Cases reported "Malaria, Cerebral"

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1/50. Cerebral uptake of mefloquine enantiomers in fatal cerebral malaria.

    patients AND methods: The brain disposition of the enantiomers of the antimalarial mefloquine was studied in two post-mortem human cerebral biopsies after oral administration of the racemic mixture. BACKGROUND: mefloquine (MQ) is an effective antimalarial drug used both for prophylaxis and treatment of chloroquine resistant plasmodium falciparum. MQ is generally well tolerated in treatment. Minor side-effects have been described. Potentially serious neuropsychiatric reactions occur. The mechanism underlying the neurotoxicity is unknown, although a dose relationship is evidently involved. RESULTS: mefloquine enantiomer concentrations were determined using a chiral liquid chromatographic method. mefloquine concentrations were higher in brain compared to plasma. Studied in one patient, white matter concentrations were higher compared to grey matter concentrations. CONCLUSION: Based on the ratios brain concentration/plasma concentration, the brain penetration of the ( ) enantiomer is much higher than that of the (-) enantiomer. ( info)

2/50. Management of severe and complicated malaria in the intensive care unit.

    malaria remains today one of the major health problems in the tropics with increased morbidity and mortality. The most serious complications are caused by plasmodium falciparum, which, in contrast to the benign malarias, may progress to a life-threatening multi-system disease. Our case concerns a young woman in the 14th week of pregnancy, admitted to the ICU in a coma, with pulmonary oedema, haemolytic anaemia, renal failure and thrombocytopenia as complications of P. falciparum malaria. The case is discussed and possible explanations for the clinical picture and complications of P. falciparum malaria are given in the light of experiences from the literature. ( info)

3/50. malaria and stroke. Case report.

    malaria is a parasitic disease with high prevalence in several regions of the world. Infestation by Plasmodium faciparum can, in some cases, affect the central nervous system producing encephalitis resulting in death or neurological sequelae. The mechanisms involved in the pathophysiology of the cerebral lesion are not totally clear and there are currently two theories (mechanical and humoral) concerning this. We report a case of malaria with an atypical evolution, with a stroke lesion in the territory of the middle cerebral artery, with no association with encephalitis. We conclude that the mechanical theory is the one applicable to this patient. ( info)

4/50. Automated RBC exchange transfusion:treatment for cerebral malaria.

    BACKGROUND: Cerebral malaria is a life-threatening complication of plasmodium falciparum infection. RBC exchange transfusion can reduce the level of parasitemia in this setting. Experience with automated RBC exchange for cerebral malaria may be limited, as most cases occur when the necessary equipment and blood components are not readily available. case reports: Three patients were admitted with cerebral malaria. parasites were found in more than 30 percent of RBCs in two cases and in more than 60 percent of RBCs in the third case. Many RBCs contained multiple organisms. In each case, antimalarial therapy was begun, and an automated RBC exchange was performed emergently with a cell separator. Exchange transfusion was repeated within 24 hours for two patients. parasitemia levels were less than 1 percent in all patients 24 hours after the last exchange. The neurologic status of these patients returned to baseline, and they were discharged 7 to 18 days after admission. CONCLUSION: Automated RBC exchange transfusion can rapidly reduce the level of parasitemia and restore neurologic functioning in patients with cerebral malaria. ( info)

5/50. Inducible nitric oxide synthase expression is increased in the brain in fatal cerebral malaria.

    AIMS: Nitric oxide (NO) has been hypothesized to play a major role in the pathogenesis of cerebral malaria caused by P. falciparum infection. NO may act as a local neuroactive mediator contributing to the coma of cerebral malaria (CM). We hypothesized that increased expression of inducible nitric oxide synthase (iNOS) may cause increased release of NO, and examined the expression and distribution of iNOS in the brain during CM. MATERIAL AND RESULTS: brain tissues from fatal cases of cerebral malaria in Thai adults were examined using immunohistochemical staining to detect iNOS. The distribution and strength of staining was compared between 14 patients with CM, three of whom were recovering from coma, and controls. iNOS expression was found in endothelial cells, neurones, astrocytes and microglial cells in CM cases. There was also strong staining in macrophages surrounding ring haemorrhages. iNOS staining was decreased in recovering malaria cases compared to acute CM, and was low in controls. Quantification showed a significant association between the intensity and number of iNOS positive vessels with the severity of malaria related histopathological changes, although the total number of cells staining was not increased compared to recovering CM cases. CONCLUSIONS: This study indicates that an acute induction of iNOS expression occurs in the brain during CM. This occurs in a number of different cells types, and is increased in the acute phase of CM compared to cases recovering from coma. As NO may activate a number of secondary neuropathological mechanisms in the brain, including modulators of synaptic function, induction of iNOS expression in cerebral malaria may contribute to coma, seizures and death. ( info)

