| Purpose:Patients with idiopathic generalized epilepsy (IGE) showed no abnormalities in routine MRI examinations. However, voxel-based morphometry studies had shown decreased gray matter volume of thalamus and frontal areas in IGE. Our purpose was to map in vivo the organization of the thalamo-cortical network in IGE in order to reveal the pathogenesis of IGE.Materials and Methods:Sixty-six patients with IGE characterized by generalized tonic-clonic seizures and sixty-six healthy controls were involved in this study. The three-dimensional high-resolution Tl structural MRI data and diffusion tensor imaging (DTI) data were acquired in 3T Siemens scanner. The T1 data was processed using Connectome Computation System. Every brain was segregated into into gray matter, white matter and cerebrospinal fluid. After that, cortex surface was rebuilt and cortex images of all subjectes were obtained by computer algorithm. The average cortical thickness and thalamic volume of every subject were calculated. Independent-samples t test was performed to compare the average cortical thicknesses and thalamic volumes between the study group and the control group. The cortical thickness differences between groups and the thalamo-cortical correlation of each group were analyzed by using Surfstat software. The cortex regions involved in the thalamo-cortical gray matter structural covariance network (SCN) were selected as seed regions for mapping the thalamo-cortical fiber network by using PANDA. If the fiber number (FN) between two regions is greater than 1, it was considered that the two regions were connected by white matter fibers. And fractional anisotropy (FA) of every fiber bundle was calculated. The differences of FN and FN of every fiber bundle between groups were analyzed by performing independent-samples t test.Results:The mean thalamic volume in IGE group (14793.68±1467.82mm3) was significantly lower than which in control group (15794.79±1500.38, P<0.001). There was no significant difference in average cortical thickness among the two groups (2.45±0.09mm vs.2.47±0.09, P=0.0226). Compared with healthy controls, IGE patients showed significant cortical thickness reductions in bilateral anterior cingulate, precentral gyrus, orbital frontal cortex, temporal pole, and right postcentral gyrus; while cortical thickness increasements were showed in bilateral posterior cingulate, precuneus, and middle occipital gyrus. In patients, thickness of bilateral middle temporal gyrus, fusiform gyms, hippocampus, and parahippocampal gyrus were positively correlated with the thalamic volumes; while bilateral anterior cingulate, middle frontal gyrus, and postcentral gyrus were negatively correlated with which. In controls, thickness of bilateral superior and inferior temporal gyrus, left postcentral gyrus, and right anterior cingulate and medial superior frontal gyrus were positively correlated with the thalamic volumes; while left cuneus and precuneus, right middle occipital gyrus and inferior parietal lobule, bilateral hippocampus and parahippocampal gyrus regions were negatively correlated with. In patients, thalamo-cortical correlation increased in bilateral left cuneus, precuneus, lingual gyrus, and inferior temporal gyrus, right hippocampus, parahippocampal gyrus, precentral gyrus, and postcentral gyrus compare to controls; while decreasements were show in bilateral medial and dorsolateral prefrontal cortex. Most regions correlated in gray matter showed corresponding fiber bundles. There were four fiber bundles showed FA decreasing, which connected from thalamus to bilateral hippocampus and parahippocampal gyrus, right insula, and left limbic lobe. The fiber bundle connecting thalamus and left limbic lobe showed FN decreased compared to controls.Conclusions:Patients with IGE showed thalamo-cortical network remodeling, including thalamus and prefrontal cortex atrophy, thickness of parietal and occipital cortex increased, and thalamo-cortical correlations decreasing in frontal cortex. White matter fiber network might be the anatomical basis of the remodeling of gray matter SCN. A small part of fiber bundles connecting the thalamus and cortex showed FA decreasing, which revealed that thalamo-cortical network remodeling exhibited a more complicated pathology.Purpose:Previous neuroimaging studies suggested that the thalamo-cortical circuit was involved in the initiation and propagation of IGE. The study aimed to demonstrate the impairments of the thalamo-cortical circuit and to investigate the effective connectivity changes between the thalamus and the whole brain in IGE as the duration of epilepsy goes on.Materials and Methods:A total of 101 patients with IGE characterized by generalized tonic clonic seizures and 101 healthy controls were recruited in the present study. The three-dimensional high-resolution T1 structural MRI data was scanned for the voxel-based morphometry analysis. After registration, segmentation, modulation and smoothing, we got the gray matter images of all subjects. A voxel-wise independent-samples t test was performed in order to compare gray matter volume differences between IGE patients and controls