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Journal articles on the topic 'Temporal lobe epilepsy'

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Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Ribbeck Lourdes, Simbrón, Sandoval Paredes Josefina, Amador Sánchez Karen, and Taboada Barajas Jesús. "Uncinate Fasciculus in Temporal Lobe Epilepsy." Brain and Neurological Disorders 2, no. 2 (October 7, 2019): 01–04. http://dx.doi.org/10.31579/2642-973x/010.

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Background and purpose: Temporal lobe epilepsy is the most common focal intractable epilepsy. Uncinate fasciculus is a white fiber bundle that connects the orbitofrontal cortex with the anterior temporal lobe, and is implicated in most of the superior mental functions. There is evidence of uncinate fasciculus as a propagation pathway of seizures from temporal lobe. The aim of the study is to determine uncinate fasciculus alterations in patients with temporal lobe epilepsy, through fractional anisotropy. Methods: Thirty-three patients with temporal lobe epilepsy (10 right and 23 left) were studied. All of them were right-handed and had left hemisphere dominance for language. A 1.5 T MR imaging scanner was used to obtain diffusion tensor imaging (DTI). Fractional anisotropy of uncinate fasciculus was calculated through TBSS (Tract Based Spatial Statistics). Statistical analysis was done using IBM SPSS (v. 25). Results: Fractional anisotropy was higher in right uncinate fasciculus, regardless of epilepsy side. Right uncinate fasciculus, at the insula level, showed lower fractional anisotropy in patients with right temporal lobe epilepsy. Conclusions: Results support the evidence of uncinate fasciculus as a pathway of propagation in temporal lobe epilepsy, specially at insular level.

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2

Engel, Jerome. "When is temporal lobe epilepsy not temporal lobe epilepsy?" Brain 139, no. 2 (January 29, 2016): 309–12. http://dx.doi.org/10.1093/brain/awv374.

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3

Grassia, Fabio, Andrew V. Poliakov, Sandra L. Poliachik, Kaitlyn Casimo, Seth D. Friedman, Hillary Shurtleff, Carlo Giussani, Edward J. Novotny, Jeffrey G. Ojemann, and Jason S. Hauptman. "Changes in resting-state connectivity in pediatric temporal lobe epilepsy." Journal of Neurosurgery: Pediatrics 22, no. 3 (September 2018): 270–75. http://dx.doi.org/10.3171/2018.3.peds17701.

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OBJECTIVEFunctional connectivity magnetic resonance imaging (fcMRI) is a form of fMRI that allows for analysis of blood oxygen level–dependent signal changes within a task-free, resting paradigm. This technique has been shown to have efficacy in evaluating network connectivity changes with epilepsy. Presurgical data from patients with unilateral temporal lobe epilepsy were evaluated using the fcMRI technique to define connectivity changes within and between the diseased and healthy temporal lobes using a within-subjects design.METHODSUsing presurgical fcMRI data from pediatric patients with unilateral temporal lobe epilepsy, the authors performed seed-based analyses within the diseased and healthy temporal lobes. Connectivity within and between temporal lobe seeds was measured and compared.RESULTSIn the cohort studied, local ipsilateral temporal lobe connectivity was significantly increased on the diseased side compared to the healthy temporal lobe. Connectivity of the diseased side to the healthy side, on the other hand, was significantly reduced when compared to connectivity of the healthy side to the diseased temporal lobe. A statistically significant regression was observed when comparing the changes in local ipsilateral temporal lobe connectivity to the changes in inter–temporal lobe connectivity. A statistically significant difference was also noted in ipsilateral connectivity changes between patients with and those without mesial temporal sclerosis.CONCLUSIONSUsing fcMRI, significant changes in ipsilateral temporal lobe and inter–temporal lobe connectivity can be appreciated in unilateral temporal lobe epilepsy. Furthermore, fcMRI may have a role in the presurgical evaluation of patients with intractable temporal lobe epilepsy.

