Cortical spreading depolarization in lesional epilepsy surgery
Introduction - Cortical spreading depressions (CSDs) are waves of near-complete cellular depolarization that spread slowly across the cortical surface (2-5mm/min) and result in transient loss of cell signaling capabilities. CSDs is a biomarker of neuronal damage described in several clinical hypoxic...
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| Hauptverfasser: | , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
May 2018
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| In: |
Clinical neurophysiology
Year: 2018, Jahrgang: 129, Pages: e144 |
| ISSN: | 1872-8952 |
| DOI: | 10.1016/j.clinph.2018.04.367 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.clinph.2018.04.367 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S1388245718306667 |
| Verfasserangaben: | Daniel San Juan Orta, Katia Márquez, Roberto Díaz Peregrino, Mario Alonso-Vanegas, Edgar Santos |
MARC
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| 520 | |a Introduction - Cortical spreading depressions (CSDs) are waves of near-complete cellular depolarization that spread slowly across the cortical surface (2-5mm/min) and result in transient loss of cell signaling capabilities. CSDs is a biomarker of neuronal damage described in several clinical hypoxic-ischemic conditions However, only has been found in one patient operated for Giant pituitary adenoma. - Methods - This is a prospective study that included adult patients undergoing elective craniotomy for epileptogenic supratentorial lesions lasting >2h. Electrocorticographic recordings were obtained from time of dural opening through the time of dural closure, using a standard 1×8 silver electrode coupled with a full-spectrum DC amplifier (0-45Hz, Notch: 60Hz). We analyzed the clinical and socio-demographic characteristics. The data were processed using the COSBID research group methodology to evaluate for slow potential changes coupled with suppression of high-frequency ECoG propagating across the electrodes. Describe statistics were used. - Results - We included 16 patients, mean age 37 (19-75) years-old, 50% male, underwent 4 callosotomies and 12 temporal lesionectomies (3 cortical dysplasia, 2 cavernomas, 5 gliomas and 2 dermoid cystic). All the patients had history of symptomatic epilepsy and none had postsurgical complications and only 2 patients post-callosotomy continued with seizures at 6months of follow-up. We didn’t find any CSD during these neurosurgeries. - Conclusion - CSDs were absent during lesional epilepsy surgery. Future studies are needed to confirm these findings. | ||
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