The Burden of Cerebral Palsy in Africa-new insight reveal more epidemiological complexity

Epidemiological studies of cerebral palsy (CP) in sub-Saharan Africa are challenging to conduct leaving us with limited insights into the most basic aspects of CP in Africa including prevalence and risk factors. If saving baby brains is a priority, understanding what injures infant nervous systems, when and how would seem a critical first step in any public health intervention aimed at improving child health. Two recent publications—a rural, population-based study in Uganda1 and a well-designed case-control study in Botswana2 offer important new findings on CP in the African setting.

In rural Uganda, Kakooza-Mwesige et al. conducted a 3-stage sampling and identification procedure aimed enumerating CP cases and assessing the underlying causes of CP in those identified. They identified a prevalence rate of 3.1 per 1.000, exceeding that typically found in high income settings. It is notable that even this figure likely underestimates the burden of CP in rural Uganda given the ample indirect evidence in their data of high early mortality in children with severe CP as more severe forms were much less represented among older pediatric populations. In medically advanced settings such as the US, prematurity is a primary contributor to the burden of CP. In contrast, in Uganda prematurity made only minuscule contributions to the burden of CP likely because survival among preemies is largely predicated upon sophisticated life support and management. In the Ugandan work, at least 25% of CP was a result of early life infections with cerebral malaria being one of most prominent contributors to early brain injury and CP. Neurologic disabilities occur in approximately  a third of cerebral malaria survivors and when the infection occurs before 2 years of age the resulting motor impairment would be indicative of CP though the adverse neurological outcomes occur across the full age range of pediatric cerebral malaria survivors 3. As such, malaria eradication efforts, if successful might be expected to lead to lower CP rates from regions of the world that have historically been heavily effected by malaria. As such, the findings in Dr. Kakooza’s study should lead us to ask if there are there neuroprotective measures beyond the delivery of antimalarials that might be added to malaria treatment protocols as well?

Compare the Uganda CP study to the case-control study conducted in urban Botswana. Botswana differs from Uganda in being middle income and relatively malaria free. In Botswana, Dr. Monokwane and colleagues identified maternal HIV infection as a major risk factor for CP even after controlling for prematurity, postnatal infection and delivery complications. The authors suggest that HIV itself may behave as a TORCH-type infection. Consideration of potential neurotoxic effects of antiretroviral agents on neonates exposed via their mother’s HIV treatment regimen also warrants evaluation. Clearly additional study is needed to confirm the finding and further elucidate the underlying mechanisms. Almost a third of pregnant women on Botswana are HIV infected and well-developed, effective HIV treatment programs are in place throughout the country. A population-based study in Botswana quantifying CP prevalence and attributable risks could help place these findings in fuller context.

As with all good research, these two studies raise as many questions as they answer. Clearly even within sub-Saharan Africa, one-size does not fit all in terms of CP risk factors and one might anticipate substantial heterogeneity in prevalence within the region if this could be assessed.

 

  1. Kakooza-Mwesige, A., et al., Prevalence of cerebral palsy in Uganda: a population-based study. Lancet Glob Health, 2017. 5(12): p. e1275-e1282.
  2. Monokwane, B., et al., Risk Factors for Cerebral Palsy in Children in Botswana. Pediatr Neurol, 2017. 77: p. 73-77.
  3. Birbeck, G.L., et al., Blantyre Malaria Project Epilepsy Study (BMPES) of neurological outcomes in retinopathy-positive paediatric cerebral malaria survivors: a prospective cohort study. Lancet Neurol, 2010. 9(12): p. 1173-1181.

 

Gretchen L. Birbeck, MD, MPH

Gretchen L. Birbeck, MD, MPH

Gretchen Birbeck is a neurologist who divides her time between the US and Africa. Her US academic home is the University of Rochester where she is the Rykenboer Professor of Neurology and Research Director for the Strong Epilepsy Center with adjunct appointments in the Center for Human Experimental Therapeutics and the Department of Public Health. Her additional skills in epidemiology, health services research, and tropical medicine are brought to bear during the 6-months annually she spends in Africa where she serves as Director for the Chikankata Epilepsy Care Team in rural Mazabuka, Zambia, an Honorary Lecturer at the University of Zambia and a consultant for the Paediatric Research Ward at Queen Elizabeth Central Hospital in Blantyre, Malawi. Gretchen’s research programs are aimed at identifying opportunities to prevent or ameliorate the medical and social morbidities of common neurologic conditions in low-income, tropical settings with the ultimate goal of developing successful interventions feasible for scale up and broad implementation. She has been recognized as an Ambassador for Epilepsy by the International League against Epilepsy, a Global Health Research Ambassador by the US Paul Rogers Society, a National Outreach Scholar by the WK Kellogg Foundation and a Leader in Medicine by the American Medical Students Association.

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