Hypoglycaemia, as a result of the inability of the liver to breakdown glucose, a fever related increase in metabolism, use of glucose by the parasites and Quinine therapy has a role in the long term sequelae of cerebral malaria. For research purposes cerebral malaria is defined as unrousable coma not attributable to any other cause in a patient with proved falciparum infection. This means that other causes of coma and convulsions viz fever, hypoglycaemia and other common CNS infections such as meningitis and encephalitis have been excluded. A functional blockade of the micro circulation is the main pathogenetic mechanism and therefore diffuse bihemispheric dysfunction is the most common manifestation of cerebral involvement. Patients become drowsy and disorientated.
Hallucinations are common.
As the disease process advances, the level of consciousness deteriorates and coma ensues. Rarely, the initial mental changes may suggest psychosis before the deterioration in the level of consciousness becomes clear. Especially when patients have high fever and with use of phenothiazine drugs. A transient paranoid psychosis may follow the acute illness. In most instances the seizures are generalised but in some instances they may have a focal onset and even persistent focal seizures have been described.