using SPM8. Following this, a voxel-based correlation analysis was carried out between gray matter volume and duration of epilepsy. According the result of independent-samples t test, impaired brain regions in IGE were selected as seed regions in order to calculat the granger causality mapping, between seed regions selected above and the whole brain gray matter, regarding the duration of epilepsy as time sequence.Results:Compared with healthy controls, patients with IGE showed significant gray matter volume reductions in right thalamus and insula, bilateral medial prefrontal cortex, orbital frontal cortex and cerebellar hemisphere; whereas there were no regions showing significantly increased gray matter volume. Voxel-based correlation analysis revealed that gray matter volumes in bilateral thalamus, hippocampus, parahippocampal gyrus, insula, paracentral lobule, and cerebellar hemisphere were significantly negatively correlated with duration of epilepsy in IGE patients. At the same threshold, there was no region with a positive correlation with duration of epilepsy. According to the result of independent-samples t test, bilateral thalamus was selected as seed region for granger causality analysis, which revealed that bilateral thalamus showed positive effect on bilateral anterior cingulate, orbital frontal cortex, precuneus, inferior parietal lobule, lingual gyrus, insula, inferior tempotal gyrus, caudate, and cerebellar hemisphere. And bilateral thalamus showed nagatively effect on regions of bilateral dorsolateral frontal lobe, parietal lobe, and temporal lobe, as well as the posterior lobe of right cerebellum.Conclusions:Patients with IGE showed thalamo-cortical circuit impaired, including thalamus and prefrontal cortex gray matter volume reduction; which may be involved in the conscious impairments of IGE patients. Along with the duration of epilepsy getting longer, the impairments of thalamo-cortical circuit getting more serious. The frontal cortex injured secondary to the thalamus, which reflected that thalamus may be the origin of brain imapairments. The specific brain structure damage and the related effective connection abnormality would help us to further understand the origin and development of IGE.Purpose:Structural MRI analysis with visual inspection usually shows a normal presentation in patients with IGE. The main therapy for IGE is pharmacotherapy. It is well-known that prolonged medication treatment can lead to hepatic and renal functional lesion. Antiepileptic drugs can also result in damage of consciousness, because of the inhibition on neuronal firing. The aim of this study is to explore the effects of valproate on the brain’s gray matter structures.Materials and Methods:19 patients with IGE characterized by generalized tonic clonic seizures who took valproate and another 19 patients unmedicated were involved in this study.19 healthy controls also included in this study. The three-dimensional high-resolution T1 structural MRI data was scanned for the voxel-based morphometry analysis. After registration, segmentation, modulation and smoothing, we got the gray matter images of all subjects. A voxel-wise variance analysis was performed in order to investigate gray matter volume differences among all group. Differences between each two groups are also analysed. For patients who took valproate, a voxel-based correlation analysis was carried out between gray matter volume and the medication duration of valproate. In order to exclude the influence of epilepsy duration to the result, we performed a correlation analysis second time with the duration of epilepsy being included as a covariate.Results:Compared with healthy controls, patients showed gray matter volume reductions in bilateral frontal lobe, while gray matter increasements showed in bilateral cerebellar hemisphere. Compared with patients took valproate, patients unmedicated showed significant gray matter reductions in bilateral dorsolateral frontal lobe, caudate and cerebellar hemisphere. When the gender, age, and whole brain volume were taken as a covariate, the volume of bilateral putamen and thalamus were positively associated with medication duration of valproate; and bilateral posterior lobe of cerebellum were positively associated with medication duration. Once the duration of epilepsy taken as a covariate as well, the volume of bilateral putamen, thalamus, and insula showed significantly positively correlated with duration of medication duration of valproate, while bilateral anterior lobe of cerebellum showed a negative correlation.Conclusions:Patients with IGE who took valproate showed gray matter volume increasements in bilateral dorsolateral frontal lobe, precuneus, caudate and cerebellar hemisphere. With the medication time increasing, the volumes of bilateral putamen and thalamus were on the rise. Putamen and thalamus were closely related to conscious system and motion control. They were also the target regions of valproate, which revealed that valproate might delay the reduction of gray matter by inhibiting neuronal firing firings and epilepsy seizures. |
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