Epilepsy affects over 50 million people worldwide. Drug-resistant epilepsy (DRE) accounts for up to a third of these cases, and neuro-inflammation is thought to play a role in such cases. Despite being a long-debated issue in the field of DRE, the mechanisms underlying neuroinflammation have yet to be fully elucidated. The pro-inflammatory microenvironment within the brain tissue of people with DRE has been probed using single-cell multimodal transcriptomics. Evidence suggests that inflammatory cells and pro-inflammatory cytokines in the nervous system can lead to extensive biochemical changes, such as connexin hemichannel excitability and disruption of neurotransmitter homeostasis. The presence of inflammation may give rise to neuronal network abnormalities that suppress endogenous antiepileptic systems. We focus on the role of neuroinflammation and brain network anomalies in DRE from multiple perspectives to identify critical points for clinical application. We hope to provide an insightful overview to advance the quest for better DRE treatments.
Humans ; Drug Resistant Epilepsy/metabolism* ; Neuroinflammatory Diseases/immunology* ; Animals ; Brain/pathology* ; Nerve Net/pathology*

Schizophrenia (SZ) stands as a severe psychiatric disorder. This study applied diffusion tensor imaging (DTI) data in conjunction with graph neural networks to distinguish SZ patients from normal controls (NCs) and showcases the superior performance of a graph neural network integrating combined fractional anisotropy and fiber number brain network features, achieving an accuracy of 73.79% in distinguishing SZ patients from NCs. Beyond mere discrimination, our study delved deeper into the advantages of utilizing white matter brain network features for identifying SZ patients through interpretable model analysis and gene expression analysis. These analyses uncovered intricate interrelationships between brain imaging markers and genetic biomarkers, providing novel insights into the neuropathological basis of SZ. In summary, our findings underscore the potential of graph neural networks applied to multimodal DTI data for enhancing SZ detection through an integrated analysis of neuroimaging and genetic features.
Humans ; Schizophrenia/pathology* ; Diffusion Tensor Imaging/methods* ; Male ; Female ; Adult ; Brain/metabolism* ; Young Adult ; Middle Aged ; White Matter/pathology* ; Gene Expression ; Nerve Net/diagnostic imaging* ; Graph Neural Networks

Adolescent ; Adult ; Brain ; abnormalities ; pathology ; physiopathology ; Child ; Female ; Humans ; Image Processing, Computer-Assisted ; Male ; Nerve Net ; pathology ; physiopathology ; Schizophrenia ; etiology ; physiopathology ; Schizophrenic Psychology

Dementia ; pathology ; Hallucinations ; pathology ; Humans ; Lewy Body Disease ; pathology ; Nerve Net ; pathology

Exploring the transition from inter-ictal to ictal epileptiform discharges (IDs) and how GABA receptor-mediated action affects the onset of IDs will enrich our understanding of epileptogenesis and epilepsy treatment. We used Mg-free artificial cerebrospinal fluid (ACSF) to induce epileptiform discharges in juvenile mouse hippocampal slices and used a micro-electrode array to record the discharges. After the slices were exposed to Mg-free ACSF for 10 min-20 min, synchronous recurrent seizure-like events were recorded across the slices, and each event evolved from inter-ictal epileptiform discharges (IIDs) to pre-ictal epileptiform discharges (PIDs), and then to IDs. During the transition from IIDs to PIDs, the duration of discharges increased and the inter-discharge interval decreased. After adding 3 μmol/L of the GABA receptor agonist muscimol, PIDs and IDs disappeared, and IIDs remained. Further, the application of 10 μmol/L muscimol abolished all the epileptiform discharges. When the GABA receptor antagonist bicuculline was applied at 10 μmol/L, IIDs and PIDs disappeared, and IDs remained at decreased intervals. These results indicated that there are dynamic changes in the hippocampal network preceding the onset of IDs, and GABA receptor activity suppresses the transition from IIDs to IDs in juvenile mouse hippocampus.
Animals ; Animals, Newborn ; Bicuculline ; pharmacology ; Disease Models, Animal ; Epilepsy ; pathology ; GABA-A Receptor Agonists ; pharmacology ; GABA-A Receptor Antagonists ; therapeutic use ; Hippocampus ; drug effects ; metabolism ; physiopathology ; In Vitro Techniques ; Magnesium ; metabolism ; pharmacology ; Male ; Membrane Potentials ; drug effects ; Mice ; Mice, Inbred C57BL ; Muscimol ; pharmacology ; Nerve Net ; drug effects ; Receptors, GABA-A ; metabolism

