Functional herniated choroid plexus in brain parenchyma following VP shunt removal

2020 ◽  
pp. 1-4
Author(s):  
Mustafa El Sheikh ◽  
Mohammed Fadelalla ◽  
Avinash Kumar Kanodia ◽  
Omar Kouli ◽  
Margaret Peebles ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Brain Parenchyma ◽  
Vp Shunt ◽  
Shunt Removal

Analysis of Changes in Signal Intensity of Choroid Plexus in MRI Using FLAIR-DW-EPI Pulse Sequence

2020 ◽  
Vol 3 (1) ◽  
pp. 9-15
Author(s):  
Jingyu Kim ◽  
◽  
Sang-Jin Im ◽  
Keyword(s):  
Choroid Plexus ◽  
Signal Intensity ◽  
Pulse Sequence ◽  
Signal Strength ◽  
Brain Parenchyma ◽  
Weighted Image ◽  
Diffusion Weighted ◽  
Water Signal ◽  
The Brain ◽  
Functional Problems

In this study, the signal intensity of choroid plexus, which is producing cerebrospinal fluid, is analyzed according to the FLAIR diffusion-weighted imaging technique. In the T2*-DW-EPI diffusion-weighted image, the FLAIR-DW-EPI technique, which suppressed the water signal, was additionally examined for subjects with high choroid plexus signals and compared and analyzed the signal intensity. As a result of the experiment, it was confirmed that the FLAIR-DW-EPI technique showed a signal strength equal to or lower than that of the brain parenchyma, and there was a difference in signal strength between the two techniques. As a result of this study, if the choroidal plexus signal is high in the T2 * -DW-EPI diffusionweighted image, additional examination of the FLAIR-DW-EPI technique is thought to be useful in distinguishing functional problems of the choroid plexus. In conclusion, if the choroidal plexus signal is high on the T2*-DW-EPI diffuse weighted image, it is thought that further examination of the FLAIR-DW-EPI technique will be useful in distinguishing functional problems of the choroidal plexus.

scholarly journals Neostigmine Attenuates Proinflammatory Cytokine Expression in Preoptic Area but Not Choroid Plexus during Lipopolysaccharide-Induced Systemic Inflammation

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Andrzej P. Herman ◽  
Dorota Tomaszewska-Zaremba ◽  
Marta Kowalewska ◽  
Aleksandra Szczepkowska ◽  
Małgorzata Oleszkiewicz ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Proinflammatory Cytokine ◽  
Preoptic Area ◽  
De Novo ◽  
Brain Parenchyma ◽  
Ache Inhibitor ◽  
Ache Inhibitors ◽  
Reproduction Process ◽  
Hypothalamic Structure ◽  
Alpha 7

The study was designed to examine whether the administration of neostigmine (0.5 mg/animal), a peripheral inhibitor of acetylcholinesterase (AChE), during an immune/inflammatory challenge provoked by intravenous injection of bacterial endotoxin—lipopolysaccharide (LPS; 400 ng/kg)—attenuates the synthesis of proinflammatory cytokines in the ovine preoptic area (POA), the hypothalamic structure playing an essential role in the control of the reproduction process, and in the choroid plexus (CP), a multifunctional organ sited at the interface between the blood and cerebrospinal fluid in the ewe. Neostigmine suppressed (p<0.05) LPS-stimulated synthesis of cytokines such as interleukin- (IL-) 1β, IL-6, and tumor necrosis factor (TNF) α in the POA, and this effect was similar to that induced by the treatment with systemic AChE inhibitor—donepezil (2.5 mg/animal). On the other hand, both AChE inhibitors did not influence the gene expression of these cytokines and their corresponding receptors in the CP. It was found that this structure seems to not express the neuronal acetylcholine (ACh) receptor subunit alpha-7, required for anti-inflammatory action of ACh. The mechanism of action involves inhibition of the proinflammatory cytokine synthesis on the periphery as well as inhibition of their de novo synthesis rather in brain microvessels and not in the CP. In conclusion, it is suggested that the AChE inhibitors incapable of reaching brain parenchyma might be used in the treatment of neuroinflammatory processes induced by peripheral inflammation.

scholarly journals Senescent Accelerated Prone 8 (SAMP8) Mice as A Model of Age Dependent Neuroinflammation

2020 ◽  
Author(s):  
Andrés Fernández ◽  
Elena Quintana ◽  
Patricia Velasco ◽  
Belén de Andrés ◽  
Maria Luisa Gaspar ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Inflammatory Cytokines ◽  
Hippocampal Formation ◽  
Morphological Changes ◽  
Interleukin 1 ◽  
Brain Parenchyma ◽  
Age Related ◽  
Inflammatory Changes ◽  
Samp8 Mice ◽  
The Brain

