Cases Of Temporal Lobe Epilepsy Research Articles

“Hu” Would Have Thought, Eh? An Interesting Case of Temporal Lobe Epilepsy in an Elderly Patient (P3-14.010)

“Hu” Would Have Thought, Eh? An Interesting Case of Temporal Lobe Epilepsy in an Elderly Patient (P3-14.010)

Morphological and metabolic asymmetries of the thalamic subregions in temporal lobe epilepsy predict cognitive functions

Both morphological and metabolic imaging were used to determine how asymmetrical changes of thalamic subregions are involved in cognition in temporal lobe epilepsy (TLE). We retrospectively recruited 24 left-TLE and 15 right-TLE patients. Six thalamic subnuclei were segmented by magnetic resonance imaging, and then co-registered onto Positron emission tomography images. We calculated the asymmetrical indexes of the volumes and normalized standard uptake value ratio (SUVR) of the entire and individual thalamic subnuclei. The SUVR of ipsilateral subnuclei were extensively and prominently decreased compared with the volume loss. The posterior and medial subnuclei had persistently lower SUVR in both TLE cases. Processing speed is the cognitive function most related to the metabolic asymmetry. It negatively correlated with the metabolic asymmetrical indexes of subregions in left-TLE, while positively correlated with the subnuclei volume asymmetrical indexes in right-TLE. Epilepsy duration negatively correlated with the volume asymmetry of most thalamic subregions in left-TLE and the SUVR asymmetry of ventral and intralaminar subnuclei in right-TLE. Preserved metabolic activity of contralateral thalamic subregions is the key to maintain the processing speed in both TLEs. R-TLE had relatively preserved volume of the ipsilateral thalamic volume, while L-TLE had relatively decline of volume and metabolism in posterior subnucleus.

(083) “TEMP”orarily Missed: A Case of Temporal Lobe Epilepsy Complicated by Hyperactive Catatonia

(083) “TEMP”orarily Missed: A Case of Temporal Lobe Epilepsy Complicated by Hyperactive Catatonia

Biomarkers of Drug Resistance in Temporal Lobe Epilepsy in Adults.

Temporal lobe epilepsy (TLE) is the most common type of focal epilepsy in adults. Experimental and clinical data indicate that neuroinflammation and neurodegeneration accompanying epileptogenesis make a significant contribution to the chronicity of epilepsy and the development of drug resistance in TLE cases. Changes in plasma and serum concentrations of proteins associated with neuroinflammation and neurodegeneration can be predictive biomarkers of the course of the disease. This study used an enzyme-linked immunosorbent assay of the following plasma proteins: brain-derived neurotrophic factor (BDNF), tumor necrosis factor alpha (TNFa), and high-mobility group protein B1 (HMGB1) in patients with mesial TLE to search for biomarkers of the disease. The objective of the study was to examine biomarkers of the neuroinflammation and neurodegeneration of plasma: BDNF, TNFa, and HMGB1. The aim of the study was to identify changes in the concentration of circulating pro-inflammatory and neurotrophic factors that are prognostically significant for the development of drug resistance and the course of TLE. A decrease in the concentration of BDNF, TNFa, and HMGB1 was registered in the group of patients with TLE compared with the control group. A significant decrease in the concentration of HMGB1 in patients with drug-resistant TLE was observed. Aberrations in plasma concentrations of BDNF, TNFa, and HMGB1 in patients with TLE compared with the controls have been confirmed by earlier studies. A decrease in the expression of the three biomarkers may be the result of neurodegenerative processes caused by the long course of the disease. The results of the study may indicate the acceptability of using HMGB1 and TNFa as prognostic biological markers to indicate the severity of the disease course and the risk of developing drug resistance.

The Glycolysis Inhibitor 2-Deoxy-D-Glucose Exerts Different Neuronal Effects at Circuit and Cellular Levels, Partially Reverses Behavioral Alterations and does not Prevent NADPH Diaphorase Activity Reduction in the Intrahippocampal Kainic Acid Model of Temporal Lobe Epilepsy.

