Temporal Lobe Epilepsy Research Articles

Face and face pareidolia in patients with temporal lobe epilepsy indicates different neural processing: an event-related potential study

BackgroundVisual perception of face images or face pareidolia can be evaluated with event-related potentials (ERP) for healthy subjects and patients with neurological conditions. In this study, we aimed to analyse event-related potential components such as P100, N100, N170, and vertex-positive potential (VPP) in response to face pareidolia perception in temporal lobe epilepsy (TLE) patients.MethodsERPs were recorded during the pareidolia test. Waveforms were analzyed and current source density (CSD) maps were generated.ResultsCSD profiles were shown to be interpretable when face and face pareidolia conditions. N100, P100, and N170 components showed larger amplitudes and longer latency in epilepsy patients in response to face pareidolia stimuli compared to real face images. However, the N170 component latency did not differ significantly between epilepsy patients and healthy participants, while the larger amplitude and longer latency of N100 and P100 responses were evoked in healthy patients.ConclusionsOur results indicate a difference in the neural mechanisms of processing real face information and pareidolia face-like information in TLE patients.

A spike is a spike: On the universality of spike features in four epilepsy models.

Frequency properties of the EEG characteristics of different seizure types including absence seizures have been described for various rodent models of epilepsy. However, little attention has been paid to the frequency properties of individual spike-wave complexes (SWCs), the constituting elements characterizing the different generalized seizure types. Knowledge of their properties is not only important for understanding the mechanisms underlying seizure generation but also for the identification of epileptiform activity in various seizure types. Here, we compared the frequency properties of SWCs in different epilepsy models. A software package was designed and used for the extraction and frequency analysis of SWCs from long-term EEG of four spontaneously seizing, chronic epilepsy models: a post-status epilepticus model of temporal lobe epilepsy, a lateral fluid percussion injury model of post-traumatic epilepsy, and two genetic models of absence epilepsy-GAERS and rats of the WAG/Rij strain. The SWCs within the generalized seizures were separated into fast (three-phasic spike) and slow (mostly containing the wave) components. Eight animals from each model were used (32 recordings, 104 510 SWCs in total). A limitation of our study is that the recordings were hardware-filtered (high-pass), which could affect the frequency composition of the EEG. We found that the three-phasic spike component was similar in all animal models both in time and frequency domains, their amplitude spectra showed a single expressed peak at 18-20 Hz. The slow component showed a much larger variability across the rat models. Despite differences in the morphology of the epileptiform activity in different models, the frequency composition of the spike component of single SWCs is identical and does not depend on the particular epilepsy model. This fact may be used for the development of universal algorithms for seizure detection applicable to different rat models of epilepsy. There is a large variety between people with epilepsy regarding the clinical manifestations and the electroencephalographic (EEG) phenomena accompanying the epileptic seizures. Here, we show that one of the EEG signs of epilepsy, an epileptic spike, is universal, since it has the same shape and frequency characteristics in different animal models of generalized epilepsies, despite differences in recording sites and location.

Overcoming Diagnostic Uncertainty: A Case of Temporal Lobe Epilepsy With Normal MRI and EEG

Overcoming Diagnostic Uncertainty: A Case of Temporal Lobe Epilepsy With Normal MRI and EEG

Association of Normative and Non-Normative Brain Networks With Cognitive Function in Patients With Temporal Lobe Epilepsy.

