Cases reported "Meningoencephalitis"

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1/196. Vascular changes in tuberculous meningoencephalitis.

    Our report refers two cases of tuberculous encephalomeningitis which differ in the course and pathological changes. In case 1 blood vessels showed features of peri, endo-, or panvasculites. In some vessels endothelium proliferation leading to the stenosis or obliteration of the vascular lumen was observed. necrosis was an effect of vessels occlusion. In case 2 many fewer vessel were involved in onflammation process. Vascular changes were also less extensive and were observed more rarely. Tuberculous infection often caused less tissue lesions than vascular changes. Different pathological changes probably depend on the type and virulence of Myobacterium tuberculosis and on the host immune response to the infection.
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2/196. Two cases of toxoplasmic encephalitis in patients with acute T-cell leukaemia and lymphoma.

    Two cases of opportunistic cerebral infections in hiv-negative cancer patients due to chemotherapy induced immunosuppression are reported. A 61-year-old patient with low grade lymphoma (immunocytoma as referred to the Kiel classification) developed stereotactical biopsy proven toxoplasmic encephalitis 6 months after initiation of fludarabine treatment. The lymphoma had been diagnosed 8 years earlier and had been treated with several different regimens. In the second case, a 55-year-old patient developed neurological symptoms while in complete remission from acute T-cell leukaemia. The patient had been treated with a multidrug chemotherapy regimen including radiotherapy of the brain and intrathecal chemotherapy. When toxoplasmic encephalitis was bioptically diagnosed the patient was on maintenance chemotherapy with methotrexate and mercaptopurine for 12 months. The patients' characteristics and outcome are reported and the potential pathogenesis is discussed.
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3/196. Cryptococcus meningoencephalitis in AIDS: parenchymal and meningeal forms.

    CT and MRI in one case of cryptococcus neoformans infection showed contrast-enhancing parenchymal lesions resembling granulomata or abscesses. After an initial phase without contrast enhancement, the full extent of the lesions was visible within 2 weeks of presentation. The enhancing masses were assumed to represent intracerebral cryptococcomas. Despite evidence of massive meningeal infection on cerebrospinal fluid (CSF) examination, no radiological signs of meningitis, invasion of the Virchow-Robin spaces or ventriculitis could be demonstrated. With antimycotic treatment the contrast enhancement disappeared and cystic, partly calcified lesions remained. recurrence of meningeal infection without radiological correlates was apparent in this stage. In a second case of proven cryptococcus meningitis, dilation of Virchow-Robin spaces or cysts in the adjacent parenchyma were the main abnormalities on MRI. Enhancing masses were not detected. These cases may represent two different reactions of the immunocompromised hosts to infection with C. neoformans: widening of the perivascular spaces as a correlate of the more typical meningeal infection and enhancing parenchymal lesions as a sign of further invasion from the CSF spaces. Enhancement of cryptococcomas, indicating an inflammatory response in the surrounding brain, is not typical in patients with impairment of immune function.
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4/196. Enteroviral meningoencephalitis as a complication of X-linked hyper IgM syndrome.

    We describe 5 children from 2 families with mutations in the cd40 ligand (CD40L) gene leading to absent expression of CD40L on activated CD4 cells. All subjects presented with interstitial pneumonia with low serum IgG and normal serum IgM. One child had normal and one child had elevated serum IgA. Four had confirmed pneumocystis carinii pneumonia. In spite of intravenous immunoglobulin treatment yielding therapeutic serum immunoglobulin levels, 3 children had enteroviral encephalitis. When assessed by flow cytometry, the 3 surviving affected male children had absent CD40L expression on activated CD4( ) T cells. The affected children from both families were shown to have the same single nucleotide insertion (codon 131) resulting in frameshift and early termination within exon 4 (extracellular domain). This observation demonstrates that persistent enteroviral infection is not only observed in X-linked agammaglobulinemia but may also occur in patients with X-linked hyper IgM syndrome.
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5/196. meningoencephalitis caused by a novel paramyxovirus: an advanced MRI case report in an emerging disease.

    Eleven abattoir workers in singapore were infected in March 1999 by an outbreak caused by the nipah virus. This newly discovered, Hendra-like paramyxovirus causes acute infection of the CNS. We present the magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (MRS) findings in a patient suffering from acute meningoencephalitis. Multiple small white matter lesions were detected on diffusion-weighted imaging (DWI) and T2-weighted images. There were no abnormalities detected on MRS. We believe this to be the first reported MRI findings in this novel zoonotic viral disease.
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6/196. mycoplasma pneumoniae: a cause of coma in the absence of meningoencephalitis.

