Clinical features, proximate causes, and consequences of active convulsive epilepsy in Africa.

Symon M Kariuki; William Matuja; Albert Akpalu; Angelina Kakooza-Mwesige; Martin Chabi; Ryan G Wagner; Myles Connor; Eddie Chengo; Anthony K Ngugi; Rachael Odhiambo; +31 more... Christian Bottomley ORCID logo; Steven White; Josemir W Sander; Brian GR Neville; Charles RJC Newton; SEEDS writing group; Rhian Twine; F Xavier Gómez Olivé; Mark Collinson; Kathleen Kahn; Stephen Tollman; Honratio Masanja; Alexander Mathew; George Pariyo; Stefan Peterson; Donald Ndyomughenyi; Evasius Bauni; Gathoni Kamuyu; Victor Mung'ala Odera; James O Mageto; Ken Ae-Ngibise; Bright Akpalu; Francis Agbokey; Patrick Adjei; Seth Owusu-Agyei; Immo Kleinschmidt; Victor CK Doku; Peter Odermatt; Thomas Nutman; Patricia Wilkins; John Noh; (2013) Clinical features, proximate causes, and consequences of active convulsive epilepsy in Africa. Epilepsia, 55 (1). pp. 76-85. ISSN 0013-9580 DOI: 10.1111/epi.12392
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PURPOSE: Epilepsy is common in sub-Saharan Africa (SSA), but the clinical features and consequences are poorly characterized. Most studies are hospital-based, and few studies have compared different ecological sites in SSA. We described active convulsive epilepsy (ACE) identified in cross-sectional community-based surveys in SSA, to understand the proximate causes, features, and consequences. METHODS: We performed a detailed clinical and neurophysiologic description of ACE cases identified from a community survey of 584,586 people using medical history, neurologic examination, and electroencephalography (EEG) data from five sites in Africa: South Africa; Tanzania; Uganda; Kenya; and Ghana. The cases were examined by clinicians to discover risk factors, clinical features, and consequences of epilepsy. We used logistic regression to determine the epilepsy factors associated with medical comorbidities. KEY FINDINGS: Half (51%) of the 2,170 people with ACE were children and 69% of seizures began in childhood. Focal features (EEG, seizure types, and neurologic deficits) were present in 58% of ACE cases, and these varied significantly with site. Status epilepticus occurred in 25% of people with ACE. Only 36% received antiepileptic drugs (phenobarbital was the most common drug [95%]), and the proportion varied significantly with the site. Proximate causes of ACE were adverse perinatal events (11%) for onset of seizures before 18 years; and acute encephalopathy (10%) and head injury prior to seizure onset (3%). Important comorbidities were malnutrition (15%), cognitive impairment (23%), and neurologic deficits (15%). The consequences of ACE were burns (16%), head injuries (postseizure) (1%), lack of education (43%), and being unmarried (67%) or unemployed (57%) in adults, all significantly more common than in those without epilepsy. SIGNIFICANCE: There were significant differences in the comorbidities across sites. Focal features are common in ACE, suggesting identifiable and preventable causes. Malnutrition and cognitive and neurologic deficits are common in people with ACE and should be integrated into the management of epilepsy in this region. Consequences of epilepsy such as burns, lack of education, poor marriage prospects, and unemployment need to be addressed.


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