Temporal lobe epilepsy is the most drug-resistant type with the highest incidence among the other focal epilepsies. Metabolic manipulations are of great interest among others, glycolysis inhibitors like 2-deoxy d-glucose (2-DG) being the most promising intervention. Here, we sought to investigate the effects of 2-DG treatment on cellular and circuit level electrophysiological properties using patch-clamp and local field potentials recordings and behavioral alterations such as depression and anxiety behaviors, and changes in nitric oxide signaling in the intrahippocampal kainic acid model. We found that epileptic animals were less anxious, more depressed, with more locomotion activity. Interestingly, by masking the effect of increased locomotor activity on the parameters of the zero-maze test, no altered anxiety behavior was noted in epileptic animals. However, 2-DG could partially reverse the behavioral changes induced by kainic acid. The findings also showed that 2-DG treatment partially suppresses cellular level alterations while failing to reverse circuit-level changes resulting from kainic acid injection. Analysis of NADPH-diaphorase positive neurons in the CA1 area of the hippocampus revealed that the number of positive neurons was significantly reduced in dorsal CA1 of the epileptic animals and 2-DG treatment did not affect the diminishing effect of kainic acid on NADPH-d+ neurons in the CA1 area. In the control group receiving 2-DG, however, an augmented NADPH-d+ cell number was noted. These data suggest that 2-DG cannot suppress epileptiform activity at the circuit-level in this model of epilepsy and therefore, may fail to control the seizures in temporal lobe epilepsy cases.

A Case of Temporal Lobe Epilepsy Associated with a Cavernous Malformation in Which Bilateral Epileptic Discharges Disappeared after Lesionectomy Alone

A Case of Temporal Lobe Epilepsy Associated with a Cavernous Malformation in Which Bilateral Epileptic Discharges Disappeared after Lesionectomy Alone

A Study of Spontaneous Brain Activity on Resting-State Functional Magnetic Resonance Imaging in Adults with MRI-Negative Temporal Lobe Epilepsy.

PurposePatients with magnetic resonance imaging (MRI)-negative temporal lobe epilepsy (TLE-N) represent an important subgroup of temporal lobe epilepsy (TLE). Here, we aimed to combine three voxel-based local brain area analysis methods of resting-state functional MRI (rs-fMRI), to examine the TLE-N patients’ resting brain function based on neural synchronization and intensity of local brain areas.MethodsThe study included 47 patients with TLE, including 28 cases of drug-controlled TLE (cTLE-N) and 19 cases of drug-resistant TLE-N (rTLE-N), as well as 30 participants in the healthy control (HC) group. To comprehensively assess the altered brain function associated with TLE-N patients, we analyzed three data-driven rs-fMRI algorithms for amplitude of low-frequency fluctuations (ALFF), fractional ALFF (fALFF) and regional homogeneity (ReHo).ResultsCompared to the HC group, the distribution of abnormal functional brain areas in cTLE-N patients was dominated by occipital lobe activation, as measured by increased fALFF values in the superior occipital gyrus (SOG) and increased ReHo values in the lingual gyrus (Lin), fusiform gyrus, and middle occipital gyrus. Patients with rTLE-N exhibited a diffuse distribution of abnormal functional brain areas, showing increased fALFF values in the SOG, Lin, superior temporal gyrus, and postcentral gyrus, and decreased fALFF values in the inferior frontal gyrus orbital, parahippocampal gyrus, and superior frontal gyrus orbital. The ReHo values were reduced in the orbital region of the middle frontal gyrus, the precuneus, and the parietal inferior angular gyrus; while ReHo values were elevated values in several frontal, temporal, occipital, and subcortical brain areas.ConclusionPatients with rTLE-N have local brain activity changes in the prefrontal limbic system and default model network dysfunction, while cTLE-N patients have local brain activity changes in the visual functional areas. Different epilepsy networks exist between cTLE-N and rTLE-N.

Mini Temporal Craniotomy Using Anatomical Surface Landmarks for Temporal Lobe Epilepsy: Technical Note and Clinical Outcomes.

