Is the anatomical lesion always guilty?: A case report.
Anatomo-electro-clinical correlations
Epilepsy surgery
Invasive investigations
“Innocent” neuroradiological lesion
Journal
Epilepsy & behavior reports
ISSN: 2589-9864
Titre abrégé: Epilepsy Behav Rep
Pays: United States
ID NLM: 101750909
Informations de publication
Date de publication:
2022
2022
Historique:
received:
30
05
2022
revised:
19
08
2022
accepted:
28
08
2022
entrez:
22
9
2022
pubmed:
23
9
2022
medline:
23
9
2022
Statut:
epublish
Résumé
During a presurgical workup, when discordant structural and electroclinical localization is identified, further evaluation with invasive EEG is often necessary. We report a 44-year-old right-handed woman without significant risk factors for epilepsy who presented at 11 years of age with focal seizures manifest as jerking of the left side of her mouth and arm with frequent evolution to bilateral tonic-clonic seizures during sleep with a weekly frequency. During video-EEG monitoring, we observed interictal left fronto-central sharp waves and some independent sharp waves in the right fronto-central region. Habitual seizures were recorded and during the post-ictal state, the patient had left arm weakness for a few minutes. The ictal discharge on EEG was characterized by a bilateral fronto-central rhythmic slow activity more prevalent over the right hemisphere. MRI of the brain revealed a left precentral structural lesion. Considering the discordant structural and electroclinical information, we performed bilateral fronto-central stereo-EEG implantation and demonstrated clear right fronto-central seizure onset. Stereo-EEG-guided radiofrequency thermocoagulation was performed in the right fronto-central leads with subsequent seizure freedom for 9 months. The patient then underwent surgery (right fronto-central cortectomy), and histology revealed focal cortical dysplasia type Ia. The post-surgical outcome was Engel Ia. This case underscores the presence of a structural lesion is not sufficient to define the epileptogenic zone if not supported by clinical and EEG evidence. In such cases, an invasive investigation is typically required.
Identifiants
pubmed: 36132992
doi: 10.1016/j.ebr.2022.100564
pii: S2589-9864(22)00041-7
pmc: PMC9483572
doi:
Types de publication
Case Reports
Langues
eng
Pagination
100564Informations de copyright
© 2022 Published by Elsevier Inc.
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Références
N Engl J Med. 1996 Mar 7;334(10):647-52
pubmed: 8592530
Brain Dev. 2013 Sep;35(8):706-20
pubmed: 23684007
Lancet Neurol. 2020 Sep;19(9):748-757
pubmed: 32822635
JAMA. 2015 Jan 20;313(3):285-93
pubmed: 25602999
Epilepsia. 2017 May;58(5):727-742
pubmed: 28266710
Neurology. 2017 Jan 17;88(3):296-303
pubmed: 27986877
Brain. 2009 Aug;132(Pt 8):2079-90
pubmed: 19506069
Epileptic Disord. 2015 Mar;17(1):19-31; quiz 31
pubmed: 25652945
N Engl J Med. 2017 Oct 26;377(17):1648-1656
pubmed: 29069555
Epileptic Disord. 2006 Aug;8 Suppl 2:S67-76
pubmed: 17012073
Arch Neurol. 2009 Dec;66(12):1491-9
pubmed: 20008653
Epilepsy Behav. 2011 Feb;20(2):190-3
pubmed: 21256814
Brain. 2001 Sep;124(Pt 9):1683-700
pubmed: 11522572
J Neurosurg. 2017 Nov;127(5):1147-1152
pubmed: 28084910
Neuroradiology. 2012 Oct;54(10):1065-77
pubmed: 22695739
Epilepsia. 2021 Jan;62(1):128-142
pubmed: 33258120
Epilepsy Res. 2010 May;89(2-3):310-8
pubmed: 20227852
Med J Aust. 2018 Mar 19;208(5):226-233
pubmed: 29540143
Epilepsia. 2011 Apr;52(4):738-45
pubmed: 21320114
Neuropathology. 2021 Feb;41(1):42-48
pubmed: 33094499
Pract Neurol. 2020 Feb;20(1):4-14
pubmed: 31420415
Epileptic Disord. 2012 Sep;14(3):257-66
pubmed: 22963868
Lancet Neurol. 2016 Apr;15(4):420-33
pubmed: 26925532
Clin Neuroradiol. 2015 Oct;25 Suppl 2:151-5
pubmed: 25850640
Epilepsia. 2012 Apr;53(4):733-40
pubmed: 22360822