    mycoplasma pneumoniae encephalitis is a recognized cause of reversible coma in children. As an etiology of infectious encephalitis, it yields a relatively poorer prognosis than most other causes of infectious encephalopathies. Encephalitis is generally diagnosed by a constellation of clinical symptoms and confirmed by a cerebrospinal fluid (CSF) examination revealing cell pleocytosis and elevated protein. That mycoplasma pneumoniae encephalopathy can occur in the presence of a normal CSF examination is less well appreciated. The authors report two children who presented with coma and normal CSF findings in whom a diagnosis of acute mycoplasma pneumoniae infection was made. The two children both had rapid and complete recovery over several days. These cases exemplify that coma can result from acute infection with mycoplasma pneumoniae in the absence of an inflammatory CSF response and that a normal CSF may herald a more favorable prognosis.
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7/196. Radiologic-pathologic findings in raccoon roundworm (Baylisascaris procyonis) encephalitis.

    A 13-month-old boy developed eosinophilic meningoencephalitis, retinitis, and a protracted encephalopathy with severe residual deficits. The initial MR examination revealed diffuse periventricular white matter disease, and follow-up images showed atrophy. brain biopsy, serology, and epidemiologic studies lead to the diagnosis of Baylisascaris procyonis infection, a parasitic disease contracted through exposure to soil contaminated by the eggs of a common raccoon intestinal roundworm. The pathologic, epidemiologic, and imaging features of this disease are herein reviewed.
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8/196. Foix-Chavany-Marie (anterior operculum) syndrome in childhood: a reappraisal of Worster-Drought syndrome.

    Foix-Chavany-Marie syndrome (FCMS) is a distinct clinical picture of suprabulbar (pseudobulbar) palsy due to bilateral anterior opercular lesions. Symptoms include anarthria/severe dysarthria and loss of voluntary muscular functions of the face and tongue, and problems with mastication and swallowing with preservation of reflex and autonomic functions. FCMS may be congenital or acquired as well as persistent or intermittent. The aetiology is heterogeneous; vascular events in adulthood, nearly exclusively affecting adults who experience multiple subsequent strokes; CNS infections; bilateral dysgenesis of the perisylvian region; and epileptic disorders. Of the six cases reported here, three children had FCMS as the result of meningoencephalitis, two children had FCMS due to a congenital bilateral perisylvian syndrome, and one child had intermittent FCMS due to an atypical benign partial epilepsy with partial status epilepticus. The congenital dysgenetic type of FCMS and its functional epileptogenic variant share clinical and EEG features suggesting a common pathogenesis. Consequently, an increased vulnerability of the perisylvian region to adverse events in utero is discussed. In honour of Worster-Drought, who described the clinical entity in children 40 years ago, the term Worster-Drought syndrome is proposed for this unique disorder in children.
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9/196. lymphocytic choriomeningitis virus: reemerging central nervous system pathogen.

    lymphocytic choriomeningitis virus (LCMV), a human zoonosis caused by a rodent-borne arenavirus, has been associated with both postnatal and intrauterine human disease. infection in man is acquired after inhalation, ingestion, or direct contact with virus found in the urine, feces, and saliva of infected mice, hamsters, and guinea pigs. Congenital LCMV infection is a significant, often unrecognized cause of chorioretinitis, hydrocephalus, microcephaly or macrocephaly, and mental retardation. Acquired LCMV infection, asymptomatic in approximately one third of individuals, is productive of central nervous system manifestations in one half of the remaining cases. Aseptic meningitis or meningoencephalitis are the predominant syndromes, although transverse myelitis, a Guillain-Barre-type syndrome, as well as transient and permanent acquired hydrocephalus have also been reported. Fatalities are rare. We report a patient with meningoencephalitis attributable to LCMV and discuss the spectrum of central nervous system disease, newer diagnostic modalities, and preventive strategies. lymphocytic choriomeningitis virus, aseptic meningitis, meningoencephalitis, zoonosis, hydrocephalus, arenavirus.
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10/196. meningoencephalitis due to blastomyces dermatitidis: case report and literature review.

    infection of the central nervous system by blastomyces dermatitidis is a rare cause of meningoencephalitis. The existence of exclusive clinical infection of the meninges in the absence of pulmonary or other foci of infection has been debated. We describe a 20-year-old man presenting with meningoencephalitis caused by B dermatitidis. Blastomycotic infection was confirmed by isolation of the organism from brain tissue obtained at biopsy. magnetic resonance imaging demonstrated progressive enhancement of basal meninges with involvement of bilateral basal ganglia and thalami. Treatment with amphotericin b arrested further neurologic decline. However, clinical and radiographic follow-up suggested damage to diencephalic structures. The diagnosis of blastomycotic meningoencephalitis is difficult to establish because no sensitive serologic test exists, and attempts to isolate the organism in cerebrospinal fluid obtained by lumbar puncture generally fail. A biopsy specimen of brain tissue is frequently necessary for the diagnosis. survival is possible with timely initiation of therapy.
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