Brain-heart functional network dysfunction in temporal lobe epilepsy: A microstate-based analysis.

To the Editor.— The report by Herzog and colleagues, Neuroendocrine Dysfunction in Temporal Lobe Epilepsy (Archives1982;39:133-135), offers a potential neuroendocrinologic basis for impaired fertility in epileptic women 1 and the frequent occurrence of hyposexuality—primarily erectile dysfunction—in men with temporal lobe epilepsy (TLE). 2 We would be interested to know whether the patient who had an elevated serum prolactin level had recently experienced a seizure. Although we agree that interictal prolactin studies are normal in this clinical population, we found postictal hyperprolactinemia after complex partial seizures in all cases studied 3 ; thus, the temporal relationship between serum prolactin determinations and the occurrence of seizures is critical. Although the clinical consequences of episodic hyperprolactinemia are uncertain, impotence and decreased libido are the most common accompaniments of sustained hyperprolactinemia in men. 4 Further studies of prolactin secretion in TLE seem warranted. Using an intravenous (IV) bolus of luteinizing hormone-releasing hormone (LH-RH) in

Cognitive dysfunction is common in people with epilepsy (PWE). Although expectations exist for deficits based on diagnosis, phenotypic variation of cognitive deficits is observed within epilepsy subtypes. Classification by severity and type of cognitive deficits has been shown across multiple studies of people with temporal lobe epilepsy (TLE). In this study, we replicate these findings using robotic assessment in TLE and apply the same method in genetic generalized epilepsy (GGE) to uncover potential cognitive phenotypes. Participants with TLE and GGE were recruited to participate in robotic assessment battery of neurocognitive function. We used 7 task scores to form clusters that includes functions from various cognitive and motor domains. Calinski-Harabasz method seeded at zero was used to find the optimal value of c, and fuzzy C-means clustering was used to assess the cluster membership from the data in c-groups. We found 3 clusters among TLE (n=33): minimal deficits (45% of participants with TLE), partial deficits (27%), and global deficits (27%). Likewise, we found 3 clusters among GGE (n=25): memory and executive deficits (40% of participants with GGE), processing speed deficits (36%), and complex motor deficits (24%). Robotic assessment can be used with clustering methods to classify cognitive dysfunction in epilepsy. These clusters show similar patterns to previous research, which suggests that robotic assessment can distinguish the cognitive phenotypes of PWE.

The goal of this work was to evaluate the relationship between neuronal injury/loss in the hippocampus, thalamus, and putamen in temporal lobe epilepsy (TLE) patients using (1)H magnetic resonance spectroscopic imaging. (1)H spectroscopic images from the hippocampus and thalamus of controls and patients with TLE were acquired at 4 T. The spectroscopic imaging data were reconstructed using an automated voxel-shifting method based on anatomic landmarks providing four, six, and three loci for the hippocampus, thalamus, and putamen, respectively. For correlation analysis, the hippocampal and striatal loci were averaged to provide single estimates of the entire structure, whereas the thalamus was divided into two regions, an anterior and posterior measure, using the average of three loci each. The ratio of N-acetyl aspartate to creatine (NAA/Cr), a measure of neuronal injury/loss, was significantly reduced in both the ipsilateral and contralateral hippocampi and thalami. NAA/Cr in the ipsilateral hippocampus was significantly correlated with the ipsilateral and contralateral anterior and posterior thalami, putamen, and contralateral hippocampus. In control subjects, the hippocampi were only correlated with each other. The data demonstrate that there is significant neuronal injury/loss in both the ipsilateral and contralateral thalami in temporal lobe epilepsy patients, with greater impairment in the anterior portions of the ipsilateral thalamus. The degree of injury/loss in the ipsilateral and contralateral thalamus and putamen is directly correlated with that of the ipsilateral hippocampus. This is consistent with the hypothesis that the impairment and damage associated with recurrent seizures as measured by N-acetyl aspartate originating in the hippocampus results in injury and impairment in other subcortical structures.

SummaryTemporal lobe epilepsy (TLE) is typically associated with long-term memory dysfunction. The frontal lobes support high-level cognition comprising executive skills and working memory that is vital for daily life functioning. Deficits in these functions have been increasingly reported in TLE. Evidence from both the neuropsychological and neuroimaging literature suggests both executive function and working memory are compromised in the presence of TLE. In relation to executive impairment, particular focus has been paid to set shifting as measured by the Wisconsin Card Sorting Task. Other discrete executive functions such as decision-making and theory of mind also appear vulnerable but have received little attention. With regard to working memory, the medial temporal lobe structures appear have a more critical role, but with emerging evidence of hippocampal dependent and independent processes. The relative role of underlying pathology and seizure spread is likely to have considerable bearing upon the cognitive phenotype and trajectory in TLE. The identification of the nature of frontal lobe dysfunction in TLE thus has important clinical implications for prognosis and surgical management. Longitudinal neuropsychological and neuroimaging studies assessing frontal lobe function in TLE patients pre- and postoperatively will improve our understanding further.

