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Cerebral Malaria

Summary

  • Severe complication of Plasmodium falciparum infection affecting the central nervous system
  • Characterised by impaired consciousness, seizures, and coma
  • Diagnosis based on clinical presentation, blood smears, and neuroimaging findings1

Pathophysiology

  • Caused by sequestration of parasitised erythrocytes in cerebral microvasculature
  • Leads to:
    • Microvascular obstruction
    • Endothelial activation
    • Blood-brain barrier disruption
    • Cerebral oedema
  • Inflammatory response contributes to neurological damage
  • Potential long-term cognitive and neurological sequelae

Demographics

  • Most common in children under 5 years in sub-Saharan Africa
  • Also affects adults in regions with lower malaria transmission
  • Travellers from non-endemic areas at risk when visiting malaria-endemic regions
  • Mortality rate ranges from 15-25% despite treatment

Diagnosis

  • Clinical criteria:
    • Unarousable coma (Glasgow Coma Scale ≤9)
    • Exclusion of other causes of encephalopathy
  • Laboratory findings:
    • Positive blood smear for P. falciparum
    • Rapid diagnostic tests for malaria antigens
  • Lumbar puncture to rule out other causes of coma
  • Neuroimaging to assess complications and exclude differential diagnoses

Imaging

  • CT findings:
    • Brain swelling (50-75% of cases)
    • Focal hypodensities suggesting infarction
    • Rarely, haemorrhage
  • MRI findings:
    • More sensitive than CT for detecting subtle abnormalities
    • T2 and FLAIR hyperintensities in:
    • Cortical grey matter
    • Basal ganglia
    • Corpus callosum
    • Brainstem
    • Diffusion-weighted imaging may show cytotoxic oedema
    • Susceptibility-weighted imaging can detect microhaemorrhages

panels-1

  • A 40-year-old patient became obtunded 1 month after return from a region endemic for malaria.
  • MRI showed the brain parenchyma appearing normal on T2 and FLAIR and DWI - there was no oedema or ischaemic changes.
  • However, SWI showed extensive juxtacortical and deep white matter foci of susceptibility artefact (representing microhaemorrhages and/or microthrombi).
  • Chest imaging showed bilateral lung consolidation, splenomegaly (with infarction) and small regions of hepatic infarcts.

Treatment

  • Prompt IV artesunate and supportive care; mortality remains high

Differential diagnosis

Differential Diagnosis Distinguishing Feature
Intracranial Haemorrhage Focal neurological deficits; CT scan shows bleeding
Acute disseminated encephalomyelitis (ADEM) Multifocal subcortical and deep white matter T2 hyperintensities, often with partial ring enhancement
Viral encephalitis (e.g. Japanese encephalitis) Bilateral thalamic and basal ganglia T2 hyperintensity; mesial temporal involvement in HSV
Osmotic demyelination Central pontine symmetric T2 hyperintensity sparing peripheral rim
Posterior reversible encephalopathy syndrome (PRES) Parieto-occipital vasogenic oedema pattern, reversible on follow-up

  1. Luzolo et al. Cerebral malaria. 2019. Brain research bulletin - Open in new tab. ↩