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*

OBJECTIVE: To study the effects of ketogenic diet (KD) on lipid metabolism in children with intractable epilepsy and the risk of atherosclerosis in children treated with KD assessed by changes in lipid profile. METHODS: The clinical data of 47 children with intractable epilepsy from 2013 to 2017 were collected. Blood lipid levels including triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL) and low-density lipoprotein (LDL), were detected before and 3 months after KD treatment. LDL/HDL ratio, arterial stiffness index (AI), atherogenic index of plasma (AIP) and lipid comprehensive index (LCI) were calculated to assess the risk of atherosclerosis. RESULTS: After 3 months of KD treatment, the TG and TC levels were slightly higher than those before treatment, and the HDL levels were slightly lower than those before treatment, but the differences were not statistically significant (P>0.05). The LDL levels of the children after 3 months of KD treatment were significantly higher than those before treatment (P<0.05). After 3 months of KD treatment, the LDL/HDL ratio and AI, AIP and LCI levels of the children were increased compared with those before treatment, but only the increase of the LDL/HDL ratio was statistically significant (P<0.05). CONCLUSIONS KD treatment may lead to increase in LDL level and LDL/HDL ratio, suggesting that KD treatment may increase the risk of atherosclerosis.
Child ; Diet, Ketogenic ; Drug Resistant Epilepsy ; Humans ; Lipid Metabolism ; Lipids ; Triglycerides

OBJECTIVETo study the clinicopathologic features of tuberous sclerosis complex (TSC).

METHODSThe clinicopathologic data of the patients diagnosed as TSC with refractory epilepsy and resection of epileptic focus were retrospectively analyzed.

RESULTSFourteen cases were included, the mean age was (15.8±12.9) years, with a male predominance (male to female ratio=10:4). Frontal lobe was the most common (13/14) site of involvement. MRI showed multiple patchy long T1 and long T2 signals. CT images showed multiple subependymal high density calcified nodules in nine cases. Histology showed mild to severe disruption of the cortical lamination, cortical and subcortical tubers with giant cells and/or dysmorphic neurons. The giant cells showed strong immunoreactivity for vimentin and nestin, while the dysmorphic neurons partially expressed MAP2 and NF. Vimentin also stained strongly the "reactive" astrocytes. Thirteen cases had follow-up information: Engel class I in six cases, Engel class II in six cases, and Engel class III in one case.

CONCLUSIONSDiagnosis of TSC relies on combined pathologic, clinical and neuroradiological features. Immunohistochemical staining can be helpful. Resection of epileptic focus is an effective method to treat refractory epilepsy in TSC.

Adolescent ; Astrocytes ; chemistry ; pathology ; Child ; Drug Resistant Epilepsy ; surgery ; Epilepsy ; complications ; metabolism ; pathology ; Epilepsy, Frontal Lobe ; complications ; metabolism ; pathology ; Female ; Giant Cells ; chemistry ; pathology ; Humans ; Magnetic Resonance Imaging ; Male ; Nestin ; analysis ; Neurons ; metabolism ; pathology ; Retrospective Studies ; Tuberous Sclerosis ; complications ; metabolism ; pathology ; Vimentin ; analysis