Aims: Survivors of cerebral malaria (CM) might develop lifelong sequelae such as cognitive deficits, altered behaviour or epilepsy. Animal models are needed to understand the underlying pathophysiology and to develop preventive or ameliorating therapies. Therefore, in this study we aimed to establish a mouse model reflecting consequences of CM. Methods: To ensure survival, C57BL/6 mice infected with P. berghei ANKA (PbANKA) were closely monitored for parasitaemia and clinical signs of CM, and rescued by artesunate treatment. Following electrode implantation, repetitive EEG-video monitoring was performed for seizure detection and assessment of response to anti-seizure drug treatment. Behavioural testing was applied to identify potential deficits in learning, as well as anxiety- or depressive-like behaviours. Age-matched naïve, sham-infected, and PbANKA-infected but CM-negative mice served as controls. Results: Tailored monitoring ensured timely artesunate treatment resulting in survival of 84.6% of CM-positive mice. Chronic epileptiform EEG activity was found in 50% of both PbANKA-infected mice with and without previous clinical CM and did not respond to phenobarbital and ethosuximide treatment. Open field test revealed reduced velocity and distance moved versus sham (-19.34%, p=0.0405 and -19.44%, p=0.0486, respectively), as well as less time spent in center (-71.15%, p=0.0111) in CM-positive mice. Acute and chronic microglial activation especially prominent in CM-positive mice was observed in areas throughout the temporal lobe. Conclusion: The CM mouse model reflects typical sequelae observed in human patients. Persistent microglial activation might be a relevant player in the pathogenesis of CM-induced seizures and behavioral changes and warrants further investigation.