Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Out of 604 Gambian children admitted with falciparum malaria to one hospital between September and December, 1988, 308 had cerebral malaria and 203 were severely anaemic (haemoglobin less than 60 g/l). 14% of those with cerebral malaria died, as did 7.8% of those with severe anaemia. 32 (12%) of children surviving cerebral malaria had residual neurological deficit. 69 other children were admitted with clinical features strongly suggestive of cerebral malaria but with negative blood films; 16 of these died and 3 had residual neurological deficits. The commonest sequelae of cerebral malaria were hemiplegia (23 cases), cortical blindness (11), aphasia (9), and ataxia (6). Factors predisposing to sequelae included prolonged coma, protracted convulsions, severe anaemia, and a biphasic clinical course characterised by recovery of consciousness followed by recurrent convulsions and coma. At follow up 1-6 months later over half these children had made a full recovery, but a quarter were left with a major residual neurological deficit. Cerebral malaria in childhood may be an important cause of neurological handicap in the tropics.
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PMID:Neurological sequelae of cerebral malaria in children. 197 27

Thirty five children aged 5 months to 15 years suffering from stroke were studied from August 1984 to July 1990 from two hospitals in order to determine the incidence, the etiological factors and the short term outcome of the stroke. The average annual incidence was 1.85 per 1000 pediatric hospitalizations. There was a progressive rise in the number of cases from 1985, with a peak in 1990. Motor impairment of one half of the body was the commonest clinical feature seen in 97.1% of the cases. Other clinical signs were: facial paralysis (62.9%) and aphasia (28.6%). The main etiological factors were: homozygous sickle cell disease (31.4%), heart disease (17.1%), cerebral malaria (14.3%) and meningitis (14.3%). No causative factor was identified in 7 patients (20%). The mortality rate was low (2.9%) and all the children had neurological deficit after a mean hospital stay of 15 days. Laboratory investigations including lipid analysis, platelet count, and skull X-rays proved to be of no diagnostic value. However, computed tomography (CT) scan confirmed the diagnosis of ischemic stroke whenever it could be done.
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PMID:Stroke in children in Yaounde, Cameroon. 789 Mar 41

Of 51 consecutive children with cerebral malaria, fever, convulsions, and drowsiness were the commonest presenting symptoms. Decerebrate and decorticate postures and absent cornea reflex were the commonest brain stem signs. Opening lumbar cerebrospinal (CSF) pressure was raised in all but one of 24 children in whom it was reliably measured [mean 15.2 +/- 5.7 mmHg, range 6-24]. Hyponatraemia occurred in 17 (33%). Acute renal failure was not uncommon; the combination of hypercreatininaemia (plasma creatinine > 100 mumol/L) and hyperkalaemia (plasma potassium > 6.0 mumol/L) was fatal in 5 out of 7 patients in whom it occurred. Disturbances of acid-base status were present in all 40 children in whom it was assessed on admission. Mortality rate was 16% (8 patients). Neurological deficits occurred in 7 (14%) of the survivors and included cortical blindness [3], aphasia [3], hypertonia [3], hearing loss [2], and dystonia [1]. In addition to the present measures aimed at reducing morbidity and morality in children with cerebral malaria, efforts should be directed at rapid assessment of renal function and prompt correction of such dysfunction if found.
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PMID:Clinical study of cerebral malaria in African children. 1089 20

Falciparum malaria is notoriously known to produce life-threatening complications. Despite growing reports of chloroquine resistance and severe disease, vivax malaria continues to be viewed as a benign disease. We report a rare case of a 47-year-old healthy man from a malaria-endemic region, presenting with intracerebral bleed, right haemiparesis, aphasia and seizures following vivax malaria. This was successfully managed conservatively, without any neurosurgical intervention, with combination therapy of intravenous artesunate, oral hydroxychloquine and primaquine. In a country where Plasmodium vivax is responsible for majority of cases of malaria, it is high time the national malaria control programmes focus on the elimination of P. vivax in addition to its more dangerous counterpart, P. falciparum.
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PMID:Intracerebral bleed, right haemiparesis and seizures: an atypical presentation of vivax malaria. 2492 May 15