Despite their temporal lobe pathology, a significant subgroup of patients with temporal lobe epilepsy (TLE) is able to maintain normative cognitive functioning. In this study, we identify patients with TLE with intact vs impaired neurocognitive profiles and interrogate for the presence of both normative and highly individual intrinsic connectivity networks (ICNs)-all toward understanding the transition from impaired to intact neurocognitive status. This retrospective cross-sectional study included patients with TLE and matched healthy controls (HCs) from the Thomas Jefferson Comprehensive Epilepsy Center. Functional MRI data were decomposed using independent component analysis to obtain individualized ICNs. In this article, we calculated the degree of match between individualized ICNs and canonical ICNs (e.g., 17 resting-state networks by Yeo et al.) and divided each participant's ICNs into normative or non-normative status based on the degree of match. 100 patients with TLE (mean age 42.0 [SD: 13.7] years, 47 women) and 92 HCs were included in this study. We found that the individualized networks matched to the canonical networks less well in the cognitively impaired (n = 24) compared with the cognitively intact (n = 63) patients with TLE by 2-way mixed-measures analysis of variance (impaired vs intact mean difference [MD] -0.165 [-0.317, -0.013], p = 0.028). The cognitively impaired patients showed significant abnormalities in the profiles of both normative (impaired vs intact MD -0.537 [-0.998, -0.076], p = 0.017, intact vs HC MD -0.221 [-0.536, 0.924], p = 0.220, and impaired vs HC MD -0.759 [-1.200, -0.319], p < 0.001) and non-normative networks (impaired vs intact MD 0.484 [0.030, 0.937], p = 0.033, intact vs HC MD 0.369 [0.059, 0.678], p = 0.014, and impaired vs HC MD 0.853 [0.419, 1.286], p < 0.001) while the intact patients showed abnormalities only in non-normative networks. At the same time, we found that normative networks held a strong, positive association with the neuropsychological measures, with this association negative in non-normative networks. Our data demonstrated that significant cognitive deficits are associated with the status of both canonical and highly individual ICNs, making clear that the transition from intact to impaired cognitive status is not simply the result of disruption to normative brain networks.

Microangiopathy in temporal lobe epilepsy with diffusion MRI alterations and cognitive decline

White matter microvascular alterations in temporal lobe epilepsy (TLE) may be relevant to acquired neurodegenerative processes and cognitive impairments associated with this condition. We quantified microvascular changes, myelin, axonal, glial and extracellular-matrix labelling in the gyral core and deep temporal lobe white matter regions in surgical resections from 44 TLE patients with or without hippocampal sclerosis. We compared this pathology data with in vivo pre-operative MRI diffusion measurements in co-registered regions and neuropsychological measures of cognitive impairment and decline. In resections, increased arteriolosclerosis was observed in TLE compared to non-epilepsy controls (greater sclerotic index, p < 0.001), independent of age. Microvascular changes included increased vascular densities in some regions but uniformly reduced mean vascular size (quantified with collagen-4, p < 0.05–0.0001), and increased pericyte coverage of small vessels and capillaries particularly in deep white matter (quantified with platelet-derived growth factor receptorβ and smooth muscle actin, p < 0.01) which was more marked the longer the duration of epilepsy (p < 0.05). We noted increased glial numbers (Olig2, Iba1) but reduced myelin (MAG, PLP) in TLE compared to controls, particularly prominent in deep white matter. Gene expression analysis showed a greater reduction of myelination genes in HS than non-HS cases and with age and correlation with diffusion MRI alterations. Glial densities and vascular size were increased with increased MRI diffusivity and vascular density with white matter abnormality quantified using fixel-based analysis. Increased perivascular space was associated with reduced fractional anisotropy as well as age-accelerated cognitive decline prior to surgery (p < 0.05). In summary, likely acquired microangiopathic changes in TLE, including vascular sclerosis, increased pericyte coverage and reduced small vessel size, may indicate a functional alteration in contractility of small vessels and haemodynamics that could impact on tissue perfusion. These morphological features correlate with white matter diffusion MRI alterations and might explain cognitive decline in TLE.

Association Between Postsurgical Functional Connectivity and Seizure Outcome in Patients With Temporal Lobe Epilepsy.

