Etiologies of non-genetic epilepsies of child and adolescent, newly diagnosed in Ouagadougou, Burkina Faso

Introduction in sub-Saharan Africa, epilepsy is common and mainly concerns children before the age of 15 years. The data on childhood epilepsy is parcel, but a high prevalence of non-genetic epilepsy is frequently reported. EEG, TDM and MRI devices are rare. The aim of this work was to study the etiological aspects of non - genetic epilepsy of the child and adolescent, newly diagnosed in Ouagadougou, Burkina Faso. Methods This was a cross-sectional, descriptive, multicentric study, from 01/01/2016 to 31/12/2016, involving patients aged 0 to 18 years old, epileptic, newly diagnosed, in the city of Ouagadougou. Each patient included in the study was to have had an EEG and brain CT scan and/or brain MRI and to gather the anamnestic and electro clinical arguments for non-genetic epilepsy. Sociodemographic, clinical, EEG and neuroradiological data were analyzed. An univariate analysis was used to determine the electro-clinical and neuro-radiological characteristics associated with epilepsies of structural causes. Results In all 115 patients were collected, with an average age of onset of epilepsy of 8.2 years, a male predominance with a sex ratio to 1.67. Risk factors of epilepsy was present in 74.8%; They were dominated by perinatal events in 79.1%. Focal seizures, daily frequency of these seizures and focal epilepsy, were predominant, respectively in 53%, 58% and 60.9% of cases. Brain scan and Brain MRI where performed in 90.4% and 9.6% of patients, respectively. The brain sequelaes of perinatal adverse events, the sequelae of central nervous system infections, and the sequelae of cranial and brain trauma, with 34.8%, 14.8%, and 5.2% respectively, were the main causes of non- genetic epilepsies of the child and adolescent. No cause was identified in 37.4% of cases. Conclusion The improvement of policies in the field of maternal and child health and the generalization of the control of infectious and parasitic diseases, including malaria, may contribute to the reduction of non-genetic epilepsy in sub-Saharan Africa.


Introduction
Epilepsy is a public health problem in developing countries, particularly in Burkina Faso, where prevalence would reach 5 to 10 times that of industrialized countries [1]. It mainly concerns children before the age of 15 years, although in sub-Saharan Africa (SSA) the available pediatric data are fragmentary [2,3]. In SSA, the causal factors of non-genetic epilepsy of the child appear to be dominated by perinatal complications and central nervous system (CNS) infections, due to the combination of several factors, such as socio-cultural burdens, the high prevalence of unassisted home births, the existence of a endemic-epidemic infectious pathologies, the lack of adequate sanitary infrastructures and qualified human resources [4]. The risk of developing epilepsy in the cohorts of survivors of CNS infections is estimated at 26% in developing countries, particularly in SSA [5], compared with 6.8% in developed countries [6]. In SSA, CT scan and particulary MRI, are little available or not accessible, whereas they are indispensable for the identification of epileptogenic brain lesions and the causal diagnosis of certainty of certain epilepsy, including epilepsy of structural causes. In the absence of these neuro-imaging examinations in most of the studies in SSA, the certainty of the causative diagnosis of epilepsy is difficult to establish, because usually based on the history of the disease, which is not always recorded and therefore subject to a recall bias [1,7]. The aim of our work was to study the causal aspects of non-genetic epilepsy of the child and adolescent, in Ouagadougou, Burkina Faso, according to electro clinical and neuroradiological diagnostic criteria.

Methods
This was a cross-sectional, descriptive, multicentric study, which took place from 01 January 2016 to 31 December 2016. It concerned all children and adolescents, aged between 0 and 18 years of age, with newly diagnosed epilepsy, followed by an external neurology consultation in the various University hospitals of the city of Ouagadougou, Yalgado Ouedraogo, Tingandogo, pediatric Charles de Gaulle, and Medical Center with surgical antenna of Schiphra. To be included in the study, each epileptic patient should benefit from at least one EEG and brain imaging (brain CT scan and/or MRI) and bring together the anamnestic and electro clinical arguments for non-genetic epilepsy. Were not included in the study, patients who had seizures whose epileptic nature was not proven, those who had genetic epilepsy on the basis of the anamnestic, clinical and EEG arguments, those for whom the EEG and the neuro Imaging were not available and finally those at which consent could not be obtained. Patients were collected consecutively in external neurology or hospitalization, by senior neurologists, at the various collection sites. The data were collected from the interrogation, the clinical examination, data from the standard EEG, which was assembled in accordance with the international system 10/20 and data from the brain CT and/or MRI.

Results
We consecutively collected 115 patients with the characteristics of a non genetic epilepsy. The average age of patients and beginning of the seizures was 9.1 years (6 months and 18 years) and 8.

Discussion
The diagnosed epilepsy etiology varies depending on the geographic locations, the authors, the study methodologies, including whether or not neuro imaging exams are available. In the absence of neuroimaging examinations in most of the studies in SSA, the certainty of the causative diagnosis of epilepsy is difficult to establish, because generally based on the history of the disease, which is not always recorded and therefore subject to a recall bias [1,7]. In our study, the etiology of non-genetic epilepsy of the child and adolescent was  [7], an implication of perinatal causes was found respectively between 1-36% and between 2%-65% of cases of epilepsy and therefore considered to be major. In our series, the sequelae of perinatal cerebral damage were the leading cause of non-genetic epilepsy of the child and adolescent, or 34.8%, after the undetermined causes, thus confirming the literature data.
Hypoxia and hypoglycemia are the frequently cited mechanisms. In the absence of neuro-imaging examinations in several studies, the causal links between a prenatal, perinatal event and epilepsy are difficult to establish. This link is usually based on the history of the disease, which is not always recorded and is subject to a recall bias [12].
Infectious pathology is the other major provider of potentially epileptogenic brain lesions, estimated to be between 1.6 and 6.3% of cases of epilepsy especially in children, in African and Asian work [13]. The history of CNS infection was 20.2% and 11.9% of the causal factors of non-genetic epilepsy in Dakar, respectively in children [8] and in children and adolescents [4] and up to 29.3% of the causative factors of focal genetic and non-genetic focal epilepsies of the child in Cameroon, including non-specific febrile seizures [9]. The sequelae of CNS infections accounted for 14.8% of the causes of non-genetic epilepsy of the child and adolescent in our series. These CNS infections are mainly represented by cerebral malaria (CM), bacterial, parasitic and viral méningoencephalitis [13].
of health services, especially in rural areas, often lead to home births without qualified assistance [7]. Certain cerebral structural causes, such as malformations of cortical development, cerebral vascular malformation, neurocutaneous syndromes, brain tumors, hippocampal sclerosis, exclusively identified by MRI, are under diagnosed in SSA, due to low availability and financial inaccessibility of this brain imaging technique [8,9]. This has been done in our series. Conversely, these causes are reported at fairly high rates in the series using brain MRI [27,28]. Structural damage such as cortical necrosis with HSV1, infarction with meningitis, hypoxoischemic lesions in the CM, and gliosis around neurocysticercosis calcifications can all constitute epileptogenic foci. It is also thought that prolonged proinflammatory stimulation or chronic inflammation, as well as recurrence of the seizures themselves, can lead to a residual pathological condition with rupture of the blood-brain barrier, neuronal death and persistence of neuronal excitability-all of which can contribute to epileptogenesis [29].

Competing interests
The author declare no competing interests.

Authors' contributions
All authors had a substantial contribution to conception and design, acquisition of data, or analysis and interpretation of data; all authors have draft the article or revised it critically for important intellectual content; and have approved the final version to be published.