Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management

*Rhoda Olowe Taiwo and Tawfeeq Shekh-Ahmad*

#### **Abstract**

Epilepsy is a neurological disorder affecting over 50 million people worldwide. Global epilepsy prevalence has been reported to be the greatest in Africa, prevalent among children living in resource-poor areas compared with all other continents. In West Africa, a meta-analysis of epilepsy prevalence was quoted to be 13–15 per 1000 persons. As a result of the lack of specialists and electroencephalographic facilities, the type of seizures that are more likely reported in rural areas is generalized tonic-clonic seizures. A high prevalence of epilepsy in low- and middleincome countries has been identified with CNS infections due to viral, bacterial, and parasitic infections. Parasitic infections including malaria, onchocerciasis, cysticercosis, and toxocariasis are believed to account for up to 27% of pediatric epilepsy cases reported in Sub-Saharan Africa, of which onchocerciasis has been more documented as a parasitic cause of epilepsy in most of west Africa. The management of epilepsy in West Africa centers around the administration of anti-seizure medications when available, and an onchocerciasis control program that has reduced onchocerciasis-associated epilepsy in these countries. However, several management options put in place still seem insufficient to curb the disease prevalence, hence improved strategy for effective control of parasite-induced epilepsy in West Africa.

**Keywords:** epilepsy, pediatric, West Africa, prevalence, parasites, general tonic-clonic seizures

#### **1. Introduction**

Epilepsy is a neurological condition affecting over 50 million people worldwide. It is characterized by recurrent seizures, following abnormal or excessive neuronal activities in the brain [1], representing a considerable healthcare burden with greater drug resistance and worse clinical outcomes than many other neurological diseases [2, 3]. It remains a global burden that knows no geographic, regional, or racial boundaries, occurring in men and women and affecting people of all ages, though more frequently affecting young people in the first two decades of life [4]. The prevalence of epilepsy has been reported to be greatest in Africa accounting for 37% of the global epilepsy burden compared to all other continents, as it has been acknowledged that more than 80% of people with epilepsy live in developing countries [5]. Typically, in Africa, the majority of people with epilepsy suffer from the disease from childhood, usually during their first few years of life. Mounting evidence from across five sites in Africa, suggested that over 60% of people with active convulsive seizures experience their first recorded seizure before age 13 [4, 6]. As a result of a lack of specialists, neurologists and electroencephalographic facilities, the type of seizures that are more likely reported in rural areas of Africa is the generalized tonic-clonic seizures (averaging 67% of individuals), because of the conspicuous presentation manifested, while partial seizures (averaging 8%) are most likely underestimated giving that their early stages recognitions are clinically difficult [7]. Although effective antiepileptic drugs are available, however, a substantial treatment gap is more evident in developing countries, mainly as a result of limited human and financial resources for diagnosis and treatment, cumulating in inadequate treatment in many cases [5]. Similarly, about 60% of patients with epilepsy receive no antiepileptic treatment, also for economic and social reasons [8]. Unfortunately, it is common that people with epilepsy left untreated to be faced with devastating social consequences, including stigma, discrimination, premature mortality, and reduced life chances for adults in terms of employment and marriage [9]. Here, we report the possible causes, prevalence, and management of pediatric epilepsy in West Africa.

#### **2. Causes**

Numerous causes have been attributed to the development of epilepsy in Africa and therefore it has been perceived that the origin of epilepsy is considered multidimensional in nature [10]. In a couple of decades ago, early knowledge of the etiology of epilepsy in most African countries has long been attributed to beliefs and spiritual reasons including spiritual attack, witchcraft, and other supernatural causes [11]. Moreover, as epidemiological studies in Africa progressed, knowledge of epilepsy prevalence begins to override beliefs, norms, and notions about epilepsy disease, highlighting other causes that might be contributory to the cause of pediatric epilepsy including obstetric injuries, frequent febrile convulsions, head trauma, and meningitis [10]. However, these aforementioned causes are only identified in less than 1% of epilepsy cases. In high-income countries, the main causes of epilepsy have been attributed to traumatic head/brain injuries and strokes [12, 13]. Whereas the high prevalence of epilepsy in low- and middle-income countries has been majorly identified with central nervous system (CNS) infections due to viral, bacterial, and parasitic infections [14].

Moreover, in recent times, the association between several parasitic diseases and epilepsy has gained new insights. Parasitic infection which remains the commonest cause of central nervous system infection and cause of symptomatic epilepsy; is believed to account for up to 27% of pediatric epilepsy cases reported in sub-saharan Africa, inclusive of West Africa [15]. Thus, updating an understanding of the etiology and epidemiology of epilepsy in West Africa. In addition, Africa has the highest burden of parasitic infections, which are associated with the development of epilepsy [16]. Among these parasitic infections are malaria, onchocerciasis, cysticercosis, and toxocariasis, infections with these organisms have been associated with epilepsy and are ubiquitous in Africa [15, 17–19].

#### **2.1 Malaria**

Malaria is one of the tropical parasitic diseases commonly thought to have a role in the development of epilepsy [20]. Majorly, most acute seizures are suggested to be caused by the malaria parasite *Plasmodium falciparum* (*P. falciparum*), usually in malaria-endemic areas, and these parasites are common in sub-Saharan Africa among people with epilepsy.

#### *2.1.1 The cell cycle of malaria*

Malaria parasites are mainly transmitted by a female anopheles mosquito. The parasite life cycle consists of a vector and human exoerythrocytic (hepatic) and erythrocytic stages [21]. The female mosquito (vector) bites the host during a blood meal, injecting mature sporozoites from its salivary glands into the host's bloodstream. These rapidly enter the liver hepatocytes and begin tissue schizogony-like asexual reproduction and proliferation (exoerythrocytic stage). Thereafter, thousands of merozoites are released into the bloodstream as the tissue schizonts burst the infected hepatocytes. The merozoites invade the erythrocytes, go through several asexual multiplication cycles (the erythrocytic stage), and then create new infectious merozoites that burst the erythrocytes to start a new infective cycle. In the long run, the parasite invades the CNS and causes some disruption of the BBB function, leading to cerebral malaria [22, 23].

Cerebral malaria is the most serious neurological complication of Plasmodium falciparum infection. In most infected children, after 1−3 days of fever, coma develops rapidly and seizures set in [24]. A defining feature of cerebral malaria is the Intravascular sequestration of circulating parasitized erythrocytes in the cerebral microcirculation.

Sequestration is a result of cytoadherence of infected erythrocytes to the vascular endothelial cells through parasite-derived proteins on the surfaces of the infected erythrocytes for example, the Plasmodium falciparum erythrocyte membrane protein-1 (PfEMP1) [25]. These are considered important pathophysiological mechanisms underlining cerebral malaria.