The impairment in episodic memory system is the best-known cognitive deficit in patients with temporal lobe epilepsy (TLE). Recent studies have shown evidence of semantic disorders, but they have been less studied than episodic memory. The semantic dysfunction in TLE has various cognitive manifestations, such as the presence of language disorders characterized by defects in naming, verbal fluency, or remote semantic information retrieval, which affects the ability of patients to interact with their surroundings. This paper is a review of recent research about the consequences of TLE on semantic processing, considering neuropsychological, electrophysiological, and neuroimaging findings, as well as the functional role of the hippocampus in semantic processing. The evidence from these studies shows disturbance of semantic memory in patients with TLE and supports the theory of declarative memory of the hippocampus. Functional neuroimaging studies show an inefficient compensatory functional reorganization of semantic networks and electrophysiological studies show a lack of N400 effect that could indicate that the deficit in semantic processing in patients with TLE could be due to a failure in the mechanisms of automatic access to lexicon.

Bipolar disorder (BD) and temporal lobe epilepsy (TLE) overlap in domains including epidemiology, treatment response, shared neurotransmitter involvement and temporal lobe pathology. Comparison of cognitive function in both disorders may indicate temporal lobe mediated processes relevant to BD. This systematic review examines neuropsychological test profiles in euthymic bipolar disorder type I (BD-I) and pre-surgical TLE and compares experimental designs used. A search of PubMed, PsychINFO, and Scopus using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines was conducted. Inclusion criteria were comparison group or pre- to post-surgical patients; reported neuropsychological tests; participants aged 18-60 years. Fifty six studies met criteria: 27 BD-I; 29 TLE. Deficits in BD-I compared to healthy controls (HC) were in executive function, attention span and verbal memory. Deficits in TLE compared to HC were in executive function and memory. In the pre- to post-surgical comparisons, verbal memory in left temporal lobe (LTL) and, less consistently, visuospatial memory in right temporal lobe (RTL) epilepsy declined following surgery. BD-I studies used comprehensive test batteries in well-defined euthymic patients compared to matched HC groups. TLE studies used convenience samples pre- to post-surgery, comparing LTL and RTL subgroups, few included comparisons to HC (5 studies). TLE studies typically examined a narrow range of known temporal lobe-mediated neuropsychological functions, particularly verbal and visuospatial memory. Both disorders exhibit deficits in executive function and verbal memory suggestive of both frontal and temporal lobe involvement. However, deficits in TLE are measured pre- to post-surgery and not controlled at baseline pre-surgery. Further research involving a head-to-head comparison of the two disorders on a broad range of neuropsychological tests is needed to clarify the nature and extent of cognitive deficits and potential overlaps.

Hypothalamic-pituitary-adrenocortical axis dysfunction in epilepsy

Electroencephalogram microstate analysis in temporal lobe epilepsy: A comparative study with and without anxiety.

Epilepsy CurrentsVolume 3, Issue 1 p. 31-32 Widespread Neuronal Dysfunction in Temporal Lobe Epilepsy Gregory D. Cascino M.D., Gregory D. Cascino M.D.Search for more papers by this author Gregory D. Cascino M.D., Gregory D. Cascino M.D.Search for more papers by this author First published: 18 September 2008 https://doi.org/10.1046/j.1535-7597.2003.03113.xRead the full textAboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume3, Issue1January 2003Pages 31-32 RelatedInformation

Mesial temporal lobe epilepsy diminishes functional connectivity during emotion perception

