Endocrine dysfunction in temporal lobe epilepsy.

Epilepsy patients face significantly elevated cardiovascular risks, with cardiac arrhythmias occurring 2-3 times more frequently than in the general population. Current knowledge of brain-heart functional coupling abnormalities in epilepsy, particularly during interictal periods, remains limited. We investigated brain-heart interplay characteristics in temporal lobe epilepsy through synchronized electroencephalographic-electrocardiographic analysis using a synthetic data generation model and microstate analysis. We enrolled 52 patients with temporal lobe epilepsy (mean age = 33.4 ± 12.7 years) and 42 age-matched healthy controls (mean age = 31.95 ± 11.03 years). Twenty-minute artifact-free electroencephalographic segments were analyzed during resting states. Four directional brain-heart coupling sequences were extracted: CBrain→HF, CBrain→LF, CHF→Brain, and CLF→Brain, representing bidirectional interactions between brain activity and cardiac components. Six microstate topologies were consistently identified across all brain-heart interplay sequences, with temporal lobe epilepsy patients demonstrating significantly more complex and unstable topological characteristics compared to healthy controls. For CBrain→HF coupling, patients exhibited significantly reduced mean duration of microstate 3 (.34 ± .09 s vs. .38 ± .07 s, p = .02), increased occurrence rates of microstates 3 and 4 (both p < .001), and altered temporal coverage patterns. Similar abnormalities were observed across all sequences, with patients showing shortened microstate durations, altered occurrence rates, and disrupted temporal coverage. Spatial dissimilarity analysis revealed significant topological abnormalities across all microstates. A logistic regression model incorporating microstate parameters achieved 94.7% diagnostic accuracy for temporal lobe epilepsy, with an F1 score of .952 and an area under the curve of .932. Temporal lobe epilepsy is characterized by profound disruptions in brain-heart functional coupling during interictal periods, manifesting as altered microstate topographies and temporal dynamics. These findings establish microstate-based analysis as a promising framework for characterizing brain-heart axis dysfunction in epilepsy.

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.

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

HYPOGONADISM, HYPERPROLACTINAEMIA, AND TEMPORAL LOBE EPILEPSY IN HYPOSEXUAL MEN

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

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.

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).

Neuron–astrocyte signaling and epilepsy

Clinical Neurophysiology: EEG–Video Monitoring

Gamma knife (GK) radiosurgery has been proposed as an alternative to classic microsurgery in mesial temporal lobe epilepsy (MTLE). Short-term follow-up studies have reported encouraging results, but long-term efficacy is not known. To report the efficacy and tolerance of GK radiosurgery in MTLE after a follow-up > 5 years. Patients with a follow-up > 5 years presenting with MTLE and treated with a marginal dose of 24 Gy were included in the study. Fifteen patients were included. Eight were treated on the left side, and 7 were treated on the right. The mean follow-up was 8 years (range 6-10 years). At the last follow-up, 9 of 16 patients (60%) were considered seizure free (Engel Class I) (4/16 in Class IA, 5/16 in Class IB). Seizure cessation occurred with a mean delay of 12 months (+/- 3) after GK radiosurgery, often preceded by a period of increasing aura or seizure occurrence (6/15 patients). The mean delay of appearance of the first neuroradiologic changes was 12 months (+/- 4). Nine patients (60%) experienced mild headache and were placed on corticosteroid treatment for a short period. All patients who were initially seizure free experienced a relapse of isolated aura (10/15, 66%) or complex partial seizures (10/15, 66%) during antiepileptic drug tapering. Restoration of treatment resulted in good control of seizures. Gamma knife radiosurgery is an effective and safe treatment for mesial temporal lobe epilepsy. Results are maintained over time with no additional side effects. Long-term results compare well with those of conventional surgery.

Recurrent spontaneous motor seizures after repeated low-dose systemic treatment with kainate: assessment of a rat model of temporal lobe epilepsy.

Elevated serum neuron-specific enolase in patients with temporal lobe epilepsy: A video–EEG study

Neuroinflammation may play a role in epilepsy. Translocator protein 18 kDa (TSPO), a biomarker of neuroinflammation, is overexpressed on activated microglia and reactive astrocytes. A preliminary positron emission tomographic (PET) imaging study using carbon 11 ([11C])-labeled PBR28 in patients with temporal lobe epilepsy (TLE) found increased TSPO ipsilateral to seizure foci. Full quantitation of TSPO in vivo is needed to detect widespread inflammation in the epileptic brain. To determine whether patients with TLE have widespread TSPO overexpression using [11C]PBR28 PET imaging, and to replicate relative ipsilateral TSPO increases in patients with TLE using [11C]PBR28 and another TSPO radioligand, [11C]DPA-713. In a cohort study from March 2009 through September 2013 at the Clinical Epilepsy Section of the National Institute of Neurological Disorders and Stroke, participants underwent brain PET and a subset had concurrent arterial sampling. Twenty-three patients with TLE and 11 age-matched controls were scanned with [11C]PBR28, and 8 patients and 7 controls were scanned with [11C]DPA-713. Patients with TLE had unilateral temporal seizure foci based on ictal electroencephalography and structural magnetic resonance imaging. Participants with homozygous low-affinity TSPO binding were excluded. The [11C]PBR28 distribution volume (VT) corrected for free fraction (fP) was measured in patients with TLE and controls using FreeSurfer software and T1-weighted magnetic resonance imaging for anatomical localization of bilateral temporal and extratemporal regions. Side-to-side asymmetry in patients with TLE was calculated as the ratio of ipsilateral to contralateral [11C]PBR28 and [11C]DPA-713 standardized uptake values from temporal regions. The [11C]PBR28 VT to fp ratio was higher in patients with TLE than in controls for all ipsilateral temporal regions (27%-42%; P < .05) and in contralateral hippocampus, amygdala, and temporal pole (approximately 30%-32%; P < .05). Individually, 12 patients, 10 with mesial temporal sclerosis, had asymmetrically increased hippocampal [11C]PBR28 uptake exceeding the 95% confidence interval of the controls. Binding of [11C]PBR28 was increased significantly in thalamus. Relative [11C]PBR28 and [11C]DPA-713 uptakes were higher ipsilateral than contralateral to seizure foci in patients with TLE ([11C]PBR28: 2%-6%; [11C]DPA-713: 4%-9%). Asymmetry of [11C]DPA-713 was greater than that of [11C]PBR28 (F = 29.4; P = .001). Binding of TSPO is increased both ipsilateral and contralateral to seizure foci in patients with TLE, suggesting ongoing inflammation. Anti-inflammatory therapy may play a role in treating drug-resistant epilepsy.

Positron emission tomography: Comparison of clinical utility in temporal lobe and extratemporal epilepsy