Furthermore, malaria can also cause different forms of seizures in the CNS, and it has already been identified as the most common cause of febrile seizures [26]. Agbéré et al., [27], reported that most febrile seizure cases occur in 55% of patients with malaria fever in Togo. Although the role of malaria in long-term epilepsy is still unclear, Preliminary studies have attributed a high risk of epilepsy to cerebral malaria, as seizures are one of the hallmarks of the clinical presentation of cerebral malaria [28]. An earlier study reporting an association between falciparum malaria and epilepsy found a 9% (4·4, 1·4–13·7) epilepsy occurrence in children exposed to cerebral malaria and 12% (6·1, 2·0–18·3) in those exposed to malaria and complex seizures [19]. However, whether they are febrile or acute symptomatic seizures, remains unclear [25, 29, 30].

#### **2.2 Onchocerciasis**

Human Onchocerciasis also referred to as "river blindness" caused by the filarial nematode; *Onchocerca volvulus* (*O. volvulus*), is a chronic parasitic infection transmitted by bites of blackflies [31]. Onchocerciasis is known as a cause of skin and eye

disease infecting a great number of people and has also been implicated in seizure disorders mainly in rural Africa. It is estimated that of the 120 million infected, 99% of them live in Africa [32].

#### *2.2.1 The cell cycle of onchocerciasis*

Several mechanisms have been proposed for the pathogenesis of onchocerciasisrelated epilepsy. However, one of the most identified mechanisms is the *O. volvulus*induced immune response via an inflammatory process or autoantibodies against neuron surface proteins such as the voltage-gated potassium channel complex (VGKC), the N-methyl-D-aspartate (NMDA), a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), gamma-aminobutyric acid (GABA)A, GABAB, and glycine receptors which are recognized causes of severe epileptic disorders [33].

Similarly, *Wolbachia* which are intracytoplasmic symbiotic bacteria found in filarial worms' endosymbiont of *O. volvulus* has also been proposed as a possible cause of onchocerciasis-related epilepsy. *O. volvulus* endemic areas, is a neuroinflammatory disorder caused by antibodies to either *O. volvulus* or its co-symbiotic bacteria, Wolbachia, cross-reacting with host neuron surface proteins, although evidence for neuroinflammation has not been established [34].

Consistent reports from epidemiological studies suggest that *O. volvulus* infection is a trigger and risk factor for epilepsy in Onchocerca endemic areas [35]. In Africa, onchocerciasis-associated epilepsy (OAE) was first documented in a populationbased epidemiological study in the Mbam valley in Cameroon between 1991 and 1992, where high epilepsy prevalence was associated with communities near Mbam River, a breeding site for black flies [36].

In addition, several studies have reported an association between the prevalence of onchocerciasis and epilepsy in different areas of east, west, and central Africa [36–38]. In West Africa, epidemiological studies have identified a high prevalence of epilepsy to a high onchocerciasis endemicity, where most infected patients experience generalized tonic-clonic seizures and the risk for children developing epilepsy has been determined by the *O. volvulus* microfilariae load [35, 39]. Although a paucity of information has been reported on *O. volvulus* penetration to the CNS, nonetheless, the presence of microfilariae from various filarial species in the human CNS has been reported. Studies suggest that since antifilariae drugs can provoke the passage of Loa Loa microfilariae (responsible for spontaneous encephalitis) into the cerebrospinal fluid (CSF) [40], therefore it does seem that *O. volvulus* would be able to penetrate the CNS since microfilariae belonging to this species have been found in the CSF of Onchocerciasis patients with or without filaricidal drugs [41, 42]. Furthermore, another explanation that *O. volvulus* could directly or indirectly cause epilepsy could be the occurrence of antibody-mediated autoinflammatory response against *O. volvulus*, cross-reacting with neuronal proteins [43] (**Figure 1**), as antibodies to voltage-gated potassium channels in neurons have recently been observed [44]. However, irrespective of this attribute, the pathophysiological mechanisms involved in onchocerciasis associated with epilepsy for seizure induction still need to be further elucidated.

#### **2.3 Neurocysticercosis**

Neurocysticercosis (Cysticercosis), remains the commonest helminthic infection of the CNS, representing an important cause of secondary epilepsy globally

*Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

#### **Figure 1.**

*The postulated scenario of infection or events of onchocerciasis associated epilepsy (AOE).*

[45, 46]. It is a cause of epilepsy in some parts of the world, and the introduction of computed tomography (CT) in the 1970s and early 1980s has allowed for its detection [47]. Cysticercosis is regarded as a Zoonotic disease, commonly caused by the larval stage (cysticercus) of the porcine tapeworm *Taenia Solium* (*T. solium*) and is said to be mainly found in the CNS including the Brain and spines. Reports of the parasite development in the brain, suggest an appearance of immature cysticerci in the brain within some weeks after ingestion of *T. Solium* eggs [48, 49].

#### *2.3.1 The cell cycle of neurocysticercosis*

In a typical life cycle of *T.* solium, following ingestion of the parasite, the adult worm is found in the small intestine of humans (the sole definite host of the parasite). The worms produce per day tens of thousands of oncospheres (eggs), They are then eliminated via feces, contaminating the food chain and water systems. Pigs (intermediate hosts of parasites) consume these oncospheres, where they are activated by bile salts and digestive enzymes in the small intestine. They subsequently go into the blood supply through the gut wall at blood vessel terminations in a variety of tissues (such as muscle, subcutaneous tissue, or nerve tissue) [50]. When a human consumes improperly cooked pork that contains a cysticercus, the scolex evaginates in the small intestine and clings to the intestinal wall where it develops into an adult worm.

However, when a person accidentally becomes an intermediate host and consumes oncospheres via tainted food or water, the oncospheres are thereafter activated in the human digestive tract just as they are in the pig, allowing them to pass into the bloodstream. They embed themselves in a variety of tissues, particularly the central nervous system. Taenia *solium* cysticerci invade and infect the brain parenchyma, of which seizures are the most common manifestation of parenchyma disease [51]. When cysticerci are present in the nervous system this is referred to as neurocysticercosis (NCC).

Although this parasite is mainly reported to cause 20–50% of all late-onset cases of epilepsy globally. Moreover, in a certain part of the world, it is assumed to be a common cause of juvenile epilepsy, majorly in the southern part of Africa [52, 53].

Nonetheless, this infection has been under-recognized in many developing countries, certainly true for Africa and more specifically West Africa, where this infection has been only reported in a few countries [47]. For instance, it is rarely reported in Nigeria unlike her neighboring countries, Cameroun, Benin, and Togo, where cysticercosis-associated epilepsy showed a significant proportion of epilepsy cases [54]. In an epidemiological study in Togo, cysticercosis prevalence was 135% among people with epilepsy (PWE) compared to 38% of the general population [55]. However, the high prevalence of neurocysticercosis is streamed lined to the rural area where a high consumption of pork infected with *T. Solium* predisposes people to epilepsy, resulting in one of the main causes of acquired epilepsy in middle-income countries around sub-Saharan Africa, inclusive of West Africa [45].

#### **2.4 Toxocariasis**

Human toxocariasis is another most prevalent helminthiasis also regarded as a parasitic zoonosis caused by the larval stages of dogs roundworm; *Toxocara canis* (*T. canis*), and by roundworm of cats; *Toxocara cati* (*T. cati*) [56]. Infections are mainly established through direct contact with the animals or via ingestion of contaminated food. Upon ingestion, eggs metamorphose into juvenile larvae capable of crossing the small intestine into the systemic circulation and then migrate to organs particularly muscles, and at times to the CNS where they invoke multisystemic inflammatory reactions [57].