Despite the success of presurgical network connectivity studies in predicting short-term (1-year) seizure outcomes, later seizure recurrence occurs in some patients with temporal lobe epilepsy (TLE). To uncover contributors to this recurrence, we investigated the relationship between functional connectivity and seizure outcomes at different time points after surgery in these patients. Patients included were clinically diagnosed with unilateral mesial TLE after a standard clinical evaluation and underwent selective amygdalohippocampectomy. Healthy controls had no history of seizures or head injury. Using resting-state fMRI, we assessed the postsurgical functional connectivity node strength, computed as the node's total strength to all other nodes, between seizure-free (Engel Ia-Ib) and nonseizure-free (Engel Ic-IV) acquisitions. The change over time after surgery in different outcome groups in these nodes was also characterized. Patients with TLE (n = 32, mean age: 43.1 ± 11.9 years; 46.8% female) and 85 healthy controls (mean age: 37.7 ± 13.5 years; 48.2% female) were included. Resting fMRI was acquired before surgery and at least once after surgery in each patient (range 1-4 scans, 5-60 months). Differences between patients with (n = 30) and without (n = 18) seizure freedom were detected in the posterior insula ipsilateral to the resection (I-PIns: 95% CI -154.8 to -50.1, p = 2.8 × 10-4) and the bilateral central operculum (I-CO: 95% CI -163.2 to -65.1, p = 2.6 × 10-5, C-CO: 95% CI -172.7 to -55.8, p = 2.8 × 10-4). In these nodes, only those who were seizure-free had increased node strength after surgery that increased linearly over time (I-CO: 95% CI 1.0-5.2, p = 4.2 × 10-3, C-CO: 95% CI 1.0-5.2, p = 5.5 × 10-3, I-PIns: 95% CI 1.6-5.5, p = 0.9 × 10-3). Different outcome groups were not distinguished by node strength before surgery. The findings suggest that network evolution in the first 5 years after selective amygdalohippocampectomy surgery is related to seizure outcomes in TLE. This highlights the need to identify presurgical and surgical conditions that lead to disparate postsurgical trajectories between seizure-free and nonseizure-free patients to identify potential contributors to long-term seizure outcomes. However, the lack of including other surgical approaches may affect the generalizability of the results.

Exploration of epileptic networks in temporal lobe encephaloceles with stereotactic EEG: Electroclinical characteristics and surgical outcomes.

Temporal lobe encephaloceles (TLEN) have been implicated as a cause of temporal lobe epilepsy (TLE), the treatment which is primarily surgical; however, there is no clear consensus on the optimal surgical approach, because it is unclear whether TLE related to TLEN can be addressed by a restricted encephalocele resection or if a more extensive resection is required. The aim of the current article is to report the clinical and electrophysiological profile of patients with TLE secondary to TLEN who underwent stereotactic electroencephalography (SEEG) implantation to identify the epileptogenic network. A retrospective review was performed of patients with TLE related to TLEN who underwent SEEG implantation. Medical charts were reviewed for demographic data, the results of noninvasive and invasive investigations, and operative details. Surgical outcomes were based on Engel classification with at least 6 months follow-up. Nine patients were identified. The mean age at epilepsy onset was 28 years (range, 15-41 years), and 7/9 patients were female. Scalp EEG revealed interictal epileptiform activity most often maximum in the frontotemporal and/or temporal regions. A discrete TLEN was often not identified on initial imaging, but was identified during re-review or at the time of surgery. Seizure onset zones during SEEG were localized to the mesial temporal structures, the temporal pole, or both. One patient became seizure-free following SEEG and another refused further surgery. Of the 7 patients who underwent epilepsy surgery, 5/7 underwent an anterior temporal lobectomy-surgical outcomes were favorable, with 5/7 achieving Engel I outcomes. Invasive SEEG monitoring demonstrated ictal onsets may not be restricted to the TLEN, and often the temporal pole and mesial structures are involved at seizure onset. Ictal propagation patterns vary significantly, which may be related to the underlying pathology and explain the variability in semiology. These findings may inform surgical treatment options. Temporal lobe encephaloceles can cause intractable epilepsy, although their presence may be missed on routine imaging. The management of encephaloceles is primarily surgical; however, the optimal surgical approach can be unclear. Invasive monitoring with SEEG may help characterize the epileptogenic network and result in more optimal surgical outcomes.

