Non-uniform propagation of epileptiform discharge in brain slices of rat neocortex

Wadman, W.J.; Gutnick, Michael J.

doi:10.1016/0306-4522(93)90154-8

Cited by 76 publications

(47 citation statements)

References 20 publications

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“…2 A). Notably, the propagation speed of the afterdischarges (29 Ϯ 18 mm/s) was similar to ictal propagation in disinhibited brain slices (20 -100 mm/s) (Chervin et al, 1988;Wadman and Gutnick, 1993;Albowitz and Kuhnt, 1995;Pinto et al, 2005).…”

Section: Different Determinants Of Propagation Speed For Tonic and CLmentioning

confidence: 64%

“…Using brain slices greatly reduces the dimensionality of the problem, essentially to analysis of a one-dimensional, horizontal propagation (Chervin et al, 1988;Traub et al, 1993;Wadman and Gutnick, 1993;Albowitz and Kuhnt, 1995;Pinto et al, 2005;Trevelyan et al, 2006Trevelyan et al, , 2007. Furthermore, these models provide far greater control of the experimental conditions than in vivo models but also allow easier access for electrophysiological recording or imaging.…”

Section: Introductionmentioning

confidence: 99%

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The Source of Afterdischarge Activity in Neocortical Tonic–Clonic Epilepsy

Trevelyan

Baldeweg²,

Drongelen³

et al. 2007

J. Neurosci.

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Tonic-clonic seizures represent a common pattern of epileptic discharges, yet the relationship between the various phases of the seizure remains obscure. Here we contrast propagation of the ictal wavefront with the propagation of individual discharges in the clonic phase of the event. In an in vitro model of tonic-clonic epilepsy, the afterdischarges (clonic phase) propagate with relative uniform speed and are independent of the speed of the ictal wavefront (tonic phase). For slowly propagating ictal wavefronts, the source of the afterdischarges, relative to a given recording electrode, switched as the wavefront passed by, indicating that afterdischarges are seeded from wavefront itself. In tissue that has experienced repeated ictal events, the wavefront generalizes rapidly, and the afterdischarges in this case show a different "flip-flop" pattern, with frequent switches in their direction of propagation. This same flip-flop pattern is also seen in subdural EEG recordings in patients suffering intractable focal seizures caused by cortical dysplasias. Thus, in both slowly and rapidly generalizing ictal events, there is not a single source of afterdischarge activity: rather, the source is continuously changing. Our data suggest a complex view of seizures in which the ictal event and its constituent discharges originate from distinct locations.

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Section: Different Determinants Of Propagation Speed For Tonic and CLmentioning

confidence: 64%

Section: Introductionmentioning

confidence: 99%

The Source of Afterdischarge Activity in Neocortical Tonic–Clonic Epilepsy

Trevelyan

Baldeweg²,

Drongelen³

et al. 2007

J. Neurosci.

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“…Such velocity, slower than conduction velocity of axons, depended on the threshold of synchronous activation of the neuronal aggregates defining each local region. Variations in latency to the threshold may have depended on local ionic concentrations, nature of lesions, or clustering of horizontal intracortical connections of intrinsically bursting cells (34)(35)(36). Such mechanisms may underlie the range of propagation speeds disclosed in each of our clinical studies.…”

Section: Discussionmentioning

confidence: 90%

“…In the subdural study, time to initial propagation ranged from 1 to 45 s, and latency to any bisynchronous discharge varied from 7 to 65 s. Assessments of propagation in the scalp study disclosed interpatient differences in onset of contiguous and bilateral ictal EEG changes, also likely reflecting a range of propagation speeds. Wadman and Gutnick (34) and Chervin gation of epileptiform events in rat cortex. Wadman and Gutnick (34) found saltatory conduction within a given pathway; conduction was divided into several sharply demarcated local regions, each with its own distinct, uniform velocity.…”

Section: Discussionmentioning

confidence: 99%

“…Wadman and Gutnick (34) and Chervin gation of epileptiform events in rat cortex. Wadman and Gutnick (34) found saltatory conduction within a given pathway; conduction was divided into several sharply demarcated local regions, each with its own distinct, uniform velocity. Such velocity, slower than conduction velocity of axons, depended on the threshold of synchronous activation of the neuronal aggregates defining each local region.…”

Section: Discussionmentioning

confidence: 99%

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Frontal Lobe Seizure Propagation: Scalp and Subdural EEG Studies

2001

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Summary:Purpose: To study propagation properties of focally originating frontal lobe seizures: principally direction and promptness of ictal spread.Method: Forty-eight scalp EEG-recorded and 17 subdurally recorded seizures in two separate groups of patients were visually scrutinized.Results: Initial propagation was directed more commonly to contiguous frontal cortex than to the opposite hemisphere in both studies: 58% and 86% for scalp and subdural recordings, respectively. Eighteen (38%) of scalp EEG seizures propagated within 5-10 s of apparent onset, whereas 16 (33%) did so after 11-20 s; no evidence of propagation could be discerned in the remaining 14 (29%). Of subdurally recorded attacks, only four (24%) propagated in the first 4 s; six (35%) did so after a delay of 5-10 s; six (35%) either failed to propagate or did so after Ն20-s latency. Latency to initial propagation was between 5 and 20 s in 41 (63%) of the 65 seizures in both studies. Ictal activity remained within the frontal lobe of origin for Ն10 s in 39 (81%) of scalp-recorded seizures and 11 (65%) of subdural seizures. It remained so confined for Ն15 s in 26 (54%) and nine (53%), respectively. Twenty-four (50%) of scalp-recorded seizures displayed evidence of opposite hemisphere (bisynchronous or other contralateral) involvement, occurring 5-10 s after onset in eight (17%) seizures and 10-20 s after onset in 16 (33%). Similarly, the subdural study documented spread to the opposite hemisphere in 11 (65%) of seizures with a latency ranging from 1 to 45 s.Conclusions: Frontal lobe seizures in this study propagated less promptly than reputed, and initial spread occurred more commonly to the frontal lobe of origin than to the opposite hemisphere. Such properties underlie the good lateralizing value of clinical semiology of frontal lobe seizures.

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