#### *2.4.1 The cell cycle of toxocariasis*

The gastrointestinal ascarid nematodes Toxocara spp., including *T.* canis and *T. cati*, are present in canids (definitive hosts), such as dogs, felids (domestic cats), as well as foxes, and jackals. They can also infect people (considered paratenic hosts) through direct contact with diseased cats and dogs as well as contaminated food, soil, and water, of which humans tend to unintentionally consume eggs containing infectious third-stage larvae [58, 59].

Eggs that have been consumed grow and hatch into larvae in the small intestine, pierce the intestinal wall, and move through the circulatory system to various tissues. This causes an immune and inflammatory tissue reaction, which can cause symptoms like fever, headaches, coughing, and abdominal or limb pains [59].

Neurotoxocariasis, also known as cerebral toxocariasis, resulting from toxocara larvae invades the brain. In the brain, the larvae can also induce epileptic convulsions, cerebral vasculitis, and eosinophilic meningitis. Similarly, reports from experimental animal models showed that the presence of Toxocara larvae in the brain leads to neuronal damage via an increase in BBB permeability, expression of proinflammatory cytokines, iNOS, and astrogliosis [60, 61]. In addition, there have also been reports of changes in the profiles of neurotransmitters such as GABA, glutamate, serotonin, dopamine, and noradrenaline [62].

In nutshell, Toxocara larvae can invade the CNS by crossing the blood-brain barrier resulting in neurotoxocariasis [63]. Seroprevalence of the parasite tends to reach up to 80−90% in tropical regions, including West Africa while seroprevalence in western countries ranges from 35 to 42% and 2 to 5% in rural and urban areas, respectively [60]. Early epidemiological studies have provided evidence of a positive association between Toxocara seropositivity and seizure in children. Arpino et al., [64], evaluated the relationship between toxocariasis infection and epilepsy

#### *Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

in children and reported that a significant (p < 0.05) association existed between seropositivity for anti-Toxocara canis and seizures and this correlation was closest in children below age five. Furthermore, an investigation on the possible association between epilepsy and toxocariasis in the kiremba population of Burundi revealed that out of the studied 191 PWE, antibodies of anti-*T. canis* were found in 114 PWE (59.7%) and multivariate analysis showed a significant association between positivity for *T.* canis and epilepsy [65]. Although, some studies have proven an association. However, reports from two other studies revealed a non-significant association between epilepsy and seropositivity (antitoxocaral antibodies) [66, 67], adding up a piece of conflicting evidence that is difficult to interpret. To gain more insights into the association of this parasite with epilepsy, further studies are necessary to clarify its potential role and activity in epilepsy.

#### **3. Prevalence**

Reports have shown that the prevalence of epilepsy is higher in less developed than in more developed countries, with prevalence estimated from door-to-door studies almost double that in Asia, Europe, and North America [45]. More precisely, in West Africa, a meta-analysis of epilepsy prevalence was quoted to be between 13.14 and 15 per 1000 persons. However, this incidence has been more prevalent among children living in resource-poor (rural) areas than in urban areas [31]. The region-specific prevalence of epilepsy has yielded a treatment gap, resulting from inadequate access to physicians trained to manage epilepsy, a lack of access to ASM, poor knowledge about epilepsy among the communities, as well as the stigma of epilepsy arising from misconceptions about; epilepsy having a supernatural origin and attributed to possession by ancestral spirits [68]. In addition, the stigma of epilepsy can be profound because it is widely thought to be contagious and associated with witchcraft [69]. This stigma surrounding the disease creates psychosocial impacts on the children, marginalizing their ability to participate in community/societal activities leading to a significant effect on their quality of life [70].

Although a paucity of information has been gathered on epilepsy prevalence in West Africa, nonetheless several studies have reported a higher occurrence of epilepsy in onchocerciasis-endemic sites across countries in West Africa. In Nigeria, epilepsy prevalence based on defined communities varies between 15 and 37 per 1000 [31, 71]. An early epidemiological survey investigating the possible relationship of epilepsy with onchocerciasis in towns and villages in Nigeria observed a 37% epilepsy prevalence in Aiyete; a rural onchocerciasis-endemic village [72] while in Igbo-Ora; a town inhabited by the same ethnic group as Aiyete, situated 20 km away recorded 5.3% epilepsy prevalence, in the age group between 10 and 19 years [72, 73]. The lower prevalence recorded in Igbo-Ora compared to Aiyete may be due to the availability of comprehensive health facilities, effective primary health care with greater emphasis on antenatal care, improved prevention of childhood infectious diseases, and a working health education system [72]. Moreover, Aiyete is said to be located closer to the Ofiki River, a known breeding site for blackflies, causing this village to pose a higher endemicity than Igbo-Ora [74]. Furthermore, in a study carried out on 13 villages in the Imo River basin; a southeastern part of Nigeria that is mesoendemic for onchocerciasis, reports revealed a 12% epilepsy prevalence in these villages with a higher prevalence of onchocerciasis ranging between 8.3 and 36% and higher microfilariae density [39].

#### *Epilepsy - Seizures without Triggers*

Furthermore, epilepsy prevalence reports in Benin; a country bordering Nigeria to the west revealed that 9/13 (69.2%) PWE in the Agbome area were associated with O. volvulus microfilariae which were detected in skin snips while 8 PWE (61.5%) presented with onchocerciasis nodules. In addition, the majority of these patients (76.9%) manifested generalized tonic-clonic seizures [75].

In Ghana, albeit a community-based survey of kintampo village, revealed a lower epilepsy prevalence of as low as 1.92%, the epilepsy cases were attributed to exposure to O. volvulus and were identified as an independent risk factor for epilepsy in children below 18 years [76].

Furthermore, in Mali, epidemiological studies conducted on the endemicity of onchocerciasis about epilepsy prevalence in 18 villages showed an epilepsy prevalence of 16.1 per 1000 in zones of high endemicity of onchocerciasis (23.0%) compared to a prevalence of 10.8 per 1000 in zones of low endemicity (9.3%). Although a non-significant difference was reported between these two zones, however, higher morbidity rates were reported in zones of high endemicity of onchocerciasis [77].

In Cameroon, an outcome of a clinical epilepsy prevalence survey of 156 PWE in selected 5 onchocerciasis-endemic villages, revealed that onchocerciasis-associated epilepsy (OAE) showed a high prevalence in epilepsy patients where 93.2% of PWE met the criteria for OAE, presenting with the most frequent seizure types being generalized tonic-clonic episodes, absences, and nodding seizures. More so, the majority of epilepsies started between the ages of 3 and 18 years [78].

In epilepsy prevalence studies in Liberia, two studies documented a high epilepsy prevalence of 27.73−49.01% in Grad Bassa, which was agreed that the prevalence was in an onchocerciasis endemic area [79, 80].