Retraction: Modulation of miR-146a/complement factor H-mediated inflammatory responses in a rat model of temporal lobe epilepsy.

Retraction: Modulation of miR-146a/complement factor H-mediated inflammatory responses in a rat model of temporal lobe epilepsy.

Clinical case of an atypical variant of Labbe's vein structure in a patient with pharmacoresistant temporal epilepsy

Among the commonly recognised structural lesions that cause drug-resistant temporal lobe epilepsy, such as mesial temporal sclerosis, focal cortical dysplasia, benign intracerebral tumors, arteriovenous malformations and cavernous angiomas, researchers have recently noted other pathologies, such as, encephalocele. There are a number of publications on the connection between epilepsy and cerebral venous angiomas. However, there are no published cases of the influence of the abnormal structure and location of normal cerebral vessels on the development of epilepsy. This article presents a case of an atypically large and unusually located vein of Labbe that may have been involved in epileptogenesis and also complicated an anteromedial temporal lobectomy. Forced coagulation and excision of the Labbe vein during surgery did not lead to venous infarction and neurological deficit.

Contribution of the Activated mTOR-STAT3 Pathway to the Pathogenesis of Focal Cortical Dysplasia Type IIIa in Pediatric Patients through Astrocyte Proliferation Mediation.

The aim of this study was to detect the association between the mTOR-STAT3 pathway and focal cortical dysplasia type IIIa (FCD IIIa) in children. A retrospective review was conducted based on 26 pediatric patients diagnosed with FCD IIIa who underwent surgical intervention. These patients were selected from a cohort of 157 individuals presenting with temporal lobe epilepsy. For comparative analysis, a control group consisting of 5 children who underwent intracranial decompression was established. Immunohistochemistry, immunofluorescence, and western blot techniques were used to assess the expression levels of mTOR, P-mTOR, P-70s6k, STAT3, P-STAT3, and GFAP in brain tissue specimens obtained from the two groups. The mTOR-STAT3 pathway exhibited activation in the FCD IIIa group (all P < 0.01). Additionally, immunofluorescence analysis revealed that cells positive for PSTAT3 were identified as astrocytes. Moreover, within the FCD IIIa group, there was a marked elevation in the expression of the mTOR-STAT3 pathway in the hippocampus compared to the brain cortex tissue. The mTOR-STAT3 pathway was demonstrated to be substantially associated with FCD IIIa in pediatric patients. The activation of the mTOR-STAT3 signaling pathway may contribute to the pathogenesis of FCD IIIa in pediatric patients by modulating the proliferation of astrocytes.

Temporal Lobe Epilepsy with Bitemporal Interictal Epileptiform Discharges: Effects of Sleep and Wakefulness

Introduction. Independent bitemporal interictal discharges are often found in patients with temporal lobe epilepsy. The likelihood of registering epileptiform activity (EA) is higher during sleep. Assessment of bitemporal interictal epileptiform discharges (BIEDs) with various discharge predominance ratio is used for presurgical evaluation of epilepsy patients and prediction of surgical outcomes. Our objective was to determine the predominant side (PS) in patients with bitemporal epilepsy using the incidence of epileptiform discharges for each sleep stage. Materials and methods. We analyzed 45 recordings of 10–24 h long-term video-EEG monitoring (LTM) in patients with bitemporal EA. For each recording, the total incidence of EA (IEA) and EA incidence for wakefulness and for each sleep stage were calculated individually. We also assessed the discharge predominance index (DPI) as a ratio of IEA in the predominant and contralateral sides for the entire recording and for each sleep stage. Results. We observed an IEA increase with sleep deepening, with maximum values observed during N2 and N3 sleep stages. The minimum IEA values were recorded during REM sleep; nevertheless, most of the REM sleep discharges were detected on the PS. DPI values were the highest and the most stable during N2 and N3 stages. Conclusion. The findings of our study demonstrate an increase in DPI values with non-rapid eye movement (NREM) sleep deepening in patients with bitemporal localization of EA. Despite the protective effects of REM sleep (i.e., reducing the likelihood of EA), it may be pivotal in lateralization of EA in patients with BIEDs. The PS is generally determined by a higher DPI during N2 and N3 stages.

