inflammatory cytokines, inhibited TRPV4-mediated activity, suggesting a link between TRPV4 and cytokine production. Contrary to published studies, the proinflammatory mediator arachidonic acid (AA) had inhibitory rather than stimulatory effects on TRPV4-mediated responses. However, inhibition of AA metabolism also caused inhibitory effects on TRPV4, suggesting a complex interaction of AA and its metabolites in the regulation of TRPV4 activity. Together these data imply that TRPV4 activity is involved in the inflammatory response; it is negatively affected by proinflammatory mediators. Furthermore, arachidonic acid metabolites, but not arachidonic acid itself, are positive regulators of TRPV4.

show abstract

“…In dogs, acquired hydrocephalus can develop at any age secondary to trauma, tumors, and meningoencephalitis leading to obstructions in the ventricular system [21]. In humans, the incidence rate of ventricular dilation occurring after a severe traumatic head injury is known to be about 39–44%, and increased ventricular size was found to be evident 4 weeks after sustaining an injury [23]. One report showed that the prevalence of hydrocephalus among dogs with head trauma was 26% (7/27), which was concluded to be an incidental finding [24].…”

Section: Discussionmentioning

confidence: 99%

Global brain ischemia in a dog with concurrent multiorgan dysfunction syndrome after bite wound trauma

2019

View full text Add to dashboard Cite

Background Bite wounds are one of the most common traumatic injuries in dogs and depending on their severity, location, etc., urgent care including antibiotic therapy may be necessary. Serious complications can result from these injuries, such as multiple organ dysfunction syndrome (MODS), as well as a generalized reduction in cerebral perfusion, e.g. during cardiac arrest, shock, or severe hypotension that may cause global brain ischemia (GBI). Case presentation A 5-year-old spayed female Maltese dog was presented with generalized seizures, ataxia, and obtunded mentation. The dog was injured by severe bite wounds that penetrated its abdomen and had received blood transfusions, antibiotic therapy (including metronidazole and cefazoline) and underwent emergency surgery 4 days before its visit. Based on a clinical examination, intracranial hypoxic damage with elevated intra-cranial pressure and MODS were highly suspected, and GBI was confirmed following magnetic resonance imaging. Increased signal intensity diffusely distributed in the olfactory bulb and frontal, temporal, and parietal grey matter was evident on the T2-weighted and fluid attenuated inversion recovery transverse images, along with corresponding high signal intensity observed on diffusion weighted imaging. During the 10-month follow-up period, the clinical signs gradually improved, but intermittent circling and cognitive dysfunction deficits remained. Conclusions GBI should be included among the differential diagnoses in case of any peracute non-progressive neurological dysfunction that occurs with episodes of hypotension or hypoxia. The abnormal signal intensity observed on diffusion weighted imaging was a useful indicator for diagnosing this condition. Long-term medical management with antibiotics and anti-convulsant and anti-oxidant therapies were considered to be helpful in managing the GBI concurrent with MODS in this dog.

show abstract

Hydrocephalus associated with childhood nonaccidental head trauma

Cited by 9 publications

References 23 publications

Inhibition of neuronal necroptosis mediated by RIP1/RIP3/MLKL provides neuroprotective effects on kaolin‐induced hydrocephalus in mice

Inhibition of neuronal necroptosis mediated by RIP1/RIP3/MLKL provides neuroprotective effects on kaolin‐induced hydrocephalus in mice

Cytokine and inflammatory mediator effects on TRPV4 function in choroid plexus epithelial cells

Global brain ischemia in a dog with concurrent multiorgan dysfunction syndrome after bite wound trauma

Contact Info

Product

Resources

About