scholarly journals Brain neuroimaging of domestic cats: correlation between computed tomography and cross- sectional anatomy

2016 ◽  
Vol 68 (5) ◽  
pp. 1105-1111
Author(s):  
A.C. Nepomuceno ◽  
R. Zanatta ◽  
D.G. Chung ◽  
P.F. Costa ◽  
M.A.R. Feliciano ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Central Nervous System ◽  
Nervous System ◽  
Clinical Symptoms ◽  
Clinical Signs ◽  
Normal Brain ◽  
Domestic Cats ◽  
Cross Sectional ◽  
Iodinated Contrast ◽  
The Brain

ABSTRACT Computed tomography of the brain is necessary as part of the diagnosis of lesions of the central nervous system. In this study we used six domestic cats, male or female, aged between one and five years, evaluated by Computed Tomography (CT) examination without clinical signs of central nervous system disorders. Two euthanized animals stating a condition unrelated to the nervous system were incorporated into this study. The proposal consisted in establishing detailed anatomical description of tomographic images of normal brain of cats, using as reference anatomical images of cross sections of the stained brain and cranial part, with thicknesses similar to the planes of the CT images. CT examinations were performed with and without intravenous iodinated contrast media for live animals. With one euthanized animal, the brain was removed and immediately preserved in 10% formalin for later achievement in cross-sectional thickness of approximately 4mm and staining technique of Barnard, and Robert Brown. The head of another animal was disarticulated in the Atlanto-occipital region and frozen at -20ºC then sliced to a thickness of about 5mm. The description of visualized anatomical structures using tomography is useful as a guide and allows transcribing with relative accuracy the brain region affected by an injury, and thus correlating it with the clinical symptoms of the patient, providing additional information and consequent improvement to veterinarians during the course of surgical clinic in this species.

scholarly journals Presence of amastigotes in the central nervous system of hamsters infected with Leishmania sp.

2011 ◽  
Vol 20 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Elisangela de Oliveira ◽  
Elisa Teruya Oshiro ◽  
Rebeca Vieira Pinto ◽  
Bruna Corrêa de Castro ◽  
Karla Borges Daniel ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Signs ◽  
Direct Examination ◽  
Mato Grosso ◽  
The Central Nervous System ◽  
Animal House ◽  
Immunohistochemical Studies ◽  
Negative Controls ◽  
The Brain

Visceral leishmaniasis (VL) is a severe chronic disease caused by Leishmania (Leishmania) infantum chagasi. Better knowledge on the effects caused by this disease can help develop adequate clinical management and treatment. Parasitological and immunohistochemical studies were performed golden hamsters Mesocricetus auratus infected with bone marrow from individuals with VL in the State of Mato Grosso do Sul, central-west Brazil. The effects of parasitism in the spleen, liver, kidneys, lungs, heart and brain of the animals were examined. Eighteen hamsters were inoculated intraperitoneally, and six healthy animals were used as negative controls. The animals were kept in the animal house and checked for clinical signs. Specimens of each organ were examined for the presence of amastigotes. Immunohistochemical technique was performed in all brain specimens and organs negative on the direct examination of parasites. Direct examination of amastigotes was positive in the spleen and liver of all infected animals; 33.3% showed the parasite in the kidneys and lungs, and 16.7% in the heart. Parasitic forms were seen in 83.3% (15/18) of the brain examined. Immunohistochemistry confirmed the results of the direct examination, except in two specimens of lung tissue and in the brain specimens. Other studies are needed to further clarify the effect of the parasite in the central nervous system.

scholarly journals Cholesterol: Its Regulation and Role in Central Nervous System Disorders

Cholesterol ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Matthias Orth ◽  
Stefano Bellosta
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Metabolic Pathways ◽  
Cholesterol Metabolism ◽  
Major Constituent ◽  
Normal Brain ◽  
Lipoprotein Receptors ◽  
Brain Cholesterol ◽  
Brain Functions ◽  
The Brain