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4

Sundram, Frederick, Mary Cannon, Colin P. Doherty, Gareth J. Barker, Mary Fitzsimons, Norman Delanty, and David Cotter. "Neuroanatomical correlates of psychosis in temporal lobe epilepsy: voxel-based morphometry study." British Journal of Psychiatry 197, no. 6 (December 2010): 482–92. http://dx.doi.org/10.1192/bjp.bp.110.080218.

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BackgroundTemporal lobe epilepsy is associated with a significant risk of psychosis but there are only limited studies investigating the underlying neurobiology.AimsTo characterise neuroanatomical changes in temporal lobe epilepsy and comorbid psychosis.MethodThe study population comprised all individuals with temporal lobe epilepsy on the epilepsy database at the National Centre for Epilepsy and Epilepsy Neurosurgery in Ireland (Beaumont Hospital) between 2002 and 2006. Ten people with temporal lobe epilepsy with psychosis were matched for age, gender, handedness, epilepsy duration, seizure laterality, severity of epilepsy and anti-epileptic medication with ten comparison participants with temporal lobe epilepsy only. Participants received a magnetic resonance imaging scan and voxel-based morphometry analyses were applied to grey and white matter anatomy.ResultsSignificant grey matter reduction was found bilaterally in those with temporal lobe epilepsy with psychosis in the temporal lobes in the inferior, middle and superior temporal gyri and fusiform gyri, and unilaterally in the left parahippocampal gyrus and hippocampus. Significant extra-temporal grey matter reduction was found bilaterally in the insula, cerebellum, caudate nuclei and in the right cingulum and left inferior parietal lobule. Significant white matter reduction in those with temporal lobe epilepsy with psychosis was found bilaterally in the hippocampus, parahippocampal/fusiform gyri, middle/inferior temporal gyri, cingulum, corpus callosum, posterior thalamic radiation, anterior limb of internal capsule and white matter fibres from the caudate nuclei, and unilaterally in the left lingual gyrus and right midbrain and superior temporal gyrus.ConclusionsSignificant grey and white matter deficits occur in temporal lobe epilepsy with psychosis. These encompass the medial temporal lobe structures but also extend to lateral temporal and extra-temporal regions. Some of these deficits overlap with those found in schizophrenia.

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Franzon, Renata C., and Marilisa M. Guerreiro. "Temporal lobe epilepsy in childhood: review article." Journal of Epilepsy and Clinical Neurophysiology 12, no. 1 suppl 1 (March 2006): 26–31. http://dx.doi.org/10.1590/s1676-26492006000200006.

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INTRODUCTION: The authors present a review article on temporal lobe epilepsy in childhood. METHODS: We performed a search in the literature. RESULTS: The main etiologies of temporal lobe epilepsy in childhood are developmental tumors and focal cortical displasia, besides temporal medial sclerosis. The clinical features may be variable particularly in children younger than six years of age. Epilepsy may present with generalized seizures. Electroencephalographic findings are also variable and show a functional dysfunction of several brain areas besides temporal lobes, especially frontal lobes. CONCLUSION: Recent advances demonstrate that temporal lobe epilepsy in childhood present with great etiologic, clinical and electroencephalographic diversity.

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6

Valente, Kette D. R., and Geraldo Busatto Filho. "Depression and temporal lobe epilepsy represent an epiphenomenon sharing similar neural networks: clinical and brain structural evidences." Arquivos de Neuro-Psiquiatria 71, no. 3 (March 2013): 183–90. http://dx.doi.org/10.1590/s0004-282x2013000300011.

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The relationship between depression and epilepsy has been known since ancient times, however, to date, it is not fully understood. The prevalence of psychiatric disorders in persons with epilepsy is high compared to general population. It is assumed that the rate of depression ranges from 20 to 55% in patients with refractory epilepsy, especially considering those with temporal lobe epilepsy caused by mesial temporal sclerosis. Temporal lobe epilepsy is a good biological model to understand the common structural basis between depression and epilepsy. Interestingly, mesial temporal lobe epilepsy and depression share a similar neurocircuitry involving: temporal lobes with hippocampus, amygdala and entorhinal and neocortical cortex; the frontal lobes with cingulate gyrus; subcortical structures, such as basal ganglia and thalamus; and the connecting pathways. We provide clinical and brain structural evidences that depression and epilepsy represent an epiphenomenon sharing similar neural networks.

