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Open Access Highly Accessed Short Report

Severe neurological sequelae and behaviour problems after cerebral malaria in Ugandan children

Richard Idro1*, Angelina Kakooza-Mwesige1, Stephen Balyejjussa1, Grace Mirembe1, Christine Mugasha1, Joshua Tugumisirize2 and Justus Byarugaba1

Author Affiliations

1 Department of Paediatrics and Child Health, Mulago Hospital and Makerere University School of Medicine, PO Box 7072, Kampala, Uganda

2 Department of Psychiatry, Mulago Hospital and Makerere University School of Medicine, PO Box 7072, Kampala, Uganda

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BMC Research Notes 2010, 3:104  doi:10.1186/1756-0500-3-104

Published: 16 April 2010

Abstract

Background

Cerebral malaria is the most severe neurological complication of falciparum malaria and a leading cause of death and neuro-disability in sub-Saharan Africa. This study aimed to describe functional deficits and behaviour problems in children who survived cerebral malaria with severe neurological sequelae and identify patterns of brain injury.

Findings

Records of children attending a specialist child neurology clinic in Uganda with severe neurological sequelae following cerebral malaria between January 2007 and December 2008 were examined to describe deficits in gross motor function, speech, vision and hearing, behaviour problems or epilepsy. Deficits were classified according to the time of development and whether their distribution suggested a focal or generalized injury. Any resolution during the observation period was also documented.

Thirty children with probable exposure to cerebral malaria attended the clinic. Referral information was inadequate to exclude other diagnoses in 7 children and these were excluded. In the remaining 23 patients, the commonest severe deficits were spastic motor weakness (14), loss of speech (14), hearing deficit (9), behaviour problems (11), epilepsy (12), blindness (12) and severe cognitive impairment (9). Behaviour problems included hyperactivity, impulsiveness and inattentiveness as in attention deficit hyperactivity disorder (ADHD) and conduct disorders with aggressive, self injurious or destructive behaviour. Two patterns were observed; a) immediate onset deficits present on discharge and b) late onset deficits. Some deficits e.g. blindness, resolved within 6 months while others e.g. speech, showed little improvement over the 6-months follow-up.

Conclusions

In addition to previously described neurological and cognitive sequelae, severe behaviour problems may follow cerebral malaria in children. The observed differences in patterns of sequelae may be due to different pathogenic mechanisms, brain regions affected or extent of injury. Cerebral malaria may be used as a new model to study the pathogenesis of ADHD.