Yayu Chen’s research while affiliated with Xiangya Hospital of Central South University and other places

Aims This study aimed to comprehensively explore the cerebellar structural and functional changes in temporal lobe epilepsy (TLE) and its association with clinical information. Methods The SUIT toolbox was utilized to perform cerebellar volume and diffusion analysis. In addition, we extracted the average diffusion values of cerebellar peduncle tracts to investigate microstructure alterations. Seed-based whole-brain analysis was used to investigate cerebellar–cerebral functional connectivity (FC). Subgroup analyses were performed to identify the cerebellar participation in TLE with/without hippocampal sclerosis (HS)/focal-to-bilateral tonic–clonic seizure (FBTCS) and TLE with different lateralization. Results TLE showed widespread gray matter atrophy in bilateral crusII, VIIb, VIIIb, left crusI, and left VIIIa. Both voxel and tract analysis observed diffusion abnormalities in cerebellar afferent peduncles. Reduced FC between the right crus II and the left parahippocampal cortex was found in TLE. Additionally, TLE showed increased FCs between left lobules VI–VIII and cortical nodes of the dorsal attention and visual networks. Across all patients, decreased FC was associated with poorer cognitive function, while increased FCs appeared to reflect compensatory effects. The cerebellar structural changes were mainly observed in HS and FBTCS subgroups and were regardless of seizure lateralization, while cerebellar–cerebral FC alterations were similar in all subgroups. Conclusion TLE exhibited microstructural changes in the cerebellum, mainly related to HS and FBTCS. In addition, altered cerebellar–cerebral functional connectivity is associated with common cognitive alterations in TLE.

Purpose Patients with temporal lobe epilepsy (TLE) are at high risk of cognitive impairment. In addition to persistent seizures and antiepileptic drugs (AEDs), genetic factors also play an important role in the progression of cognitive deficits in TLE patients. Defining a cognitive endophenotype for TLE can provide information on the risk of cognitive impairment in patients. This study investigated the cognitive endophenotype of TLE by comparing neuropsychological function between patients with TLE, their unaffected siblings, and healthy control subjects. Patients and Methods A total of 46 patients with TLE, 26 siblings, and 33 control subjects were recruited. Cognitive function (ie, general cognition, short- and long-term memory, attention, visuospatial and executive functions, and working memory) was assessed with a battery of neuropsychological tests. Differences between groups were evaluated by analysis of covariance, with age and years of education as covariates. The Kruskal–Wallis test was used to evaluate data that did not satisfy the homogeneity of variance assumption. Pairwise comparisons were adjusted by Bonferroni correction, with a significance threshold of P<0.05. Results Patients with TLE showed deficits in the information test (P<0.001), arithmetic test (P=0.003), digit symbol substitution test (P=0.001), block design test (BDT; P=0.005), and backward digit span test (P=0.001) and took a longer time to complete the Hayling test Part A (P=0.011) compared to controls. Left TLE patients tended to have worse executive function test scores than right TLE patients. The siblings of TLE patients showed deficits in the BDT (P=0.006, Bonferroni-corrected) relative to controls. Conclusion Patients with TLE exhibit cognitive impairment. Executive function is worse in patients with left TLE than in those with right TLE. Siblings show impaired visuospatial function relative to controls. Thus, cognitive deficits in TLE patients have a genetic component and are independent of seizures or AED use.