In Ivory Coast, an epidemiological survey carried out in a village less than 10 km from M'Brou, where a high burden of epilepsy had previously been reported for decades with a microfilariae prevalence of 76%, revealed an epilepsy prevalence of 41% (38 of 920) and 73.7% fulfilled the OAE criteria [81].

In Burkina Faso, a prevalence study of epilepsy in three villages has specifically identified epilepsy prevalence with a positive reaction to cysticercosis Ag-ELISA serology with an association with past pork consumption. The findings reported that 39 of 70 that screened positive for cysticercosis were confirmed to have epilepsy, suggesting the presence of neurocysticercosis as the cause of epilepsy. Collectively, a total of 70 (7.9%) of 888 persons interviewed for epilepsy or seizure screened positive and 29 (74.4%) were reported to have experienced generalized seizures [82]*.*

Epilepsy prevalence in almost all study sites in Togo was reported to be below 20%, however, these epilepsies were said to be associated with cysticercosis, where its prevalence was 135% among PWE compared to 38% of the whole population [83]. In addition, an epilepsy management study in the Batamariba district of Togo revealed an epilepsy prevalence estimation of 15.7% of 98 patients, where the etiologies of 14/98 PWE (14.3%) were confirmed to be associated with neurocysticercosis (subcutaneous cysticercus cyst) [55]. However, in rural Gambia, a lower active epilepsy prevalence of 4.3/1000 was reported which is non-endemic for neither Neurocysticercosis nor onchocerciasis. In patients whose etiology could be suggested, etiology was only attributed to febrile illness in childhood and antenatal or perinatal brain insult [84].

Similarly, in Senegal, in the early 60s, a lower epilepsy prevalence of 1.92% was reported in an area non-endemic for onchocerciasis located in the Moyenne Vallée of Senegal. However, a more recent study from Pikine Health District of Senegal reported an epilepsy prevalence of 14.22% also in a non-endemic area [85].

*Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*


#### **Table 1.**

*Summary of identified prevalence and cause of epilepsy in west African countries.*

The majority of these findings strongly incriminate onchocerciasis as an important yet neglected contributor to the epilepsy burden in West Africa (**Table 1**).

#### **4. Management**

Management of Epilepsy in West Africa centers around the administration of ASM to control seizures as epilepsy surgery is rarely available in most parts of Africa [86]. However, in rural areas, a wide treatment gap is usually reported, and a systemic review has identified several reasons for this treatment gap including scarcity of knowledgeable staff, lack of investigative resources to ensure a diagnosis, cost of treatment, far-flung distance to health care facilities, cultural beliefs and inadequate availability of anti-seizure medications [87]. The presence of treatment gaps in West Africa has accounted for a high mortality rate related to poorly controlled epilepsy, with a greater proportion of children dying from status epilepticus compared to other continents [88]. In addition, in a systematic review, the World Health Organization (WHO) reported a greater treatment gap of 95% in some African countries including Ethiopia, Nigeria, Togo, Uganda, Tanzania, Gambia, and Zambia [89]. In most developing countries, available medications in the treatment and management of partial seizures include but are not limited to Carbamazepine, Phenobarbital, and Phenytoin, while drugs of choice for patients with tonic-clonic seizures are Valproic acid and Phenobarbital [90, 91]. However, Phenobarbital is the single most commonly prescribed anti-seizure medication for reasons due to availability, economic considerations, and its effectiveness in reducing the frequency of partial and generalized tonic-clonic seizures [92]. Moreover, the WHO has recommended Phenobarbital as the first-line therapy for convulsive epilepsy in Africa since it's the most readily

available and cost-effective ASM for seizure management [93]. Furthermore, another management practice particularly influenced by the introduction of the vector control program, that has been deployed in West Africa is the OCP (1974–2002), executed through a largescale onchocerciasis elimination control measure, followed by annual microfilaricidal treatment with Ivermectin distribution [94]. These control measures have significantly reduced OAE and drastically decrease the incidence of epilepsy in 11 countries in West Africa [95, 96]. However, despite the documented success, several challenges remain unmet, including banishing the stigma associated with epilepsy and dealing with cultural and social beliefs culminating in poor help-seeking behaviors among family and community of epilepsy patients. Ensuring easy access to anti-seizure medications at a cheaper or subsidized cost; Improving sensitization on relying on the primary health care system for treatments in rural areas.

#### **5. Discussion**

In most developing countries like West Africa, epilepsy disease remains prevalent in the younger population of resource-deprived communities. The majority of epidemiological studies indicate that the age of epilepsy onset is younger in underdeveloped countries than in areas with greater access to resources [97]. The survey methodology commonly employed in population studies of epilepsy is the door-todoor epidemiological survey, where a questionnaire is provided to screen members of a household with epilepsy [98].

However, this survey method poses a likely problem of underestimation as the screening tends to identify majorly individuals with generalized tonic-clonic seizure, and under-recognition is given to individuals with partial complex, dyscognitive, or myoclonic seizures, thereby underestimating the prevalence of the disease [99]. Additionally, people who have children with epilepsy tend not to declare the condition in a bid to avoid epilepsy-associated stigmas. The stigma attached to epilepsy may make people reluctant to acknowledge that someone in their home has the illness, thus resulting in the unavailability of epidemiological data [45].

Although, about three decades ago, epilepsy patients are rarely stigmatized because the condition is believed to be of demonic origin, attributed as being possessed and it is only combated with sorcery and traditional medicines with no seeming solutions [72, 73]. Just in recent times, following community sensitization about the disease condition and communities were enlightened on the disease being of medical origin, identified as epilepsy, bringing about the stigmatization of the disease. It is commonly established that epilepsy stigma has an impact on many aspects of its victim's life, such as social isolation, low self-esteem, worse psychological function, and increased future uncertainty [100]. Nonetheless, a well establishes effective epilepsy enlightenment campaign, as well as epilepsy education, could help patients and their families have comprehensive information on epilepsy disorder, avoid misconceptions and overcome the challenge of stigma in the resource-poor areas where epilepsy prevalence is pronounced [101].

Moreover, it is known that 80% of people with epilepsy reside in resource-poor, developing countries, however, a huge treatment gap exists, where epilepsy care in these regions remains limited and a majority of epilepsy patients go untreated [8]. Treatment gaps resulting from weak healthcare structures, inadequate financial resources, unreliable supply and quality of pharmaceuticals, the high rate of inappropriate self-medication, unavailability of ASM, inadequate ASM storage conditions are

#### *Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

likely to lead to ineffective and possibly dangerous ASMs [102], and even when goodquality ASMs are initially imported. Highlighting the difficulties with antiepileptics and, indeed, all drug use in developing countries [103].

To overcome these challenges, sustainable epilepsy care services that can deliver first-line antiepileptic drugs through established primary healthcare facilities, are needed to reduce these treatment gaps. Furthermore, Neurologists with knowledge of the culture and local experiences, who are willing to serve as advocates, educators, and policy advisors, can help make a difference. Nonetheless, a more sophisticated approach to overcoming the hurdles of epilepsy treatment in resource-poor nations is the availability of expertise for reliable EEG video interpretation of different seizure types for effective treatment and the establishment of a sustainable epilepsy monitor program.