Cholesterol is a major constituent of the human brain, and the brain is the most cholesterol-rich organ. Numerous lipoprotein receptors and apolipoproteins are expressed in the brain. Cholesterol is tightly regulated between the major brain cells and is essential for normal brain development. The metabolism of brain cholesterol differs markedly from that of other tissues. Brain cholesterol is primarily derived by de novo synthesis and the blood brain barrier prevents the uptake of lipoprotein cholesterol from the circulation. Defects in cholesterol metabolism lead to structural and functional central nervous system diseases such as Smith-Lemli-Opitz syndrome, Niemann-Pick type C disease, and Alzheimer’s disease. These diseases affect different metabolic pathways (cholesterol biosynthesis, lipid transport and lipoprotein assembly, apolipoproteins, lipoprotein receptors, and signaling molecules). We review the metabolic pathways of cholesterol in the CNS and its cell-specific and microdomain-specific interaction with other pathways such as the amyloid precursor protein and discuss potential treatment strategies as well as the effects of the widespread use of LDL cholesterol-lowering drugs on brain functions.

Microglia and the Brain: Complementary Partners in Development and Disease

2018 ◽  
Vol 34 (1) ◽  
pp. 523-544 ◽  
Author(s):  
Timothy R. Hammond ◽  
Daisy Robinton ◽  
Beth Stevens
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Disease ◽  
Immune Cells ◽  
New Technologies ◽  
Normal Brain ◽  
The Central Nervous System ◽  
Synaptic Maturation ◽  
The Brain ◽  
Normal Brain Development

An explosion of findings driven by powerful new technologies has expanded our understanding of microglia, the resident immune cells of the central nervous system (CNS). This wave of discoveries has fueled a growing interest in the roles that these cells play in the development of the CNS and in the neuropathology of a diverse array of disorders. In this review, we discuss the crucial roles that microglia play in shaping the brain—from their influence on neurons and glia within the developing CNS to their roles in synaptic maturation and brain wiring—as well as some of the obstacles to overcome when assessing their contributions to normal brain development. Furthermore, we examine how normal developmental functions of microglia are perturbed or remerge in neurodevelopmental and neurodegenerative disease.

scholarly journals Physiology of Microglia

2011 ◽  
Vol 91 (2) ◽  
pp. 461-553 ◽  
Author(s):  
Helmut Kettenmann ◽  
Uwe-Karsten Hanisch ◽  
Mami Noda ◽  
Alexei Verkhratsky
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Cell ◽  
Brain Parenchyma ◽  
Microglial Cells ◽  
Activation Process ◽  
Normal Brain ◽  
The Central Nervous System ◽  
Cellular Compartments ◽  
The Brain

Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

Effects of an aqueous extract of North American ginseng on MOG(35–55)-induced EAE in mice

2012 ◽  
Vol 90 (7) ◽  
pp. 933-939 ◽  
Author(s):  
Laura E. Bowie ◽  
Wendi A. Roscoe ◽  
Ed M.K. Lui ◽  
Robin Smith ◽  
Stephen J. Karlik
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Aqueous Extract ◽  
Clinical Symptoms ◽  
Clinical Signs ◽  
American Ginseng ◽  
Chronic Inflammatory Disease ◽  
Spinal Cord Tissue ◽  
Tissue Samples ◽  
The Central Nervous System

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system, in which the release of reactive oxygen species by infiltrating immune cells contributes to demyelination. American ginseng ( Panax quinquefolius ) is a natural health product with numerous beneficial properties, including anti-inflammatory and anti-oxidant effects. The purpose of this study was to determine whether ginseng could influence the course of the disease experimental autoimmune encephalomyelitis (EAE), an animal model of MS. C57BL/6J mice were immunized with MOG(35–55) peptide to induce EAE. After clinical disease appeared, mice received either oral doses of an aqueous extract of ginseng (150 mg/kg body mass), or the vehicle. Clinical symptoms were recorded, and spinal cord tissue samples were analyzed for pathological signs of disease. The aqueous extract of ginseng significantly decreased (i) clinical signs of EAE, (ii) levels of circulating TNF-α, and (iii) central nervous system immunoreactive iNOS and demyelination scores, without a change in other neuropathological measures. This study shows that an aqueous extract of ginseng may be able to attenuate certain signs of EAE, suggesting that it may be a useful adjuvant therapy for MS.