Patients with temporal lobe epilepsy are subjected to standard temporal lobectomy wherever indicated. This is performed using a reverse question mark flap and a standard frontotemporal craniotomy. We describe the technique of minitemporal craniotomy (3 × 3cms) for temporal lobe epilepsy (TLE) and analyze the clinical outcomes of patients operated using this approach. To describe the technique of minitemporal craniotomy for TLE without navigation guidance and to analyze the clinical outcomes of patients operated using this approach. This was a retrospective analysis of all consecutive TLE cases operated at our institute from 2014 to 2019, via minitemporal craniotomy, using surface landmarks only without navigation guidance. The surgical technique, indications for surgery, and their clinical outcomes were analyzed. A total number of 48 patients underwent surgery for TLE. There were no complications except three patients who had transient hemiparesis. The average duration of hospital stay was 4 days following surgery. Out of 28 patients with mesial temporal sclerosis, 22 (82%) had international league against epilepsy, Class I seizure outcome, 4 (12.5%) had Class II outcome and 2 (5.5%) had Class III outcome. 9 patients with dysembryoplastic neurectodermal tumor (DNET), 4 gangliogliomas, 2 neurocystecercosis (NCC), all had Class I outcome. Out of the five patients with MTS and associated anterior temporal focal cortical dysplasia (FCD), four (80%) had a Class I outcome, whereas one (20%) had Class II outcome. Utilizing surface anatomical landmarks, minitemporal craniotomy can be performed in even peripheral centers without neuronavigation, with good cosmesis, seizure outcomes.

Radiological identification of temporal lobe epilepsy using artificial intelligence: a feasibility study.

Temporal lobe epilepsy is associated with MRI findings reflecting underlying mesial temporal sclerosis. Identifying these MRI features is critical for the diagnosis and management of temporal lobe epilepsy. To date, this process relies on visual assessment by highly trained human experts (e.g. neuroradiologists, epileptologists). Artificial intelligence is increasingly recognized as a promising aid in the radiological evaluation of neurological diseases, yet its applications in temporal lobe epilepsy have been limited. Here, we applied a convolutional neural network to assess the classification accuracy of temporal lobe epilepsy based on structural MRI. We demonstrate that convoluted neural networks can achieve high accuracy in the identification of unilateral temporal lobe epilepsy cases even when the MRI had been originally interpreted as normal by experts. We show that accuracy can be potentiated by employing smoothed grey matter maps and a direct acyclic graphs approach. We further discuss the foundations for the development of computer-aided tools to assist with the diagnosis of epilepsy.

P.189 Unruptured Posterior Cerebral Artery aneurysm causing temporal lobe epilepsy

Background: Cerebral aneurysms are an unusal cause of epilepsy. To date, several groups have reported temporal lobe seizures caused by aneurysms projecting into the parahippocampal gyrus. Given the low incidence of posterior cerebral artery aneurysms, they are a very rare cause of temporal lobe seizures. Methods: Here, we report a rare case of temporal lobe epilepsy caused by an unruptured aneurysm. We also present a review of the literature yielding two similar cases. Results: A previosuly well 56 year old male presented to a neurologist with symptoms consistent with temporal lobe epilepsy. He was started on carbamzepine and underwent imaging and neuropsychological assessments. An MRI suggested the existance of a 7mm posterior cerebral artery aneurysm arising from the P2 segment of the posterior cerebral artery and projecting into the parahippocampal gyrus. This was also confirmed with CT angiography and the patient elected to have the aneurysm clipped. Conclusions: Temporal lobe epilepsy is an uncommon presentation for unruptured cerebral aneurysms. We report a rare case wherein a laterally pointing PCA aneurysm was buried in the posterior parahippocampal gyrus. This aneurysm had caused perifocal gliosis leading to stereotyped seizures. Post-operatively, the patient has been seizure free.

Skull-base temporal encephalocele: Hidden cause of temporal lobe epilepsy

Among patients with Temporal lobe epilepsy (TLE), up to 30% can have normal (non-lesional) MRI scans. With increased use of high resolution MRI (3 T) scans, many of the MRI‐negative TLE cases turn out to be lesional TLE. Skull-base temporal encephalocele (TE), has to be suspected and specifically searched for among patients with apparent MRI negative TLE. The study aims to analyse patients with TLE for temporal lobe encephalocoele.

Genetic influence of Apolipoprotein E gene ε2/ε3/ε4 isoforms on odds of mesial temporal lobe epilepsy.

