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MRI Findings in a Cohort of Brain Injured Survivors of Pediatric Cerebral Malaria

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  • Department of Radiology, Queen Elizabeth Central Hospital, Blantyre, Malawi; Department of Radiology, Michigan State University, East Lansing, Michigan; Department of Eye and Vision Science, Institute of Aging and Chronic Disease, University of Liverpool, United Kingdom; Department of Osteopathic Medical Specialties, College of Osteopathic Medicine, Michigan State University, East Lansing, Michigan; Ophthalmology Department, Raigmore Hospital, Inverness, United Kingdom; Blantyre Malaria Project, University of Malawi College of Medicine, Blantyre, Malawi; International Neurologic and Psychiatric Epidemiology Program, Michigan State University, East Lansing, Michigan
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A prospective cohort study of retinopathy-confirmed cerebral malaria (CM) survivors identified 42 of 132 with neurologic sequelae. The 38 survivors with sequelae who were alive when magnetic resonance imaging (MRI) technology became available underwent brain MRIs. Common MRI abnormalities included periventricular T2 signal changes (53%), atrophy (47%), subcortical T2 signal changes (18%), and focal cortical defects (16%). The χ2 tests assessed the relationship between chronic MRI findings, acute clinical and demographic data, and outcomes. Children who were older at the time of CM infection (P = 0.01) and those with isolated behavioral problems (P = 0.02) were more likely to have a normal MRI. Acute focal seizures were associated with atrophy (P = 0.05). Acute papilledema was associated with subcortical T2 signal changes (P = 0.02). Peripheral retinal whitening (P = 0.007) and a higher admission white blood cell count (P = 0.02) were associated with periventricular T2 signal changes. Chronic MRI findings suggest seizures, increased intracranial pressure, and microvascular ischemia contribute to clinically relevant structural brain injury in CM.

Author Notes

* Address correspondence to Gretchen L. Birbeck, International Neurologic and Psychiatric Epidemiology Program, Michigan State University, 909 Fee Road, West Fee Hall, Room 324, East Lansing, MI 48824. E-mail: birbeck@msu.edu

Financial support: NIH K23NS046086, NIH 5R01AI034969, and Intramural Michigan State University funding CDFP App #: 09-CDFP-1771.

Disclosure: S. Kampondeni received research funding from the U.S. National Institute of Health. G. L. Birbeck received research funding from the U.S. National Institute of Health and the Dana Foundation. N. A. V. Beare received research funding from The Wellcome Trust, and has received travel expenses to attend scientific conferences from Novartis. K. B. Seydel and M. J. Potchen received research funding from the U.S. NIH and the Dana Foundation. S. Glover received research funding from the Wellcome Trust. T. E. Taylor received research funding from the U.S. NIH.

Authors' addresses: Sam D. Kampondeni, Blantyre Malaria Project, Blantyre, Malawi, E-mail: s.kampo154@gmail.com. Michael J. Potchen, Department of Radiology Michigan State University, East Lansing MI, E-mail: mjp@rad.msu.edu. Nicholas A. V. Beare, FRCOphth, St. Paul's Eye Unit, Royal Liverpool University Hospital, Liverpool, UK, E-mail: nbeare@btinternet.com. Karl B. Seydel, Department of Osteopathic Medical Specialties, College of Osteopathic Medicine, Michigan State University, East Lansing, MI, E-mail: seydel@msu.edu. Simon J. Glover, Ophthalmology Department, Raigmore Hospital, Inverness, UK, E-mail: Simontheeyeman@hotmail.com. Terrie E. Taylor, Department of Osteopathic Specialties Michigan State University, East Lansing, MI, E-mail: ttmalawi@msu.edu. Gretchen L. Birbeck, Department of Neurology & Ophthalmology and Department of Epidemiology & Biostatistics International Neurologic and Psychiatric Epidemiology Program, Michigan State University, East Lansing, MI, E-mail: birbeck@msu.edu.

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