Temporal Lobe Surgery in Pediatric Patients: From Temporal Lobe Epilepsy to Temporal Plus Epilepsy

Purpose: Temporal lobe resection can be categorized as either temporal lobe epilepsy (TLE), which involves cortical resection confined to the temporal lobe, or temporal plus epilepsy (TPE), which entails temporal resection along with involvement of additional extratemporal regions. We compared these forms within a pediatric population.Methods: We identified 136 patients who underwent temporal resection over a 17-year period and investigated the differences in the clinical profiles and seizure outcomes between TLE and TPE.Results: Of the total sample, 110 patients (80.9%) presented with TLE and 26 (19.1%) with TPE. Significant differences were observed between the groups in age at seizure onset (TLE: 6.3 years, TPE: 0.9 years; P=0.001), age at epilepsy surgery (TLE: 14.2 years, TPE: 9.2 years; P=0.002), the proportion of patients with a history of infantile epileptic spasm syndrome (IESS) (TLE: 6 [5.5%], TPE: 8 [30.3%]; P&lt;0.001), electroclinical presentation with IESS or Lennox-Gastaut syndrome (LGS) (TLE: 11 [10.0%], TPE: 13 [50.0%]; P&lt;0.001), the presence of focal temporal hypometabolism on positron emission tomography (TLE: 74 [68.5%], TPE: 11 [44.0%], P=0.021), and the use of intracranial electroencephalogram monitoring (TLE: 58 [52.7%], TPE: 21 [80.8%]; P=0.009). Furthermore, multivariate analysis identified the epileptic presentation of IESS or LGS as a significant predictor of TPE (P=0.049). The rates of seizure outcomes of International League Against Epilepsy class 1–3 at 1 year of follow-up were 83.8% for the entire cohort, 89.1% for TLE, and 61.5% for TPE (P=0.002).Conclusion: TPE appears to represent a substantial subset of pediatric temporal resections. The variation in seizure outcomes between groups underscores the importance of predicting TPE in advance, with implications for effective treatment planning.

Exercise, memory, and the hippocampus: Uncovering modifiable lifestyle reserve factors in refractory epilepsy

Physical exercise is an emerging target for improving cognition in aging and neurological disease. Due to the beneficial impact of exercise on hippocampal health and the vulnerability of the hippocampus in medication-resistant temporal lobe epilepsy (TLE), exercise could present a promising intervention in TLE. We investigated whether exercise engagement is associated with verbal memory function and hippocampal integrity in 29 young to middle-aged adults with refractory TLE and 21 demographically matched controls. Participants completed a self-reported questionnaire of weekly exercise, three tests of verbal memory, and a subset (n = 44) underwent structural MRI. Individuals with TLE self-reported lower exercise scores than controls across all levels of exercise intensity (p < 0.001). In TLE, greater exercise engagement was associated with better verbal memory (word-list recall and associative learning; rho = 0.46–0.47; ps FDR < 0.05), and with larger contralateral hippocampal volumes (rho = 0.61; p < 0.01). These effects remained significant when controlling for several clinical and demographic factors. These findings suggest that exercise may be a cognitive reserve factor in TLE, potentially mitigating memory decline by enhancing contralateral hippocampal integrity. With future replication and longitudinal investigation, exercise holds promise as a low-cost and accessible modifiable lifestyle target for improving cognitive health in individuals with refractory TLE

Sex-Dependent Changes in Gonadotropin-Releasing Hormone Neuron Voltage-Gated Potassium Currents in a Mouse Model of Temporal Lobe Epilepsy.