The potential correlation between the ε2/ε3/ε4 variants of the ApoE (Apolipoprotein E) gene and the odds of mesial temporal lobe epilepsy was investigated. The database searching for eligible studies was performed in October 2020. A series of pooling analyses were conducted. We enrolled a total of twelve case-control studies for pooling. Within the pooling analysis of ε4, there was an increased risk of mesial temporal lobe epilepsy in cases under the models of carrier ε4 vs. ε3, ε3ε4 vs. ε3ε3, and ε3ε4+ε4ε4 vs. ε3ε3 [P < 0.05, odds ratio (OR) > 1], compared with controls. Moreover, we observed similar positive results in the subgroup analyses of "China" and "Population-based control" under the genetic models of ε4 (P < 0.05, OR > 1). Nevertheless, we did not detect the significant difference between the mesial temporal lobe epilepsy cases and controls in the pooling analyses of ε2 (all P > 0.05). The ε3ε4 genotype of ApoE seems to be linked to the risk of mesial temporal lobe epilepsy for patients in China. More sample sizes are required to confirm the potential role of ApoE isoforms in the susceptibility to diverse types of epilepsy from different origins.

Feature of cognitive dysfunction in patients with temporal lobe epilepsy and its clinical influencing factors.

To comprehensively analyze the characteristics of cognitive impairment of temporal lobe epilepsy (TLE), and to explore the effects of different lateral patients' cognitive impairment and different clinical factors on cognitive impairment of TLE. A total of 84 patients, who met the diagnostic criteria for TLE in the Department of Neurology, Xiangya Hospital, were collected as a patient group, with 36 cases of left TLE and 48 cases of right TLE. A total of 79 healthy volunteers with matching gender, age and education level were selected as a control group. The Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and the scores of Arithmetic Test, Information Test, Digit Symbol Substitution Test (DSST), Block Design Test (BDT), Hayling Test and Verbal Fluency Test (VFT) of the revised Chinese Adult Wechsler Intelligence scale were retrospectively analyzed in the 2 groups.Multiple regression analysis was used to analyze the relationship between the clinical factors and the cognitive impairment score. Compared with the control group, the TLE patient group had low scores in all neuropsychological tests, with significant difference (all P<0.05). Compared with the control group, there was significant difference in different neuropsychological tests in the patients with TLE on different sides (all P<0.05). In the left TLE, there were low scores in Information Test, arithmetic, VFT, the completion time of Hayling Test part A, the completion time of Hayling Test part B, the correct number of Hayling Test part A, the correct number of Hayling Test part B, BDT, Forward Digit Span Test (FDST) and Backward Digit Span Test (BDST). While in the right TLE, there were low scores in Information Test, arithmetic, DSST, VFT, the completion time of Hayling Test part A, the correct number of Hayling Test part A, the completion time of Hayling Test part B, the correct number of Hayling Test part B, BDT, FDST and BDST. There are multiple cognitive domain dysfunctions in TLE, including language, short-term memory, long-term memory, attention, working memory, executive function and visual space function. Left TLE has greater impairment of executive function and right TLE has greater damage in working memory. Long pathography of disease, hippocampal sclerosis and a history of febrile convulsions may lead to more severe cognitive impairment. Earlier identification and earlier intervention are needed to improve prognosis of patients.

Temporal and extratemporal atrophic manifestation of temporal lobe epilepsy using voxel-based morphometry and corticometry: clinical application in lateralization of epileptogenic zone.

