Metabolic covariance networks combining graph theory measuring aberrant topological patterns in mesial temporal lobe epilepsy

Abstract

Summary Objective We aimed to study the networks’ mechanism of metabolic covariance networks in mesial temporal lobe epilepsy (mTLE), through examining the brain value of fluorine‐18‐fluorodeoxyglucose positron emission tomography (18F‐FDG‐PET). Methods 18F‐FDG‐PET images from 16 patients with mTLE were analyzed using local and global metabolic covariance network (MCN) approaches, including whole metabolic pattern analysis (WMPA), hippocampus‐based (h‐) MCN, whole brain (w‐) MCN, and edge‐based connectivity analysis (EBCA). Results WMPA showed a typical ipsilateral hypometabolism and contralateral hypermetabolism pattern to epileptic zones in mTLE. h‐MCN revealed decreased hippocampus‐based synchronization in contralateral regions. w‐MCN exhibited a disrupted metabolic network with globally increased small‐world properties and regionally decreased nodal metrics in the ipsilateral hemisphere. Hippocampus (h)‐EBCA and whole brain EBCA (w‐EBCA) both detected a reduced‐connectivity dominated metabolic covariant network. Moreover, the reduced interhemisphere connectivity seemingly played a major role in the aberrant epileptic topological pattern. Conclusion From a metabolic point of view, we demonstrated the damaging effects with reduced contralateral intranetwork metrics properties and the compensatory effects in contralateral intranetworks with increased network properties. However, the import role of significant reduced interhemisphere connection has rarely been reported in other mTLE studies. Taken together, 18F‐FDG‐PET MCN analysis provides new evidence that the mTLE is a system neurological disorder with disrupted networks.

Alterations in the metabolic networks of temporal lobe epilepsy patients: A graph theoretical analysis using FDG-PET

“…Multiple studies on the structural and functional connectivity in patients with focal epilepsy based on DTI, EEG, functional MRI, and MEG have been done. However, only a few studies on the metabolic connectivity based on FDG-PET in patients with drug-resistant TLE have been carried out ( Wang et al, 2019 , Vanicek et al, 2016 ). These previous studies have demonstrated a disrupted metabolic network in patients with TLE ( Wang et al, 2019 , Vanicek et al, 2016 ).…”

“…However, only a few studies on the metabolic connectivity based on FDG-PET in patients with drug-resistant TLE have been carried out ( Wang et al, 2019 , Vanicek et al, 2016 ). These previous studies have demonstrated a disrupted metabolic network in patients with TLE ( Wang et al, 2019 , Vanicek et al, 2016 ). However, no researches have investigated the differences of the metabolic network based on FDG-PET between TLE patients with and without HS.…”

In vivo Characterization of MRI-based T1w/T2w Ratios and Covariance Network in Temporal Lobe Epilepsy

“…Focke et al also found that the WM tract of arcuate fasciculus was more affected in LTLE [35]. Wang and colleagues reported aberrant topological patterns of metabolic covariance networks in TLE [36]. In addition, Campos et al indicated that LTLE had a more intricate bilateral bi-hemispheric dysfunction compared to RTLE using resting-state fMRI [9].…”

Rosiglitazone polarizes microglia and protects against pilocarpine‐induced status epilepticus

“…As early as 8 hours following seizure, activated microglia are found in the hippocampal cornu ammonis (CA)1 and CA3 regions, the reorganization of which can cause hyper‐excitability and seizure generation . Patients with hippocampal sclerosis and TLE exhibit high level of activated microglia in the hippocampi, and many of them do not respond well to antiepileptic medications …”

“…[8][9][10][11] Patients with hippocampal sclerosis and TLE exhibit high level of activated microglia in the hippocampi, and many of them do not respond well to antiepileptic medications. [12][13][14][15] Microglia are sedentary immunomodulatory cells in our central nervous system (CNS) that play critical roles in host defence and immune surveillance and harmonize innate and adaptive immune responses, which involve antigen presentation, phagocytosis, cell proliferation, cell migration, and cytokine production. 16,17 Under normal circumstances, microglial cells not only perform immune surveillance but also react to danger signals owing to distinct microglial phenotypes, including proinflammatory M1 and antiinflammatory M2 phenotypes.…”