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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Travel is associated with a number of neurological disorders that can be divided into two categories: (1) Neurological infections including encephalitides, neurotuberculosis, neurobrucellosis, cysticercosis and trichinosis. Some of these disorders can be prevented by vaccinations, such as Japanese B encephalitis and rabies, some by the use of insect repellents and some by avoiding raw milk products and undercooked meat. (2) Non-infective neurological disorders, such as acute mountain sickness and high altitude cerebral oedema, problems occurring during air travel such as syncope, seizures, strokes, nerve compression, barotrauma and vertigo, motion sickness and foodborne neurotoxic disorders such as ciguatera, shellfish poisoning and intoxication by cassava. This group of diseases and disorders could be prevented if the traveller knows about them, applies simple physiological rules, takes some specific medications and knows how to avoid intoxications in certain geographical areas. Meningococcal meningitis, malaria and jet lag syndrome are extensively discussed in other articles of this issue. The discussion in this paper will be limited to the other disorders.
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PMID:Neurological disorders and travel. 1261 85

Physiologically in the brain, cytokines such as tumor necrosis factor-alpha (TNalpha) are released by the immune system and can modulate neurological responses. Conversely, the central nervous system (CNS) is also able to modulate cytokine production. In the case of CNS disorders, cytokine release may be modified. Cerebral malaria (CM) is a complication of Plasmodium falciparum infection in humans and is characterized by a reversible encephalopathy with seizures and loss of consciousness. Central clinical signs are partly due to sequestration of parasitized red blood cells in the brain microvasculature due to interactions between parasite proteins and adhesion molecules. TNFalpha is produced and released by host cells following exposure to various malarial antigens. The increase of TNFalpha release is responsible for the overexpression of adhesion molecules. This article reviews the involvement of TNFalpha in cerebral malaria and the relation with all the processes involved in this pathology. It shows that (i). TNFalpha levels are increased in plasma and brain but with no clear correlation between TNFalpha levels and occurrence and severity of CM; (ii). TNFalpha is responsible for intercellular adhesion molecule-1 upregulation in CM, the relation being less clear for other adhesion molecules; (iii). TNFalpha receptors are upregulated in CM, with TNF receptor 2 (TNFR2) showing a higher upregulation than TNFR1 in vivo; (iv). in murine CM, low doses of TNFalpha seem to protect from CM, whereas excess TNFalpha induces CM and anti-TNFalpha therapies (antibodies, pentoxifylline) did not show any efficiency in protection from CM. Moreover, the involvement of lymphotoxin a, which shares with TNFalpha the same receptors with similar affinity, appears to be an interesting target for further investigation.
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PMID:Tumor necrosis factor alpha in the pathogenesis of cerebral malaria. 1450 53

Infections are probably the most common preventable cause of epilepsy worldwide. There are concerns that endemic infections and infestations, such as malaria and neurocysticercosis, could be responsible for the increased incidence of epilepsy in the developing world. Cases of epilepsy associated with neurocysticercosis are also being seen increasingly in developed countries due to migration from, and travel to, endemic areas. When prescribing antimicrobial agents in patients with epilepsy a number of issues need to be considered, such as potential adverse effects on seizure control and interactions with concomitant antiepileptic drugs (AEDs). Some antimicrobial agents, including penicillins, cephalosporins, carbapenems, quinolones and antimalarials, can have proconvulsant activity and may precipitate seizures, even in patients who do not have epilepsy. Moreover, many antimicrobials increase or decrease the plasma levels of AEDs, whereas some AEDs may adversely affect the efficacy of antimicrobials.
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PMID:Epilepsy and comorbidity: infections and antimicrobials usage in relation to epilepsy management. 1451 Aug 16

A 3 year review of neurologic admissions into the adult medical wards at the UCH, Ibadan, Nigeria between January 1998 and December 2000 is presented. The study design involved the scrutiny of the records of all the neurological admissions, male and female to the medical ward. The identified cases were then classified and only cases confirmed as neurological were further analysed. Stroke, predominantly non-hemorrhagic accounted for 50.4% of cases for the period of study. Stroke is therefore the most common cause of adult neurologic admissions on medical wards of UCH. Central nervous system infections, comprising mainly of tetanus and meningitis accounted for 14.2% (111) and 12.4% (97) of case respectively. The myelopathies were the cause of neurologic admissions in 8.1% (63) of cases followed by seizure disorders. Headache was the reason for admission in 0.9% (7) of cases. Parkinsons disease, hypertensive encephalopathy, Guillian Barne syndrome, seasonal ataxic neuropathy, cavernous sinus thrombophlebitis, normal pressure hydrocephalus were rarely the cause of admission. Similarly, dystonia, and cerebral malaria recorded 0.13% (1) of cases each. A case is made for the establishment of regional stroke units in Nigeria.
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PMID:A 3-year review of neurologic admissions in University College Hospital Ibadan, Nigeria. 1452 26

Malaria continues to be a problem for children returning or immigrating to industrialized countries from tropical regions. Proper diagnosis begins with clinical suspicion. In nonimmune children, malaria typically presents with high fever that might be accompanied by chills and headache. Symptoms and signs may be more subtle in partially immune children, and anemia and hepatosplenomegaly may also be present. Children may present with respiratory distress and/or rapidly progressing cerebral malaria that manifests as altered sensorium and, sometimes, seizures. Thick blood smears help to determine when infection is present, but a single smear without parasites is not sufficient to rule out malaria. Thin blood smears aid in identifying the species of parasite. Treatment must include careful supportive care, and intensive care measures should be available for treating children with complicated Plasmodium falciparum malaria. Medical regimens can include mefloquine, atovaquone-proguanil, sulfadoxine-pyrimethamine, quinine or quinidine, clindamycin, doxycycline, chloroquine, and primaquine.
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PMID:Diagnosis and treatment of malaria in children. 1458 68

