Exploring the neuropathology and treatment of Plasmodium vivax malaria

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Abstract Plasmodium vivax malaria remains a significant global health burden, with recurrent relapses contributing to morbidity and complicating elimination efforts. While traditionally considered less severe than P. falciparum , emerging evidence has indicated that P. vivax can affect the central nervous system (CNS). Neurological effects range from subtle cognitive and attention deficits to severe complications such as diffuse encephalopathy, seizures and cerebral involvement. The pathophysiology of brain involvement is multifactorial, involving microvascular obstruction, systemic inflammation, cytokine-mediated neurotoxicity and oxidative stress, which collectively contribute to neuronal injury and altered brain function. Antimalarial agents used in the treatment and radical cure of P. vivax , including chloroquine, primaquine and tafenoquine, differ in their pharmacological and neuropharmacological properties. Radical cure requires 8-aminoquinolines (primaquine or tafenoquine) to eliminate dormant hepatic hypnozoites, as chloroquine is limited to blood-stage activity and does not prevent relapse. These agents exhibit distinct neuropharmacological profiles, influenced by factors such as blood-brain barrier penetration, metabolic activation and receptor interactions. In silico analyses and clinical data suggest that primaquine and its metabolites have the highest potential for CNS interactions, with tafenoquine showing a comparatively generally acceptable neuropsychiatric safety profile, and chloroquine with identifiable CNS and cardiac risks. These findings underscore the importance of glucose-6-phosphate dehydrogenase deficiency and psychiatric screening, monitoring for neuropsychiatric adverse effects and tailoring therapy to patient-specific risk factors. Integrating pharmacogenetic insights and neurotoxicity considerations into treatment strategies may optimize efficacy and safety in the management of P. vivax malaria.

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