Abstract Background: Aging and age related diseases are strong risk factors for the development of neurodegenerative diseases. Neuroinflammation (NIF), as the brain's immune response, plays an important role in aged associated degeneration of central nervous system (CNS). The need of animal models that will allow us to understand and modulate this process is required for the scientific community. Methods: We have analyzed aging-phenotypical and inflammatory changes of brain myeloid cells (bMyC) in a senescent accelerated prone aged (SAMP8) mouse model, and compared with their resistant to senescence control (SAMR1). We have performed morphometric methods to evaluate the architecture of cellular prolongations and analyzed Iba1+ clustered cells with aging. To analyse specific constant brain areas we have performed stereology measurements of Iba1+ cells in the hippocampal formation. We have isolated bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch), and analyzed their response to systemic LPS- driven inflammation.Results: Aged 10 month old SAMP8 mice presents many of the hallmarks of aging-dependent neuroinflammation when compared with their senescence resistant control (SAMR1); ie, increase of protein aggregates, presence of Iba1+ clusters, but not increase in the number of Iba1+ cells. We have further observed and increased of main inflammatory mediator IL-1β, and augment of border MHCII+Iba1+ cells. Isolated CD45+ bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch) have been analyzed showing that there is not significant increase of CD45+ from the periphery. Our data support that aged-driven pro-inflammatory cytokine interleukin 1 beta (IL1β) transcription is mainly enhanced in CD45+BP cells. Furthermore, we are showing that LPS-driven systemic inflammation produces inflammatory cytokines mainly in the border bMyC, sensed to a lesser extent by the BP bMyC, and is enhanced in aged SAMP8 compared to control SAMR1.Conclusion: Our data validate the SAMP8 model to study age-associated neuroinflammatory events, but careful controls for age and strain are required. These animals show morphological changes in their bMyC cell repertoires associated to age, corresponding to an increase in the production of main pro inflammatory cytokines such as IL-1β, which predispose the brain to an enhanced inflammatory response after LPS-systemic challenge.

scholarly journals Wandering Distal End of Ventriculo-Peritoneal Shunt: Our Experience with Five Cases and Review of Literature

2013 ◽  
Vol 32 (3) ◽  
pp. 266-269 ◽  
Author(s):  
Vijay Kumar Kundal ◽  
Mufique Gajdhar ◽  
Chetan Sharma ◽  
Deepak Agrawal ◽  
Raksha Kundal
Keyword(s):  
Inguinal Hernia ◽  
The Other ◽  
Unusual Complication ◽  
Shunt Surgery ◽  
Review Of Literature ◽  
Hernia Sac ◽  
Vp Shunt ◽  
The Past ◽  
Shunt Removal ◽  
Ventriculo Peritoneal Shunt

Ventriculo-peritoneal (VP) shunt is the most commonly performed procedure for the management of hydrocephalus. Although shunts have improved the morbidity and mortality associated with disordered Cerebrospinal fluid (CSF) mechanics over the past 30 years, they still are associated with many potentially avoidable complications in clinical practice. However, extrusion of VP shunt catheter is an unusual complication of VP shunt Surgery. We are presenting this unusual complication in five patients. The lower end of the shunt was seen extruding from anal opening in one patient, umbilicus in one, urethra in one, inguinal hernia sac in one and oral cavity in one patient. All of these patients were managed by shunt removal, intra venous antibiotics followed by shunt replacement on the other side except the patient with inguinal hernia sac. DOI: http://dx.doi.org/10.3126/jnps.v32i3.6935 J. Nepal Paediatr. SocVol.32(3) 2012 266-269

Translational value of choroid plexus imaging for tracking neuroinflammation in mice and humans

2021 ◽  
Vol 118 (36) ◽  
pp. e2025000118
Author(s):  
Vinzenz Fleischer ◽  
Gabriel Gonzalez-Escamilla ◽  
Dumitru Ciolac ◽  
Philipp Albrecht ◽  
Patrick Küry ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Choroid Plexus ◽  
Mouse Models ◽  
Functional Impairment ◽  
Brain Parenchyma ◽  
Autoimmune Encephalomyelitis ◽  
Inflammatory Conditions ◽  
Brain Responses ◽  
Experimental Mouse ◽  
Multiple Sclerosis Patients