Temporal lobe epilepsy (TLE) is the most common focal epilepsy in adults, and people with TLE exhibit higher rates of reproductive endocrine dysfunction. Hypothalamic gonadotropin-releasing hormone (GnRH) neurons regulate reproductive function in mammals by regulating gonadotropin secretion from the anterior pituitary. Previous research demonstrated GnRH neuron hyperexcitability in both sexes in the intrahippocampal kainic acid (IHKA) mouse model of TLE. Fast-inactivating A-type (I A) and delayed rectifier K-type (I K) K+ currents play critical roles in modulating neuronal excitability, including in GnRH neurons. Here, we tested the hypothesis that GnRH neuron hyperexcitability is associated with reduced I A and I K conductances. At 2 months after IHKA or control saline injection, when IHKA mice exhibit chronic epilepsy, we recorded GnRH neuron excitability, I A, and I K using whole-cell patch-clamp electrophysiology. GnRH neurons from both IHKA male and diestrus female GnRH-GFP mice exhibited hyperexcitability compared with controls. In IHKA males, although maximum I A current density was increased, I K recovery from inactivation was significantly slower, consistent with a hyperexcitability phenotype. In IHKA females, however, both I A and I K were unchanged. Sex differences were not observed in I A or I K properties in controls, but IHKA mice exhibited sex effects in I A properties. These results indicate that although the emergent phenotype of increased GnRH neuron excitability is similar in IHKA males and diestrus females, the underlying mechanisms are distinct. This study thus highlights sex-specific changes in voltage-gated K+ currents in GnRH neurons in a mouse model of TLE and suggesting potential sex differences in GnRH neuron ion channel properties.

Evaluating the Efficacy of CortexID Quantitative Analysis in Localization of the Epileptogenic Zone in Patients with Temporal Lobe Epilepsy.

There remains a critical need for precise localization of the epileptogenic foci in individuals with drug-resistant epilepsy (DRE). 18F-Fluorodeoxyglucose positron emission tomography (FDG-PET) imaging can reveal hypometabolic regions during the interval between seizures in patients with epilepsy. However, visual-based qualitative analysis is time-consuming and strongly influenced by physician experience. CortexID Suite is a quantitative analysis software that helps to evaluate PET imaging of the human brain. Therefore, we aimed to evaluate the efficacy of CortexID quantitative analysis in the localization of the epileptogenic zone in patients with temporal lobe epilepsy (TLE). A total of 102 patients with epilepsy who underwent 18F-FDG-PET examinations were included in this retrospective study. The PET visual analysis was interpreted by two nuclear medicine physicians, and the quantitative analysis was performed automatically using CortexID analysis software. The assumed epileptogenic zone was evaluated comprehensively by two skilled neurologists in the preoperative assessment of epilepsy. The accuracy of epileptogenic zone localization in PET visual analysis was compared with that in CortexID quantitative analysis. The diagnostic threshold for the difference in the metabolic Z-score between the right and left sides of medial temporal lobe epilepsy (MTLE) was calculated as 0.87, and that for lateral temporal lobe epilepsy (LTLE) was 2.175. In patients with MTLE, the area under the curve (AUC) was 0.922 for PET visual analysis, 0.853 for CortexID quantitative analysis, and 0.971 for the combined diagnosis. In patients with LTLE, the AUC was 0.842 for PET visual analysis, 0.831 for CortexID quantitative analysis, and 0.897 for the combined diagnosis. These results indicate that the diagnostic efficacy of CortexID quantitative analysis is not inferior to PET visual analysis (p > 0.05), while combined analysis significantly increases diagnostic efficacy (p < 0.05). Among the 23 patients who underwent surgery, the sensitivity and specificity of PET visual analysis for localization were 95.4% and 66.7%, and the sensitivity and specificity of CortexID quantitative analysis were 100% and 50%. The diagnostic efficacy of CortexID quantitative analysis is comparable to PET visual analysis in the localization of the epileptogenic zone in patients with TLE. CortexID quantitative analysis combined with visual analysis can further improve the accuracy of epileptogenic zone localization.