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7

Carne, Ross P., Terence J. O'Brien, Christine J. Kilpatrick, Lachlan R. MacGregor, Rodney J. Hicks, Michael A. Murphy, Stephen C. Bowden, Andrew H. Kaye, and Mark J. Cook. "Temporal Lobe Epilepsy." Journal of Neurosurgery 103, no. 4 (October 2005): 768–69. http://dx.doi.org/10.3171/jns.2005.103.4.0768.

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Abstract Object. The syndrome of medial temporal lobe epilepsy (MTLE) may occur in patients in whom magnetic resonance (MR) images demonstrate normal findings. In these patients, there is no evidence of hippocampal sclerosis on neuroimaging, and histopathological examination of the resected hippocampus does not reveal significant neuron loss. In this paper the authors describe the distinct clinical features of this MTLE subtype, referred to as paradoxical temporal lobe epilepsy (PTLE). Methods. The authors selected 12 consecutive patients with preoperative findings consistent with MTLE in whom MR imaging did not demonstrate any hippocampal abnormality. Onset of hippocampal seizure was confirmed by long-term intracranial monitoring. There were six female and six male patients with a mean age of 32 ± 11 years (mean ± standard deviation [SD]) at presentation. These patients' seizure histories, available hippocampal volumetric measurements, and hippocampal cell densities in different subfields were reviewed. Sharp electrode recordings from dentate granule cells that had been maintained in hippocampal slices provided a measure of excitation and inhibition in the tissue. We compared these data with those of a cohort of 50 randomly selected patients who underwent anteromedial temporal resection for medial temporal sclerosis (MTS) during the same time period (1987–1999). The durations of follow up (means ± SDs) for the PTLE and MTS groups were 51 ± 59 months and 88 ± 44 months, respectively. A history of febrile seizure was present less frequently in the PTLE group (8%) than in the MTS group (34%). Other risk factors for epilepsy such as trauma, meningoencephalitis, or perinatal injuries were present more frequently in the PTLE group (50%) than in the MTS cohort (36%). In patients in the PTLE group the first seizure occurred later in life (mean age at seizure onset 14 years in the PTLE group compared with 9 years in the MTS group, p = 0.09). Ten patients (83%) in the PTLE cohort and 23 patients (46%) in the MTLE cohort had secondary generalization of their seizures. Among patients with PTLE, volumetric measurements (five patients) and randomized blinded visual inspection (seven patients) of the bilateral hippocampi revealed no atrophy and no increased T2 signal change on preoperative MR images. All patients with PTLE underwent anteromedial temporal resection (amygdalohippocampectomy, in five patients on the left side and in seven on the right side). Electrophysiological studies of hippocampal slices demonstrated that dentate granule cells from patients with PTLE were significantly less excitable than those from patients with MTS. The mean pyramidal cell loss in the CA1 subfield in patients in the PTLE group was 20% (range 0–59%) and that in patients in the MTS group was 75% (range 41–90%) (p < 0.001). Maximal neuron loss (mean loss 38%) occurred in the CA4 region in six patients with PTLE (end folium sclerosis). At the last follow-up examination, six patients (50%) in the PTLE group were seizure free compared with 38 patients (76%) in the MTS group. Conclusions. Clinical PTLE is a distinct syndrome with clinical features and surgical outcomes different from those of MTS.

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8

Beit-Jones, Meredith S., and Lissa Robins Kapust. "Temporal Lobe Epilepsy." Social Work in Health Care 11, no. 2 (March 10, 1986): 17–33. http://dx.doi.org/10.1300/j010v11n02_02.