Neuroinflammation is a pathophysiological hallmark of multiple sclerosis and has a close mechanistic link to neurodegeneration. Although this link is potentially targetable, robust translatable models to reliably quantify and track neuroinflammation in both mice and humans are lacking. The choroid plexus (ChP) plays a pivotal role in regulating the trafficking of immune cells from the brain parenchyma into the cerebrospinal fluid (CSF) and has recently attracted attention as a key structure in the initiation of inflammatory brain responses. In a translational framework, we here address the integrity and multidimensional characteristics of the ChP under inflammatory conditions and question whether ChP volumes could act as an interspecies marker of neuroinflammation that closely interrelates with functional impairment. Therefore, we explore ChP characteristics in neuroinflammation in patients with multiple sclerosis and in two experimental mouse models, cuprizone diet-related demyelination and experimental autoimmune encephalomyelitis. We demonstrate that ChP enlargement—reconstructed from MRI—is highly associated with acute disease activity, both in the studied mouse models and in humans. A close dependency of ChP integrity and molecular signatures of neuroinflammation is shown in the performed transcriptomic analyses. Moreover, pharmacological modulation of the blood–CSF barrier with natalizumab prevents an increase of the ChP volume. ChP enlargement is strongly linked to emerging functional impairment as depicted in the mouse models and in multiple sclerosis patients. Our findings identify ChP characteristics as robust and translatable hallmarks of acute and ongoing neuroinflammatory activity in mice and humans that could serve as a promising interspecies marker for translational and reverse-translational approaches.

scholarly journals The Role of the Choroid Plexus in Neutrophil Invasion after Traumatic Brain Injury

2009 ◽  
Vol 29 (9) ◽  
pp. 1503-1516 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Nathalie Strazielle ◽  
Brian J Zink ◽  
Jean-François Ghersi-Egea ◽  
Adam Chodobski
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Choroid Plexus ◽  
Neutrophil Migration ◽  
Inflammatory Cells ◽  
Brain Parenchyma ◽  
Electron Microscopic ◽  
Epithelial Barriers

Traumatic brain injury (TBI) frequently results in neuroinflammation, which includes the invasion of neutrophils. After TBI, neutrophils infiltrate the choroid plexus (CP), a site of the blood—cerebrospinal fluid (CSF) barrier (BCSFB), and accumulate in the CSF space near the injury, from where these inflammatory cells may migrate to brain parenchyma. We have hypothesized that the CP functions as an entry point for neutrophils to invade the injured brain. Using the controlled cortical impact model of TBI in rats and an in vitro model of the BCSFB, we show that the CP produces CXC chemokines, such as cytokine-induced neutrophil chemoattractant (CINC)-1 or CXCL1, CINC-2α or CXCL3, and CINC-3 or CXCL2. These chemokines are secreted both apically and basolaterally from the choroidal epithelium, a prerequisite for neutrophil migration across epithelial barriers. Consistent with these findings, we also provide electron microscopic evidence that neutrophils infiltrate the choroidal stroma and subsequently reach the intercellular space between choroidal epithelial cells. This is the first detailed analysis of the BCSFB function related to neutrophil trafficking. Our observations support the role of this barrier in posttraumatic neutrophil invasion.

scholarly journals Distribution of Suramin, an Antitrypanosomal Drug, across the Blood-Brain and Blood-Cerebrospinal Fluid Interfaces in Wild-Type and P-Glycoprotein Transporter-Deficient Mice

2007 ◽  
Vol 51 (9) ◽  
pp. 3136-3146 ◽  
Author(s):  
Lisa Sanderson ◽  
Adil Khan ◽  
Sarah Thomas
Keyword(s):  
Choroid Plexus ◽  
Brain Perfusion ◽  
Brain Parenchyma ◽  
Sleeping Sickness ◽  
New Drugs ◽  
Wild Type ◽  
P Glycoprotein ◽  
Blood Brain ◽  
Targeted Mutation ◽  
The Brain

ABSTRACT Although 60 million people are exposed to human African trypanosomiasis, drug companies have not been interested in developing new drugs due to the lack of financial reward. No new drugs will be available for several years. A clearer understanding of the distribution of existing drugs into the brains of sleeping sickness patients is needed if we are to use the treatments that are available more safely and effectively. This proposal addresses this issue by using established animal models. Using in situ brain perfusion and isolated incubated choroid plexus techniques, we investigated the distribution of [3H]suramin into the central nervous systems (CNSs) of male BALB/c, FVB (wild-type), and P-glycoprotein-deficient (Mdr1a/Mdr1b-targeted mutation) mice. There was no difference in the [3H]suramin distributions between the three strains of mice. [3H]suramin had a distribution similar to that of the vascular marker, [14C]sucrose, into the regions of the brain parenchyma that have a blood-brain barrier. However, the association of [3H]suramin with the circumventricular organ samples, including the choroid plexus, was higher than that of [14C]sucrose. The association of [3H]suramin with the choroid plexus was also sensitive to phenylarsine oxide, an inhibitor of endocytosis. The distribution of [3H]suramin to the brain was not affected by the presence of other antitrypanosomal drugs or the P-glycoprotein efflux transporter. Overall, the results confirm that [3H]suramin would be unlikely to treat the second or CNS stage of sleeping sickness.

