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      Continuous EEG monitoring in Kenyan children with non-traumatic coma

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          Abstract

          Background

          The aim of this study was to describe the EEG and clinical profile of seizures in children with non-traumatic coma, compare seizure detection by clinical observations with that by continuous EEG, and relate EEG features to outcome.

          Methods

          This prospective observational study was conducted at the paediatric high dependency unit of Kilifi District Hospital, Kenya. Children aged 9 months to 13 years presenting with acute coma were monitored by EEG for 72 h or until they regained consciousness or died. Poor outcome was defined as death or gross motor deficits at discharge.

          Results

          82 children (median age 2.8 (IQR 2.0–3.9) years) were recruited. An initial medium EEG amplitude (100–300 mV) was associated with less risk of poor outcome compared to low amplitude (≤100 mV) (OR 0.2, 95% CI 0.1 to 0.7; p<0.01). 363 seizures in 28 (34%) children were observed: 240 (66%) were electrographic and 112 (31%) electroclinical. In 16 (20%) children, electrographic seizures were the only seizure types detected. The majority (63%) of electroclinical seizures had focal clinical features but appeared as generalised (79%) or focal with secondary generalisation (14%) on EEG. Occurrence of any seizure or status epilepticus during monitoring was associated with poor outcome (OR 3.2, 95% CI 1.2 to 8.7; p=0.02 and OR 4.5, 95% CI 1.3 to 15.3; p<0.01, respectively).

          Conclusion

          Initial EEG background amplitude is prognostic in paediatric non-traumatic coma. Clinical observations do not detect two out of three seizures. Seizures and status epilepticus after admission are associated with poor outcome.

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          Most cited references27

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          Severe falciparum malaria. World Health Organization, Communicable Diseases Cluster.

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            Pathogenesis, clinical features, and neurological outcome of cerebral malaria.

            Cerebral malaria is the most severe neurological complication of Plasmodium falciparum malaria. Even though this type of malaria is most common in children living in sub-Saharan Africa, it should be considered in anybody with impaired consciousness that has recently travelled in a malaria-endemic area. Cerebral malaria has few specific features, but there are differences in clinical presentation between African children and non-immune adults. Subsequent neurological impairments are also most common and severe in children. Sequestration of infected erythrocytes within cerebral blood vessels seems to be an essential component of the pathogenesis. However, other factors such as convulsions, acidosis, or hypoglycaemia can impair consciousness. In this review, we describe the clinical features and epidemiology of cerebral malaria. We highlight recent insights provided by ex-vivo work on sequestration and examination of pathological specimens. We also summarise recent studies of persisting neurocognitive impairments in children who survive cerebral malaria and suggest areas for further research.
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              Blantyre Malaria Project Epilepsy Study (BMPES) of neurological outcomes in retinopathy-positive paediatric cerebral malaria survivors: a prospective cohort study

              Summary Background Cerebral malaria, a disorder characterised by coma, parasitaemia, and no other evident cause of coma, is challenging to diagnose definitively in endemic regions that have high rates of asymptomatic parasitaemia and limited neurodiagnostic facilities. A recently described malaria retinopathy improves diagnostic specificity. We aimed to establish whether retinopathy-positive cerebral malaria is a risk factor for epilepsy or other neurodisabilities. Methods Between 2005 and 2007, we did a prospective cohort study of survivors of cerebral malaria with malaria retinopathy in Blantyre, Malawi. Children with cerebral malaria were identified at the time of their index admission and age-matched to concurrently admitted children without coma or nervous system infection. Initially matching of cases to controls was 1:1 but, in 2006, enrolment criteria for cerebral malaria survivors were revised to limit inclusion to children with cerebral malaria and retinopathy on the basis of indirect ophthalmoscopic examination; matching was then changed to 1:2 and the revised inclusion criteria were applied retrospectively for children enrolled previously. Clinical assessments at discharge and standardised nurse-led follow-up every 3 months thereafter were done to identify children with new seizure disorders or other neurodisabilities. A Kaplan-Meier survival analysis was done for incident epilepsy. Findings 132 children with retinopathy-positive cerebral malaria and 264 age-matched, non-comatose controls were followed up for a median of 495 days (IQR 195–819). 12 of 132 cerebral malaria survivors developed epilepsy versus none of 264 controls (odds ratio [OR] undefined; p<0·0001). 28 of 121 cerebral malaria survivors developed new neurodisabilities, characterised by gross motor, sensory, or language deficits, compared with two of 253 controls (OR 37·8, 95% CI 8·8–161·8; p<0·0001). The risk factors for epilepsy in children with cerebral malaria were a higher maximum temperature (39·4°C [SD 1·2] vs 38·5°C [1·1]; p=0·01) and acute seizures (11/12 vs 76/120; OR 6·37, 95% CI 1·02–141·2), and male sex was a risk factor for new neurodisabilities (20/28 vs 38/93; OR 3·62, 1·44–9·06). Interpretation Almost a third of retinopathy-positive cerebral malaria survivors developed epilepsy or other neurobehavioural sequelae. Neuroprotective clinical trials aimed at managing hyperpyrexia and optimising seizure control are warranted. Funding US National Institutes of Health and Wellcome Trust.
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                Author and article information

                Journal
                Arch Dis Child
                Arch. Dis. Child
                archdischild
                adc
                Archives of Disease in Childhood
                BMJ Group (BMA House, Tavistock Square, London, WC1H 9JR )
                0003-9888
                1468-2044
                1 April 2012
                10 February 2012
                : 97
                : 4
                : 343-349
                Affiliations
                [1 ]Centre for Geographic Medicine Research – Coast, Kenya Medical Research Institute–Wellcome Trust Research Programme, Kilifi, Kenya
                [2 ]Department of Clinical Research, Afya Research Africa, Nairobi, Kenya
                [3 ]Department of Paediatrics and Child Health, Mulago Hospital/Makerere University, Kampala, Uganda
                [4 ]Centre for Clinical Vaccinology and Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK
                [5 ]Department of Clinical Neurophysiology, Great Ormond Street Hospital for Children, London, UK
                [6 ]Department of Child Health, Southampton General Hospital, Southampton, UK
                [7 ]Neurosciences Unit, University College London Institute of Child Health, London, UK
                [8 ]Department of Psychiatry, University of Oxford, Oxford, UK
                Author notes
                Correspondence to Dr Samson Gwer, Centre for Geographic Medicine Research – Coast, Kenya Medical Research Institute–Wellcome Trust Research Programme, PO Box 230, Kilifi, Kenya; samgwer@ 123456gmail.com
                Article
                archdischild-2011-300935
                10.1136/archdischild-2011-300935
                3329232
                22328741
                27a17c44-d7b9-487e-8b72-32620a242cfa
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode.

                History
                : 30 August 2011
                : 11 December 2011
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