Correlations between ictal propagation and response to electrical cortical stimulation: A cortico-cortical evoked potential study
書誌事項
- 公開日
- 2012-08
- 権利情報
-
- https://www.elsevier.com/tdm/userlicense/1.0/
- https://www.elsevier.com/legal/tdmrep-license
- https://doi.org/10.15223/policy-017
- https://doi.org/10.15223/policy-037
- https://doi.org/10.15223/policy-012
- https://doi.org/10.15223/policy-029
- https://doi.org/10.15223/policy-004
- DOI
-
- 10.1016/j.eplepsyres.2012.03.004
- 公開者
- Elsevier BV
この論文をさがす
説明
To better understand the process of ictal propagation in epilepsy by using cortico-cortical evoked potential (CCEP), which reveals the brain networks.Intracranial EEG recordings of 11 seizures from 11 patients with pharmacoresistant focal epilepsy were studied to identify the propagation sites and times. Six patients had a history of secondary generalization (Gen (+) group) and five patients did not (Gen (-) group). Thereafter repetitive 1Hz bipolar electrical stimuli were applied to the ictal onset zones and CCEPs were recorded by averaging electrocorticograms.The propagation of contiguous spread was significantly faster than non-contiguous spread (p=0.033). In four patients, CCEP amplitudes were significantly larger in the ictal propagation area than out of the propagation area. However, the distribution of CCEP responses was not necessarily consistent with the ictal propagation area as a whole. Furthermore, the ictal propagation areas out of CCEP-positive areas were significantly broader in Gen (+) group than Gen (-) group (p=0.017).The present findings suggest that contiguous spread is faster than non-contiguous spread, which can be explained by the enhancement of excitability around the ictal onset area. Furthermore, there is a group of fibers that is "closed" during the seizures and secondary generalization might be more associated with the impairment of cortical inhibition over the broad cortical area rather than direct connection.
収録刊行物
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- Epilepsy Research
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Epilepsy Research 101 (1-2), 76-87, 2012-08
Elsevier BV