#### **6. Conclusions**

Epilepsy in West Africa remains an undebatable challenge majorly in children in their first few years of life. Knowing fully that prevalence studies are a prerequisite for successful intervention. The primary purpose of this report was to assess the prevalence, causes, and management of pediatric epilepsy in West African countries at a community level and to bring to the limelight the available knowledge with previously existing data on this subject that dates way back to over 3 decades ago. We have recalled a parasitic cause of epilepsy that has been the main concern in tropical countries like West Africa. Parasitic infections including malaria, onchocerciasis, cysticercosis, and toxocariasis remain a common cause of CNS infection and cause of symptomatic epilepsy; where onchocerciasis is believed to account for up to 27% of pediatric epilepsy cases. These findings strongly incriminate onchocerciasis as an important yet neglected contributor to epilepsy in West Africa. Parasite-induced epilepsy remains a burden in many parts of West Africa, where generalized tonic-clonic and partial seizures were the predominant seizure types that have been reported. So far, the main achievements in dealing with epilepsy in West Africa involve the administration of available ASM such as Carbamazepine, Phenobarbital, Valproic acid, and Phenytoin, albeit a wide treatment gap is usually reported. Currently, resource-poor communities in low-income nations are unable to fund desirable but expensive initiatives like specialized epilepsy centers, which would appear to be the best method to assist epileptic patients in poor nations. Nonetheless, subsidized antiseizure medications could be provided to community health care centers so as to be at the disposal of the patients. More so, a national organization that is associated with international organizations for epilepsy could solicit and receive support and encouragement from international bodies like the International Bureau of Epilepsy. In addition, the introduction of the onchocerciasis control program has been deployed in West Africa as a parasitic control measure for onchocerciasis-induced seizures.

However, pediatric epilepsy in West Africa has long been underestimated as a paucity of information has only been gathered so far on its prevalence, causes, and management. It could be a result of the lower number of epidemiological studies carried out, arising from the stigma attached to epilepsy, as some people still hide the diagnosis; hence contributing to the underestimated prevalence of the disease. To overcome this challenge, education relevant to epilepsy health education such as patient-centered care allows individuals with epilepsy and their families to access usable information including Knowledge of epilepsy in general, an explanation of what happens during a seizure, and the importance of getting medical help, the significance of trigger factors that may

induce a seizure, a guide to ASMs; how they work, their side effects and the importance of compliance, orientations on improved quality of life, managing lifestyle and wellness should be encouraged at all levels to debunk wrong notions and myths about epilepsy as well to control the stigmatization of affected people. Furthermore, more epidemiological studies for improved interventions are required.

#### **Acknowledgements**

The authors are thankful to The Neubauer Family Foundation for their generous support of our research.

We also acknowledge the David R. Bloom Center for Pharmacy for financial support. The research also received support from The Israel Science Foundation (grant no. 1976/20 to TSA).

## **Conflict of interest**

The authors declare no conflict of interest.

## **Acronyms and abbreviations**


*Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

#### **Author details**

Rhoda Olowe Taiwo and Tawfeeq Shekh-Ahmad\* The Institute for Drug Research, The School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel

\*Address all correspondence to: tawfeeq.shekh-ahmad@mail.huji.ac.il

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

#### **References**

[1] Huang LG, Zou J, Lu QC. Silencing rno-miR-155-5p in rat temporal lobe epilepsy model reduces pathophysiological features and cell apoptosis by activating Sestrin-3. Brain Research. 2018;**1689**:109-122

[2] Sun H, Ma L, Zhang Y, Pan X, Wang C, Zhang J, et al. A purinergic P2 receptor family-mediated increase in Thrombospondin-1 bolsters synaptic density and epileptic seizure activity in the amygdala-kindling rat model. Frontiers in Cellular Neuroscience. 2018;**12**:302

[3] Zhang Y, Zhang M, Zhu W, Yu J, Wang Q, Zhang J, et al. Succinate accumulation induces mitochondrial reactive oxygen species generation and promotes status epilepticus in the kainic acid rat model. Redox Biology. 2020;**28**:101365

[4] Sander JW. The epidemiology of epilepsy revisited. Current Opinion in Neurology. 2003;**16**(2):165-170

[5] Meinardi H, Scott RA, Reis R, Sander JWAS, World ICD. The treatment gap in epilepsy: The current situation and ways forward. Epilepsia. 2001;**42**(1):136-149

[6] Duncan JS, Sander JW, Sisodiya SM, Walker MC. Adult epilepsy. Lancet. 2006;**367**(9516):1087-1100

[7] Kaiser C, Benninger C, Asaba G, Mugisa C, Kabagambe G, Kipp W, et al. Clinical and electro-clinical classification of epileptic seizure in West Uganda. Bulletin de la Societe de Pathologie Exotique. 2000;**93**(4):255-259

[8] Ngugi AK, Bottomley C, Kleinschmidt I, Sander JW, Newton CR. Estimation of the burden of active and life-time epilepsy: A meta-analytic approach. Epilepsia. 2010;**51**(5):883-890

[9] Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: A systematic analysis for the global burden of disease study 2010. Lancet. 2012;**380**(9859):2163-2196

[10] Osakwe C, Otte WM, Alo C. Epilepsy prevalence, potential causes and social beliefs in Ebonyi state and Benue state, Nigeria. Epilepsy Research. 2014;**108**(2):316-326

[11] Komolafe M, Sunmonu T, Fabusiwa F, Komolafe E, Afolabi O, Kett M, et al. Women's perspectives on epilepsy and its sociocultural impact in south western Nigeria. African Journal of Neurological Sciences. 2011;**30**(2):39-48

[12] Garcia-Martin G, Perez-Errazquin F, Chamorro-Munoz MI, Romero-Acebal M, Martin-Reyes G, Dawid-Milner MS. Prevalence and clinical characteristics of epilepsy in the south of Spain. Epilepsy Research. 2012;**102**(1-2):100-108

[13] Rai D, Kerr MP, McManus S, Jordanova V, Lewis G, Brugha TS. Epilepsy and psychiatric comorbidity: A nationally representative population-based study. Epilepsia. 2012;**53**(6):1095-1103

[14] Forsgren L. Estimations of the prevalence of epilepsy in sub-Saharan Africa. Lancet Neurology. 2008;**7**(1):21-22

[15] Ngugi AK, Bottomley C, Kleinschmidt I, Wagner RG, Kakooza-Mwesige A, Ae-Ngibise K, et al. *Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

Prevalence of active convulsive epilepsy in sub-Saharan Africa and associated risk factors: Cross-sectional and casecontrol studies. Lancet Neurology. 2013;**12**(3):253-263

[16] Birbeck G, Chomba E, Atadzhanov M, Mbewe E, Haworth A. The social and economic impact of epilepsy in Zambia: A cross-sectional study. Lancet Neurology. 2007;**6**(1):39-44

