Very high-frequency rhythmic activity during SEEG suppression in frontal lobe epilepsy

Allen, Philip J.; Fish, D. R.; Smith, S. J. M.

doi:10.1016/0013-4694(92)90160-j

Cited by 231 publications

(132 citation statements)

References 2 publications

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“…Clinical studies based on longterm intracranial depth recordings from the epileptogenic zone during presurgical stereo-EEG monitoring confirmed that the most common pattern at seizure onset is characterized by the abolition of background activity that is replaced by low-voltage fast activity at 20 -100 Hz ("bg" range) (Allen et al 1992;Fisher et al 1992;Gotman et al 1995;Gnatkovsky et al 2011), which is often superimposed to a very slow potential (Ikeda et al 1999;Bragin et al 2007;Gnatkovsky et al 2014;Wu et al 2014). Lowvoltage fast activity has a critical localizing/ lateralizing value, and is detected in the large majority of intracranially explored partial epilepsies, such as TLEs, focal cortical dysplasias, and postanoxic lesions (Gotman et al 1995;Pelliccia et al 2013).…”

Section: Seizure Onsetmentioning

confidence: 99%

Initiation, Propagation, and Termination of Partial (Focal) Seizures

Curtis

Avoli

2015

Cold Spring Harb Perspect Med

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The neurophysiological patterns that correlate with partial (focal) seizures are well defined in humans by standard electroencephalogram (EEG) and presurgical depth electrode recordings. Seizure patterns with similar features are reproduced in animal models of partial seizures and epilepsy. However, the network determinants that support interictal spikes, as well as the initiation, progression, and termination of seizures, are still elusive. Recent findings show that inhibitory networks are prominently involved at the onset of these seizures, and that extracellular changes in potassium contribute to initiate and sustain seizure progression. The end of a partial seizure correlates with an increase in network synchronization, which possibly involves both excitatory and inhibitory mechanisms.

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Section: Seizure Onsetmentioning

confidence: 99%

Initiation, Propagation, and Termination of Partial (Focal) Seizures

Curtis

Avoli

2015

Cold Spring Harb Perspect Med

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“…The burst waves often have a frequency at about 40 Hz and high amplitudes. Increasing competition as a consequence of failure of associative connections without possibility to agree on a common frequency of oscillations may lead after extremely intense and hypersynchronous gamma rhythms to epileptiform discharges and decreasing gamma oscillations (Medvedev, 2001(Medvedev, , 2002Alarcon et al, 1995;Allen et al, 1992;Fisher et al, 1992;Huang & White, 1989). In this context, epileptiform activity has been suggested as an antibinding mechanism which is related to a failure of associative connections between neural assemblies (Medvedev, 2001(Medvedev, , 2002 and corresponding fragmentation of related mental representations characteristic for dissociative states.…”

Section: Binding Of Neural Assemblies Chaos and Dissociation: A Neurmentioning

confidence: 99%

Dissociation, Epileptiform Discharges and Chaos in the Brain: Toward a Neuroscientific Theory of Dissociation

Bob

2012

Act Nerv Super

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Dissociated states represent pathological conditions when psychological trauma may emerge in a variety of forms such as psychic dissociative symptoms or, on the contrary, as paroxysms or other somatoform symptoms. There is evidence that epileptic activity plays an important role in the generation of dissociative states and it is able to generate various psychopathological processes as well as a wide spectrum of somatic symptoms or seizures. For the explanation of these connections between dissociative states and epileptic discharges the author proposes a neuroscientific model of dissociation based on the theory of competitive neural assemblies which can lead to chaotic self-organization in brain neural networks. This model is suggested as an integrative view interconnecting the various psychopathological and somatoform manifestations of dissociative states and suggests further possibilities for future research regarding common pathogenic mechanisms among epilepsy and mental disorders.

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“…High-frequency oscillations (HFOs), also called ripples, at 80-200 Hz or even higher frequencies (250-600 Hz), are ensembles of repeated and synchronous firing in many neurons. Because they have been recorded immediately preceding seizure onset in vivo [129,130] , in vitro [101,131] and in human clinical electroencephalograms (EEGs) [132][133][134][135][136] , HFOs are thought to be an indication of an epileptiform network mechanism in seizure initiation [137][138][139][140][141][142][143] . An increasing number of studies suggests that gap junctions interconnecting neurons, rather [144] .…”

Section: Role Of Neuronal Network In Oscillations and Seizure Synchrmentioning

confidence: 99%

Role of gap junctions in epilepsy

Jin

Chen

2011

Neurosci. Bull.

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Epilepsy is a common neurological disorder characterized by periodic and unpredictable seizures. Gap junctions have recently been proposed to be involved in the generation, synchronization and maintenance of seizure events.The present review mainly summarizes recent reports concerning the contribution of gap junctions to the pathophysiology of epilepsy, together with the regulation of connexin after clinical and experimental seizure activity. The anticonvulsant effects of gap junction blockers both in vitro and in vivo suggest that the gap junction is a candidate target for the development of antiepileptic drugs. It is also of interest that the roles of neuronal and astrocytic gap junctions in epilepsy have been investigated independently, based on evidence from pharmacological manipulations and connexin-knockout mice.Further studies using more specific manipulations of gap junctions in different cell types and in human epileptic tissue are needed to fully uncover the role of gap junctions in epilepsy.

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Very high-frequency rhythmic activity during SEEG suppression in frontal lobe epilepsy

Cited by 231 publications

References 2 publications

Initiation, Propagation, and Termination of Partial (Focal) Seizures

Initiation, Propagation, and Termination of Partial (Focal) Seizures

Dissociation, Epileptiform Discharges and Chaos in the Brain: Toward a Neuroscientific Theory of Dissociation

Role of gap junctions in epilepsy

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