1/25. 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.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/25. 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.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
3/25. 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.- - - - - - - - - - ranking = 3.5keywords = coma (Clic here for more details about this article) |
4/25. A case of balamuthia mandrillaris meningoencephalitis.balamuthia mandrillaris is a newly described pathogen that causes granulomatous amebic encephalitis, an extremely rare clinical entity that usually occurs in immunosuppressed individuals. We report a case of pathologically proven Balamuthia encephalitis with unusual laboratory and radiologic findings. A 52-year-old woman with idiopathic seizures and a 2-year history of chronic neutropenia of unknown cause had a subacute illness with progressive lethargy, headaches, and coma and died 3 months after the onset of symptoms. Cerebrospinal fluid (CSF) glucose concentrations were extremely low or unmeasurable, a feature not previously described (to our knowledge). Cranial magnetic resonance imaging scans showed a single large temporal lobe nodule, followed 6 weeks later by the appearance of 18 ring-enhancing lesions in the cerebral hemispheres that disappeared after treatment with antibiotics and high-dose corticosteroids. The initial brain biopsy specimen and analysis of CSF samples did not demonstate amebae, but a second biopsy specimen and the postmortem pathologic examination showed Balamuthia trophozoites surrounded by widespread granulomatous inflammation and vasculitis. The patient's neutropenia and antibiotic use may have caused susceptibility to this organism. Amebic meningoencephalitis should be considered in cases of subacute meningoencephalitis with greatly depressed CSF glucose concentrations and multiple nodular lesions on cerebral imaging. Arch Neurol. 2000;57:1210-1212- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
5/25. magnetic resonance imaging in a patient with X-linked agammaglobulinemia and chronic meningoencephalitis.The case of a boy with congenital agammaglobulinemia is reported. In spite of regular immunoglobulin replacement therapy (fresh plasma transfusion from family donors--20 ml/kg/month), he developed chronic meningoencephalitis (ME). Besides characteristic clinical signs of ME, he also presented at cerebrospinal fluid analysis pleocytosis with lymphocyte predominance and class II cytomorphology, and delta and theta waves in the EEG. Computerized tomography showed dilatation of the ventricles and marked cortical fissures (sulci). magnetic resonance imaging showed a disease affecting white and gray matter. After diagnosis of ME, replacement therapy with Sandoglobulin (700 mg/kg every 2 weeks) was started. His condition gradually worsened, and coma and death occurred after a follow-up of 18 months. The etiological agent could not be identified.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
6/25. Fatal fulminant pan-meningo-polioencephalitis due to west nile virus.We report a case of fatal fulminant west nile virus (WNV) meningoencephalitis in an 87-year-old white male gardener. The pennsylvania patient presented with a 3-day history of flu-like symptoms. His hospital course was gravely precipitous with onset of coma, ventilator dependence, loss of cortical and brainstem functions within ten days of admission. Acute serum and cerebrospinal fluid samples revealed elevated levels of WNV IgM antibodies by ELISA as well as elevated CSF white blood cells, protein and glucose. A complete autopsy revealed a multifocal lymphocytic myocarditis and severe chronic tubulointerstitial nephritis. Viral culture and PCR analysis of post-mortem samples of the spleen, kidney and brain were positive for WNV. Histological sections from all regions of the brain and spinal cord demonstrated a severe, non-necrotizing, subacute, polio-meningoencephalitis. While both gray and white matter were inflamed, gray matter was much more severely involved. Many gray matter nuclei showed severe neuronal loss with residual dying neurons surrounded by activated microglia. Immunohistochemical stains revealed profuse infiltration of the meninges and cerebral parenchyma by CD8 t-lymphocytes and perivascular b-lymphocytes. Electron micrographs revealed diffuse intracellular and extracellular edema but no viral particles were identified. Immunohistochemical and immunofluorescent staining for WNV filled the cytoplasm of residual neurons. west nile virus mediates a predominantly polioencephalitis secondary to direct infection of neurons.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