scholarly journals Naphthoquine-induced Central Nervous System and Hepatic Vasculocentric Toxicity in the Beagle Dog

2016 ◽  
Vol 44 (8) ◽  
pp. 1128-1136 ◽  
Author(s):  
Jean-Rene Galarneau ◽  
Emily K. Meseck ◽  
Robert L. Hall ◽  
Wenkui Li ◽  
Margaret L. Weaver
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Signs ◽  
Drug Candidate ◽  
Oral Gavage ◽  
Plasma Exposure ◽  
Toxicology Study ◽  
The Central Nervous System ◽  
The Brain ◽  
Microscopic Findings

Naphthoquine phosphate (NP) was considered as a partner drug with a promising antimalarial drug candidate. Here we report unexpected adverse clinical signs and microscopic findings in a canine pilot toxicology study with NP. Male and female dogs were dosed daily by oral gavage with NP at 2, 10, or 50 mg/kg/day for a maximum of 14 days. NP was not tolerated at ≥10 mg/kg/day; several animals were sacrificed in moribund condition and marked neurological clinical signs were noted at 50 mg/kg/day. The main microscopic observation was central nervous system vasculocentric inflammation (mainly lymphocytes and macrophages) in the white and gray matter of various regions of the brain at ≥2 mg/kg/day and at lower incidence in the spinal cord at ≥10 mg/kg/day. Vasculocentric microscopic changes predominantly centered on the centrilobular vein were also observed in the liver at ≥2 mg/kg/day. Females were more sensitive than males with comparable NP plasma exposure. In conclusion, under the conditions of this study, the administration of NP to dogs via daily oral gavage for up to 2 weeks was not tolerated causing moribundity, marked neurological clinical signs, and vasculocentric microscopic changes in the central nervous system and the liver.

scholarly journals Serum Procalcitonin Levels in Patients with Acute Central Nervous System Infections

2020 ◽  
Vol 8 (B) ◽  
pp. 1251-1255
Author(s):  
Yordan Kalchev ◽  
Tsetsa Petkova ◽  
Ralitsa Raycheva ◽  
Bothwell Kabayira ◽  
Tanya Deneva ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Bacterial Infections ◽  
Clinical Symptoms ◽  
Discriminatory Power ◽  
Cns Infection ◽  
Microbiological Analysis ◽  
Significant Difference ◽  
Serum Crp ◽  
The Brain

BACKGROUND: Bacterial infections of the brain are associated with high mortality and neurological sequelae, whereas viral diseases are usually self-limiting. A fast and easy-to-perform biomarker is needed to improve management in these patients. AIM: Procalcitonin (PCT) testing has already been implemented in many laboratories for evaluating septic patients and it is an easily accessible biomarker, so we aimed to examine its role specifically in discriminating acute bacterial from viral infections of the central nervous system (CNS). MATERIALS AND METHODS: This prospective study included 80 patients with both clinical symptoms and laboratory findings suggesting acute CNS infection. The microbiological analysis included direct microscopy, culturing, latex-agglutination test, and multiplex polymerase chain reaction. PCT levels were measured by enzyme-linked fluorescent assay technology. RESULTS: Following the results of the microbiological analysis, the cases were divided into three groups – bacterial 26.3% (n = 21), viral 17.5% (n = 14), and unidentified neuroinfections – 56.2% (n = 45). A statistically significant difference in the median serum PCT was observed between the bacterial and viral neuroinfections (p = 0.004) as well as between bacterial and unidentified infections of the brain (p = 0.000). No significant difference was found (p = 1.000) when comparing viral and unidentified neuroinfection. The area under the receiver operating characteristic curve for serum PCT was 0.823 but could be increased to 0.929 when combining serum PCT and C-reactive protein (CRP). CONCLUSION: Serum PCT levels are significantly higher in patients with acute bacterial infections of the brain. As a stand-alone biomarker, its discriminatory power is not superior to the classical laboratory parameters in the cerebrospinal fluid and serum CRP. However, when combined with serum CRP, excellent discriminatory power is observed.

