Clinical History
A 1-year-old boy suffered from several fever episodes during and after a holiday in Africa. After a few days, neurological symptoms including general tonic-clonic seizures and general muscular hypotonia arose. The child had no relevant medical history or history of neurological problems.
Imaging Findings
MRI of the brain.
a) Axial T2-weighted image at the level of the thalami shows marked bilateral hyperintensity in the posterior part of the thalamus.
b) Axial inversion recovery T1-weighted image at the same level shows corresponding hypointensity.
c) Axial diffusion-weighted (b1000) image at the same level shows no diffusion restriction.
Discussion
Background
Malaria, caused by infection with the protozoan parasite Plasmodium, is a major health problem in tropical countries. Cerebral complications of an acute Plasmodium falciparum infection occur in approximately 2% of patients. Usually young children are affected, and to a lesser extent adults visiting endemic regions [1].
Clinical perspective
Symptoms start after an incubation period of 1-3 weeks and are variable and non-specific. They include headache, nausea, photophobia, seizures, decreased consciousness and coma.
Imaging perspective
The lesions are the result of capillary occlusion by infected red blood cells and presumably also of an immune inflammatory response [1]. Imaging findings are variable and non-specific. The cortex and deep white matter are frequently affected. Symmetrical thalamic lesions are typical as well [2]. The cerebellum is less involved. Findings on NECT vary from normal to focal infarcts. On MRI T2-weighted and FLAIR images demonstrate focal hyperintensities in the affected areas. Diffusion restriction on diffusion-weighted images (DWI) may be seen but is not invariably present [2, 3]. Susceptibility-sensitive sequences (GRE/SWI) will reveal ‘blooming’ in case of petechial haemorrhages [4]. Generally there is no enhancement after gadolinium administration.
Differential diagnosis
Bilateral thalamic T2 or FLAIR hyperintense lesions in an infant with fever or other symptoms of infection/inflammation have a broad differential diagnosis [5]. Acute disseminated encephalomyelitis (ADEM) is usually encountered a few weeks after viral infection or vaccination. Asymmetric involvement of the grey and white matter is more frequently seen than bilateral thalamic lesions, commonly showing some enhancement or diffusion-restriction. Acute haemorrhagic leukoencephalopathy (AHLE), a hyperacute form of ADEM, affects the thalami in a bilateral manner as part of diffuse leukoencephalopathy, often with diffusion-restriction and haemorrhagic components. Symmetric thalamic lesions, with peripheral ring-like enhancement suggesting necrosis, are a distinctive finding of acute necrotizing encephalopathy of childhood (ANEC). The vast majority of ANEC cases are found in Asia. A host of viral encephalitides may affect the thalami, mimicking other aetiologies. Travel and clinical history may be helpful.
Outcome
Even with adequate therapy, 15-20% of cerebral malaria patients do not survive. Most survivors have minimal or no long-term sequelae.
Take home messages
The imaging findings of cerebral malaria are not specific and overlap among several entities.
Bilateral thalamic hyperintensities on T2-WI and FLAIR is such a non-specific but typical manifestation of cerebral malaria. Radiologists should be aware of this possible diagnosis, especially in patients with fever who have recently travelled to an endemic region.
Differential Diagnosis List
Cerebral malaria (in a patient with confirmed Plasmodium falciparum malaria)
Acute disseminated encephalomyelitis (ADEM)
Acute haemorrhagic leukoencephalitis (AHLE)
Acute necrotizing encephalopathy of childhood (ANEC)
Cerebral malaria
Viral encephalitis
Final Diagnosis
Cerebral malaria (in a patient with confirmed Plasmodium falciparum malaria)
