Pathophysiology of encephalopathy related to continuous spike and waves during sleep: the contribution of neuroimaging (notice n° 612471)
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| fixed length control field | 02606cam a2200205 4500500 |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20250121162833.0 |
| 041 ## - LANGUAGE CODE | |
| Language code of text/sound track or separate title | fre |
| 042 ## - AUTHENTICATION CODE | |
| Authentication code | dc |
| 100 10 - MAIN ENTRY--PERSONAL NAME | |
| Personal name | Siniatchkin, Michael |
| Relator term | author |
| 245 00 - TITLE STATEMENT | |
| Title | Pathophysiology of encephalopathy related to continuous spike and waves during sleep: the contribution of neuroimaging |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. | |
| Date of publication, distribution, etc. | 2019.<br/> |
| 500 ## - GENERAL NOTE | |
| General note | 61 |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | In the last three decades, studies on functional neuroimaging have helped us to understand pathophysiological mechanisms responsible for electro-clinical patterns associated with epileptic encephalopathies with continuous spikes and waves during slow sleep (ECSWS). MEG and EEG source reconstruction have revealed sources of pathological brain activity associated with epileptiform discharges in the perisylvian region pointing to the significance of this brain area for ECSWS. PET studies have revealed areas of focal hypermetabolism in perisylvian, superior temporal and inferior parietal regions as well as central cortices which were related to epileptic activity. The widespread hypometabolism in regions that belong to the default network (prefrontal and posterior cingulate cortices, parahippocampal gyrus and precuneus) was interpreted as remote inhibition following epileptic activity, which could contribute to cognitive deficits in affected individuals. Note that the described metabolic changes were functional and disappeared after successful treatment and recovery of ECSWS and were found in both sleep and wakefulness which may account for cognitive deficits in patients during the day. EEG-fMRI studies have revealed a functional fingerprint of epileptic encephalopathy: significant positive BOLD signal changes were identified in the perisylvian regions, prefrontal cortex and anterior cingulate as well as thalamus and negative BOLD signal changes in the regions of the default mode network. The pattern of activation represents a propagation of epileptic activity specific to encephalopathy, which is independent of etiology and type of seizure associated with ECSWS. In summary, methods of neuroimaging have shed light on pathogenic mechanisms of ECSWS which may account for a number of clinical phenomena associated with this condition. |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | ESES |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | encephalopathy related to status epilepticus during slow sleep |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | neuroimaging |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Van Bogaert, Patrick |
| Relator term | author |
| 786 0# - DATA SOURCE ENTRY | |
| Note | Epileptic Disorders | Vol 21 | N° Supp | 2019-07-01 | p. 48-53 | 1294-9361 |
| 856 41 - ELECTRONIC LOCATION AND ACCESS | |
| Uniform Resource Identifier | <a href="https://shs.cairn.info/revue-epileptic-disorders-2019-HS1-page-48?lang=fr&redirect-ssocas=7080">https://shs.cairn.info/revue-epileptic-disorders-2019-HS1-page-48?lang=fr&redirect-ssocas=7080</a> |
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