Acute Viral Meningitis

2018 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Meningitis ◽  
Viral Pathogen ◽  
Meningeal Irritation ◽  
Nuchal Rigidity ◽  
Common Causes ◽  
Neurologic Sequelae ◽  
Control And Prevention ◽  
Csf Pleocytosis ◽  
The Brain

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This review contains 4 highly rendered figures, 8 tables, and 17 references.

Acute Viral Meningitis

2015 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Meningitis ◽  
Viral Pathogen ◽  
Meningeal Irritation ◽  
Nuchal Rigidity ◽  
Common Causes ◽  
Neurologic Sequelae ◽  
Control And Prevention ◽  
Csf Pleocytosis ◽  
The Brain

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This chapter contains 4 highly rendered figures, 7 tables, 16 references, and 5 MCQs.

Acute Viral Meningitis

2018 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Meningitis ◽  
Viral Pathogen ◽  
Meningeal Irritation ◽  
Nuchal Rigidity ◽  
Common Causes ◽  
Neurologic Sequelae ◽  
Control And Prevention ◽  
Csf Pleocytosis ◽  
The Brain

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This review contains 4 highly rendered figures, 8 tables, and 17 references.

scholarly journals Glucose status in cerebrospinal fluid (CSF) in different meningitic children in a hospital in Chittagong, Bangladesh

2013 ◽  
Vol 6 (1-2) ◽  
pp. 41-49
Author(s):  
Sharmistha Mitra ◽  
Robiul Hasan Bhuiyan ◽  
Md Arifuzzaman ◽  
Mohammad Sayedul Islam ◽  
Mahmood A Chowdhury ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Glucose Level ◽  
Viral Meningitis ◽  
Pyogenic Meningitis ◽  
Detailed Medical History ◽  
Different Types ◽  
The Brain ◽  
Very High ◽  
Potential Tool ◽  
Glucose Status

Meningitis is referred to as an inflammatory process of the leptomeninges and cerebrospinal fluid (CSF) within the sub-arachnoid space of the brain. We have investigated glucose status in CSF in different types of meningitis together with detailed medical history in children. In addition, we have also carried out the detailed cytological and microbiological examinations. A total of 40 subjects were investigated. We observed that the glucose level was significantly decreased (<20 mg/dl) in 65%, moderately decreased (20-40 mg/dl) in 20% and mildly decreased (40-50mg/dl) in 15% of the patients in our study. Patients with Pyogenic meningitis had tremendously reduced glucose level (9.0 mg/dl) in their CSF whereas in viral meningitis the CSF glucose level is highly variable (10 to 65 mg/dl). Furthermore, 5 (12.5%) patients showed high lymphocyte counts and 34 (85%) patients showed high neutrophil counts. Interestingly, in Pyogenic meningitis, the neutrophil count was very high compared to that in viral meningitis. The present study clearly demonstrates that biochemical parameters such as glucose level in CSF might be a potential tool for detecting meningitis and as well as differentiation of the different types of meningitis. DOI: http://dx.doi.org/10.3329/cujbs.v6i1-2.17080 The Chittagong Univ. J. B. Sci.,Vol. 6(1&2):41-49, 2011

Naegleria fowleri Hemorrhagic Meningoencephalitis: Report of Two Fatalities in Children

2004 ◽  
Vol 19 (3) ◽  
pp. 231-233 ◽  
Author(s):  
Darin T. Okuda ◽  
Hank J. Hanna ◽  
Stephen W. Coons ◽  
John B. Bodenstelner
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Stem ◽  
Mass Effect ◽  
Severe Headache ◽  
Neurologic Examination ◽  
Naegleria Fowleri ◽  
Neck Stiffness ◽  
Nuchal Rigidity ◽  
Nægleria Fowleri ◽  
The Brain

Two cases of hemorrhagic meningoencephalitis secondary to Naegleria fowleri infection confirmed by postmortem analysis are described. The first patient is a 5-year-old boy who presented with a severe headache, neck stiffness, and lethargy. His neurologic examination was significant for somnolence and nuchal rigidity. Cerebrospinal fluid studies and structural neuroimaging were consistent with hemorrhagic meningoencephalitis. Another 5-year-old boy presented to a different institution 2 miles away in the same week with similar complaints. Both patients declined rapidly and expired within 48 hours of admission secondary to transtentorial herniation caused by the mass effect of inflammation, edema, and hemorrhage with displacement of the brain stem. Histopathologic and immunochemistry analysis of brain tissue revealed the presence of Naegleria trophozoites in both cases.

scholarly journals Follistatin (FS) in human cerebrospinal fluid and regulation of FS expression in a mouse model of meningitis