It has been well established that high fever can cause substantial damage to the cerebellum and also cause multiple small vascular lesions in neocortex and subcortical white matter. Beyond acute effects, the neuropsychological sequelae of these latter cortical and subcortical lesions have not been studied. The investigation reported involved 36 VA patients with a history of serious febrile illness. The febrile illnesses of the pyrexic subjects did not cause febrile seizures and resulted from diseases that did not directly involve the brain (e.g., encephalitis, meningitis, malaria). Control subjects were combat veterans who had suffered gunshot wounds, but who had no history of febrile illness. Pyrexic patients performed worse than controls on a variety of measures including language, memory, concentration, and word finding as well as failing a test of dichotic listening for words. Results demonstrate that hyperpyrexia can have lasting neuropsychological sequelae, and suggest that history of serious febrile illness be considered as an exclusionary criterion for participation in neuropsychological research concerning other topics or disorders.
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PMID:Long-term neuropsychological sequelae of fever associated with amnesia. 1458 27

Common causes of coma in falciparum malaria are cerebral malaria, hypoglycaemia and electrolyte disturbances. Focal deficits due to arterial infarcts may sometimes occur in children, but are rare in adults. Three adults with falciparum malaria who had fever, altered consciousness and focal neurological deficits (one of whom also had seizures) are being reported here. CT scan of the brain revealed haemorrhagic infarction of the cerebral cortex and subcortical white matter with surrounding oedema suggestive of venous infarction in all three patients. The diagnosis of cerebral venous thrombosis was missed in the first patient, and was detected only at autopsy. In the next two patients, superior sagittal sinus thrombosis was confirmed angiographically. Only one patient survived; the other two died of increased intracranial pressure. Two of the three patients also had Plasmodium vivax co-infection. A hypercoagulable state resulting from severe malaria may be responsible for this rare and potentially fatal complication. Cerebral malaria may be associated with raised intracranial pressure due to cerebral oedema. Cerebral venous thrombosis may worsen this and adversely affect outcome. This diagnosis should be suspected in patients with severe malaria who develop focal neurological deficits and confirmed by appropriate imaging; judicious use of local thrombolytic therapy may help improve outcome.
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PMID:Cerebral venous and dural sinus thrombosis in severe falciparum malaria. 1466 96

Plasmodium falciparum is the most common cause of severe and life-threatening malaria. Falciparum malaria causes over one million deaths every year. In Africa, a vast majority of these deaths occur in children under five years of age. The presentation of severe malaria varies with age and geographical distribution. The mortality rate is higher in adults than in children but African children develop neuro-cognitive sequelae following severe malaria more frequently. The management of severe malaria includes prompt administration of appropriate parenteral anti-malarial agents and early recognition and treatment of the complications. In children, the complications include metabolic acidosis (often caused by hypovolaemia), hypoglycaemia, hyperlacticacidaemia, severe anaemia, seizures and raised intracranial pressure. In adults, renal failure and pulmonary oedema are more common causes of death. In contrast, concomitant bacterial infections occur more frequently in children and are associated with mortality in children. Admission to critical or intensive care units may help reduce the mortality, and the frequency and severity of sequelae related to severe malaria.
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PMID:Management of severe falciparum malaria. 1504 99

Falciparum malaria affect all ages with multiple-systemic complications which varies in different age group. We studied 242 children with complicated Falciparum malaria with a median age of 6.5 years to look for occurrence of different complications in younger and older age groups and overall mortality picture. Unarousable coma (40.5%), severe anemia (26.03%), repeated seizures (46.2%) and hepatopathy (32.2%) were commonest complications. Under five children had higher risk of development of cerebral malaria (P<0.01), severe anemia (P<0.05) and seizures (P<0.001); whereas above five children had higher risk of acute renal failure (P<0.05) and malarial hepatopathy (P<0.02). Over all mortality was 9.9%, cerebral malaria being the commonest cause (6.6%). Multi-system involvement was seen in 58.4% cases of death. Children having pulmonary edema, shock and cerebral malaria had high case fatality rate.
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PMID:Severe falciparum malaria. 1505 76

Falciparum malaria is the most common cause of convulsions in children admitted to hospital in malaria endemic areas. Detection of convulsions requires close monitoring and one should be on the look out for signs of subtle convulsions. About a third of acute seizures in children with cerebral malaria, do not manifest as convulsions, but as changes in eye deviation, salivation and/or eye deviation. It is important to terminate convulsions lasting more than 5 min, since prolonged convulsions are associated with neurological deficits in survivors of children with severe malaria. Initial management should include putting the child into the left lateral position, checking the blood glucose and administering oxygen if hypoxic. The benzodiazepines, particularly diazepam, are used as the initial anticonvulsants. Phenobarbital and phenytoin are used as second-line treatments. Prompt and effective management of falciparum malaria associated convulsions may contribute to a better outcome in children with severe malaria.
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PMID:Management of seizures in children with falciparum malaria. 1511 28


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