Institutional members access full text with Ovid®

Share this article on:

Children With Retinopathy-negative Cerebral Malaria: A Pathophysiologic Puzzle

Postels, Douglas G. MD; Birbeck, Gretchen L. MD, MPH, DTMH

The Pediatric Infectious Disease Journal: November 2011 - Volume 30 - Issue 11 - p 953-956
doi: 10.1097/INF.0b013e3182271c69
Original Studies

Background: Cerebral malaria, defined as otherwise unexplained coma in a patient with circulating parasitemia, is a common disease in the developing world. The clinical diagnosis lacks specificity and children with other underlying causes of coma might be misdiagnosed as having cerebral malaria. The presence of malarial retinopathy can be used to differentiate children whose comas are caused by Plasmodium falciparum and its attendant pathophysiologies from those with other reasons for their abnormal mental status. Children with cerebral malaria who lack malarial retinopathy have not previously been described.

Methods: All patients admitted to Queen Elizabeth Central Hospital in Blantyre, Malawi, during a 12-month period with a clinical diagnosis of cerebral malaria were evaluated for the presence of malarial retinopathy. Thirty-two patients lacked retinopathy findings. Clinical, laboratory, and radiologic information data were collected.

Results: Thirty-two cases of retinopathy-negative cerebral malaria are presented.

Conclusions: Children with retinopathy-negative cerebral malaria share a common clinical phenotype with lower rates of mortality compared with those who have malarial retinopathy. There are at least 4 possible pathophysiologic explanations for this common condition.


From the Department of Neurology and Ophthalmology, Michigan State University, International Neurologic and Psychiatric Epidemiology Program (INPEP), East Lansing, MI.

Accepted for publication May 31, 2011.

Data collection for the primary study was supported by NIH grant number 5R01AI34969–14 as well as the Wellcome Trust.

The authors have no other funding or conflicts of interest to disclose.

This study is a secondary data analysis.

Address for correspondence: Douglas G. Postels, MD, International Neurologic and Psychiatric Epidemiology Program, Michigan State University, 324 West Fee Hall, East Lansing, MI 48824. E-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

© 2011 by Lippincott Williams & Wilkins, Inc.