2000 ◽  
pp. 809-816 ◽  
Author(s):  
U Michel ◽  
S Ebert ◽  
O Schneider ◽  
Y Shintani ◽  
S Bunkowski ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Specific Binding ◽  
In Situ Hybridisation ◽  
Viral Meningitis ◽  
Csf Analysis ◽  
Mrna And Protein Expression ◽  
Leukocyte Counts ◽  
The Brain

OBJECTIVE: Follistatin (FS) is the specific binding protein of activin and expression of both factors is regulated by inflammatory agents. Therefore, FS concentrations were determined in cerebrospinal fluid (CSF) of patients with bacterial and viral meningitis or multiple sclerosis (MS), as well as in the CSF of patients without meningial inflammation or autoimmune diseases. Furthermore, a mouse pneumococcal meningitis model was used to localise the cellular sources of FS in brains of normal and meningitic mice. METHODS: FS concentrations in CSF were determined by ELISA; FS in mice was localised by in situ hybridisation and immunohistochemistry. RESULTS: FS concentrations were > or =0.4 microg/l in 22 of 66 CSF samples of meningitis patients versus 2 of 27 CSF samples from patients with multiple sclerosis (P<0.05) and 2 of 41 CSF specimen from patients without neuroinflammatory diseases (P<0.01). In the CSF of patients with meningitis, the concentration of FS was correlated with total protein (P<0.005) and lactate concentrations (P<0.05), but not with leukocyte counts, interval between onset of disease and CSF analysis, or clinical outcome. The CSF-to-serum ratios of FS and albumin also correlated significantly (P<0.0005). In some patients with meningitis the CSF-to-serum ratios suggested that the elevated FS in CSF did not originate from serum alone. FS was localised in mice brains to neurones of the hippocampus, dentate gyrus, neocortex, and to the choroid plexus. Analyses of brains and other organs from uninfected and infected animals sacrificed 6-36 h after infection did not reveal any obvious differences in the distribution and intensity of FS mRNA and protein expression. CONCLUSIONS: The concentration of FS in humans is elevated during meningitis. In some patients the increase is caused by a release of FS from brain into CSF. Data from the mouse meningitis model suggest that increased CSF concentrations of FS in meningitis appear not to be accompanied by an elevated number of cells containing FS mRNA or protein in the brain.

scholarly journals The Prevalence of Viruses in the Cerebrospinal Fluid of Children with Aseptic Meningitis in Shiraz, Iran

2020 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Anahita Sanaei Dashti ◽  
Masoomeh Khalifeh ◽  
Elham Yousefifar ◽  
Mohammad Rahim Kadivar ◽  
Marzieh Jamalidoust ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Real Time ◽  
Aseptic Meningitis ◽  
Real Time Pcr ◽  
Laboratory Data ◽  
Rapid Test ◽  
Viral Meningitis ◽  
Common Causes ◽  
Causative Agents ◽  
Meningitis In Children

Objectives: The current study aimed to evaluate the causative agents of viral meningitis through real-time PCR among children with aseptic meningitis. Methods: Children aged 1 month to 16 years with suspected viral meningitis were enrolled in this study (March 2014-February 2015). Cerebrospinal fluid samples were analyzed by real-time PCR for detection of enterovirus, mumps, measles, adenovirus, EBV, CMV, VZV, hhv 6, and rubella viruses. Demographic information, laboratory data, and clinical presentations of patients were also collected. Results: Of 56 patients suspected to viral meningitis, 21 (38.9 %) had a positive PCR result. Enterovirus (42.85%) and mumps (38.1%) were the most prevalent viruses, and VZV and measles were not detected. Three children were coinfected with enterovirus/hhv6, enterovirus/EBV, and mump/adenovirus. Fever, headache, and nausea/vomiting were the most common symptoms in children. The rates of symptoms were not statistically significant among children with positive and negative PCR tests. Conclusions: In the present study Enterovirus and mumps viruses were the most common causes of viral meningitis in children. PCR, as a rapid test for the diagnosis of viral meningitis, can be used to decrease hospitalization length.

Fibrinolytic Activity of Cerebro-Spinal Fluid and the Development of Artificial Cerebral Haematomas in Dogs

1969 ◽  
Vol 21 (02) ◽  
pp. 294-303 ◽  
Author(s):  
H Mihara ◽  
T Fujii ◽  
S Okamoto
Keyword(s):  
Cerebrospinal Fluid ◽  
Carboxylic Acid ◽  
Fibrinolytic Activity ◽  
Clinical Implications ◽  
Trans Form ◽  
Plate Method ◽  
Blood Samples ◽  
Fibrin Plate ◽  
The Brain

SummaryBlood was injected into the brains of dogs to produce artificial haematomas, and paraffin injected to produce intracerebral paraffin masses. Cerebrospinal fluid (CSF) and peripheral blood samples were withdrawn at regular intervals and their fibrinolytic activities estimated by the fibrin plate method. Trans-form aminomethylcyclohexane-carboxylic acid (t-AMCHA) was administered to some individuals. Genera] relationships were found between changes in CSF fibrinolytic activity, area of tissue damage and survival time. t-AMCHA was clearly beneficial to those animals given a programme of administration. Tissue activator was extracted from the brain tissue after death or sacrifice for haematoma examination. The possible role of tissue activator in relation to haematoma development, and clinical implications of the results, are discussed.