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9

Bernhardt, Boris C., Fatemeh Fadaie, Min Liu, Benoit Caldairou, Shi Gu, Elizabeth Jefferies, Jonathan Smallwood, Danielle S. Bassett, Andrea Bernasconi, and Neda Bernasconi. "Temporal lobe epilepsy." Neurology 92, no. 19 (April 19, 2019): e2209-e2220. http://dx.doi.org/10.1212/wnl.0000000000007447.

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ObjectiveTo assess whether hippocampal sclerosis (HS) severity is mirrored at the level of large-scale networks.MethodsWe studied preoperative high-resolution anatomical and diffusion-weighted MRI of 44 temporal lobe epilepsy (TLE) patients with histopathologic diagnosis of HS (n = 25; TLE-HS) and isolated gliosis (n = 19; TLE-G) and 25 healthy controls. Hippocampal measurements included surface-based subfield mapping of atrophy and T2 hyperintensity indexing cell loss and gliosis, respectively. Whole-brain connectomes were generated via diffusion tractography and examined using graph theory along with a novel network control theory paradigm that simulates functional dynamics from structural network data.ResultsCompared to controls, we observed markedly increased path length and decreased clustering in TLE-HS compared to controls, indicating lower global and local network efficiency, while TLE-G showed only subtle alterations. Similarly, network controllability was lower in TLE-HS only, suggesting limited range of functional dynamics. Hippocampal imaging markers were positively associated with macroscale network alterations, particularly in ipsilateral CA1-3. Systematic assessment across several networks revealed maximal changes in the hippocampal circuity. Findings were consistent when correcting for cortical thickness, suggesting independence from gray matter atrophy.ConclusionsSevere HS is associated with marked remodeling of connectome topology and structurally governed functional dynamics in TLE, as opposed to isolated gliosis, which has negligible effects. Cell loss, particularly in CA1-3, may exert a cascading effect on brain-wide connectomes, underlining coupled disease processes across multiple scales.

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10

Garyfallos, George, Nikolas Manos, and Aravela Adamopoulou. "Temporal Lobe Epilepsy." British Journal of Psychiatry 153, no. 6 (December 1988): 852–53. http://dx.doi.org/10.1192/bjp.153.6.852.

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11

Hermann, Bruce, and Michael Seidenberg. "Neuropsychology and Temporal Lobe Epilepsy." CNS Spectrums 7, no. 5 (May 2002): 343–48. http://dx.doi.org/10.1017/s1092852900017806.

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ABSTRACTThe purpose of this article is to review aspects of the neuropsychology of temporal lobe epilepsy. Evidence will be presented to demonstrate that the cognitive consequences of this focal seizure disorder can be more generalized in nature than expected. Consistent with the extratemporal neurocognitive findings, careful quantitative magnetic resonance imaging volumetrics have shown that structural brain changes may be detected outside the temporal lobes. Many factors can potentially affect cognition and brain structure. We focus on the potential neurodevelopmental impact of early-onset temporal lobe epilepsy on brain structure and cognition positing that this disorder can have both immediate and lifespan implications for cognition and psychosocial status.

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12

Fried, Itzhak. "Anatomic Temporal Lobe Resections for Temporal Lobe Epilepsy." Neurosurgery Clinics of North America 4, no. 2 (April 1993): 233–42. http://dx.doi.org/10.1016/s1042-3680(18)30590-4.

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13

Blair, Robert D. G. "Temporal Lobe Epilepsy Semiology." Epilepsy Research and Treatment 2012 (March 7, 2012): 1–10. http://dx.doi.org/10.1155/2012/751510.

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Epilepsy represents a multifaceted group of disorders divided into two broad categories, partial and generalized, based on the seizure onset zone. The identification of the neuroanatomic site of seizure onset depends on delineation of seizure semiology by a careful history together with video-EEG, and a variety of neuroimaging technologies such as MRI, fMRI, FDG-PET, MEG, or invasive intracranial EEG recording. Temporal lobe epilepsy (TLE) is the commonest form of focal epilepsy and represents almost 2/3 of cases of intractable epilepsy managed surgically. A history of febrile seizures (especially complex febrile seizures) is common in TLE and is frequently associated with mesial temporal sclerosis (the commonest form of TLE). Seizure auras occur in many TLE patients and often exhibit features that are relatively specific for TLE but few are of lateralizing value. Automatisms, however, often have lateralizing significance. Careful study of seizure semiology remains invaluable in addressing the search for the seizure onset zone.

