PPubMed21 Jan 2021Cited 8×

Focal to bilateral tonic–clonic seizures are associated with widespread network abnormality in temporal lobe epilepsy SINHA et al.

Nishant Sinha, Natalie Peternell, Gabrielle M. Schroeder, Jane de Tisi, Sjoerd B. Vos, Gavin P. Winston, John S. Duncan, Yujiang Wang, Peter N. Taylor

Abstract

4## DISCUSSION We investigated whether widespread brain network abnormalities were present in patients with a history of FBTCS and drug-resistant TLE. By comparing controls and patients with and without FBTCS, we mapped alterations in brain networks at the resolution of individual connections, nodes, lobes, and the whole brain. In patients without a history of FBTCS, abnormalities were localized mainly in temporal and frontal areas. In contrast, abnormalities were widespread and bilateral in patients with FBTCS. Regions in the subcortical and parietal lobes showed a marked increase in node abn

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Patients with TLE and focal to bilateral tonic‑clonic seizures show far more widespread whole‑brain structural network abnormalities than those without such seizures.

What’s new

i.Demonstrated that whole‑brain structural network alterations differ between TLE patients with and without FBTCS.
ii.Introduced a patient‑specific node abnormality metric to quantify abnormality load.
iii.Showed that FBTCS+ patients have a markedly larger altered subnetwork (441 connections) versus FBTCS− patients (21 connections).
iv.Made the anonymized diffusion‑MRI brain networks of all participants publicly available.

How they did it

The study recruited 83 drug‑resistant unilateral TLE patients (60 FBTCS+ and 23 FBTCS−) and 29 matched healthy controls, acquiring diffusion‑weighted MRI to construct 90‑node whole‑brain structural networks weighted by fractional anisotropy and mean diffusivity. Network‑based statistics identified altered subnetworks, and a node abnormality metric quantified patient‑specific abnormality load by comparing each connection to control distributions.

What they found

FBTCS+ patients exhibited 441 altered connections (t > 3, p < .001) compared to 21 altered connections in FBTCS− patients (t > 3, p = .01).
Whole‑brain abnormality load was significantly higher in FBTCS+ patients (p < .001, d = .82, 95% CI = .32‑1.3).
Direct comparison between FBTCS+ and FBTCS− groups showed p = .03, d = .44 (95% CI = -.07‑.92).
Abnormal nodes in FBTCS+ patients were widespread, including subcortical and parietal regions, whereas FBTCS− abnormalities were confined to temporal and frontal lobes.

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