Epilepsy Research Journal
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Maximal/Exhaustive Treadmill Test Features in Patients with Temporal Lobe Epilepsy: Search for Sudden Unexpected Death Biomarkers
Epilepsy is one of the most important neurological diseases in clinical practice, being the second most common neurological disease in primary care. All over the world, around 65 million individuals suffer from epilepsy (Thurman et al., 2011) and patients with epilepsy (PWE) have a 20 to 40-fold increased risk for sudden death (Ficker et al., 1998; Mohanraj et al., 2006). In fact, Sudden Unexpected Death in Epilepsy (SUDEP) is responsible for 17 to 38% of deaths in PWE. SUDEP has been defined as the sudden, unexpected, witnessed or unwitnessed, non-traumatic, and non-drowning death in PWE, with or without evidence for a seizure, with exclusion of documented status epilepticus, and when post-mortem examination does not reveal a structural or toxicological cause for death (Nashef, 2012, 1997).
Changes in the interictal and early postictal diffusion and perfusion magnetic resonance parameters in familial spontaneous epileptic cats
Epilepsy research - Full-length Paper
A Survey of Medical Examiner Death Certification of Vignettes on Death in Epilepsy: Gaps in Identifying SUDEP
Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in individuals with chronic, uncontrolled epilepsy (Tomson et al., 2005, 2008). These poorly understood deaths can occur in anyone with epilepsy of any kind, and both high and low risk groups have been identified (So, 2006; Tomson et al., 2005). The specific mechanism of death is unknown for SUDEP cases and likely multifactorial, with evidence suggesting brainstem dysfunction and cardiorespiratory dysregulation as a final common pathway associated with sudden death in these individuals (de la Grandmaison, 2006; Partemi et al., 2015; So, 2008; Tu et al., 2011).
Reduced Abnormal Integration of Adult-Generated Granule Cells does not Attenuate Spontaneous Recurrent Seizures in Mice
Neurogenesis in the subgranular zone (SGZ) of the dentate gyrus (DG) persists throughout life in a wide variety of mammalian species. In rodent temporal lobe epilepsy (TLE) models, initial status epilepticus (SE) insult lead to augmented DG neurogenesis and abnormal integrations of newly generated granule cells, including hilar ectopic cells (HECs), hilar basal dendrites (HBDs) and mossy fiber sprouting (MFS), which potentially mediate the formation of hyperexcitable DG circuits (Parent et al., 1997; Murphy et al., 2011; Pun et al., 2012).
Sporadic periventricular nodular heterotopia: Classification, phenotype and correlation with Filamin A mutations
Heterotopia is defined by the presence of groups of normal neurons in an inappropriate location, which results from a primary failure of neuronal migration, including periventricular, subcortical and leptomeningeal glioneuronal varieties (Barkovich et al., 2001; Barkovich et al., 2005; Barkovich et al., 2012; Guerrini and Barba, 2010). The most common clinical manifestations of heterotopia are epileptic seizures, mainly resistant focal seizures, neurological deficits, systemic malformations and developmental delays (Barkovich et al., 2012; Guerrini and Parrini, 2010).
Medically refractory focal epilepsy is associated with decreased brain-wide volumetric measures and cognitive function, both of which are also observed in normal aging (Dabbs et al., 2012; Hoppe et al., 2007; Sowell et al., 2003; Salthouse, 2004). Prior studies have noted that epilepsy-related neuroanatomical and cognitive changes are greater than those observed in normal aging and therefore may be conceptualized as accelerated aging (Breuer et al., 2016; Lin et al., 2012; Bernhardt et al., 2009; Helmstaedter et al., 2003).