Advances in MRI acquisition and data processing have become important for revealing brain structural changes. Previous studies have reported widespread structural brain abnormalities and cortical thinning in patients with temporal lobe epilepsy (TLE), as the most common form of focal epilepsy. In this research, healthy control cases (n = 20) and patients with left TLE (n = 19) and right TLE (n = 14) were recruited, all underwent 3.0T MRI with magnetization-prepared rapid gradient echo sequence to acquire T1-weighted images. Morphometric alterations in gray matter were identified using voxel-based morphometry (VBM). Volumetric alterations in subcortical structures and cortical thinning were also determined. Patients with left TLE demonstrated more prevailing and widespread changes in subcortical volumes and cortical thickness than right TLE, mainly in the left hemisphere, compared to the healthy group. Both VBM analysis and subcortical volumetry detected significant hippocampal atrophy in ipsilateral compared to contralateral side in TLE group. In addition to hippocampus, subcortical volumetry found the thalamus and pallidum bilaterally vulnerable to the TLE. Furthermore, the TLE patients underwent cortical thinning beyond the temporal lobe, affecting gray matter cortices in frontal, parietal, and occipital lobes in the majority of patients, more prevalently for left TLE cases. Exploiting volume changes in individual patients in the hippocampus alone led to 63.6% sensitivity and 100% specificity for lateralization of TLE. Alteration of gray matter volumes in subcortical regions and neocortical temporal structures and also cortical gray matter thickness were evidenced as common effects of epileptogenicity, as manifested by the majority of cases in this study.

Resective surgery prevents progressive cortical thinning in temporal lobe epilepsy.

Focal epilepsy in adults is associated with progressive atrophy of the cortex at a rate more than double that of normal ageing. We aimed to determine whether successful epilepsy surgery interrupts progressive cortical thinning. In this longitudinal case-control neuroimaging study, we included subjects with unilateral temporal lobe epilepsy (TLE) before (n = 29) or after (n = 56) anterior temporal lobe resection and healthy volunteers (n = 124) comparable regarding age and sex. We measured cortical thickness on paired structural MRI scans in all participants and compared progressive thinning between groups using linear mixed effects models. Compared to ageing-related cortical thinning in healthy subjects, we found progressive cortical atrophy on vertex-wise analysis in TLE before surgery that was bilateral and localized beyond the ipsilateral temporal lobe. In these regions, we observed accelerated annualized thinning in left (left TLE 0.0192 ± 0.0014 versus healthy volunteers 0.0032 ± 0.0013 mm/year, P < 0.0001) and right (right TLE 0.0198 ± 0.0016 versus healthy volunteers 0.0037 ± 0.0016 mm/year, P < 0.0001) presurgical TLE cases. Cortical thinning in these areas was reduced after surgical resection of the left (0.0074 ± 0.0016 mm/year, P = 0.0006) or right (0.0052 ± 0.0020 mm/year, P = 0.0006) anterior temporal lobe. Directly comparing the post- versus presurgical TLE groups on vertex-wise analysis, the areas of postoperatively reduced thinning were in both hemispheres, particularly, but not exclusively, in regions that were affected preoperatively. Participants who remained completely seizure-free after surgery had no more progressive thinning than that observed during normal ageing. Those with postoperative seizures had small areas of continued accelerated thinning after surgery. Thus, successful epilepsy surgery prevents progressive cortical atrophy that is observed in TLE and may be potentially neuroprotective. This effect was more pronounced in those who remained seizure-free after temporal lobe resection, normalizing the rate of atrophy to that of normal ageing. These results provide evidence of epilepsy surgery preventing further cerebral damage and provide incentives for offering early surgery in refractory TLE.

Diagnosis and surgical treatment of non-lesional temporal lobe epilepsy with unilateral amygdala enlargement

Exploring the role of amygdala enlargement (AE) in temporal lobe epilepsy (TLE) without ipsilateral mesial temporal sclerosis (MTS) using comprehensive presurgical workup tools including traditional tools, automatically volumetric analysis, high-density EEG (HD-EEG) source imaging (HD-ESI), and stereoelectroencephalography (SEEG). Nine patients diagnosed with TLE-AE who underwent resective surgeries encompassing the amygdala were retrospectively studied. HD-ESI was obtained using 256-channel HD-EEG on the individualized head model. For automatic volumetric analysis, 48 matched controls were enrolled. Diagnosis and surgical strategies were based on a comprehensive workup following the anatomo-electro-clinical principle. At post-operative follow-up (average 30.9months), eight patients had achieved Engel class I and one Engel class II recovery. HD-ESI yielded unifocal source estimates in anterior mesial temporal region in 85.7% of cases. Automatic volumetric analysis showed the AE sides were consistent with the values determined through other preoperative workup tools. Furthermore, the amygdala volume of the affected sides in AE was significantly greater than that of the larger sides in controls (p < 0.001). Meanwhile, the amygdala volume lateral index (LI) of AE was significantly higher than in controls (p < 0.001). SEEG analysis showed that ictal onsets arose from the enlarged amygdala (and hippocampus) in all cases. In addition to traditional workup tools, automatic volumetric analysis, HD-ESI on individualized head model, and invasive SEEG can provide evidence of epileptogenicity in TLE-AE. Resective surgical strategies encompassing the amygdala result in better prognosis. In suspected TLE cases, more attention should be focused on detecting enlargement of amygdala which sometimes is "hidden" in "MR-negative" non-MTS cases.

