Cases reported "meningoencephalitis"

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1/482. 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. ( info)

2/482. 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. ( info)

3/482. 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. ( info)

4/482. trypanosoma cruzi meningoencephalitis in hiv-infected patients.

    Five cases of trypanosoma cruzi meningoencephalitis in hiv-infected patients are reported. All patients presented with mass lesions on head computed tomographic scan, trypanosomes in the cerebrospinal fluid and failure to respond to antitoxoplasmosis therapy. Benznidazole therapy was associated with clinical improvement in 1 patient. Another 4 patients had T cruzi identified in a peripheral smear. T cruzi needs to be considered in the differential diagnosis of hiv-infected patients with central nervous system mass lesions if they have a history of appropriate exposure. ( info)

5/482. anthrax meningitis. Report of two cases with autopsies.

    The authors report two cases of occupation-related anthrax meningitis; one was direct contamination from a diseased animal; the second was due to handling of bone powder imported from india. The pathological pattern of involvement of the meninges and brain is described and discussed. ( info)

6/482. 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. ( info)

7/482. Epstein-Barr virus meningoencephalitis with a lymphoma-like response in an immunocompetent host.

    We report the clinical and neuropathological findings in an immunocompetent 19-year-old patient with a fatal acute Epstein-Barr virus (EBV) meningoencephalitis and a lymphoma-like B-lymphocyte response. Our results suggest that an immunotoxic rather than direct viral neuronal invasion mediates brain damage in EBV encephalitis and rule out primary central nervous system lymphoma (PCNSL) in our patient. We discuss immunosuppression as a therapeutic option, because present strategies mainly consist of symptomatic therapy due to unclear pathogenesis and nonavailability of effective antiviral agents. ( info)

8/482. Meningotheliomatous meningioma accompanied by aspergillosis at the skull base.

    A 73-year-old man was admitted because of right frontal headache and gradual loss of right visual acuity, which had been occurring for 1 year. He had been treated with corticosteroids under the diagnosis of retrobulbar optic neuritis at a nearby clinic. magnetic resonance imaging (MRI) revealed a nodular lesion at the tuberculum sellae, which showed isointensity on T1-weighted images, iso- to low-intensity on T2-weighted images, and heterogeneous enhancement with Gd-DTPA. meningioma was diagnosed, and surgery was performed but was limited to biopsy because of intraoperative detection of purulent inflammation of the nodule. Histologic examination revealed aspergillosis in a portion of the meningotheliomatous meningioma. The patient died of meningoencephalitis about 1 month after surgery in spite of extensive treatment with antifungal agents. MRI findings of meningioma and aspergillosis are similar, thus making preoperative diagnosis difficult. However, this case provides evidence that aspergillosis should be included in the differential diagnosis when a skull-base meningioma-like nodule is noted if sinusitis is revealed in the sphenoid sinus. ( info)

9/482. Persistent trigeminal neuralgia after removal of contralateral posterior cranial fossa tumor. Report of two cases.

    BACKGROUND: Contralateral trigeminal neuralgia as a false localizing sign in patients with posterior cranial fossa tumors is rare. Persistent contralateral trigeminal neuralgia after removal of the posterior fossa expanding lesion with microsurgical exploration of the affected trigeminal nerve root has been described in only a few reports. Displacement of the brainstem and the trigeminal nerve root, arachnoid adhesions, and vascular compression of the nerve root entry zone have been reported as causes of persistent contralateral trigeminal neuralgia. methods: One patient developed transformation of the contralateral constant burning facial pain into trigeminal neuralgia after removal of a posterior fossa meningioma. A typical right-sided tic douloureux in our second patient did not disappear after removal of a left acoustic neurinoma. CT scan revealed brainstem displacement to the side of trigeminal neuralgia. Microsurgical exploration in both cases demonstrated the squeezed and distorted trigeminal nerve root and displaced brain stem with no vascular involvement. Both patients underwent partial trigeminal rhizotomy for pain control. RESULTS: Complete disappearance of the trigeminal neuralgia was evident in both cases with postoperative facial sensory loss. The postoperative course in the first case was uneventful; the second patient died from purulent meningoencephalitis. CONCLUSION: Persistent contralateral trigeminal neuralgia after removal of a posterior fossa tumor is caused by distortion of the fifth nerve root by the displaced brainstem. Partial trigeminal rhizotomy can be performed for alleviation of facial neuralgic pain in cases without neurovascular compression. ( info)

10/482. Primary amebic meningoencephalitis due to naegleria fowleri: an autopsy case in japan.

    Free-living amebas represented by naegleria fowleri, acanthamoeba and Balamutia have been known to cause fatal meningoencephalitis since Fowler and Carter (1965) reported the first four human cases. An autopsy case of a 25-year-old female with primary amebic meningoencephalitis (PAM) due to naegleria fowleri is described. headache, lethargy and coma developed in this patient, and her condition progressed to death 8 days after the onset of clinical symptoms. Cerebral spinal fluid examination confirmed clusters of amebas, which were grown in culture and identified as naegleria fowleri. At autopsy, lesions were seen in the central nervous system (CNS) and the ethmoid sinus. The CNS had severe, suppurative meningoencephalitis with amebic trophozoites mingled with macrophages. This case is the first report of PAM due to naegleria fowleri in japan. ( info)
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