Celebral Malaria

To investigate auto-reactive antibodies against dendrites of neurons (AAD) previously reported in cerebral malaria (CM) for their functional biological activity, a serological study was conducted in a larger cohort of patients with CM and uncomplicated falciparum malaria (UM).

Excessive release of proinflammatory cytokines by innate immune cells is an important component of the pathogenic basis of malaria.

Children who suffer retinopathy-positive CM at preschool age are at greater risk of developmental delay, particularly with respect to language development.

Cerebral malaria is the most severe neurologic complication in children and young adults infected with Plasmodium falciparum.

Clinical manifestations of Plasmodium falciparum infection are induced by the asexual stages of the parasite that develop inside red blood cells (RBCs).

The small sample size does not permit definitive conclusions, but the mortality rate was unexpectedly high in the PTX group.

Cerebral malaria (CM) is the most severe complication of Plasmodium infection. Although inappropriate immune responses to Plasmodium falciparum are reported as the major causes of CM, the precise mechanisms for development remain unclear.

Cerebral malaria (CM) and severe anemia (SA) are the most severe complications of Plasmodium falciparum infections.

Although the peak age of CM will increase as transmission intensity decreases in Africa, more than 75% of all paediatric hospital admissions of severe malaria are likely to remain in under five year olds in most epidemiological settings.

As we close the gaps in the fight against global malaria, the question of cerebral malaria mortality remains a source of great concern.