Purpose The purpose of the present study was to identify abnormal areas of regional synchronization in patients with mesial temporal lobe epilepsy and hippocampus sclerosis (mTLE-HS) compared to healthy controls, by applying a relatively novel method, the Regional Homogeneity (ReHo) method to resting state fMRI(RS-fMRI) data. Methods Eyes closed RS-fMRI data were acquired from 10 mTLE-HS patients (4 right-side, 6 left-side) and 15 age and gender matched healthy subjects, and were analyzed by using ReHo. For group analysis, 4 right-side MTLE-HS patients’ functional images were flipped, so that a homogeneous left MTLE-HS group with 10 cases were made. Key Findings Compared to the healthy control group, patients showed significantly increased ReHo in ipsilateral parahippocampal gyrus, midbrain, insula, corpus callosum, bilateral sensorimotor cortex and fronto-parietal subcortical structures, while decreased ReHo was mainly observed in default model network (DMN) (including precuneous and posterior cingulate gyrus, bilateral inferior lateral parietal and mesial prefrontal cortex) and cerebellum in patients relative to the control group. Significance This study identified that ReHo pattern in mTLE-HS patients was altered compared to healthy controls. We consider decreased ReHo in DMN to be responsible for wide functional impairments in cognitive processes. We propose that the increased ReHo in specific regions may compose a network which might be responsible for seizure genesis and propagation.

Objective The purpose of this study was to investigate regional homogeneity (ReHo) in children with new-onset drug-naïve Benign Epilepsy with Centrotemporal Spikes (BECTS), chronic BECTS and healthy controls (HC) using the Regional Homogeneity (ReHo) method applied to resting state fMRI data. Methods Resting state fMRI data was collected from three groups of children aged 6 to13, including new onset drug naïve BECTS, chronic BECTS with medication, and HC; the data analyzed by ReHo method. Mandarin school exams scores were acquired and compared across groups. Results There were three main findings. Firstly, compared with HC, abnormally increased ReHo was observed in bilateral sensorimotor regions in new onset BECTS which normalized or even reversed in the chronic BECTS group. Secondly, enhanced ReHo was found in the left frontal language region in the two BECTS groups, with even higher ReHo value in the chronic group. Lastly, decreased ReHo was found in regions of the default mode network (DMN), bilateral occipital lobes and cerebellum in both the new onset and chronic BECTS groups, lower in chronic BECTS. Behavioral analyses of school scores showed the chronic BECTS group presented significantly lower scores compared to HC (p < .05). Significance The coherence of low frequency fluctuations is disrupted in sensorimotor, language and DMN-related regions in new-onset BECTS. Some of these effects seem to be selectively normalized in chronic BECTS, thus allowing us to explore possible chronicity and AED-induced effects on BECTS. Abnormal ReHo in left language and DMN regions could be responsible for impairments of cognitive function.

Objective Parkinson's disease (PD) episodic memory impairments are common; however, it is not known whether these impairments are due to hippocampal pathology. Hippocampal Lewy-bodies emerge by Braak stage 4, but are not uniformly distributed. For instance, hippocampal CA1 Lewy-body pathology has been specifically associated with pre-mortem episodic memory performance in demented patients. By contrast, the dentate gyrus (DG) is relatively free of Lewy-body pathology. In this study, we used ultra-high field 7-Tesla to measure hippocampal subfields in vivo and determine if these measures predict episodic memory impairment in PD during life. Methods We studied 29 participants with PD (age 65.5 ± 7.8 years; disease duration 4.5 ± 3.0 years) and 8 matched-healthy controls (age 67.9 ± 6.8 years), who completed comprehensive neuropsychological testing and MRI. With 7-Tesla MRI, we used validated segmentation techniques to estimate CA1 stratum pyramidale (CA1-SP) and stratum radiatum lacunosum moleculare (CA1-SRLM) thickness, dentate gyrus/CA3 (DG/CA3) area, and whole hippocampus area. We used linear regression, which included imaging and clinical measures (age, duration, education, gender, and CSF), to determine the best predictors of episodic memory impairment in PD. Results In our cohort, 62.1% of participants with PD had normal cognition, 27.6% had mild cognitive impairment, and 10.3% had dementia. Using 7-Tesla MRI, we found that smaller CA1-SP thickness was significantly associated with poorer immediate memory, delayed memory, and delayed cued memory; by contrast, whole hippocampus area, DG/CA3 area, and CA1-SRLM thickness did not significantly predict memory. Age-adjusted linear regression models revealed that CA1-SP predicted immediate memory (beta[standard error]10.895[4.215], p < .05), delayed memory (12.740[5.014], p < .05), and delayed cued memory (12.801[3.991], p < .05). In the fully-adjusted models, which included all five clinical measures as covariates, only CA1-SP remained a significant predictor of delayed cued memory (13.436[4.651], p < .05). Conclusions In PD, we found hippocampal CA1-SP subfield thickness estimated on 7-Tesla MRI scans was the best predictor of episodic memory impairment, even when controlling for confounding clinical measures. Our results imply that ultra-high field imaging could be a sensitive measure to identify changes in hippocampal subfields and thus probe the neuroanatomical underpinnings of episodic memory impairments in patients with PD.