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14

Barba, Carmen, Sylvain Rheims, Lorella Minotti, Marc Guénot, Dominique Hoffmann, Stephan Chabardès, Jean Isnard, Philippe Kahane, and Philippe Ryvlin. "Temporal plus epilepsy is a major determinant of temporal lobe surgery failures." Brain 139, no. 2 (December 23, 2015): 444–51. http://dx.doi.org/10.1093/brain/awv372.

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Abstract See Engel (doi:10.1093/awv374) for a scientific commentary on this article. Reasons for failed temporal lobe epilepsy surgery remain unclear. Temporal plus epilepsy, characterized by a primary temporal lobe epileptogenic zone extending to neighboured regions, might account for a yet unknown proportion of these failures. In this study all patients from two epilepsy surgery programmes who fulfilled the following criteria were included: (i) operated from an anterior temporal lobectomy or disconnection between January 1990 and December 2001; (ii) magnetic resonance imaging normal or showing signs of hippocampal sclerosis; and (iii) postoperative follow-up ≥ 24 months for seizure-free patients. Patients were classified as suffering from unilateral temporal lobe epilepsy, bitemporal epilepsy or temporal plus epilepsy based on available presurgical data. Kaplan-Meier survival analysis was used to calculate the probability of seizure freedom over time. Predictors of seizure recurrence were investigated using Cox proportional hazards model. Of 168 patients included, 108 (63.7%) underwent stereoelectroencephalography, 131 (78%) had hippocampal sclerosis, 149 suffered from unilateral temporal lobe epilepsy (88.7%), one from bitemporal epilepsy (0.6%) and 18 (10.7%) from temporal plus epilepsy. The probability of Engel class I outcome at 10 years of follow-up was 67.3% (95% CI: 63.4–71.2) for the entire cohort, 74.5% (95% CI: 70.6–78.4) for unilateral temporal lobe epilepsy, and 14.8% (95% CI: 5.9–23.7) for temporal plus epilepsy. Multivariate analyses demonstrated four predictors of seizure relapse: temporal plus epilepsy (P < 0.001), postoperative hippocampal remnant (P = 0.001), past history of traumatic or infectious brain insult (P = 0.022), and secondary generalized tonic-clonic seizures (P = 0.023). Risk of temporal lobe surgery failure was 5.06 (95% CI: 2.36–10.382) greater in patients with temporal plus epilepsy than in those with unilateral temporal lobe epilepsy. Temporal plus epilepsy represents a hitherto unrecognized prominent cause of temporal lobe surgery failures. In patients with temporal plus epilepsy, anterior temporal lobectomy appears very unlikely to control seizures and should not be advised. Whether larger resection of temporal plus epileptogenic zones offers greater chance of seizure freedom remains to be investigated.

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Bercovici, Eduard, Balagobal Santosh Kumar, and Seyed M. Mirsattari. "Neocortical Temporal Lobe Epilepsy." Epilepsy Research and Treatment 2012 (July 16, 2012): 1–15. http://dx.doi.org/10.1155/2012/103160.

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Complex partial seizures (CPSs) can present with various semiologies, while mesial temporal lobe epilepsy (mTLE) is a well-recognized cause of CPS, neocortical temporal lobe epilepsy (nTLE) albeit being less common is increasingly recognized as separate disease entity. Differentiating the two remains a challenge for epileptologists as many symptoms overlap due to reciprocal connections between the neocortical and the mesial temporal regions. Various studies have attempted to correctly localize the seizure focus in nTLE as patients with this disorder may benefit from surgery. While earlier work predicted poor outcomes in this population, recent work challenges those ideas yielding good outcomes in part due to better localization using improved anatomical and functional techniques. This paper provides a comprehensive review of the diagnostic workup, particularly the application of recent advances in electroencephalography and functional brain imaging, in neocortical temporal lobe epilepsy.