[17] Matuja WB, Kilonzo G, Mbena P, Mwango'mbola RL, Wong P, Goodfellow P, et al. Risk factors for epilepsy in a rural area in Tanzania. A community-based case-control study. Neuroepidemiology. 2001;**20**(4):242-247

[18] Birbeck GL. Epilepsy in Africa: Caution and optimism. Lancet Neurology. 2013;**12**(3):220-222

[19] Carter JA, Neville BG, White S, Ross AJ, Otieno G, Mturi N, et al. Increased prevalence of epilepsy associated with severe falciparum malaria in children. Epilepsia. 2004;**45**(8):978-981

[20] Ngoungou EB, Dulac O, Poudiougou B, Druet-Cabanac M, Dicko A, Traore AM, et al. Epilepsy as a consequence of cerebral malaria in the area in which malaria is endemic in Mali, West Africa. Epilepsia. 2006;**47**(5):873-879

[21] Sinka ME, Bangs MJ, Manguin S, Rubio-Palis Y, Chareonviriyaphap T, Coetzee M, et al. A global map of dominant malaria vectors. Parasites & Vectors. 2012;**5**:69

[22] Cowman AF, Healer J, Marapana D, Marsh K. Malaria: Biology and disease. Cell. 2016;**167**(3):610-624

[23] Venugopal K, Hentzschel F, Valkiūnas G, Marti M. Plasmodium asexual growth and sexual development in the haematopoietic niche of the host. Nature Reviews. Microbiology. 2020;**18**(3):177-189

[24] Idro R, Marsh K, John CC, Newton CRJ. Cerebral malaria: Mechanisms of brain injury and strategies for the improved neurocognitive outcome. Pediatric Research. 2010;**68**(4):267-274

[25] Idro R, Jenkins NE, Newton CR. Pathogenesis, clinical features, and neurological outcome of cerebral malaria. Lancet Neurology. 2005;**4**(12):827-840

[26] Waller D, Krishna S, Crawley J, Miller K, Nosten F, Chapman D, et al. Clinical features and outcome of severe malaria in Gambian children. Clinical Infectious Diseases. 1995;**21**(3):577-587

[27] Agbéré A, Tatagan K, Madikorai M, Eklu-Avlasu E, Balaka B, Bakondé B. Les crises convulsives de l'enfant dans le service de Pédiatrie du centre hospitalier régional de Kara (Nord-Togo). Médecine d'Afrique Noire. 1995;**42**(6):310-314

[28] Ngoungou EB, Druet-Cabanac M, Dulac O, Kombila M, Doumbo O, Preux P-M, editors. Cerebral malaria and epilepsy in a cohort of 322 Malian children. In: Abstract from the 25th International Epilepsy Congress, Lisbon, Portugal, 12-16 October, 2003. Vol. 44, Supplement 8. Epilepsia: Wiley Online Library; 2003. p. 60

[29] Winkler AS. Neurocysticercosis in sub-Saharan Africa: A review of prevalence, clinical characteristics, diagnosis, and management. Pathog Global Health. 2012;**106**(5):261-274

[30] Quattrocchi G, Nicoletti A, Marin B, Bruno E, Druet-Cabanac M, Preux PM. Toxocariasis and epilepsy:

Systematic review and meta-analysis. PLoS Neglected Tropical Diseases. 2012;**6**(8):e1775

[31] Siewe Fodjo JN, Remme JHF, Preux PM, Colebunders R. Meta-analysis of epilepsy prevalence in West Africa and its relationship with onchocerciasis endemicity and control. International Health. 2020;**12**(3):192-202

[32] Duke BOL. Human onchocerciasis - an overview of the disease. Acta Leidensia. 1990;**59**(1-2):9-24

[33] Vincent A, Bien CG, Irani SR, Waters P. Autoantibodies associated with diseases of the CNS: New developments and future challenges. The Lancet Neurology. 2011;**10**(8):759-772

[34] Galán-Puchades MT. Onchocerciasisassociated epilepsy. The Lancet Infectious Diseases. 2019;**19**(1):21-22

[35] Chesnais CB, Nana-Djeunga HC, Njamnshi AK, Lenou-Nanga CG, Boulle C, Bissek ACZK, et al. The temporal relationship between onchocerciasis and epilepsy: A population-based cohort study. Lancet Infectious Diseases. 2018;**18**(11):1278-1286

[36] Boussinesq M, Pion SDS, Demanga-Ngangue KJ. Relationship between onchocerciasis and epilepsy: A matched case-control study in the Mbam Valley, Republic of Cameroon. Transactions of the Royal Society of Tropical Medicine and Hygiene. 2002;**96**(5):537-541

[37] Pion SD, Kaiser C, Boutros-Toni F, Cournil A, Taylor MM, Meredith SE, et al. Epilepsy in onchocerciasis endemic areas: Systematic review and metaanalysis of population-based surveys. PLoS Neglected Tropical Diseases. 2009;**3**(6):e461

[38] Pion SDS, Boussinesq M. Significant association between epilepsy and presence of Onchocercal nodules: Casecontrol study in Cameroon. American Journal of Tropical Medicine and Hygiene. 2012;**86**(3):557

[39] Dozie IN, Onwuliri CO, Nwoke BE, Chukwuocha UM, Chikwendu CI, Okoro I, et al. Onchocerciasis and epilepsy in parts of the Imo river basin, Nigeria: A preliminary report. Public Health. 2006;**120**(5):448-450

[40] Ducorps M, Gardon-Wendel N, Ranque S, Ndong W, Boussinesq M, Gardon J, et al. Effets secondaires du traitement de la loase hypermicrofilarémique par l'ivermectine. Bulletin Society Pathology Exotic. 1995;**88**:105-112

[41] Mazzoti L. Presencia de microfilariasis de Onchocerca volvulus en al liquids cefalorraquides de enfrmos tratados con hetrazan. Revista del Instituto Salubridad Enfermedades Tropicales Mexico. 1959;**19**:1-5

[42] Duke BO, Vincelette J, Moore PJ. Microfilariae in the cerebrospinal fluid, and neurological complications, during treatment of onchocerciasis with diethylcarbamazine. Tropenmedizin und Parasitologie. 1976;**27**(2):123-132

[43] Johnson TP, Tyagi R, Lee PR, Lee MH, Johnson KR, Kowalak J, et al. Nodding syndrome may be an autoimmune reaction to the parasitic worm Onchocerca volvulus. Science Translational Medicine. 2017;**9**(377):eaaf6953

[44] Idro R, Opar B, Wamala J, Abbo C, Onzivua S, Mwaka DA, et al. Is nodding syndrome an Onchocerca volvulus-induced neuroinflammatory disorder? Uganda's story of research in understanding the disease. International *Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

Journal of Infectious Diseases. 2016;**45**:112-117

[45] Preux PM, Druet-Cabanac M. Epidemiology and aetiology of epilepsy in sub-Saharan Africa. Lancet Neurology. 2005;**4**(1):21-31