Vasopressin enhances the clearance of β-endorphin immunoreactivity from rat cerebrospinal fluid

1990 ◽  
Vol 122 (2) ◽  
pp. 191-200 ◽  
Author(s):  
C. G. J. Sweep ◽  
Margreet D. Boomkamp ◽  
István Barna ◽  
A. Willeke Logtenberg ◽  
Victor M. Wiegant
Keyword(s):  
Cerebrospinal Fluid ◽  
Receptor Antagonist ◽  
Short Duration ◽  
Lateral Ventricle ◽  
Underlying Mechanism ◽  
Terminal Phase ◽  
Intracerebroventricular Injection ◽  
Intracerebroventricular Administration ◽  
Biphasic Pattern ◽  
The Brain

Abstract The effect of intracerebroventricular (lateral ventricle) administration of arginine8-vasopressin (AVP) on the concentration of β-endorphin immunoreactivity in the cerebrospinal fluid obtained from the cisterna magna was studied in rats. A decrease was observed 5 min following injection of 0.9 fmol AVP. No statistically significant changes were found 5 min after intracerebroventricular treatment of rats with 0.09 or 9 fmol. The decrease induced by 0.9 fmol AVP was of short duration and was found 5 min after treatment but not 10 and 20 min. Desglycinamide9-AVP (0.97 fmol), [pGlu4, Cyt6]-AVP-(4–9) (1.44 fmol), Nα-acetyl-AVP (0.88 fmol), lysine8-vasopressin (0.94 fmol) and oxytocin (1 fmol) when intracerebroventricularly injected did not affect the levels of β-endorphin immunoreactivity in the cerebrospinal fluid 5 min later. This suggests that the intact AVP-(1–9) molecule is required for this effect. Intracerebroventricular pretreatment of rats with the vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)AVP (8.63 fmol) completely blocked the effect of AVP (0.9 fmol). In order to investigate further the underlying mechanism, the effect of AVP on the disappearance from the cerebrospinal fluid of exogenously applied β-endorphin was determined. Following intracerebroventricular injection of 1.46 pmol camel β-endorphin-(1–31), the β-endorphin immunoreactivity levels in the cisternal cerebrospinal fluid increased rapidly, and reached peak values at 10 min. The disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid then followed a biphasic pattern with calculated half-lifes of 28 and 131 min for the initial and the terminal phase, respectively. Treatment of rats with AVP (0.9 fmol; icv) during either phase (10, 30, 55 min following intracerebroventricular administration of 1.46 pmol β-endorphin-(1–31)) significantly enhanced the disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid. The data suggest that vasopressin plays a role in the regulation of β-endorphin levels in the cerebrospinal fluid by modulating clearance mechanisms via V1-receptors in the brain.

Mechanical Choices

2020 ◽  
Author(s):  
Michael S. Moore
Keyword(s):  
Common Sense ◽  
Legal Punishment ◽  
Common Causes ◽  
Moral Blame ◽  
The Brain ◽  
Common Sense Psychology

This book assays how the remarkable discoveries of contemporary neuroscience impact our conception of ourselves and our responsibility for our choices and our actions. Dramatic (and indeed revolutionary) changes in how we think of ourselves as agents and as persons are commonly taken to be the implications of those discoveries of neuroscience. Indeed, the very notions of responsibility and of deserved punishment are thought to be threatened by these discoveries. Such threats are collected into four groupings: (1) the threat from determinism, that neurosciences shows us that all of our choices and actions are caused by events in the brain that precede choice; (2) the threat from epiphenomenalism, that our choices are shown by experiment not to cause the actions that are the objects of such choice but are rather mere epiphenomena, co-effects of common causes in the brain; (3) the threat from reductionist mechanism, that we and everything we value is nothing but a bunch of two-valued switches going off in our brains; and (4) the threat from fallibilism, that we are not masters in our own house because we lack the privileged knowledge of our own minds needed to be such masters. The book seeks to blunt such radical challenges while nonetheless detailing how law, morality, and common-sense psychology can harness the insights of an advancing neuroscience to more accurately assign moral blame and legal punishment to the truly deserving.

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