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Sato, Mitsumoto, and Matsue Miyasaka. "Symposium: Temporal Lobe Epilepsy." Psychiatry and Clinical Neurosciences 48, no. 2 (June 1994): 203–4. http://dx.doi.org/10.1111/j.1440-1819.1994.tb03051.x.

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17

Benbadis, S. R., W. A. Gerson, J. H. Harvey, and H. O. Luders. "Photosensitive temporal lobe epilepsy." Neurology 46, no. 6 (June 1, 1996): 1540–42. http://dx.doi.org/10.1212/wnl.46.6.1540.

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18

Bernasconi, A., F. Andermann, F. Cendes, F. Dubeau, E. Andermann, and A. Olivier. "Nocturnal temporal lobe epilepsy." Neurology 50, no. 6 (June 1, 1998): 1772–77. http://dx.doi.org/10.1212/wnl.50.6.1772.

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19

Gambardella, Antonio, Demetrio Messina, Emilio Le Piane, R. Luciano Oliveri, Grazia Annesi, Mario Zappia, Eva Andermann, Aldo Quattrone, and Umberto Aguglia. "Familial temporal lobe epilepsy." Epilepsy Research 38, no. 2-3 (February 2000): 127–32. http://dx.doi.org/10.1016/s0920-1211(99)00080-7.

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20

Gordon, Neil. "Familial temporal-lobe epilepsy." Developmental Medicine & Child Neurology 41, no. 7 (July 1999): 501–2. http://dx.doi.org/10.1017/s0012162299001073.

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21

Tatum, William O. "Mesial Temporal Lobe Epilepsy." Journal of Clinical Neurophysiology 29, no. 5 (October 2012): 356–65. http://dx.doi.org/10.1097/wnp.0b013e31826b3ab7.

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22

Kennedy, Jeffrey D., and Stephan U. Schuele. "Neocortical Temporal Lobe Epilepsy." Journal of Clinical Neurophysiology 29, no. 5 (October 2012): 366–70. http://dx.doi.org/10.1097/wnp.0b013e31826bd78b.

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23

Gambardella, Antonio. "Benign temporal lobe epilepsy." Epilepsia 51 (February 2010): 45–46. http://dx.doi.org/10.1111/j.1528-1167.2009.02444.x.

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Gordon, Neil. "Familial temporal-lobe epilepsy." Developmental Medicine & Child Neurology 41, no. 7 (July 1999): 501–2. http://dx.doi.org/10.1111/j.1469-8749.1999.tb00645.x.

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Panday, Avidesh, Chrystal Calderon, Sherry Sandy, and Devindra Ramnarine. "Mesial temporal lobe epilepsy." International Journal of Surgery Case Reports 65 (2019): 275–78. http://dx.doi.org/10.1016/j.ijscr.2019.10.063.

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26

Gerson, W., S. Benbadis, J. Harvey, and H. Lüders. "Photosensitive temporal lobe epilepsy." Electroencephalography and Clinical Neurophysiology 95, no. 2 (August 1995): P39. http://dx.doi.org/10.1016/0013-4694(95)98027-6.

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27

Schofield, G. M. "Mesial Temporal Lobe Epilepsy." Archives of Neurology 55, no. 5 (May 1, 1998): 754. http://dx.doi.org/10.1001/archneur.55.5.754.

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28

Landazuri, Patrick. "Mesial Temporal Lobe Epilepsy: A Distinct Electroclinical Subtype of Temporal Lobe Epilepsy." Neurodiagnostic Journal 54, no. 3 (September 2014): 274–88. http://dx.doi.org/10.1080/21646821.2014.11106809.

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Chandanala, Shashank, Harishchandra Prasad YS, Chiatra Venugopal, and Anandh Dhanushkodi. "Stem Cells Based Therapy for Temporal Lobe Epilepsy." JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 04, no. 2 (June 15, 2014): 267–71. http://dx.doi.org/10.58739/jcbs/v04i2.12.