STEREOTACTIC RADIOSURGERY: ADJACENT TISSUE INJURY AND RESPONSE AFTERHIGH-DOSE SINGLE FRACTION RADIATION

Neurosurgery ◽  
2007 ◽  
Vol 60 (1) ◽  
pp. 31-45 ◽  
Author(s):  
Bryan C. Oh ◽  
Paul G. Pagnini ◽  
Michael Y. Wang ◽  
Charles Y. Liu ◽  
Paul E. Kim ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tissue Injury ◽  
Molecular Data ◽  
Benign Tumors ◽  
Normal Brain ◽  
Clinical Scenarios ◽  
The Central Nervous System ◽  
Brain Parenchymal ◽  
The Brain

Abstract RADIOSURGERY IS NOW the preferred treatment modality for many intracranial disease processes. Although almost 50 years have passed since it was introduced as a tool to treat neurological disease, investigations into its effects on normal tissues of the central nervous system are still ongoing. The need for these continuing studies must be underscored. A fundamental understanding of the brain parenchymal response to radiosurgery would permit development of strategies that would enhance and potentiate the radiosurgical treatment effects on diseased tissue while mitigating injury to normal structures. To date, most studies on the response of the central nervous system to radiosurgery have been performed on brain tissue in the absence of pathological lesions, such as benign tumors or metastases. Although instructive, these investigations fail to emulate the majority of clinical scenarios that involve radiosurgical treatment of specific lesions surrounded by normal brain parenchyma. This article is the first in a two-part series that addresses the brain parenchyma's response to radiosurgery. This first article analyzes the histological, radiographic, and molecular data gathered regarding the brain parenchymal response to radiosurgery and aims to suggest future studies that could enhance our understanding of the topic. The second article in the series begins by discussing strategies for radiosurgical therapeutic enhancement. It concludes by focusing on strategies for mitigation and repair of radiation-induced brain injury.

scholarly journals Tuberculosis of the central nervous system in cattle in Paraíba, Brazil

2018 ◽  
Vol 38 (11) ◽  
pp. 2092-2098 ◽  
Author(s):  
Aline M. Silveira ◽  
Eduardo M. Nascimento ◽  
Guilherme Konradt ◽  
Eldinê G. Miranda Neto ◽  
David Driemeier ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Bovine Tuberculosis ◽  
Clinical Signs ◽  
Northeastern Brazil ◽  
Focal Lesion ◽  
Mediastinal Lymph Nodes ◽  
The Central Nervous System ◽  
The Brain ◽  
Hematogenous Route

ABSTRACT: This paper describes six cases of tuberculosis in the central nervous system (CNS) of cattle in the state of Paraíba in northeastern Brazil. We reviewed the autopsy reports of 851 bovine necropsies performed from 2003 to 2016. Seventy-three (8.6%) cattle were diagnosed with tuberculosis and six showed lesions in the CNS. Three cases affected cattle up to two-year-old and other three affected adults. Three cattle presented exclusively nervous signs, two had respiratory signs and weight loss and one did not present any clinical signs. At necropsy, five cattle had thickening of the leptomeninges of the cerebellum, pons, obex, spinal cord and cortex, mainly, in the region near the brain basilar Willis´ circle. Another animal, presented a single focal lesion in the cerebellum. Microscopically we observed moderate to severe granulomatous meningitis and encephalitis. Five cattle presented lesions in the lungs and mediastinal lymph nodes and three of them had disseminated lesions in other organs. In all cattle acid-fast bacilli were observed in the lesions and marked positive for immunohistochemistry with polyclonal antibody anti-Mycobacterium tuberculosis. It is concluded that bovine tuberculosis of central nervous system occurs sporadically in Paraíba, in cattle of different ages, most of them with disseminate lesions in other organs. The location of the lesions suggests that the agent invaded the brain by hematogenous route through the circle of Willis.

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