ObjectiveSeveral neuroimaging studies have examined language reorganization in stroke patients with aphasia. However, few studies have examined language reorganization in stroke patients without aphasia. Here, we investigated functional connectivity (FC) changes after stroke in the language network using resting-state fMRI and performance on a verbal fluency (VF) task in patients without clinically documented language deficits.MethodsEarly-stage ischemic stroke patients (N = 26) (average 5 days from onset), 14 of whom were tested at a later stage (average 4.5 months from onset), 26 age-matched healthy control subjects (HCs), and 12 patients with cerebrovascular risk factors (patients at risk, PR) participated in this study. We examined FC of the language network with 23 seed regions based on a previous study. We evaluated patients' behavioral performance on a VF task and correlation between brain resting-state FC (rsFC) and behavior.ResultsCompared to HCs, early stroke patients showed significantly decreased rsFC in the language network but no difference with respect to PR. Early stroke patients showed significant differences in performance on the VF task compared to HCs but not PR. Late-stage patients compared to HCs and PR showed no differences in brain rsFC in the language network and significantly stronger connections compared to early-stage patients. Behavioral differences persisted in the late stage compared to HCs. Change in specific connection strengths correlated with changes in behavior from early to late stage.ConclusionsThese results show decreased rsFC in the language network and verbal fluency deficits in early stroke patients without clinically documented language deficits.

To identify clinically implementable biomarkers of cognitive impairment in Parkinson's Disease (PD) derived from resting state-functional MRI (rs-fMRI) and CSF protein analysis. Methods: In this single-center longitudinal cohort study, we analyzed rs-fMRI and CSF biomarkers from 50 PD patients (23 cognitively normal, 18 mild cognitive impairment, 9 dementia) and 19 controls, who completed comprehensive neuropsychological testing. A subgroup of participants returned for follow-up cognitive assessments three years later. From rs-fMRI, we studied the connectivity within two distinct Default Mode Network subsystems: left-to-right hippocampus (LHC-RHC) and medial prefrontal cortex-to-posterior cingulate cortex (mPFC-PCC). We used regression analyses to determine whether imaging (LHC-RHC, mPFC-PCC), clinical (CSF Aβ-42:40, disease duration), and demographic (age, sex, education) variables were associated with global and domain-specific cognitive impairments. Results: LHC-RHC (F 3,67 = 3.41,p=0.023) and CSF Aβ-42:40 (χ 2 (3) = 8.77,p = 0.033) were reduced across more cognitively impaired PD groups. Notably, LHC-RHC connectivity was significantly associated with all global and domain-specific cognitive impairments (attention/executive, episodic memory, visuospatial, and language) at the baseline visit. In an exploratory longitudinal analysis, mPFC-PCC was associated with future global and episodic memory impairment. Conclusion:We used biomarker techniques that are readily available in clinical and research facilities to shed light on the pathophysiologic basis of cognitive impairment in PD. Our findings suggest that there is a functionally distinct role of the hippocampal subsystem within the DMN resting state network, and that intrinsic connectivity between the hippocampi is critically related to a broad range of cognitive functions in PD.