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CUKIERT, ARTHUR, CASSIO FORSTER, MARIO S. D. ANDRIOLI, and LEILA FRAYMAN. "Insular epilepsy: similarities to temporal lobe epilepsy case report." Arquivos de Neuro-Psiquiatria 56, no. 1 (March 1998): 126–28. http://dx.doi.org/10.1590/s0004-282x1998000100022.

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Insular epilepsy has been rarely reported and its clinical and electrographic features are poorly understood. The electrographic study of the insula is difficult since it is hidden from the brain surface by the frontal and temporal lobe. A 48 years-old woman started having simple partial autonomic and complex partial seizures with automatisms and ictal left arm paresis 8 years prior to admission. Seizure's frequency was 1 per week. Pre-operative EEG showed a right temporal lobe focus. Neuropsychological testing disclosed right fronto-temporal dysfunction. MRI showed a right anterior insular cavernous angioma. Intraoperative ECoG obtained after spliting of the sylvian fissure showed independent spiking from the insula and temporal lobe and insular spikes that spread to the temporal lobe. The cavernous angioma and the surrounding gliotic tissue were removed and the temporal lobe was left in place. Post-resection ECoG still disclosed independent temporal and insular spiking with a lower frequency. The patient has been seizure-free since surgery. Insular epilepsy may share many clinical and electroencephalographic features with temporal lobe epilepsy.

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Ferreira, Fabio Thadeu, Eliane Kobayashi, Iscia Lopes-Cendes, and Fernando Cendes. "Structural Abnormalities are Similar in Familial and Nonfamilial Mesial Temporal Lobe Epilepsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 31, no. 3 (August 2004): 368–72. http://dx.doi.org/10.1017/s0317167100003462.

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Background/Objective:Diffuse temporal lobe abnormalities can be observed on MRI of patients with mesial temporal lobe epilepsy (MTLE). Our objective was to perform qualitative and quantitative analyses of temporal lobe structures in patients with familial MTLE (FMTLE) and nonfamilial MTLE.Methods:Two groups of patients were ascertained: 67 FMTLE patients (14 with refractory seizures) and 30 patients with nonfamilial refractory MTLE. We performed qualitative analyses of MRI (with multiplanar reconstruction) and volumes of hippocampi and anterior temporal lobes in all patients, and in a normal control group of 23 individuals. We used the Chi-square test and ANOVA for statistical analyses.Results:We identified anterior temporal lobe abnormalities by visual analysis in only 4% of FMTLE patients and atrophy of the anterior temporal lobe by volumetric analysis in 19%. In the group of nonfamilial MTLE patients we found anterior temporal lobe abnormalities by visual analysis in 17% of patients and anterior temporal lobe atrophy in 13%. Hippocampal atrophy was present in 90% of FMTLE and in 83% of nonfamilial MTLE. No signs of cortical dysplasia were observed.Conclusion:Anterior temporal lobe atrophy and other abnormalities outside the mesial portion of temporal lobes were infrequent in both familial and nonfamilial MTLE patients. Despite the genetic basis, hippocampal atrophy in FMTLE is not associated with other abnormalities outside the mesial temporal regions.

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Halász, Péter. "The medial temporal lobe epilepsy is a bilateral disease – novel aspects." Journal of Epileptology 24, no. 2 (December 1, 2016): 141–55. http://dx.doi.org/10.1515/joepi-2016-0010.

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SummaryIntroduction.Medial temporal lobe epilepsy (MTLE) is the most frequent form of epilepsy in adulthood. It is classified as local/regional epilepsy. However, there is increasing evidence of the involvement of both temporal lobes and this provides abundant arguments to question this view, and consider MTLE as one of the typical bilateral system epilepsies.Aim.To provide a contemporary review of medial temporal lobe epilepsy, discussing the bilateral aspects, with reference to epilepsy surgery.Methods.A literature review and a resume of the author’s own experiences with MTLE patients.Results.Recent electrophysiological and neuroimaging data provide convincing data supporting that MTLE is a bilateral disease. The uni-and bilateral features form a continuum and the participation rate of the two temporal lobes determine course and surgical perspective of the individual patient.Conclusions.The contradictory data of invasive presurgical evaluations of MTLE patients suggest that there need to identify further indicatory markers of bilaterality and thus change the presurgical evaluation from the non-invasive towards the invasive ways. The mechanisms of the interrelationship between the two temporal lobes in MTLE warrants further research.