Drebrin expression patterns in patients with refractory temporal lobe epilepsy and hippocampal sclerosis

Drebrins are crucial for synaptic function and dendritic spine development, remodeling, and maintenance. In temporal lobe epilepsy (TLE) patients, a significant hippocampal synaptic reorganization occurs, and synaptic reorganization has been associated with hippocampal hyperexcitability. This study aimed to evaluate, in TLE patients, the hippocampal expression of drebrin using immunohistochemistry with DAS2 or M2F6 antibodies that recognize adult (drebrin A) or adult and embryonic (pan-drebrin) isoforms, respectively. Hippocampal sections from drug-resistant TLE patients with hippocampal sclerosis (HS; TLE, n=33), of whom 31 presented with type 1 HS and two with type 2 HS, and autopsy control cases (n=20) were assayed by immunohistochemistry and evaluated for neuron density, and drebrin A and pan-drebrin expression. Double-labeling immunofluorescences were performed to localize drebrin A-positive spines in dendrites (MAP2), and to evaluate whether drebrin colocalizes with inhibitory (GAD65) and excitatory (VGlut1) presynaptic markers. Compared to controls, TLE patients had increased pan-drebrin in all hippocampal subfields and increased drebrin A-immunopositive area in all hippocampal subfields but CA1. Drebrin-positive spine density followed the same pattern as total drebrin quantification. Confocal microscopy indicated juxtaposition of drebrin-positive spines with VGlut1-positive puncta, but not with GAD65-positive puncta. Drebrin expression in the dentate gyrus of TLE cases was associated negatively with seizure frequency and positively with verbal memory. TLE patients with lower drebrin-immunopositive area in inner molecular layer (IML) than in outer molecular layer (OML) had a lower seizure frequency than those with higher or comparable drebrin-immunopositive area in IML compared with OML. Our results suggest that changes in drebrin-positive spines and drebrin expression in the dentate gyrus of TLE patients are associated with lower seizure frequency, more preserved verbal memory, and a better postsurgical outcome.

A Combination of Particle Swarm Optimization and Minkowski Weighted K-Means Clustering: Application in Lateralization of Temporal Lobe Epilepsy

K-Means is one of the most popular clustering algorithms that partitions observations into nonoverlapping subgroups based on a predefined similarity metric. Its drawbacks include a sensitivity to noisy features and a dependency of its resulting clusters upon the initial selection of cluster centroids resulting in the algorithm converging to local optima. Minkowski weighted K-Means (MWK-Means) addresses the issue of sensitivity to noisy features, but is sensitive to the initialization of clusters, and so the algorithm may similarly converge to local optima. Particle Swarm Optimization (PSO) uses a globalized search method to solve this issue. We present a hybrid Particle Swarm Optimization (PSO) + MWK-Means clustering algorithm to address all the above problems in a single framework, while maintaining benefits of PSO and MWK Means methods. This study investigated the utility of this approach in lateralizing the epileptogenic hemisphere for temporal lobe epilepsy (TLE) cases using magnetoencephalography (MEG) coherence source imaging (CSI) and diffusion tensor imaging (DTI). Using MEG-CSI, we analyzed preoperative resting state MEG data from 17 adults TLE patients with Engel class I outcomes to determine coherence at 54 anatomical sites and compared the results with 17 age- and gender-matched controls. Fiber-tracking was performed through the same anatomical sites using DTI data. Indices of both MEG coherence and DTI nodal degree were calculated. A PSO + MWK-Means clustering algorithm was applied to identify the side of temporal lobe epileptogenicity and distinguish between normal and TLE cases. The PSO module was aimed at identifying initial cluster centroids and assigning initial feature weights to cluster centroids and, hence, transferring to the MWK-Means module for the final optimal clustering solution. We demonstrated improvements with the use of the PSO + MWK-Means clustering algorithm compared to that of K-Means and MWK-Means independently. PSO + MWK-Means was able to successfully distinguish between normal and TLE in 97.2% and 82.3% of cases for DTI and MEG data, respectively. It also lateralized left and right TLE in 82.3% and 93.6% of cases for DTI and MEG data, respectively. The proposed optimization and clustering methodology for MEG and DTI features, as they relate to focal epileptogenicity, would enhance the identification of the TLE laterality in cases of unilateral epileptogenicity.

