Mechanisms of Epileptogenesis

Avanzini, G.; Franceschetti, Silvana

doi:10.1002/9781118936979.ch3

Cited by 2 publications

(1 citation statement)

References 121 publications

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“…Indeed, models of seizure propagation and clinically recorded networks show rapid spread of disruptions through small-world networks as a result of their long-range connectivity and hub structure (Netoff et al, 2004 ; Ponten et al, 2007 ). With the reliance of seizure spread on network topology, epileptogenesis can occur as a result of disruptions to functional and structural connectivity (Avanzini and Franceschetti, 2009 ; Terry et al, 2012 ; Fornito et al, 2015 ). Functional connectivity mapping in stroke patients often reveals hyperconnectivity, where functional network components paradoxically show an increase in connectivity post-stroke (Hillary and Grafman, 2017 ).…”

Section: Brain Disorders and Disruptions To Criticalitymentioning

confidence: 99%

Criticality, Connectivity, and Neural Disorder: A Multifaceted Approach to Neural Computation

Heiney

Ramstad

Fiskum

et al. 2021

Front. Comput. Neurosci.

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It has been hypothesized that the brain optimizes its capacity for computation by self-organizing to a critical point. The dynamical state of criticality is achieved by striking a balance such that activity can effectively spread through the network without overwhelming it and is commonly identified in neuronal networks by observing the behavior of cascades of network activity termed “neuronal avalanches.” The dynamic activity that occurs in neuronal networks is closely intertwined with how the elements of the network are connected and how they influence each other's functional activity. In this review, we highlight how studying criticality with a broad perspective that integrates concepts from physics, experimental and theoretical neuroscience, and computer science can provide a greater understanding of the mechanisms that drive networks to criticality and how their disruption may manifest in different disorders. First, integrating graph theory into experimental studies on criticality, as is becoming more common in theoretical and modeling studies, would provide insight into the kinds of network structures that support criticality in networks of biological neurons. Furthermore, plasticity mechanisms play a crucial role in shaping these neural structures, both in terms of homeostatic maintenance and learning. Both network structures and plasticity have been studied fairly extensively in theoretical models, but much work remains to bridge the gap between theoretical and experimental findings. Finally, information theoretical approaches can tie in more concrete evidence of a network's computational capabilities. Approaching neural dynamics with all these facets in mind has the potential to provide a greater understanding of what goes wrong in neural disorders. Criticality analysis therefore holds potential to identify disruptions to healthy dynamics, granted that robust methods and approaches are considered.

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Section: Brain Disorders and Disruptions To Criticalitymentioning

confidence: 99%

Criticality, Connectivity, and Neural Disorder: A Multifaceted Approach to Neural Computation

Heiney

Ramstad

Fiskum

et al. 2021

Front. Comput. Neurosci.

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Effect of carbamazepine-beta-cyclodextrin inclusion complex on seizure-like events in an in vitro model of temporal lobe epilepsy

Kiss,

Csüdör,

Sárosi

et al. 2024

Acta Marisiensis - Seria Medica

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Objective: Pharmacoresistant epilepsy represents a significant global health challenge, necessitating novel therapeutic approaches. Despite advances in antiseizure medications, many patients remain treatment-resistant partially due to complex pharmacokinetic issues. Beta-cyclodextrin, known for enhancing drug solubility and stability, offers potential solutions by forming inclusion complexes, thereby improving anti-seizure medication’s efficacy. This study aimed to investigate the effect of beta-cyclodextrin and beta-cyclodextrin-complexed carbamazepine on epileptiform activities, using an in vitro model of temporal lobe epilepsy. Methods: Seizure-like neuronal activity was induced using the low-magnesium model. Local field potentials were recorded from transverse rat hippocampal slices immersed in epileptogenic artificial cerebrospinal fluid, followed by the administration of either beta-cyclodextrin or carbamazepine, the latter in 100 micromolar concentration. Results: Beta cyclodextrin, applied alone, significantly reduced the duration of interictal and ictal phases while increasing the frequency of seizure-like events. Carbamazepine exhibited an important anticonvulsant effect, significantly reducing ictal and postictal phase durations. However, the frequency of seizure-like events was increased. Notably, in some of the slices, carbamazepine completely suppressed epileptiform activity. Conclusions: Beta cyclodextrin had an effect on its own; it shortened seizure durations and increased their frequency. Carbamazepine in complexed form, as used in our study, exhibited anticonvulsant efficacy, emphasizing the feasibility of solubility enhancement by this method. This study provides insights into potential therapeutic strategies for pharmacoresistant temporal lobe epilepsy, improving the pharmacological properties of the drugs. As cyclodextrins emerge as promising excipients for antiepileptic drugs with poor solubility, more effort is needed in order to elucidate the underlying mechanisms of their effects.

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Mechanisms of Epileptogenesis

Cited by 2 publications

References 121 publications

Criticality, Connectivity, and Neural Disorder: A Multifaceted Approach to Neural Computation

Criticality, Connectivity, and Neural Disorder: A Multifaceted Approach to Neural Computation

Effect of carbamazepine-beta-cyclodextrin inclusion complex on seizure-like events in an in vitro model of temporal lobe epilepsy

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