[46] Del Brutto OH, Santibanez R, Idrovo L, Rodriguez S, Diaz-Calderon E, Navas C, et al. Epilepsy and neurocysticercosis in Atahualpa: A door-to-door survey in rural coastal Ecuador. Epilepsia. 2005;**46**(4):583-587

[47] Zoli A, Shey-Njila O, Assana E, Nguekam JP, Dorny P, Brandt J, et al. Regional status, epidemiology and impact of Taenia solium cysticercosis in Western and Central Africa. Acta Tropica. 2003;**87**(1):35-42

[48] Carpio A, Hauser WA. Prognosis for seizure recurrence in patients with newly diagnosed neurocysticercosis. Neurology. 2002;**59**(11):1730-1734

[49] Del Brutto OH. Clinical management of neurocysticercosis. Expert Review of Neurotherapeutics. 2014;**14**(4):389-396

[50] White AC. Neurocysticercosis: Updates on epidemiology, pathogenesis, diagnosis, and management. Annual Review of Medicine. 2000;**51**(1):187-206

[51] Ndimubanzi PC, Carabin H, Budke CM, Nguyen H, Qian Y-J, Rainwater E, et al. A systematic review of the frequency of neurocysticercosis with a focus on people with epilepsy. PLoS Neglected Tropical Diseases. 2010;**4**(11):e870

[52] Grill J, Rakotomalala W, Andriantsimahavandy A, Boisier P, Guyon P, Roux J, et al. High prevalence of serological markers of cysticercosis among epileptic Malagasy children.

Annals of Tropical Paediatrics. 1996;**16**(3):185-191

[53] Mafojane NA, Appleton CC, Krecek RC, Michael LM, Willingham AL 3rd. The current status of neurocysticercosis in eastern and southern Africa. Acta Tropica. 2003;**87**(1):25-33

[54] Balogou A, Grunitzky K, Beketi K, Bouteille B, Dumas M. Cysticercosis and epilepsy in the city of tone, north of Togo. Revue Neurologique. 2000;**156**(3):270-273

[55] Balogou AA, Grunitzky EK, Belo M, Sankaredja M, Djagba DD, Tatagan-Agbi K, et al. Management of epilepsy patients in Batamariba district, Togo. Acta Neurologica Scandinavica. 2007;**116**(4):211-216

[56] Luna J, Cicero CE, Rateau G, Quattrocchi G, Marin B, Bruno E, et al. Updated evidence of the association between toxocariasis and epilepsy: Systematic review and meta-analysis. PLoS Neglected Tropical Diseases. 2018;**12**(7):e0006665

[57] Schantz PM, Glickman LT. Toxocaral visceral larva migrans. The New England Journal of Medicine. 1978;**298**(8):436-439

[58] Ma G, Holland CV, Wang T, Hofmann A, Fan C-K, Maizels RM, et al. Human toxocariasis. The Lancet Infectious Diseases. 2018;**18**(1):e14-e24

[59] Rostami A, Ma G, Wang T, Koehler AV, Hofmann A, Chang BCH, et al. Human toxocariasis – A look at a neglected disease through an epidemiological 'prism'. Infection, Genetics and Evolution. 2019;**74**:104002

[60] Fan C-K, Holland CV, Loxton K, Barghouth U. Cerebral Toxocariasis:

Silent progression to neurodegenerative disorders? Clinical Microbiology Reviews. 2015;**28**(3):663-686

[61] Meliou M, Mavridis IN, Pyrgelis E-S, Agapiou E. Toxocariasis of the nervous system. Acta Parasitologica. 2020;**65**(2):291-299

[62] Othman AA, Abdel-Aleem GA, Saied EM, Mayah WW, Elatrash AM. Biochemical and immunopathological changes in experimental neurotoxocariasis. Molecular and Biochemical Parasitology. 2010;**172**(1):1-8

[63] Sanchez SS, Garcia HH, Nicoletti A. Clinical and magnetic resonance imaging findings of Neurotoxocariasis. Frontiers in Neurology. 2018;**9**:53

[64] Arpino C, Gattinara GC, Piergili D, Curatolo P. Toxocara infection and epilepsy in children: A case-control study. Epilepsia. 1990;**31**(1):33-36

[65] Nicoletti A, Bartoloni A, Sofia V, Mantella A, Nsengiyumva G, Frescaline G, et al. Epilepsy and toxocariasis: A case-control study in Burundi. Epilepsia. 2007;**48**(5):894-899

[66] Akyol A, Bicerol B, Ertug S, Ertabaklar H, Kiylioglu N. Epilepsy and seropositivity rates of *Toxocara canis* and toxoplasma gondii. Seizure-European Journal of Epilepsy. 2007;**16**(3):233-237

[67] Winkler AS, Blocher J, Auer H, Gotwald T, Matuja W, Schmutzhard E. Anticysticercal and antitoxocaral antibodies in people with epilepsy in rural Tanzania. Transactions of the Royal Society of Tropical Medicine and Hygiene. 2008;**102**(10):1032-1038

[68] Birbeck GL. Seizures in rural Zambia. Epilepsia. 2000;**41**(3):277-281 [69] Mushi D, Hunter E, Mtuya C, Mshana G, Aris E, Walker R. Socialcultural aspects of epilepsy in Kilimanjaro region, Tanzania: Knowledge and experience among patients and carers. Epilepsy & Behavior. 2011;**20**(2):338-343

[70] Nsengiyumva G, Druet-Cabanac M, Nzisabira L, Preux PM, Vergnenegre A. Economic evaluation of epilepsy in Kiremba (Burundi): A case-control study. Epilepsia. 2004;**45**(6):673-677

[71] Ogunrin OA. Epilepsy in Nigeria-a review of etiology; epidemiology and management. Benin Journal of Postgraduate Medicine. 2006;**8**(1):27-51

[72] Osuntokun BO, Adeuja AO, Nottidge VA, Bademosi O, Olumide A, Ige O, et al. Prevalence of the epilepsies in Nigerian Africans: A community-based study. Epilepsia. 1987;**28**(3):272-279

[73] Osuntokun BO, Schoenberg BS, Nottidge VA, Adeuja A, Kale O, Adeyefa A, et al. Research protocol for measuring the prevalence of neurologic disorders in developing countries. Neuroepidemiology. 1982;**1**(3):143-153

[74] Brieger WR, Oshiname FO, Ososanya OO. Stigma associated with onchocercal skin disease among those affected near the Ofiki and Oyan Rivers in Western Nigeria. Social Science & Medicine. 1998;**47**(7):841-852

[75] Gbenou H. Contribution à l'étude de l'association onchocercose-épilepsie. Résultats préliminaires d'une enquête neuroépidémiologique à Agbogbomé commune de Paouignan, sous-préfecture de Dassa-Zoumé, au Bénin [MD Thesis]. Cotonou: Cotonou Univ Natl du; 1995

[76] Ae-Ngibise KA, Akpalu B, Ngugi A, Akpalu A, Agbokey F, Adjei P, et al. Prevalence and risk factors for active

*Pediatric Epilepsy in West Africa: Prevalence, Causes, and Management DOI: http://dx.doi.org/10.5772/intechopen.108255*

convulsive epilepsy in Kintampo, Ghana. The Pan African Medical Journal. 2015;**21**:29