In 1905, Henry Head first suggested that transmission of pain-related protopathic information can be negatively modulated by inputs from afferents sensing innocuous touch and temperature. In 1965, Melzak and Wall proposed a more concrete gate control theory of pain that highlights the interaction between unmyelinated C fibers and myelinated A fibers in pain transmission. Here we review the current understanding of the spinal microcircuits transmitting and gating mechanical pain or itch. We also discuss how disruption of the gate control could cause pain or itch evoked by innocuous mechanical stimuli, a hallmark symptom for many chronic pain or itch patients.
Animals ; Humans ; Nerve Net ; pathology ; physiopathology ; Pain ; pathology ; Pruritus ; pathology ; Spinal Cord ; pathology ; Synaptic Transmission ; physiology

In this study, the automatic segmentation of the irregular lesion region in the image of fundus fluorescence angiography was actualized by means of the modified Back Propagation (BP) neural network method. Combining the transfer scaling coefficient between pixel of the image and the actual size, the area of the irregular lesion region was measured. The results may provide valuable data for the clinical diagnosis, treatment and prognostic evaluation.
Algorithms ; Fluorescein Angiography ; methods ; Nerve Net ; Retinal Diseases ; diagnosis ; pathology

Many functional magnetic resonance imaging (fMRI) studies have revealed the deactivation phenomenon of default mode network in the patients with epilepsy; however, nearly not any of the reports has focused on the dorsal attention network of epilepsy. In this paper, independent component analysis (ICA) was used to isolate the dorsal attention network of 16 patients with temporal lobe epilepsy (TLE) and of 20 healthy normals; and a goodness-of-fit analysis was applied at the individual subject level to choose the interesting component. Intra-group analysis and inter-group analysis were performed. The results indicated that the dorsal attention network included bilateral intraparietal sulcus, middle frontal gyrus, human frontal eye field, posterior lobe of right cerebellum, etc. The TLE group showed decreased functional connectivity in most of the dorsal attention regions with the predominance in the bilateral intraparietal sulcus, middle frontal gyrus, and posterior lobe of right cerebellum. These data suggested that the intrinsic organization of the brain function might be disrupted in TLE. In addition, the decrease of goodness-of-fit scores suggests that activity in the dorsal attention network may ultimately prove a sensitive biomarker for TLE.
Adolescent ; Adult ; Attention ; physiology ; Attention Deficit and Disruptive Behavior Disorders ; etiology ; physiopathology ; Brain Mapping ; Epilepsy, Temporal Lobe ; pathology ; physiopathology ; psychology ; Female ; Humans ; Image Interpretation, Computer-Assisted ; Image Processing, Computer-Assisted ; methods ; Magnetic Resonance Imaging ; methods ; Male ; Nerve Net ; physiopathology ; Principal Component Analysis ; methods ; Young Adult

AIMTo study the role of epileptic neural networks reestablished in contralateral caudate putamen (CPu)-hippocampus(HPC) by using chronic tetanization of the right corpus callosum (CTRCC).

METHODSExperiments were performed on 50 SD rats under anaesthesia. The left CPu (LCPu) and the left HPC(LHPC) electrographs were synchronously recorded after acute tetanization following CTRCC (60 Hz, 0.4-0.6 mA, 2 s).

RESULTS(1) In contralateralization to the side implanted interconvertible network inhibition between the CPu and the HPC were induced by combinedly using chronic and acute tetanization of the RCC. (2) Electrographic kindling in the LCPu or in the LHPC was recorded after CTRCC. (3) In case the LCPu or the LHPC electrographs were not kindled after CTRCC, hypsarrhythmia in the LCPu and reduced sharp waves in the HPC were induced b y repetitive tetanization of the RCC once again. Primary afterdischarges in the LCPu or in the LHPC electrographs were evoked by combinedly using chronic and acute tetanization of the RCC.

CONCLUSIONPathophysiological neural networks in the CPu and in the HPC might be reestablished in another side of hemispheres by chronic over-activation of the right CC, which is related to epileptogenesis. Abnormal interactions between the two functional neural networks might be involved in formation of secondary epileptic focus.

Animals ; Caudate Nucleus ; pathology ; physiopathology ; Corpus Callosum ; pathology ; physiopathology ; Disease Models, Animal ; Electric Stimulation ; Epilepsy ; pathology ; physiopathology ; Hippocampus ; pathology ; physiopathology ; Male ; Nerve Net ; Putamen ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley