Status epilepticus and thinning of the entorhinal cortex

TL;DR

This study found that individuals with temporal lobe epilepsy and a history of status epilepticus exhibit significant atrophy in the entorhinal cortex, especially on the same side as the seizure focus, indicating its involvement in prolonged seizures.

Contribution

It provides the first large-cohort evidence linking entorhinal cortex atrophy specifically to history of status epilepticus in TLE patients.

Findings

Entorhinal cortex atrophy is greater in TLE patients with SE.

Atrophy is more pronounced ipsilaterally, especially in left TLE.

Other brain regions did not show SE-related atrophy.

Abstract

Status epilepticus (SE) carries risks of morbidity and mortality. Experimental studies have implicated the entorhinal cortex in prolonged seizures; however, studies in large human cohorts are limited. We hypothesised that individuals with temporal lobe epilepsy (TLE) and a history of SE would have more severe entorhinal atrophy compared to others with TLE and no history of SE. 357 individuals with drug resistant temporal lobe epilepsy (TLE) and 100 healthy controls were scanned on a 3T MRI. For all subjects the cortex was segmented, parcellated, and the thickness calculated from the T1-weighted anatomical scan. Subcortical volumes were derived similarly. Cohen's d and Wilcoxon rank-sum tests respectively were used to capture effect sizes and significance. Individuals with TLE and SE had reduced entorhinal thickness compared to those with TLE and no history of SE. The entorhinal cortex was more atrophic ipsilaterally (d=0.51, p<0.001) than contralaterally (d=0.37, p=0.01). Reductions in ipsilateral entorhinal thickness were present in both left TLE (n=22:176, d=0.78, p<0.001), and right TLE (n=19:140, d=0.31, p=0.04), albeit with a smaller effect size in right TLE. Several other regions exhibited atrophy in individuals with TLE, but these did not relate to a history of SE. These findings suggest potential involvement or susceptibility of the entorhinal cortex in prolonged seizures.