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In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
Published on: June 8, 2017
Imaging analysis of the brain in a primate model of cerebral malaria
Satoru Kawai1, Munehiro Sugiyama
1Center for Tropical Medicine and Parasitology, Dokkyo Medical University, Mibu, Tochigi, Japan. skawai@dokkyomed.ac.jp
Abstract:
This paper reviews our studies concerning imaging analysis of the brain in a primate model of cerebral malaria. To elucidate the clinical features of cerebral malaria, we performed positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) scanning and magnetic resonance imaging (MRI) of the brain in Japanese macaques (Macaca fuscata) infected with Plasmodium coatneyi, a primate model of severe human malaria with cerebral involvement. On FDG-PET scanning, we observed diffuse and heterogeneous reduction of metabolism in the cerebral cortex in the acute phase of malaria infection. Although the monkey exhibited severe clinical signs, MR imaging did not reveal any significant changes during the course of infection. Histopathologic examination frequently revealed preferential sequestration of PRBCs in the cerebral and cerebellum capillaries, but neither parenchymal injury nor neuronal necrosis was found in the tissues. These results suggest that heterogeneous metabolic reduction and lack of abnormalities on MRI in the acute phase of CM may be due to any avoidance mechanisms from ischemia caused by sequestration. This may be one reason why more than half of CM patients have no neurological sequelae following recovery.
Insights
Cerebral malaria imaging in macaques showed reduced brain metabolism but no MRI changes, suggesting protective mechanisms against ischemia. This may explain why many cerebral malaria patients recover without lasting neurological damage.
Area of Science:
- Neuroscience
- Infectious Diseases
- Medical Imaging
Background:
- Cerebral malaria (CM) is a severe complication of malaria, often leading to neurological deficits.
- Understanding the pathophysiology of CM is crucial for developing effective treatments.
- Primate models offer valuable insights into human diseases.
Purpose of the Study:
- To investigate brain changes in a primate model of cerebral malaria using advanced imaging techniques.
- To correlate imaging findings with clinical and histopathological observations.
- To explore potential mechanisms underlying neurological recovery in CM.
Main Methods:
- Positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) scanning was used to assess brain metabolism.
- Magnetic resonance imaging (MRI) was employed to detect structural brain abnormalities.
- Japanese macaques infected with Plasmodium coatneyi served as the CM model.
- Histopathological examination of brain tissue was performed.
Main Results:
- FDG-PET revealed diffuse and heterogeneous reduction in cerebral cortex metabolism during acute malaria infection.
- MRI scans showed no significant structural changes despite severe clinical signs in the infected macaques.
- Histopathology indicated preferential sequestration of Plasmodium-infected red blood cells (PRBCs) in capillaries, but without parenchymal injury or neuronal necrosis.
Conclusions:
- The observed metabolic reductions and lack of MRI abnormalities in acute CM may indicate protective mechanisms against ischemia.
- These findings suggest that the brain may employ strategies to mitigate damage from parasite sequestration.
- This could explain the frequent absence of neurological sequelae in human CM patients upon recovery.