Surgical Treatment of Temporal Lobe Epilepsy and Micro-Neuroanatomical Details of the Medial Temporal Region.

To evaluate the long-term efficacy of temporal lobe epilepsy (TLE) surgery, and to emphasize the factors affecting seizure outcomes such as surgical technique nuances and micro-neuroanatomical details in TLE cases. In this retrospective analysis, 238 patients who underwent epilepsy surgery at Ankara University (Faculty of Medicine, Department of Neurosurgery) between 1990 and 2019 were included. All patients presented with symptoms of TLE. They were divided into two groups: those with neoplastic lesions and those with non-neoplastic brain lesions presenting with medically intractable epilepsy. In the non-neoplastic group, the patients underwent anterior temporal lobectomy with amygdalohippocampectomy (ATL+AH), whereas in the neoplastic group, the patients underwent tumor resection in addition to ATL+AH. This study included 126 female (52.9%) and 112 male (47.1%) patients. The mean duration of epilepsy was 14.65 ± 9.29 years (0.08?46 years). The number of patients in the non-neoplastic and neoplastic groups was 190 and 48, respectively. The mean duration of follow-up was 15.82 ± 6.55 years (1?28 years). In the neoplastic and non-neoplastic groups, the Engel I seizure-free rates were 91.6% (44/48) and 90.5% (172/190), respectively. Furthermore, no mortality was observed among the groups. Overall, effective seizure control was achieved with acceptable morbidity and complication rates in the neoplastic and non-neoplastic groups with surgical and micro-neuroanatomical nuances.

Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy.

Temporal lobe epilepsy represents a major cause of drug-resistant epilepsy. Cognitive impairment is a frequent comorbidity, but the mechanisms are not fully elucidated. We hypothesized that the cognitive impairment in drug-resistant temporal lobe epilepsy could be due to perturbations of amyloid and tau signalling pathways related to activation of stress kinases, similar to those observed in Alzheimer's disease. We examined these pathways, as well as amyloid-β and tau pathologies in the hippocampus and temporal lobe cortex of drug-resistant temporal lobe epilepsy patients who underwent temporal lobe resection (n = 19), in comparison with age- and region-matched samples from neurologically normal autopsy cases (n = 22). Post-mortem temporal cortex samples from Alzheimer's disease patients (n = 9) were used as positive controls to validate many of the neurodegeneration-related antibodies. Western blot and immunohistochemical analysis of tissue from temporal lobe epilepsy cases revealed increased phosphorylation of full-length amyloid precursor protein and its associated neurotoxic cleavage product amyloid-β*56. Pathological phosphorylation of two distinct tau species was also increased in both regions, but increases in amyloid-β1-42 peptide, the main component of amyloid plaques, were restricted to the hippocampus. Furthermore, several major stress kinases involved in the development of Alzheimer's disease pathology were significantly activated in temporal lobe epilepsy brain samples, including the c-Jun N-terminal kinase and the protein kinase R-like endoplasmic reticulum kinase. In temporal lobe epilepsy cases, hippocampal levels of phosphorylated amyloid precursor protein, its pro-amyloidogenic processing enzyme beta-site amyloid precursor protein cleaving enzyme 1, and both total and hyperphosphorylated tau expression, correlated with impaired preoperative executive function. Our study suggests that neurodegenerative and stress-related processes common to those observed in Alzheimer's disease may contribute to cognitive impairment in drug-resistant temporal lobe epilepsy. In particular, we identified several stress pathways that may represent potential novel therapeutic targets.