meningitis/edém

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Antibody neutralization of vascular endothelial growth factor (VEGF) fails to attenuate vascular permeability and brain edema in experimental pneumococcal meningitis.

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To determine the contribution of vascular endothelial growth factor (VEGF) to cerebral edema formation in bacterial meningitis, we used a VEGF neutralizing antibody to block VEGF in rabbits, following induction of meningitis by intracisternal inoculation with 10(9) heat-killed pneumococci. At 8 h,

Fluid administration, brain edema, and cerebrospinal fluid lactate and glucose concentrations in experimental Escherichia coli meningitis.

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The effect of no fluids versus liberal fluid supplementation on brain edema and cerebrospinal fluid (CSF) lactate and glucose concentrations was compared in rabbits with experimental Escherichia coli meningitis. Fluid restriction for the duration of the experiment (19 h) led to a decrease in body

Sudden death in toddlers with viral meningitis, massive cerebral edema, and neurogenic pulmonary edema and hemorrhage: report of two cases.

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Viral (lymphocytic) meningitis typically does not cause sudden death, especially in the absence of severe inflammation in the brain or other organs. We report 2 toddlers with clinical evidence of a viral infection who died unexpectedly and were found at autopsy to have lymphocytic meningitis

Idiopathic hypertrophic cranial pachymeningitis with perifocal brain edema.

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Idiopathic hypertrophic cranial pachymeningitis (IHCP) consists of meningeal thickening due to chronic inflammation for which no cause such as infection, specific granulomatous disease, or malignancy is demonstrable. We present a case of IHCP with perifocal brain edema suggesting mass lesion with

Neurogenic pulmonary edema associated with meningitis.

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A 17-year-old man presented with acute febrile, obtundation, nuchal rigidity and CSF pleocytosis with polymorphonuclear cell predominate. He developed acute pulmonary edema which could not be explained by other mechanisms. Meningitis appears to be another cause of neurogenic pulmonary edema.

Invasive pressure monitoring saves from tuberculous meningitis with fulminant generalized brain edema.

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We report a 57-year old female patient with a rapid and dramatic dynamic of whole brain edema caused by tuberculous meningitis. After initiation of tuberculostatic medication, general condition of the patient worsened and finally she was intubated due to a progredient loss of consciousness and

Contribution of lethal toxin and edema toxin to the pathogenesis of anthrax meningitis.

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Bacillus anthracis is a Gram-positive spore-forming bacterium that causes anthrax disease in humans and animals. Systemic infection is characterized by septicemia, toxemia, and meningitis, the main neurological complication associated with high mortality. We have shown previously that B. anthracis

Combined lung injury, meningitis and cerebral edema: how permissive can hypercapnia be?

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We describe a patient with combined meningococcal septicemia and meningitis, cerebral edema and acute respiratory distress syndrome, in whom we balanced the conflicting carbon dioxide strategies for optimal pulmonary and neurological management using jugular oxygen saturation (SjvO2) monitoring to

Late Recovery from Severe Streptococcus pneumoniae Comatose Meningitis with Concomitant Diffuse Subcortical Cytotoxic Edema and Cortical Hypometabolism.

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A 75-year-old woman was admitted to ICU with coma following Streptococcus pneumoniae meningitis with bacteremia. Her Glasgow Coma Scale (GCS) score fluctuated around 4 to 6 over the next four weeks. There was no evidence of increased intracranial pressure (ICP). Electroencephalogram (EEG) showed

Superior effect of hypertonic saline over mannitol to attenuate cerebral edema in a rabbit bacterial meningitis model.

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OBJECTIVE Adjunctive therapies that reduce the cerebral edema in bacterial meningitis include osmotic agents. There is a lack of information comparing mannitol vs. hypertonic saline as an osmotic agent for adjunctive therapy of bacterial meningitis. We attempted to elucidate the impact of hypertonic

Minocycline-induced hypersensitivity syndrome presenting with meningitis and brain edema: a case report.

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BACKGROUND Hypersentivity Syndrome (HS) may be a life-threatening condition. It frequently presents with fever, rash, eosinophilia and systemic manifestations. Mortality can be as high as 10% and is primarily due to hepatic failure. We describe what we believe to be the first case of

Cervicomedullary injury after pneumococcal meningitis with brain edema.

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OBJECTIVE To demonstrate a rare but potential mechanism of quadriplegia in a patient with fulminant pneumococcal meningitis complicated by severe intracranial hypertension. METHODS Case report. METHODS Intensive care unit. METHODS A 21-year-old man who presented with 3 days of headache,

Transforming growth factor beta 2 inhibits cerebrovascular changes and brain edema formation in the tumor necrosis factor alpha-independent early phase of experimental pneumococcal meningitis.

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Macrophages and granulocytes seem to play a key role in the pathogenesis of bacterial meningitis. Transforming growth factor beta (TGF-beta) leads to macrophage deactivation, as well as to inhibition of cytokine production and of endothelial granulocyte adhesion. We have investigated the influence

Bilateral Frontal Lobe Vasogenic Edema Resulting from Hypertrophic Pachymeningitis due to Granulomatosis with Polyangiitis.

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A 61-year-old woman presented with a 1-month history of decreased activities of daily living. Magnetic resonance imaging revealed abnormal intensities of the bilateral frontal lobes and enhancement of the thickened dura matter. A biopsy of the dura mater revealed multinucleated giant cells. She had

[Fulminating meningitis caused by Haemophilus influenzae with rapid progression of severe brain edema similar to acute encephalopathy].

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We report a 4-year-old boy with fulminating meningitis caused by Haemophilus influenzae (Hib). He suddenly developed fever, vomiting and then somnolence. As bacterial meningitis was suspected, treatment with antibiotics was started at 12 hours after the onset. However, there was a rapid progression

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