Vascular structures may play a significant role in epileptic pathology. Although previous attempts to characterize vasculature relative to epileptogenic zones and hippocampal sclerosis have been inconsistent, an in vivo method of analysis would assist in resolving these inconsistencies and facilitate a comparison against healthy controls in a human model. Magnetic resonance imaging is a noninvasive technique that provides excellent soft tissue contrast, and the relatively recent development of susceptibility-weighted imaging has dramatically improved the visibility of small veins. We built and tested a Hessian-based segmentation technique, which takes advantage of the increased signal and contrast available at 7 T to detect venous structures in vivo. We investigate the ability of this technique to quantify vessels in the brain and apply it to an asymmetry analysis of vessel density in the hippocampus in patients with mesial temporal lobe epilepsy (MTLE) and neocortical epilepsy. Vessel density was highly symmetric in the hippocampus in controls (mean asymmetry=0.080±0.076, median=0.05027), whereas average vessel density asymmetry was greater in neocortical (mean asymmetry=0.23±0.17, median=0.14) and MTLE (mean asymmetry=0.37±0.46, median=0.26) patients, with the decrease in vessel density ipsilateral to the suspected seizure onset zone. Post hoc testing with one-way analysis of variance and Tukey post hoc test indicated significant differences in the group means (P<.02) between MTLE and the control group only. Asymmetry in vessel density in the hippocampus is visible in patients with MTLE, even when qualitative and quantitative measures of hippocampal asymmetry show little volumetric difference between epilepsy patients and healthy controls.

Category-specific naming impairment in temporal lobe epilepsy through cortical electrical stimulation: Case report

SummaryNeural stem cells (NSCs) are one of the candidates for grafting in the realm of cell‐based therapy for temporal lobe epilepsy (TLE). Because NSCs can produce neurons synthesizing the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) and cells secreting multiple neurotrophic factors, NSC grafting therapy has promise for restraining seizures and easing cognitive dysfunction in TLE. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).

The role of the orbitofrontal cortex and insula for prognosis of mesial temporal lobe epilepsy

The hippocampus is a highly epileptogenic brain region, yet over 90% of hippocampal epileptiform activity (HEA) cannot be identified on scalp electroencephalogram (EEG) by human experts. Currently, detection of HEA requires intracranial electrodes, which limits our understanding of the role of HEA in brain diseases. To develop and validate a machine learning algorithm that accurately detects HEA from a standard scalp EEG, without the need for intracranial electrodes. In this diagnostic study, conducted from 2008 to 2021, EEG data were used from patients with temporal lobe epilepsy (TLE) and healthy controls (HCs) to train and validate a deep neural network, HEAnet, to detect HEA on scalp EEG. Participants were evaluated at tertiary-level epilepsy centers at 2 academic hospitals: Massachusetts General Hospital (MGH) or Brigham and Women's Hospital (BWH). Included in the study were patients aged 12 to 78 years with a clinical diagnosis of TLE and HCs without epilepsy. Patients with TLE and HCs with a history of intracranial surgery were excluded from the study. Simultaneous intracranial EEG and/or scalp EEG. Performance was assessed using cross-validated areas under the receiver operating characteristic curve (AUC ROC) and precision-recall curve (AUC PR) and additional clinically relevant metrics. HEAnet was trained and validated using data sets that were derived from a convenience sample of 141 eligible participants (97 with TLE and 44 HCs without epilepsy) whose retrospective EEG data were readily available. Data set 1 included the simultaneous scalp EEG and intracranial electrode recordings of 51 patients with TLE (mean [SD] age, 40.7 [15.9] years; 30 men [59%]) at MGH. An automatically generated training data set with 972 095 positive HEA examples was created, in addition to a held-out expert-annotated testing data set with 22 762 positive HEA examples. HEAnet's performance was validated on 2 independent scalp EEG data sets: (1) data set 2 (at MGH; 24 patients with TLE and 20 HCs; mean [SD] age, 42.3 [16.2] years; 17 men [39%]) and (2) data set 3 (at BWH; 22 patients with TLE and 24 HCs; mean [SD] age, 43.0 [14.4] years; 20 men [43%]). For single-event detection of HEA on data set 1, HEAnet achieved a mean (SD) AUC ROC of 0.89 (0.01) and a mean (SD) AUC PR of 0.39 (0.03). On external validation with data sets 2 and 3, HEAnet accurately distinguished TLE from HC (AUC ROC of 0.88 and 0.95, respectively) and predicted epilepsy lateralization with 100% and 92% accuracy, respectively. HEAnet tracked dynamic changes in HEA in response to seizure medication adjustments and performed comparably with human experts in diagnosing TLE from 1-hour scalp EEG recordings, diagnosing TLE in several individuals that experts missed. Without reducing specificity, addition of HEAnet to human expert EEG review increased sensitivity for diagnosing TLE in humans from 50% to 58% to 63% to 67%. Results of this diagnostic study suggest that HEAnet provides a novel, noninvasive, quantitative, and clinically relevant biomarker of hippocampal hyperexcitability in humans.