Late drug-resistance in mild MTLE: Can it be influenced by preexisting white matter alterations?


Journal

Epilepsia
ISSN: 1528-1167
Titre abrégé: Epilepsia
Pays: United States
ID NLM: 2983306R

Informations de publication

Date de publication:
05 2020
Historique:
received: 22 01 2020
revised: 21 03 2020
accepted: 23 03 2020
pubmed: 21 4 2020
medline: 1 12 2020
entrez: 21 4 2020
Statut: ppublish

Résumé

To identify early structural alterations preceding the development of drug-resistance in mild mesial temporal lobe epilepsy (mMTLE), a drug-responsive syndrome ideal for investigating epilepsy pathophysiology and potential prognostic markers of long-term clinical outcome, using magnetic resonance imaging (MRI) at baseline and after 12-year follow-up. Since 2002, a total of 55 participants with a baseline diagnosis of mMTLE underwent three-dimensional (3D) T1 1.5T MRI. Based on long-term outcome (follow-up 12 ± 3 years), we identified 39 patients with stable mMTLE (smMTLE) and 16 patients who had developed drug-resistance overtime (refractory MTLE [rMTLE]). At follow-up, 21 smMTLE and 13 rMTLE patients underwent 3T-MRI including diffusion-weighted scans. Structural images were processed using longitudinal voxel-based morphometry and standard Freesurfer analysis. Statistical analyses were carried out accounting for age, age at onset, gender, hippocampal volume, and hippocampal sclerosis (Hs). Patients presented similar demographic, clinical, and Hs features. White matter volume of the arcuate fasciculi, corticospinal tracts, left retrosplenial cingulum, and left inferior longitudinal fasciculus was reduced only in rMTLE patients before the development of drug-resistance. At follow-up, rMTLE showed decreased fractional anisotropy in the corpus callosum, superior longitudinal fasciculi, and major bundles of the right hemisphere. White matter temporal and extratemporal abnormalities are preexisting in patients with mild MTLE who will develop drug-resistance, independently from the presence of Hs. Thus, these changes might be due to an inherited genetic alteration rather than a subordinate worsening after repeated seizures, multiple antiepileptic drugs, or initial precipitating factors.

Identifiants

pubmed: 32311085
doi: 10.1111/epi.16503
doi:

Substances chimiques

Anticonvulsants 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

924-934

Informations de copyright

© 2020 International League Against Epilepsy.

Références

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Auteurs

Angelo Labate (A)

Institute of Neurology, University Magna Graecia, Catanzaro, Italy.
Neuroscience Research Center, University Magna Graecia, Catanzaro, Italy.

Maria Eugenia Caligiuri (ME)

Neuroscience Research Center, University Magna Graecia, Catanzaro, Italy.

Francesco Fortunato (F)

Institute of Neurology, University Magna Graecia, Catanzaro, Italy.

Edoardo Ferlazzo (E)

Institute of Neurology, University Magna Graecia, Catanzaro, Italy.
Regional Epilepsy Centre, Great Metropolitan Hospital of Reggio Calabria, Reggio Calabria, Italy.

Umberto Aguglia (U)

Institute of Neurology, University Magna Graecia, Catanzaro, Italy.
Regional Epilepsy Centre, Great Metropolitan Hospital of Reggio Calabria, Reggio Calabria, Italy.

Antonio Gambardella (A)

Institute of Neurology, University Magna Graecia, Catanzaro, Italy.
Neuroscience Research Center, University Magna Graecia, Catanzaro, Italy.

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