Tropisetron, an Antiemetic Drug, Exerts an Anti-Epileptic Effect Through the Activation of α7nAChRs in a Rat Model of Temporal Lobe Epilepsy.

Temporal lobe epilepsy (TLE), a prevalent chronic neurological disorder, affects millions of individuals and is often resistant to anti-epileptic drugs. Increasing evidence has shown that acetylcholine (ACh) and cholinergic neurotransmission play a role in the pathophysiology of epilepsy. Tropisetron, an antiemetic drug used for chemotherapy in clinic, has displayed potential in the treatment of Alzheimer's disease, depression, and schizophrenia in animal models. However, as a partial agonist of α7 nicotinic acetylcholine receptors (α7nAChRs), whether tropisetron possesses the therapeutic potential for TLE has not yet been determined. In this study, tropisetron was intraperitoneally injected into pilocarpine-induced epileptic rats for 3 weeks. Alpha-bungarotoxin (α-bgt), a specific α7nAChR antagonist, was applied to investigate the mechanism of tropisetron. Rats were assessed for spontaneous recurrent seizures (SRS) and cognitive function using video surveillance and Morris's water maze testing. Hippocampal impairment and synaptic structure were evaluated by Nissl staining, immunohistochemistry, and Golgi staining. Additionally, the levels of glutamate, γ-aminobutyric acid (GABA), ACh, α7nAChRs, neuroinflammatory cytokines, glucocorticoids and their receptors, as well as synapse-associated protein (F-actin, cofilin-1) were quantified. The results showed that tropisetron significantly reduced SRS, improved cognitive function, alleviated hippocampal sclerosis, and concurrently suppressed synaptic remodeling and the m6A modification of cofilin-1 in TLE rats. Furthermore, tropisetron lowered glutamate levels without affecting GABA levels, reduced neuroinflammation, and increased ACh levels and α7nAChR expression in the hippocampi of TLE rats. The effects of tropisetron treatment were counteracted by α-bgt. In summary, these findings indicate that tropisetron exhibits an anti-epileptic effect and provides neuroprotection in TLE rats through the activation of α7nAChRs. The potential mechanism may involve the reduction of glutamate levels, enhancement of cholinergic transmission, and suppression of synaptic remodeling. Consequently, the present study not only highlights the potential of tropisetron as an anti-epileptic drug but also identifies α7nAChRs as a promising therapeutic target for the treatment of TLE.

Machine learning localization to identify the epileptogenic side in mesial temporal lobe epilepsy

BackgroundMesial temporal sclerosis (MTS) is the most common pathology associated with drug-resistant mesial temporal lobe epilepsy (mTLE) in adults.Most atrophic hippocampi can be identified using MRI based on standard epilepsy protocols; however, difficulties can arise in cases where sclerotic changes in the hippocampus are subtle or non-epilepsy-specific protocols have been implemented. In such cases, quantitative methods, such as T1-weighted axial series MRIs, are valuable additional tools to complement epilepsy-specific protocols. In the current study, we applied machine learning (ML) techniques to the analysis of brain regions of interest (ROIs), including the hippocampus, thalamus, and cortical areas, to enhance the accuracy of lesion lateralization in MRI. MethodsThis study included 104 patients diagnosed with mTLE, including 55 with lesions on the right side and 49 with lesions on the left side. FreeSurfer software was used to extract features from high-resolution T1-weighted axial brain MRI scans for use in computing lateralization indices (LI) for various brain regions. After using feature selection to pinpoint critical ROIs, the corresponding LI values were used as parameters in training the ML model. ResultsThe proposed ML model demonstrated exceptional performance in the lateralization of mTLE, achieving test accuracy of 92.38 % with an AUROC of 0.97. ConclusionThis study demonstrated the efficacy of ML in detecting instances of MTS from thin-slice T1 images. The proposed method provides valuable insights for surgical planning and treatment. Nonetheless, additional research will be required to enhance the robustness of the model and rigorously validate its effectiveness and applicability in clinical settings.

