**4. Acknowledgment**

186 Novel Aspects on Epilepsy

pilot study made five years back (Foyaca-Sibat & Ibañez-Valdés, 2006) and based on those results we refined our selecting criteria. Our prevalence of ILE is low because it is an

Previous studies based on video ictal recordings, and direct electric insular stimulation of the insular cortex for presurgical evaluation of temporal lobe epilepsy described clinical features of ictal manifestation on IL eventually followed by dysarthric speech and focal motor convulsive symptoms no present in our series. Other clinical manifestation in our series including speech problems, neurogenic heart and sudden unexpected death were not included for statistical analysis at this time because were not considered in our objectives. Some patients became a little bit surprised when we asked for some symptoms that they did not expressed before because these symptoms did not recall attention from patients and relatives which may contribute to an underestimate prevalence of this type of seizures mainly in patients presenting it sporadically . A fully conscious patient with laryngeal discomfort, dyspnea, unpleasant perioral or somatic paresthesia, and dysarthric speech, followed by somatomotor symptoms, implies an insular onset and a good respond to

Antiparasitic treatment for NC at the IL should be prescribed with caution because the risk of developing complications such as: the neurogenic heart and/or SUDEP. One patient from this series died because subendocardic hemorrhage probable due to active and calcified NC on the

Fig. 6. Lateral view of the right insular lobe fixed in formalin. One cyst with the scolex inside (in vesicualr stage) on anterior insula is seen, another cyst without scolex with turbid fluidfilled oval cysts and local inflammatory reaction on the middle-anterior (agranular) insula is observed. Left insula was normal and no other cysts were found all over the brain. Cause of

Although largely neglected in earlier literature, sudden unexpected death in epilepsy (SUDEP) is the most important epilepsy-related mode of death, and is the leading cause of death in people with chronic uncontrolled epilepsy. Research during the past two to three decades has shown that incidence varies substantially depending on the epilepsy population studied, ranging from 0—09 per 1000 patients-years in newly diagnosed patients to 9 per

**3.3.1 Sudden unexpected death in epilepsy secondary to neurocysticercosis** 

1000 patient-years in candidates for epilepsy surgery.(Tomson et al., 2008)

right insula cortex documented by postmortem examination (See figure 6)

death: SUDEP/Neurogenic heart (subendocardial hemorrhage)

uncommon epileptic disorder.

antiepileptic treatment can help to confirm it.

We like to express our gratitude to all veterinarian doctors working in this field particularly: Professors Rosina Tammi Krecek, Albert Lee Willingham, Linda Cowan, Samson Mukaratiwua and other members of the Cysticercosis Working Group for Eastern and Southern Africa (CWGESA) for their dedications and commitment.

Special thanks to Professor Helen Carabin from the Department of Biostatistics and Epidemiology College of Public Health University of Oklahoma Health Sciences Center for her invaluable enthusiasm, persistence, and leadership in our research team.

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We want to thanks to all radiologists and radiographers from Nelson Mandela Academic Hospital and Inkhosi Albert Luthuli Central Hospital in South Africa for their contribution to this study.

Special thanks are due to the Cuban Ministry of Health, the Institute of Tropical Medicine Pedro Kouri, authorities of Faculty of Health Sciences and Directorate: Research Development from Walter Sisulu University and Nelson Mandela Academic Hospital for their unconditional support.

We also acknowledge financial support from, Directorate of Research Development from Walter Sisulu University in South Africa, and South African Medical Research Council.

The founder had no role in study design, data collection and analysis, decision to publish, or the preparation of manuscript.

Finally, we wish to declare our eternal and deepest gratitude to our family, relatives, and colleagues for their unconditional and permanent support.

Finally, we wish to declare our eternal, deepest love and gratitude to Lorna María Foyaca García, Thabo Humberto Jorge Foyaca Ibañez and Fátima Susana Adolfina Foyaca Ibañez, because without their love and unconditional support this chapter would not have been written.

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**11** 

*1Switzerland 2Denmark* 

**Epileptic Channelopathies and** 

**Mutations to Novel Treatments** 

Sigrid Marie Blom1 and Henrik Sindal Jensen2

*1Department of Physiology, University of Bern 2Neuroscience Drug Discovery, H. Lundbeck A/S* 

**Dysfunctional Excitability - From Gene** 

Epilepsy is not a single disorder, but a collection of disorders that all are characterized by episodic abnormal synchronous electrical activity in the brain. This abnormal activity represents a disturbance of the balance between excitatory and inhibitory neurotransmission. The majority (50%) of epilepsies are cryptogenic, meaning there is a presumptive but no identifiable underlying etiology. Approximately 20% of epilepsies have an identifiable cause (i.e. they are symptomatic) and are usually a result of trauma to the head, stroke, brain tumours, or infections. The remaining 30% are idiopathic, meaning there is no apparent underlying cause (Berg et al., 1999). However, as they are usually associated with a family history of similar seizures, they are mostly considered to be genetic. Mutations in over 70 genes have been found to cause epilepsy (Noebels, 2003). Given the dependence of seizures on synaptic transmission and neuronal excitability, it is not surprising that many of these mutations affect the function of ion channels. Since the identification of the first epilepsycausing ion channel mutation, scientists have come a long way in the understanding of the pathogenesis of the disease. This chapter deals with some of the main questions that have been asked, and looks at some of the proposed answers to the questions. How do mutations in certain ion channels lead to hyperexcitability and seizures? Why do mutations in one ion channel cause a particular epilepsy syndrome? Why are the seizures often initiated during specific physiological events? And why do most of the childhood epilepsies remit with age?

Furthermore, ion channels as targets for antiepileptic drugs will be discussed.

In most cases genetic epilepsy syndromes have a complex rather than a simple inheritance pattern. Although the epilepsies described here are thought to be monogenic, not even those considered inherited in a dominant fashion have a penetrance of 100%. Mutations within the same gene can result in clinically distinct phenotypes. Variable expressivity is also a common feature of inherited epilepsy demonstrated by family members with the same mutation that exhibit differences in the clinical severity of the disease (Hayman et al., 1997).

**1. Introduction** 

**2. Idiopathic epilepsies** 