7/25. Unusual presentation of life-threatening Toscana virus meningoencephalitis.This case report describes a brother and a sister with severe meningoencephalitis caused by Toscana virus (TOSv). The clinical presentation was characterized by stiff neck, deep coma, maculopapular rash, diffuse lymphadenopathy, hepatosplenomegaly, renal involvement, tendency to bleeding, and diffuse intravascular coagulation. The boy had epididymo-orchitis. Recovery with neurologic sequelae as hydrocephalus was observed. Microbiological diagnosis was obtained by serological tests and reverse transcriptase-polymerase chain reaction. Sequencing of polymerase chain reaction products from the S and M segments was carried out. TOSv may be a causative agent in severe meningoencephalitis.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
8/25. Post-mortem diagnosis of encephalitis in a 75-year-old man associated with human herpesvirus-6 variant A.An HHV-6 variant A infection is described in a 75 year-old man in association with meningoencephalitis identified at autopsy. The patient presented with fever and anorexia, then he developed altered consciousness, motor weakness, progressive lethargy, and coma, and died 21 days after hospital admission. Histopathological examination showed perivascular lymphocytic infiltrates in the central nervous system (CNS). serum and cerebral spinal fluid (CSF) samples drawn from the patient were tested for viruses by a nested polymerase chain reaction (nPCR). HHV-6 primers A and C [Aubin et al., 1991: J Clin Microb 29: 367-372] and HS6AE and HS6AF from [Dewhurst et al. (1993): J Clin Microb 31: 416-418] disclosed a 750 bp genomic product of HHV-6 in both types of biological samples. Restricted site analysis showed that the HHV-6 dna amplified belonged to the variant A of the virus. Short sequences of HHV-6 dna could also be detected in the dna extracted from formalin-fixed, paraffin-embedded sections of CNS tissues by use of one (GM5 and GM6) of three pairs of HHV-6 primers that were selected. Immunohistochemical examination of brain sections, employing a specific monoclonal antibody directed against the HHV-6 gp 102 protein, detected the viral antigen in neurons and glial cells.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
9/25. syndrome of inappropriate antidiuretic hormone secretion in a patient with cryptococcal meningoencephalitis: a hidden mediastinal small cell carcinoma.We report a 59-year-old man with cryptococcal meningoencephalitis who presented with typical features of syndrome of inappropriate antidiuretic hormone secretion (SIADH). There was no evidence of lung disease or drugs causing SIADH. Studies for endocrine functions and tumor markers were normal. The patient's hyponatremia was refractory to treatment (Na 120-125 mmol/L) after resolution of the cryptococcal infection. Three months after completion of antifungal treatment, a radiograph of the chest disclosed widening of the mediastinum. Computed tomography revealed a mediastinal mass. A tentative diagnosis of extrapulmonary cryptococcoma or a tumor was made. Positron emission tomography using F-fluorodeoxy glucose demonstrated an intense uptake mass in the mediastinum without lesions elsewhere in the body. A biopsy of the mass clearly showed small cell carcinoma (SCC) with positive immunoreactivity for arginine vasopressin and atrial natriuretic peptide. The hyponatremia completely resolved and tumor size dramatically decreased after chemotherapy. To the best of our knowledge, this is the first case of mediastinal SCC associated with SIADH. patients with otherwise unexplained SIADH should be meticulously scrutinized for a possible malignancy.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
10/25. Eosinophilic myelomeningoencephalitis caused by angiostrongylus cantonensis: a report of three cases.Three members of a family developed eosinophilic myelomeningoencephalitis following ingestion of Pila snails. They were father, daughter and son and had similar clinical presentations. Two days after ingestion of snails, they developed a generalized itchy maculopapular rash followed by myalgia, marked paresthesia, fever and headache. Two days later there was weakness of the extremities which was progressive in severity involving the legs more than the arms. They later developed urine retention and cloudiness of consciousness. Two patients progressed to coma, one of whom died after 3 weeks and the other died at home 9 months after the onset. autopsy of the fatal case revealed multiple tracks and cavities with the presence of angiostrongylus cantonensis in the brain and various levels of the spinal cord.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
| | Next -> |