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

Infections with malaria are increasing in Europe and Northern America and are also spreading in tropical endemic areas. A falciparum variety of malaria known as cerebral malaria is the most well-known neurological complication, caused by Plasmodium falciparum and characterised by a fulminant course with disturbances of consciousness and facultative seizures or focal neurological deficits. 50% of deaths caused by malaria are due to cerebral involvement. Pathologically a disseminated vasculomyelinopathic disorder is seen. Immunological changes, vascular-hypoxic disturbances and metabolic-toxic factors contribute to these pathological findings. Facts on diagnostic, differential diagnostic and therapeutic procedures are presented. Beside the severe and life-threatening cerebral malaria some unspecific cerebral symptoms are seen, such as cerebellar ataxia and chorea. Spinal disease and peripheral nerve involvement, polyradiculitis and especially psychiatric disorders have also been described. Every neurological and psychiatric disorder presented first in tropical areas or malaria-endemic regions requires malaria diagnostic tests. In our geographical region, any previous history of a journey to the tropics is an important pointer; in particular, neurological or psychiatric symptoms can be important pointers to malaria.
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PMID:[Neurologic complications of malaria infection]. 844 77

Electroencephalography (EEG) was performed in 13 male patients with cerebral malaria during the first 24 hours of admission, using a 10-channel, 10-20 system EEG machine (6 montages, 20 minute duration). The EEG patterns were of theta and delta waves from both sides of cerebral hemisphere suggesting diffused cortical dysfunction. No epileptic pattern was found in patients who had seizures prior to, or after admission. The initial EEG performed on the day of admission did not show any specific pattern attributable to any pathological condition. It was also unable to predict the prognosis of the 2 dead patients. However, one cerebral malaria patient with left hemiplegia was subsequently found to have right basal ganglia hemorrhage in CAT scan, high amplitude delta waves and theta waves in the tracings of the right hemisphere. The study suggests that a single EEG data on admission can hardly give enough information for prediction of the clinical course and outcome of cerebral malaria. Serial EEGs probably provide more useful information regarding the prognostic signs in this group of patients. Nevertheless, EEG could be useful to rule out some cerebral pathology such as space occupying lesions, epilepsy or any other causes of unconsciousness that could produce similar cerebral symptoms in malaria patients.
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PMID:Electroencephalography in cerebral malaria. 852 17

The clinical and laboratory features of severe falciparum malaria in 180 Gambian children were studied between 1985 and 1989. Of the 180 children, 118 (66%) presented with seizures, 77 (43%) had cerebral malaria, 35 (20%) had witnessed seizures after admission, 29 (16%) were hypoglycemic, and 27 (15%) died. Respiratory distress was a common harbinger of a fatal outcome. The differences in admission parasite counts in the blood, hematocrit, and opening cerebrospinal pressures for patients who died and survivors were not significant. A multiple logistic regression model identified neurological status (coma, particularly if associated with extensor posturing), stage of parasite development on the peripheral blood film, pulse rate of > 150 or respiratory rate of > 50, hypoglycemia, and hyperlactatemia (plasma lactate level, > 5 mmol/L) as independent indicators of a fatal outcome. Biochemical evidence of hepatic and renal dysfunction was an additional marker of a poor prognosis, but, in contrast to severe malaria in adults, none of these children with severe malaria had acute renal failure.
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PMID:Clinical features and outcome of severe malaria in Gambian children. 852 47

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25

Between October 1990 and November 1991 data were collected on the frequency, causes, and nature of epileptic seizures in children admitted to the paediatric ward at Kilifi District Hospital, Kenya, from a defined study area. During this period, 1324 children were studied, of whom 15.8% had seizures as part of their illness. Malaria was by far the commonest cause of seizures, accounting for 69.0%; no other single condition caused more than 4.4%. The proportion of respiratory infections complicated by seizures was 4.0% compared to 31.3% for malaria. Only 25% of malaria-related epileptic seizures were associated with cerebral malaria; the remainder were associated with otherwise uncomplicated malaria and, in this group, 84% had complex seizures, with 47% being partial and over 70% repetitive. There was no relationship with fever, with 54% of observed seizures occurring at rectal temperatures below 38 degrees C. The minimum community incidence of complex seizures in association with non-cerebral malaria was 5.8 per 1000 per year. Complex epileptic seizures in association with otherwise uncomplicated malaria are common and may be a significant cause of longer term morbidity in malaria endemic areas.
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PMID:Epileptic seizures and malaria in Kenyan children. 876 76

The mechanisms of death and neurologic sequelae in African children with cerebral malaria are undetermined. Because pathologic features are confined to the cerebral vasculature, perturbations in cerebral hemodynamics may be responsible. We compared the transcranial Doppler findings in 50 children with cerebral malaria with those of 115 conscious Kenyan children. In addition, 10 children with cerebral malaria were studied during intracranial pressure monitoring and nine children were studied during the agonal stages. In the children with cerebral malaria, cerebral blood flow velocity was increased in 30%, usually associated with seizures. Of the 11 children who developed neurologic sequelae, six had sonographic abnormalities associated with lateralizing deficits, including four children with hemiparesis (in two children the contralateral middle cerebral artery could not be insonated and two had transient increases in blood flow velocity associated with seizures). In the children with severe intracranial hypertension, there was a significant linear relationship between the cerebral perfusion pressure and blood flow velocity, suggesting that autoregulation was impaired. Sonographic features of progressive intracranial hypertension, were observed in three children with cerebral malaria who died. Perturbations of cerebral hemodynamics are associated with a poor outcome in Kenyan children with cerebral malaria.
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PMID:Perturbations of cerebral hemodynamics in Kenyans with cerebral malaria. 885

