Authors :
Presenting Author: Rasesh Joshi, MD, PhD – Boston Children's Hospital, Harvard Medical School, Boston, MA, USA
Suzanna Mwanza, MBBS MMed – Chipata Central Hospital, Chipata, Zambia
Joseph Kasolo, - – Chipata Central Hospital, Chipata, Zambia
Angela Masempela, - – Chipata Central Hospital, Chipata, Zambia
Thelma Musakanya, - – Chipata Central Hospital, Chipata, Zambia
Tina Mwale, - – Chipata Central Hospital, Chipata, Zambia
Violet Nambeye, - – Chipata Central Hospital, Chpiata, Zambia
Rosemary Nyirongo, - – Chipata Central Hospital, Chipata, Zambia
Ruth Tembo, - – Chipata Central Hospital, Chipata, Zambia
Christopher Cortina, MS – Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA
Bo Zhang, PhD – Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA
Hitten Zaveri, PhD – Yale School of Medicine, New Haven, CT, USA
Gretchen Birbeck, MD, MPH – University of Rochester, Rochester, NY, USA
Alexander Rotenberg, MD, PhD – Boston Children's Hospital, Harvard Medical School, Boston, MA, USA
Archana Patel, MD, MPH, MSc – Boston Children's Hospital, Harvard Medical School, Boston, MA, USA
Rationale:
Severe malaria with neurologic involvement (CNS malaria) accounts for a significant proportion of the global burden of acquired pediatric epilepsy. The pathogenesis of post-malarial epilepsy (PME) is multifactorial, including microvascular sequestration and resultant ischemic injury, neuroinflammation and blood-brain barrier breakdown, and excitotoxicity, all of which likely contribute to short- and long-term network-level remodeling. In this study, we examined long-term EEG network changes in post-malarial epileptogenesis using connectivity measures across multiple timescales, including conventional EEG frequency bands (delta, theta, alpha, beta, and gamma) and in the infraslow (< 0.15 Hz) range.