Is Spreading Depolarization a Risk Factor for Late Epilepsy? A Prospective Study in Patients with Traumatic Brain Injury and Malignant Ischemic Stroke Undergoing Decompressive Craniectomy.


Journal

Neurocritical care
ISSN: 1556-0961
Titre abrégé: Neurocrit Care
Pays: United States
ID NLM: 101156086

Informations de publication

Date de publication:
06 2021
Historique:
received: 17 05 2020
accepted: 05 09 2020
pubmed: 2 10 2020
medline: 30 9 2021
entrez: 1 10 2020
Statut: ppublish

Résumé

Spreading depolarizations (SDs) have been described in patients with ischemic and haemorrhagic stroke, traumatic brain injury, and migraine with aura, among other conditions. The exact pathophysiological mechanism of SDs is not yet fully established. Our aim in this study was to evaluate the relationship between the electrocorticography (ECoG) findings of SDs and/or epileptiform activity and subsequent epilepsy and electroclinical outcome. This was a prospective observational study of 39 adults, 17 with malignant middle cerebral artery infarction (MMCAI) and 22 with traumatic brain injury, who underwent decompressive craniectomy and multimodal neuromonitoring including ECoG in penumbral tissue. Serial electroencephalography (EEG) recordings were obtained for all surviving patients. Functional disability at 6 and 12 months after injury were assessed using the Barthel, modified Rankin (mRS), and Extended Glasgow Outcome (GOS-E) scales. SDs were recorded in 58.9% of patients, being more common-particularly those of isoelectric type-in patients with MMCAI (p < 0.04). At follow-up, 74.7% of patients had epileptiform abnormalities on EEG and/or seizures. A significant correlation was observed between the degree of preserved brain activity on EEG and disability severity (R [mRS]: + 0.7, R [GOS-E, Barthel]: - 0.6, p < 0.001), and between the presence of multifocal epileptiform abnormalities on EEG and more severe disability on the GOS-E at 6 months (R: - 0.3, p = 0.03) and 12 months (R: - 0.3, p = 0.05). Patients with more SDs and higher depression ratios scored worse on the GOS-E (R: - 0.4 at 6 and 12 months) and Barthel (R: - 0.4 at 6 and 12 months) disability scales (p < 0.05). The number of SDs (p = 0.064) and the depression ratio (p = 0.1) on ECoG did not show a statistically significant correlation with late epilepsy. SDs are common in the cortex of ischemic or traumatic penumbra. Our study suggests an association between the presence of SDs in the acute phase and worse long-term outcome, although no association with subsequent epilepsy was found. More comprehensive studies, involving ECoG and EEG could help determine their association with epileptogenesis.

Identifiants

pubmed: 33000378
doi: 10.1007/s12028-020-01107-x
pii: 10.1007/s12028-020-01107-x
doi:

Types de publication

Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

876-888

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Auteurs

Maria Sueiras (M)

Department of Clinical Neurophysiology, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain. msueiras@vhebron.net.
Neurotrauma and Neurosurgery Research Unit (UNINN), Vall d'Hebron Research Institute (VHIR), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain. msueiras@vhebron.net.
Universitat Autònoma de Barcelona (UAB), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain. msueiras@vhebron.net.

Vanessa Thonon (V)

Department of Clinical Neurophysiology, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Estevo Santamarina (E)

Epilepsy Unit, Department of Neurology, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Ángela Sánchez-Guerrero (Á)

Neurotrauma and Neurosurgery Research Unit (UNINN), Vall d'Hebron Research Institute (VHIR), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Marilyn Riveiro (M)

Neurotrauma Intensive Care Unit, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Maria-Antonia Poca (MA)

Neurotrauma and Neurosurgery Research Unit (UNINN), Vall d'Hebron Research Institute (VHIR), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.
Universitat Autònoma de Barcelona (UAB), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.
Department of Neurosurgery, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Manuel Quintana (M)

Epilepsy Unit, Department of Neurology, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Dario Gándara (D)

Neurotrauma and Neurosurgery Research Unit (UNINN), Vall d'Hebron Research Institute (VHIR), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.
Department of Neurosurgery, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

Juan Sahuquillo (J)

Neurotrauma and Neurosurgery Research Unit (UNINN), Vall d'Hebron Research Institute (VHIR), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.
Universitat Autònoma de Barcelona (UAB), Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.
Department of Neurosurgery, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain.

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