Choroid plexus coagulation in infants with extreme hydrocephalus or hydranencephaly

2014 ◽  
Vol 14 (1) ◽  
pp. 55-57 ◽  
Author(s):  
Sylvia Shitsama ◽  
Nunthasiri Wittayanakorn ◽  
Humphrey Okechi ◽  
A. Leland Albright
Keyword(s):  
Choroid Plexus ◽  
Medical Records ◽  
Congenital Hydrocephalus ◽  
Shunt Insertion ◽  
Radiographic Images ◽  
Vp Shunt ◽  
Shunt Placement ◽  
Csf Leakage ◽  
Lost To Follow Up ◽  
Severe Hydrocephalus

Object Severe hydrocephalus and hydranencephaly are common congenital conditions in Kenya. In patients with these conditions, ventriculoperitoneal (VP) shunts are associated with appreciable complications and endoscopic third ventriculostomies (ETVs) have limited success. Endoscopic choroid plexus coagulation (CPC) to diminish CSF production is a potential treatment option. The purpose of this study was to evaluate the effect of CPC without ETV in infants with severe hydrocephalus or hydranencephaly. Methods Medical records of infants with severe congenital hydrocephalus or hydranencephaly who underwent CPC in Kijabe Hospital from November 2010 to April 2013 were reviewed retrospectively. Thirty-three patients with complete medical records and preoperative radiographic images were identified. After CPC, the infants were followed in the Kijabe Hospital outpatient department, in mobile clinics, or by telephone. Success of the CPC was defined as resolution of preoperative symptoms, stabilization of head size, and avoidance of VP shunt placement. Results Patients were followed from 30 to 608 days (median of 120 days). Three patients were lost to follow-up. Of the 30 evaluable patients, CPC was considered to be successful in 13 (43.3%), including 8 of 20 patients with severe hydrocephalus and 5 of 10 with hydranencephaly. Failure of CPC was evident from increased head circumference in 14 (82%) of 17 patients and from CSF leakage in 3. Of the 17 failures, 13 occurred within 3 months of surgery. Six patients died: 3 whose CPC procedures were failures, 2 whose CPC was successful, and 1 postoperatively. Of the 17 in whom CPC failed, 10 subsequently underwent VP shunt insertion. Conclusions CPC stabilizes macrocephaly in approximately 40% of infants with severe congenital hydrocephalus and hydranencephaly and can be considered as an alternative to VP shunt placement.

scholarly journals Spike protein multiorgan tropism suppressed by antibodies targeting SARS-CoV-2

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Molly Brady ◽  
Conor McQuaid ◽  
Alexander Solorzano ◽  
Angelique Johnson ◽  
Abigail Combs ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Imaging System ◽  
Brain Parenchyma ◽  
Dynamic Imaging ◽  
Spike Protein ◽  
Tissue Analysis ◽  
Organ Uptake ◽  
Organ Specific ◽  
The Brain

AbstractWhile there is SARS-CoV-2 multiorgan tropism in severely infected COVID-19 patients, it’s unclear if this occurs in healthy young individuals. In addition, for antibodies that target the spike protein (SP), it’s unclear if these reduce SARS-CoV-2/SP multiorgan tropism equally. We used fluorescently labeled SP-NIRF to study viral behavior, using an in vivo dynamic imaging system and ex in vivo tissue analysis, in young mice. We found a SP body-wide biodistribution followed by a slow regional elimination, except for the liver, which showed an accumulation. SP uptake was highest for the lungs, and this was followed by kidney, heart and liver, but, unlike the choroid plexus, it was not detected in the brain parenchyma or CSF. Thus, the brain vascular barriers were effective in restricting the entry of SP into brain parenchyma in young healthy mice. While both anti-ACE2 and anti-SP antibodies suppressed SP biodistribution and organ uptake, anti-SP antibody was more effective. By extension, our data support the efficacy of these antibodies on SARS-CoV-2 multiorgan tropism, which could determine COVID-19 organ-specific outcomes.

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