6/50. Adhesion molecule detection in a case of early cerebral malaria: immunohistochemical and electron microscopic findings.

    A case of early cerebral malaria caused by plasmodium falciparum was studied. p-selectin glycoprotein ligand 1 (PL1) was detected along the inner surface of the infected red blood cells (IRBCs), which ordinarily are not positive for PL1 immunohistochemically, suggesting PL1 being the product of parasite. The electron microscopic finding showed granular deposits in the corresponding lesion, consistent with PL1 deposition, in the IRBCs firmly attached to the endothelium of small cerebral vessels. Most of the IRBCs were round shaped as though they lost their capacity to change shape. The therapeutic strategy was expected against adhesion molecules such as PL1 and for maintaining or restoring the metamorphic capacity of IRBCs. ( info)

7/50. pleural effusion in childhood falciparum malaria.

    Pulmonary complication is a rare manifestation of childhood malaria and isolated pleural effusion without pulmonary edema has never been reported in children. We report here an 11-year-old boy who suffered from cerebral malaria and massive right pleural effusion. The patient was treated with intravenous artesunate, albumin, and other supportive treatments. He recovered completely after eight days. The clinical and laboratory courses suggested that the plasma leakage played a role in the pathogenesis of pleural effusion. ( info)

8/50. Postmortem diagnosis of cerebral malaria.

    Human cerebral malaria is a frequent encephalopathy that occurs in the endemic tropical-subtropical zones. There are a smaller number of imported cases in continental zones where the diagnosis sometimes remains difficult to establish. Fifteen days after the death of a 36-year-old male French citizen in africa, an investigation to determine the cause of death was conducted. Histologic examination of the brain permitted the diagnosis of cerebral malaria. Because of the popularity of overseas tourism and because this disorder may appear as "sudden death," these victims may be referred to a forensic pathologist. This case demonstrates the role a forensic pathologist may play in determining the cause of death in cerebral malaria. ( info)

9/50. Erythrocytapheresis for plasmodium falciparum infection complicated by cerebral malaria and hyperparasitemia.

    In malaria due to plasmodium falciparum, life-threatening complications are in part related to the degree of parasitemia. Whole blood exchange and red blood cell exchange (RCE) have been used for the rapid removal of parasites from the circulation of patients with a high parasite load complicated by cerebral, pulmonary, and renal dysfunction. We have treated three 5-45-year-old patients with hyperparasitemia and end-organ dysfunction with red cell exchange by automated apheresis as an adjunct to specific anti-malarial chemotherapy. parasitemia dropped more than 80% in all three patients immediately after the exchange, and all patients had an uneventful and full recovery. In combination with effective anti-malarial chemotherapy, apheresis RCE is a safe and rapid approach to treat complicated malaria due to P. falciparum. ( info)

10/50. Severe falciparum malaria in five soldiers from east timor: a case series and literature review.

    Despite chemoprophylaxis, malaria remains a serious threat for large numbers of non-immune soldiers deployed in endemic areas. Five adult cases of severe falciparum malaria are reported. Three cases were complicated by multiorgan failure and one of these patients died from cerebral malaria. These cases serve to highlight issues, in an Australian intensive care unit, associated with the management of severe malaria, an uncommon disease in our country. The need for rapid diagnosis and commencement of appropriate treatment is paramount in preventing further morbidity and mortality. Understanding and management of malaria continues to evolve rapidly. The pathophysiology of acute lung injury, shock and brain injury associated with malaria are examined in light of recent research. This article discusses the current controversies of exchange blood transfusion and the use of the new artemisinin derivatives. ( info)
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