[77] Farnarier G, Diop S, Coulibaly B, Arborio S, Dabo A, Diakite M, et al. Onchocerciasis and epilepsy. Epidemiological survey in Mali. Medicine Tropical (Mars). 2000;**60**(2):151-155

[78] Siewe JFN, Ngarka L, Tatah G, Mengnjo MK, Nfor LN, Chokote ES, et al. Clinical presentations of onchocerciasisassociated epilepsy (OAE) in Cameroon. Epilepsy & Behavior. 2019;**90**:70-78

[79] Gerrits C. A west African epilepsy focus. Lancet. 1983;**1**(8320):358

[80] Goudsmit J, van der Waals FW, Gajdusek C. Epilepsy in the Gbawein and Wroughbarh clan of Grand Bassa County, Liberia: The endemic occurrence of 'See-ee' in the native population. Neuroepidemiology. 1983;**2**(1-2):24-34

[81] Kaudjhis P. Les agrégats de l'épilepsie de M'brou: approche électroclinique et étiologique. Medical Thesis. Abidjan, Côte-d'Ivoire: Université Nationale de Côte d'Ivoire; 1995

[82] Nitiema P, Carabin H, Hounton S, Praet N, Cowan LD, Ganaba R, et al. Prevalence case-control study of epilepsy in three Burkina Faso villages. Acta Neurologica Scandinavica. 2012;**126**(4):270-278

[83] Balogou AA, Doh A, Grunitzky KE. Neurological disorders and endemic goiter: Comparative analysis of 2 provinces in Togo. Bulletin de la Societe de Pathologie Exotique. 2001;**94**(5):406-410

[84] Coleman R, Loppy L, Walraven G. The treatment gap and primary health care for people with epilepsy in rural Gambia. Bulletin of the World Health Organization. 2002;**80**(5):378-383

[85] Ndoye NF, Sow AD, Diop AG, Sessouma B, Sene-Diouf F, Boissy L, et al. Prevalence of epilepsy its treatment gap and knowledge, attitude and practice of its population in sub-urban Senegal an ILAE/IBE/WHO study. Seizure. 2005;**14**(2):106-111

[86] De Toffol B. Epilepsies: étiologie, diagnostic, évolution, pronostic, traitement. La Revue du praticien (Paris). 1995;**45**(7):885-891

[87] Mbuba CK, Ngugi AK, Newton CR, Carter JA. The epilepsy treatment gap in developing countries: A systematic review of the magnitude, causes, and intervention strategies. Epilepsia. 2008;**49**(9):1491-1503

[88] Ascoli M, Ferlazzo E, Gasparini S, Mastroianni G, Citraro R, Roberti R, et al. Epidemiology and outcomes of status epilepticus. International Journal of General Medicine. 2021;**14**:2965-2973

[89] Meyer AC, Dua T, Ma J, Saxena S, Birbeck G. Global disparities in the epilepsy treatment gap: A systematic review. Bulletin of the World Health Organization. 2010;**88**(4):260-266

[90] Mattson RH, Cramer JA, Collins JF, Smith DB, Delgado-Escueta AV, Browne TR, et al. Comparison of carbamazepine, phenobarbital, phenytoin, and primidone in partial and secondarily generalized tonic-clonic seizures. The New England Journal of Medicine. 1985;**313**(3):145-151

[91] Richens A, Davidson DL, Cartlidge NE, Easter DJ. A multicentre comparative trial of sodium valproate and carbamazepine in adult onset epilepsy. Adult EPITEG collaborative group. Journal of Neurology, Neurosurgery, and Psychiatry. 1994;**57**(6):682-687

[92] Ogunniyi A, Osuntokun BO. Effectiveness of anticonvulsant therapy in the epilepsies in Nigerian Africans. East African Medical Journal. 1991;**68**(9):707-713

[93] Wilmshurst JM, Cross JH, Newton C, Kakooza AM, Wammanda RD, Mallewa M, et al. Children with epilepsy in Africa: Recommendations from the international child neurology association/African child neurology association workshop. Journal of Child Neurology. 2013;**28**(5):633-644

[94] Boussinesq M, Chippaux JP, Ernould JC, Quillevere D, Prodhon J. Effect of repeated treatments with Ivermectin on the incidence of onchocerciasis in northern Cameroon. American Journal of Tropical Medicine and Hygiene. 1995;**53**(1):63-67

[95] Boatin BA. The current state of the onchocerciasis control Programme in West Africa. Tropical Doctor. 2003;**33**(4):209-214

[96] Leveque C. The use of insecticides in the onchocerciasis control programme and aquatic monitoring in West Africa. Ecotoxicology and Climate. 1989;**317**:335

[97] Nimaga K, Desplats D, Doumbo O, Farnarier G. Treatment with phenobarbital and monitoring of epileptic patients in rural Mali. Bulletin of the World Health Organization. 2002;**80**:532-537

[98] Placencia M, Sander JWAS, Shorvon SD, Ellison RH, Cascante SM. Validation of a screening questionnaire for the detection of epileptic seizures in epidemiological studies. Brain. 1992;**115**(3):783-794

[99] Boling W, Means M, Fletcher A. Quality of life and stigma in epilepsy, perspectives from selected regions of

Asia and sub-Saharan Africa. Brain Sciences. 2018;**8**(4):59

[100] Jacoby A. Felt versus enacted stigma: A concept revisited. Social Science & Medicine. 1994;**38**(2):269-274

[101] Cochrane J. Patient education: Lessons from epilepsy. Patient Education and Counseling. 1995;**26**(1-3):25-31

[102] Newton CR, Garcia HH. Epilepsy in poor regions of the world. The Lancet. 2012;**380**(9848):1193-1201

[103] Otte WM, van Diessen E, van Eijsden P, van der Maas F, Patsalos PN, Newton PN, et al. Counterfeit antiepileptic drugs threaten community services in Guinea-Bissau and Nigeria. The Lancet Neurology. 2015;**14**(11):1075-1076

## *Edited by Kaneez Fatima Shad*

According to the World Health Organization, nearly 80% of people with epilepsy live in low- and middle-income countries and could live seizure-free if properly diagnosed and treated. Among the structural and genetic triggers that may lead to epilepsy are head trauma, abnormal synaptic connectivity, receptor subunits anomalies, and atypical ionic channel function. Developing brains are specifically susceptible to seizures for many reasons, for example, the presence of enhanced excitation due to the early production of excitatory neurotransmitters, and the fact that the inhibitory neurotransmitter GABA causes excitation early in life. These studies help to clarify why the very young brain is exceptionally prone to seizures. The chapters presented in this book describe how structural, genetic, infectious, and metabolic abnormalities can lead to epileptogenesis. Nevertheless, many underlying disease mechanisms that can lead to epilepsy remain unknown.

Published in London, UK © 2023 IntechOpen © ktsimage / iStock

Epilepsy - Seizures without Triggers

Epilepsy

Seizures without Triggers

*Edited by Kaneez Fatima Shad*