Prolonged, multiple seizures complicate a high proportion of cases of childhood cerebral malaria, and several studies have shown an association between these and neurological sequelae. We prospectively studied 65 patients (38 female) admitted to Kilifi Hospital in 1994. Electroencephalographic recordings (EEGs) were made at 12-hourly intervals, with continuous recordings made on a cerebral function analysing monitor (CFAM). Survivors were seen one month after discharge. Cerebral computerized tomography was performed on children with neurological sequelae. Sixty-two percent of patients had seizures following admission, of whom half had an episode of status epilepticus. Fifty-two percent of seizures were partial motor, 34% generalized tonic-clonic, and 14% partial with secondary generalization. In 22%, coma appeared to be due to a prolonged postictal state. Ten children had subtle motor seizures. Posterior parieto-temporal discharges were the most common EEG finding. Seven children died, eight developed neurological sequelae, and 50 (77%) recovered fully. Status epilepticus was associated with the development of neurological sequelae. Prolonged, multiple seizures may play an important part in the pathogenesis of coma in childhood cerebral malaria, and are likely to contribute to both the morbidity and mortality of this disease.
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PMID:Seizures and status epilepticus in childhood cerebral malaria. 934 57

A prospective study was undertaken to determine the clinical pattern and outcome among children admitted with acute severe malaria into the emergency paediatric unit (EPU) at the Jos University Teaching Hospital (JUTH) over a 15-month period (between August 1991-October 1992). Five hundred and one (25%) children were admitted with acute severe malaria, out of a total of 2008 admissions into the EPU during the study period. Blood smears for malaria parasites were positive in 287 (57.7%) of the children and P. falciparum was the only species identified in the study. Seventy one percent of the children admitted were aged 5 years and below. Febrile convulsions was the commonest manifestation of acute severe malaria, accounting for 49.7% of the cases. Majority (97.8%) of the children responded satisfactorily to chloroquine therapy with clearance of parasitaemia. Associated bacteraemia was documented in 35 (7%) of the 501 children. Sixteen out of the 501 children died, giving a mortality of 3.2%. Cerebral malaria, which accounted for only 17.6% of the admissions, was responsible for 56.3% of all the deaths. Mortality was also associated with hypoglycaemia, severe anaemia, shock and repeated, prolonged seizures.
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PMID:Clinical pattern and outcome in children with acute severe falciparum malaria at Jos University Teaching Hospital, Nigeria. 910 94

In a prospective study, hyponatraemia was observed in 52.6% of 19 children with cerebral malaria on admission, the plasma sodium ranging from 117 to 129 mumol/l. In addition, a further 10% developed hyponatraemia between 48 and 96 hrs after admission; in half of these, there was continuing urinary sodium loss. The clinical presentation of hypo- and normonatraemic children was similar except for vomiting and hypoglycaemia which were commoner in the normonatraemic and irritability and signs of lower respiratory tract infection which were commoner in the hyponatraemic groups. In hyponatraemic and normonatraemic children, there was a negative correlation between hyponatraemia and parasite density (r = -0.503, P < 0.05) and (r = -0.14, P < 0.05 respectively) and between parasite density and urinary sodium concentration during the first 24 hours of admission (r = -0.034; P < 0.05 and r = -0.045, P > 0.05 respectively). Irrespective of group, a relative increase in plasma sodium in the first 24 hours of admission (positive delta Na 24 h) was associated with a reduction in seizure frequency during this period as compared to the reported 24 hour of pre-admission seizure frequency, and, vice-versa. It is concluded that hyponatraemia is not uncommon in childhood cerebral malaria; urinary sodium loss may be contributory to the hyponatraemia seen in this condition.
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PMID:Hyponatraemia in severe falciparum malaria: a clinical study of nineteen comatose African children. 911 54

The Blantyre coma scale (BCS) is used to assess children with severe falciparum malaria, particularly as a criterion for cerebral malaria, but it has not been formally validated. We compared the BCS to the Adelaide coma scale (ACS), for Kenyan children with severe malaria. We examined the inter-observer agreement between 3 observers in the assessment of coma scales on 17 children by measuring the proportion of agreement (PA), disagreement rate (DR) and fixed sample size kappa (kappa n). We assessed the sensitivity and specificity of the scales in detecting events (seizures and hypoglycaemia) in 240 children during admission and the usefulness of the scales in predicting outcome. There was considerable disagreement between observers in the assessment of both scales (BCS: PA = 0.55, DR = 0.09 and kappa n = 0.27; ACS: PA = 0.36, DR = 0.31, and kappa n = 0.31), particularly with the verbal component of the BCS (kappa n = 0.02). Compared to the ACS, the BCS was more specific (0.85 for BCS and 0.80 for ACS), but less sensitive (0.25-0.69 vs. 0.38-0.88 respectively) in detecting events and was a worse predictor of neurological sequelae. The BCS provided a better overall assessment of a child's incapacity from falciparum malaria, but the ACS was more useful in assessing neurological disturbances.
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PMID:Coma scales for children with severe falciparum malaria. 919 57


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