Subcortical alterations in tissue microstructure adjacent to focal cortical dysplasia: detection at diffusion-tensor MR imaging by using magnetoencephalographic dipole cluster localization.
ABSTRACT To determine whether changes at diffusion-tensor magnetic resonance (MR) imaging were present in children with intractable epilepsy and focal cortical dysplasia (FCD) in (a) subcortical white matter subjacent to MR imaging-visible areas of FCD, (b) subcortical white matter beyond the MR imaging-visible abnormality but subjacent to a magnetoencephalographic (MEG) dipole cluster, and (c) deep white matter tracts.
The study protocol had institutional research ethics board approval, and written informed consent was obtained. Fifteen children with FCD and intractable epilepsy (mean age, 11.6 years; range, 3.6-18.3 years) underwent diffusion-tensor MR imaging and MEG. Regions of interest were placed in (a) the subcortical white matter subjacent to the MR imaging-visible abnormality, as well as the contralateral side; (b) the subcortical white matter beyond the MR imaging-visible abnormality but subjacent to a MEG dipole cluster, as well as the contralateral side; and (c) deep white matter tracts projecting to or from the MR imaging-visible FCD, as well as the contralateral side. Fractional anisotropy (FA), mean diffusivity, and eigenvalues (lambda(1), lambda(2), lambda(3)) were evaluated.
Eleven of 15 children had MEG dipole clusters, and four children had MEG scatter. There were significant differences in FA, mean diffusivity, lambda(2), and lambda(3) of the subcortical white matter subjacent to the MR imaging-visible FCD (P < .001 for all), as well as that beyond the MR imaging-visible FCD but subjacent to a MEG dipole cluster (P = .001, P = .036, P < .001, and P = .002, respectively), compared with the contralateral side. There were also significant differences in FA (P < .001), mean diffusivity (P = .008), lambda(2) (P < .001), and lambda(3) (P = .001) of the deep white matter tracts projecting to or from the MR imaging-visible FCD compared with the contralateral side.
With use of MEG dipole clusters to localize the epileptogenic zone, diffusion-tensor imaging can help identify alterations in tissue microstructure beyond the MR imaging-visible FCD.
SourceAvailable from: Boris Bernhardt[Show abstract] [Hide abstract]
ABSTRACT: The advent of MRI has revolutionized the evaluation and management of drug-resistant epilepsy by allowing the detection of the lesion associated with the region that gives rise to seizures. Recent evidence indicates marked chronic alterations in the functional organization of lesional tissue and large-scale cortico-subcortical networks. In this review, we focus on recent methodological developments in functional MRI (fMRI) analysis techniques and their application to the two most common drug-resistant focal epilepsies, i.e., temporal lobe epilepsy related to mesial temporal sclerosis and extra-temporal lobe epilepsy related to focal cortical dysplasia. We put particular emphasis on methodological developments in the analysis of task-free or "resting-state" fMRI to probe the integrity of intrinsic networks on a regional, inter-regional, and connectome-wide level. In temporal lobe epilepsy, these techniques have revealed disrupted connectivity of the ipsilateral mesiotemporal lobe, together with contralateral compensatory reorganization and striking reconfigurations of large-scale networks. In cortical dysplasia, initial observations indicate functional alterations in lesional, peri-lesional, and remote neocortical regions. While future research is needed to critically evaluate the reliability, sensitivity, and specificity, fMRI mapping promises to lend distinct biomarkers for diagnosis, presurgical planning, and outcome prediction.Frontiers in Neuroscience 12/2014; 8. DOI:10.3389/fnins.2014.00411
[Show abstract] [Hide abstract]
ABSTRACT: Purpose Diffusion tensor imaging (DTI) is a magnetic resonance imaging (MRI) technique that can characterize white matter (WM) architecture and microstructure. DTI has demonstrated extensive WM changes in patients with several epileptic syndromes, but few studies have focused on patients with malformations of cortical development (MCD). Our aim was to investigate the quantitative diffusion properties of the corpus callosum (CC), a major commissural bundle critical in inter-hemispheric connectivity, in a large group of patients with MCD. Methods Thirty-two MCD patients and 32 age and sex-matched control subjects were evaluated with DTI at 3.0 T. We analyzed the three major subdivisions of the CC (genu, body, and splenium) with deterministic tractography to yield fractional anisotropy (FA), mean diffusivity (MD), parallel diffusivity (λ||) and perpendicular diffusivity (λ⊥). We further assessed the CC with region of interest (ROI)-based analyses and evaluated different subgroups of MCD (polymicrogyria/schizencephaly, heterotopia, and cortical dysplasia). Partial correlations between diffusion changes and clinical parameters (epilepsy duration and age at disease onset) were also queried. Results There were significant reductions of FA, accompanied by increases in MD and λ⊥ in all segments of the CC in the patients group with both analytical methods. The absolute differences in FA were greater on ROI-analyses. There were no significant differences between the MCD subgroups, and no correlations between clinical parameters of epilepsy and FA. Conclusions Our study indicates DTI abnormalities consistent with microstructural changes in the corpus callosum of MCD patients. The findings support the idea that patients with epilepsy secondary to cortical malformations present widespread WM changes that extend beyond the macroscopic MRI-visible lesions.Epilepsy Research 11/2014; 108(9):1533-1542. DOI:10.1016/j.eplepsyres.2014.08.023 · 2.19 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Once patients have a diagnosis of localization related epilepsy (LRE), it is critical to further classify those patients into lesional or nonlesional for treatment and prognostic reasons. An individual with LRE may be classified as nonlesional for two reasons: 1) a lesion may not exist; that is, the structural abnormality that gives rise to seizures may be at the channel level or be spatially distributed in such a way that it would not be accurately termed a lesion, or 2) a lesion exists but is so subtle that standard clinical imaging is not sensitive enough to discriminate between the lesion and surrounding healthy brain tissue. As with any technology and disease process, this definition is dynamic, as we know that future imaging techniques will be developed and new disease mechanisms will be discovered, making detection of the epileptogenic underlying abnormality an ever-changing target.Epilepsy Currents 05/2014; 14(3):121. DOI:10.5698/1535-7597-14.3.121 · 2.95 Impact Factor