Investigation of the cingulate cortex in idiopathic generalized epilepsy

Abstract

SUMMARYObjective: Studies using quantitative neuroimaging have shown subtle abnormalities in patients with idiopathic generalized epilepsy (IGE). These findings have several locations, but the midline parasagittal structures are most commonly implicated. The cingulate cortex is related and may be involved. The objective of the current investigation was to perform a comprehensive analysis of the cingulate cortex using multiple quantitative structural neuroimaging techniques. Methods: Thirty-two patients (18 women, 30 AE 10 years) and 36 controls (18 women, 32 AE 11 years) were imaged by 3 Tesla magnetic resonance imaging (MRI). A volumetric three-dimensional (3D) sequence was acquired and used for this investigation. Regions-of-interest were selected and voxel-based morphometry (VBM) analyses compared the cingulate cortex of the two groups using Statistical Parametric Mapping (SPM8) and VBM8 software. Cortical analyses of the cingulate gyrus was performed using Freesurfer. Images were submitted to automatic processing using built-in routines and recommendations. Structural parameters were extracted for individual analyses, and comparisons between groups were restricted to the cingulate gyrus. Finally, shape analyses was performed on the anterior rostral, anterior caudal, posterior, and isthmus cingulate using spherical harmonic description (SPHARM). Results: VBM analyses of cingulate gyrus showed areas of gray matter atrophy, mainly in the anterior cingulate gyrus (972 mm 3 ) and the isthmus (168 mm 3 ). Individual analyses of the cingulate cortex were similar between patients with IGE and controls. Surface-based comparisons revealed abnormalities located mainly in the posterior cingulate cortex (718.12 mm 2 ). Shape analyses demonstrated a predominance of anterior and posterior cingulate abnormalities. Significance: This study suggests that patients with IGE have structural abnormalities in the cingulate gyrus mainly localized at the anterior and posterior portions. This finding is subtle and variable among patients.

Analysis of fractional anisotropy and mean diffusivity in refractory and non-refractory idiopathic generalized epilepsies

“…Other advanced neuroimaging studies in IGEs have disclosed more widespread involvement of white matter tract and fiber involvement, not traditionally included in IGE networks [7]. Our findings did not disclose more pronounced white matter abnormalities in patients with a less favorable treatment response, while on an adequate antiepileptic drug regimen [8][9][10]. Treatment refractoriness in epilepsy is usually defined as absence of seizure control after two appropriate treatment regimens in appropriate doses [11].…”

Disruption of the ATP/adenosine balance in CD39−/− mice is associated with handling‐induced seizures

“…The absence of sclerosis and inflammation in CD39 −/− mice may be due to the acute and idiopathic nature of their seizures. In fact, neuronal damage correlates with frequency and duration of seizures; brief seizures result in necrosis and minimal apoptosis and patients with idiopathic epilepsy have subtle brain abnormalities . Future studies could investigate potentially microscopic differences in microglia–neuron interactions, astrocytic phyllopodia, vasculature or number of excitatory/inhibitory synapses.…”

Nicotinic receptor abnormalities as a biomarker in idiopathic generalized epilepsy

“…The mesiofrontal regions, including the ACC, are known to play a role in the spreading of epileptic discharges (Zhang, Liao et al 2011). A frontal cortical onset was also suggested in childhood absence epilepsy by a magnetoencephalographical and an fMRI study, respectively (Westmijse, Ossenblok et al 2009, Bai, Vestal et al 2010 (Braga, Fujisao et al 2015), or an increased gray matter volume in mesiofrontal cortical structures (Woermann, Free et al 1999, Alhusaini, Ronan et al 2013 including the ACC (Cao, Tang et al 2013, Braga, Fujisao et al 2015), associated to a bilateral reduction in thalamic volume (Alhusaini, Ronan et al 2013, Cao, Tang et al 2013.…”