This study investigates the pathogenesis of cerebral malaria by examining ultrastructural changes in brain and other tissues from patients who died with *Plasmodium falciparum* malaria, both with and without cerebral malaria (CM). The researchers found that the proportion of parasitized erythrocytes (PRBCs) was higher in CM patients compared to non-cerebral malaria (NCM) patients, and that PRBCs were more tightly packed in CM patients' cerebral vessels. However, there was no significant difference in endothelial damage or the presence of endothelial pseudopodia between CM and NCM patients. Fibrillar deposits were observed in a small proportion of vessels, but no thrombosis or acute/chronic inflammation was noted. Leukocytes were absent within or outside cerebral vessels, and there was no immune complex deposition. The parasites in cerebral vessels were primarily trophozoites or schizonts, and some parasites showed signs of degeneration. PRBCs adhered to the endothelium via surface knobs. The study concludes that there is no evidence for an inflammatory or immune pathogenesis in human cerebral malaria, suggesting that the clinical effects are likely due to anoxia and the metabolic activities of the parasites.This study investigates the pathogenesis of cerebral malaria by examining ultrastructural changes in brain and other tissues from patients who died with *Plasmodium falciparum* malaria, both with and without cerebral malaria (CM). The researchers found that the proportion of parasitized erythrocytes (PRBCs) was higher in CM patients compared to non-cerebral malaria (NCM) patients, and that PRBCs were more tightly packed in CM patients' cerebral vessels. However, there was no significant difference in endothelial damage or the presence of endothelial pseudopodia between CM and NCM patients. Fibrillar deposits were observed in a small proportion of vessels, but no thrombosis or acute/chronic inflammation was noted. Leukocytes were absent within or outside cerebral vessels, and there was no immune complex deposition. The parasites in cerebral vessels were primarily trophozoites or schizonts, and some parasites showed signs of degeneration. PRBCs adhered to the endothelium via surface knobs. The study concludes that there is no evidence for an inflammatory or immune pathogenesis in human cerebral malaria, suggesting that the clinical effects are likely due to anoxia and the metabolic activities of the parasites.