Cerebral malaria

Last revised by Rohit Sharma on 21 Feb 2024

Cerebral malaria is a rare intracranial complication of a malarial infection.

Cerebral malaria is mainly encountered in young children and adults living or traveling in malaria-endemic areas. It is estimated to occur in ~2% of patients with acute Plasmodium falciparum infection, the most common species of Plasmodium that causes malaria.

Cerebral malaria should be suspected when there are neurological symptoms on a background of malarial infection. Clinical presentations include: headache, altered state of consciousness, seizures, backache, vomiting, nausea, etc.

It can at times be characterized by diffuse petechial hemorrhages on postmortem pathological specimens which are often difficult to identify retrospectively on imaging 1,2.

The hemorrhages are thought to occur when cerebral capillaries and small veins are occluded by sequestered Plasmodium-infected erythrocytes. Hence, this pathological process may lead to areas of infarction.

Imaging features on its own are often non-specific and correlation with travel history or exposure in an endemic area is mandatory 7. Most published articles are based on case reports and small case series.

The most common findings are related to ischemia involving: deep white matter, cortex, basal ganglia, thalami and cerebellum. These areas of ischemia can be hemorrhagic 6.

CT findings do not appear to correlate with the degree of parasitemia and can sometimes be normal 1. However, reported features include 1:

  • cerebral edema

  • thalamic hypoattenuation from infarcts

  • cerebellar white matter hypoattenuation from infarcts

Described features include:

  • T2/FLAIR: non-specific hyperintensities located in the bilateral periventricular white matter, corpus callosum, occipital subcortex, basal, ganglia, and/or bilateral thalamic regions 3,8,10

  • DWI: high diffusion signal if cortical infarcts are present

  • SWI: regions of hypointensity representing either petechial microbleeds or regions of hemorrhage in infarcted tissue 6

Treatment is with parenteral artemisinin derivatives and electrolyte correction, usually in the setting of an intensive care unit, as well as symptomatic treatment (e.g. use of antiseizure medications) 9.

It is often associated with a high mortality rate (20-50%). However, those patients who survive often have a full recovery with minimal or no long-term sequelae.

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