Abstract
Patients with acute uncomplicated Plasmodium falciparum malaria have no evident neurologic disorder, vital organ dysfunction, or other severe manifestations of infection. Nonetheless, parasitized erythrocytes cytoadhere to the endothelium throughout their microvasculature, especially within the brain. We aimed to determine if 3 Tesla magnetic resonance imaging studies could detect evidence of cerebral abnormalities in these patients. Within 24 hours of admission, initial magnetic resonance imaging examinations found a lesion with restricted water diffusion in the mid-portion of the splenium of the corpus callosum of 4 (40%) of 10 male patients. The four patients who had a splenial lesion initially had evidence of more severe hemolysis and thrombocytopenia than the six patients who had no apparent abnormality. Repeat studies four weeks later found no residua of the lesions and resolution of the hematologic differences. These observations provide evidence for acute cerebral injury in the absence of severe or cerebral malaria.
Highlights
Worldwide, the most important parasitic disease infecting the central nervous system is Plasmodium falciparum malaria.[1]
In 4 of the 10 patients (40%), the initial magnetic resonance study showed a hyperintense, symmetrical oval lesion in the midline of the splenium of the corpus callosum on images derived from T2-weighted fluid-attenuated inversion recovery (T2FLAIR) sequences (Figure 1)
Using maps of the apparent diffusion coefficient (ADC) of water derived from the diffusion-weighted echoplanar imaging studies, we found that measurements of the corresponding regions of interest within the mid portion of the splenium of the corpus callosum showed a decrease in the ADC for each patient in whom a lesion was seen on the T2FLAIR examination
Summary
The most important parasitic disease infecting the central nervous system is Plasmodium falciparum malaria.[1]. Microvascular obstruction by sequestered parasitized erythrocytes leading to axonal damage has been proposed as a principal pathway responsible for coma and neurologic dysfunction, possibly in concert with a variety of immunopathologic mechanisms.[1,7,8,9,10] Sequestration and cerebral damage have been documented at autopsy in patients who died of cerebral or other forms of severe malaria.[3,11,12,13]
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