Epilepsy and Epileptic Syndrome

Abstract

Epilepsy is one of the most common neurological disorders. In most patients with epilepsy, seizures respond to available medications. However, a significant number of patients, especially in the setting of medically-intractable epilepsies, may experience different degrees of memory or cognitive impairment, behavioral abnormalities or psychiatric symptoms, which may limit their daily functioning. As a result, in many patients, epilepsy may resemble a neurodegenerative disease. Epileptic seizures and their potential impact on brain development, the progressive nature of epileptogenesis that may functionally alter brain regions involved in cognitive processing, neurodegenerative processes that relate to the underlying etiology, comorbid conditions or epigenetic factors, such as stress, medications, social factors, may all contribute to the progressive nature of epilepsy. Clinical and experimental studies have addressed the pathogenetic mechanisms underlying epileptogenesis and neurodegeneration.We will primarily focus on the findings derived from studies on one of the most common causes of focal onset epilepsy, the temporal lobe epilepsy, which indicate that both processes are progressive and utilize common or interacting pathways. In this chapter we will discuss some of these studies, the potential candidate targets for neuroprotective therapies as well as the attempts to identify early biomarkers of progression and epileptogenesis, so as to implement therapies with early-onset disease-modifying effects.

The vicious circle of hypometabolism in neurodegenerative diseases: Ways and mechanisms of metabolic correction

“…Major preconditioning risk factors such as cardiovascular dysfunction, diabetes, metabolic syndrome, traumatic brain injury, and stroke are shared by the sporadic AD (Biessels and Reagan, 2015;Chakrabarti et al, 2015;de la Torre, 2012;Patterson et al, 2007) and PD (Athauda and Foltynie 2016;Daneshvar et al, 2015;Jabir et al, 2015;Jha et al, 2016;Santiago and Potashkin, 2013;Santiago and Potashkin, 2014), in addition to being associated with AE (Chou et al, 2016;Kalra et al, 2016;Ono and Galanopoulou, 2012;Pitkanen et al, 2015;Verrotti et al, 2012;Waldbaum and Patel, 2010b). These factors are characterized by common brain pathologies such as chronic hypoperfusion (Scholz and Hanefeld, 2016;Zlokovic, 2011), neuro-inflammation, and insulin resistance (Rosales-Corral et al, 2015;Straub 2014;Yamagata et al, 2017), all leading to energy deficiency and oxidative stress.…”

Neural ECM and epilepsy

“…For example, patients with TLE suffer from hippocampal degeneration and learning and memory deficits (Ono and Galanopoulou, 2012), while individual with frontal lobe epilepsy often experience difficulties in performing tasks that require executive functions and decision making (Patrikelis et al, 2009). For example, patients with TLE suffer from hippocampal degeneration and learning and memory deficits (Ono and Galanopoulou, 2012), while individual with frontal lobe epilepsy often experience difficulties in performing tasks that require executive functions and decision making (Patrikelis et al, 2009).…”

Identification of the antiepileptic racetam binding site in the synaptic vesicle protein 2A by molecular dynamics and docking simulations

“…However, a significant number of patients -especially in the setting of medical-intractable epilepsies- may experience different degrees of memory or cognitive impairment, behavioral abnormalities or psychiatric symptoms, which limit their daily functioning. As a result, in many patients, epilepsy may resemble a neurodegenerative disease ( Ono and Galanopoulou, 2012 ). Epileptic seizures and/or epileptogenesis may functionally alter brain regions involved in cognitive processing, contributing to the progressive nature of epilepsy; additionally neurodegenerative cellular mechanisms may also participate.…”