Objective To examine the shared familial contribution to hippocampal and extrahippocampal morphological abnormalities in patients with sporadic temporal lobe epilepsy (TLE) and their unaffected siblings. Methods We collected clinical, electrophysiological, and T1‐weighted magnetic resonance imaging (MRI) data of 18 sporadic patients with TLE without lesions other than hippocampal sclerosis (12 right, 6 left), their 18 unaffected full siblings, and 18 matched healthy volunteers. We compared between‐group differences in cortical thickness and volumes of five subcortical areas (hippocampus, amygdala, thalamus, putamen, and pallidum). We determined the subregional extent of hippocampal abnormalities using surface shape analysis. All our imaging results were corrected for multiple comparisons using random field theory. Results We detected smaller hippocampal volumes in patients (right TLE: median right hippocampus 1.92 mL, interquartile range [IQR] 1.39‐2.62, P < .001; left TLE: left hippocampus 2.05 mL, IQR 1.99‐2.33, P = .01) and their unaffected siblings (right hippocampus 2.65 mL, IQR 2.32‐2.80, P < .001; left hippocampus 2.39 mL, IQR 2.18‐2.53, P < .001) compared to healthy controls (right hippocampus 2.94 mL, IQR 2.77‐3.24; left hippocampus 2.71 mL, IQR 2.37‐2.89). Surface shape analysis showed that patients with TLE had bilateral subregional atrophy in both hippocampi (right > left). Similar but less‐pronounced subregional atrophy was detected in the right hippocampus of unaffected siblings. Patients with TLE had reduced cortical thickness in bilateral premotor/prefrontal cortices and the right precentral gyrus. Siblings did not show abnormalities in cortical or subcortical areas other than the hippocampus. Significance Our results demonstrate a shared vulnerability of the hippocampus in both patients with TLE and their unaffected siblings, pointing to a contribution of familial factors to hippocampal atrophy. This neuroimaging trait could represent an endophenotype of TLE, which might precede the onset of epilepsy in some individuals.

Purpose: To study the clinical characteristics of patients with game-induced seizures in the Chinese population. Method: We assessed 51 patients with various game-induced epileptic seizures. Based on whether they had spontaneous seizures, these 51 patients were classified as two groups. Twenty-seven patients who had both game-induced and spontaneous seizures were referred to as Group I, whereas twenty-four patients that had experienced seizures exclusively while playing specific games were assigned to Group II. All of the related clinical data of the patients was collected and evaluated. Results: The patients in Group I presented with adolescent-onset and related to photosensitive idiopathic generalized epilepsy (IGE), were responsive to valproic acid (VPA) or magnesium valproate (VPA-Mg) therapy, and presented a major seizure-precipitating factor in response to electronic games. While patients in Group II were adult onset and not associated with IGE, showed uncertain responses to VPA and a benign prognosis, and presented major seizure-precipitating factors in response to non-electronic games. Conclusion: There are obvious genetic differences between patients with game-induced epilepsy. It is necessary to differentiate between various types of game-induced seizures and select the corresponding treatment.

Purpose Clinically diagnosed partial epilepsy is hard to be functionally diagnosed by regular electroencephalograph (EEG) and conventional magnetic resonance imaging (MRI). By collecting transient brain regional signals, blood oxygenation level-dependent (BOLD) function MRI (BOLD-fMRI) can provide brain function change information with high accuracy. By using resting state BOLD-fMRI technique, we aim to investigate the changes of brain function in partial epilepsy patients. Methods BOLD-fMRI scanning was performed in 70 partial epilepsy and 70 healthy people. BOLD-fMRI data was analyzed by using the Regional Homogeneity (ReHo) method and functional connectivity of Default Mode Network (DMN) methods. The abnormal brain functional connectivity in partial epilepsy patients was detected by Statistical Parametric Mapping 8 (SPM8) analysis. Results Compared to healthy group, epilepsy patients showed significant decreased ReHo in left inferior parietal lobule/pre- and post-central gyrus, right thalamus/paracentral lobule/Cerebellum anterior and posterior Lobe, bilateral insula. The DMN functional connectivity regions decreased significantly in right uncus, left Inferior parietal lobule, left supramarginal gyrus, left uncus, left parahippocampa gyrus, and left superior temporal gyrus, in epilepsy patients, compared to healthy controls. Significance This study clarified that both ReHo and functional connectivity of DMN decreased in partial epilepsy patients compared to healthy controls. While left inferior parietal lobule was detected in both ReHo and DMN, many other identified regions were different by using these two BOLD-fMRI techniques. We propose that both ReHo and DMN patterns in BOLD-fMRI may suggest networks responsible for partial epilepsy genesis or progression.