ID: 332409 Shape Analysis and Tractography of the Visual Pathway in Temporal Lobe Epilepsy

ID: 332409 Shape Analysis and Tractography of the Visual Pathway in Temporal Lobe Epilepsy

Hippocampal dentate granule cells in temporal lobe epilepsy: A morphometry and transcriptomic study.

The dentate gyrus (DG) plays a critical role in hippocampal circuitry, providing a "gate-like" function to the downstream cornu ammonis (CA) sectors. Despite this critical role, pathologies in DG are less commonly described than those in the CA sectors in the diagnosis of mesial temporal lobe epilepsy (mTLE). To elucidate the role of the DG in mTLE, we analysed hippocampal sclerosis (HS), no-HS, non-TLE epilepsy control, and non-epilepsy control cohorts using morphometry and gene expression profiling techniques. Morphometry techniques analysed DG cell spacing, nucleus size, and nucleus circularity. Our data show distinct DG morphometry and RNA expression profiles between HS and No-HS. Dentate granule cells are more dispersed in patients with HS, and the DG shows an elevated expression of the complement system, apoptosis, and extracellular matrix remodelling-related RNA. We also observe an overall decrease in neurogenesis-related RNA in HS DG. Interestingly, regardless of the pathological diagnosis, the DG morphometry correlates with post-operative outcomes. Increased cell spacing is observed in the DG of mTLE cases that achieve seizure freedom post-operatively. This study reveals the possible prognostic value of DG morphometry, as well as supporting the notion that HS and no-HS TLE may be distinct disease entities with differing contributing mechanisms.

Antiepileptic and anti-inflammatory effects of Lippia multiflora moldenke (Verbenaceae) in mice model of chronic temporal lobe epilepsy induced by pilocarpine

Lippia multiflora Moldenke (Verbenaceae) is an aromatic plant used as a popular medicine with antidepressant, antispasmodic, antifungal, anti-inflammatory, and antioxidant properties. In this study, we explored the effects of L. multiflora in mice chronic model of temporal lobe epilepsy induced by pilocarpine and kindled with pentylenetetrazol. Mice were divided into 7 groups of 10 animals, and received a single dose of pilocarpine (360 mg/kg, i.p.), 20 min after the administration of N-methyl-scopolamine (1 mg/kg, i.p). Thirty days after the induction of status epilepticus, animals were daily treated for 60 days with distilled water (10 mL/kg, per os) for the negative control group, extract (23.07, 57.69, 115.39 and 230.78 mg/kg, per os) for the test groups, and sodium valproate (300 mg/kg, i.p) for the positive control group. On every 10th day, animals were injected with a sub-convulsive dose of pentylenetetrazol (15 mg/kg, i.p) 1 h after the administration of the various treatments to assess the susceptibility of animals to seizures. At the end of behavioural tests, animals were sacrificed and the level of inflammatory cytokines was assessed in the hippocampus. The plant extract reduced (p < 0.001) the occurrence of seizures and the number of spontaneous recurrent seizures induced by pilocarpine in mice. It ameliorated the levels of inflammatory cytokines (TNF-α, INF- γ, IL-1β, IL-6, and IL-10) in the hippocampus. The in vitro studies show that L. multiflora have a high amount of total phenolic content, flavonoids and tannins and also have some good antioxidant properties. These results suggest that L. multiflora aqueous extracts has the potential to be a promising complementary and alternative medicine for the treatment of epilepsy, due to its antiepileptic, anti-inflammatory and antioxidant effects.