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Al Sufiani, Fahd, and Lee Cyn Ang. "Neuropathology of Temporal Lobe Epilepsy." Epilepsy Research and Treatment 2012 (April 12, 2012): 1–13. http://dx.doi.org/10.1155/2012/624519.

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Pathologic findings in surgical resections from patients with temporal lobe epilepsy include a wide range of diagnostic possibilities that can be categorized into different groups on the basis of etiology. This paper outlines the various pathologic entities described in temporal lobe epilepsy, including some newly recognized epilepsy-associated tumors, and briefly touch on the recent classification of focal cortical dysplasia. This classification takes into account coexistent pathologic lesions in focal cortical dysplasia.

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Peplow, PhilipV, and Bridget Martinez. "MicroRNAs as potential biomarkers in temporal lobe epilepsy and mesial temporal lobe epilepsy." Neural Regeneration Research 18, no. 4 (2023): 716. http://dx.doi.org/10.4103/1673-5374.354510.

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35

Bertram, Edward H. "Extratemporal lobe circuits in temporal lobe epilepsy." Epilepsy & Behavior 38 (September 2014): 13–18. http://dx.doi.org/10.1016/j.yebeh.2014.07.012.

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Stretton, J., and P. J. Thompson. "Frontal lobe function in temporal lobe epilepsy." Epilepsy Research 98, no. 1 (January 2012): 1–13. http://dx.doi.org/10.1016/j.eplepsyres.2011.10.009.

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37

Leblanc, Richard, Donatella Tampieri, Yves Robitaille, André Olivier, Frederick Andermann, and Alan Sherwin. "Developmental anterobasal temporal encephalocele and temporal lobe epilepsy." Journal of Neurosurgery 74, no. 6 (June 1991): 933–39. http://dx.doi.org/10.3171/jns.1991.74.6.0933.

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✓ The authors describe the association between an anterobasal temporal lobe encephalocele and medically intractable temporal lobe epilepsy in three patients treated successfully by surgery. Two men and one woman, aged 26 to 37 years (mean 31 years), had onset of complex automatism and generalized seizures in their second and fourth decades (mean age 22.7 years). They had been epileptic for 6 to 14 years (mean 8.3 years) before surgery. Preoperative electroencephalograms localized ictal epileptic activity to the left mesial temporal lobe in all cases, and neuropsychological testing revealed dominant temporal lobe dysfunction. Magnetic resonance (MR) imaging demonstrated an anteromedial basal temporal encephalocele extending into the pterygopalatine fossa through a bone defect at the base of the greater sphenoid wing in the region of the foramen rotundum and pterygoid process, a discrete center of embryonal chondrification. At surgery, the encephaloceles were found in front of the uncus, and an area of gliosis extended from the encephalocele to the amygdalohippocampal region. All patients have been seizure-free following anterior temporal resection and amygdalohippocampectomy including the encephalocele. These three cases delineate a condition of disordered embryogenesis wherein a developmental anterobasal temporal encephalocele acts as the substrate for temporal lobe epilepsy. This lesion may be diagnosed preoperatively with MR imaging and should be considered in the differential diagnosis of late-onset temporal lobe epilepsy.

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Chen, Feng, Xi Dong, Zhenhuan Wang, Tongrui Wu, Liangpeng Wei, Yuanyuan Li, Kai Zhang, et al. "Regulation of specific abnormal calcium signals in the hippocampal CA1 and primary cortex M1 alleviates the progression of temporal lobe epilepsy." Neural Regeneration Research 19, no. 2 (July 7, 2023): 425–33. http://dx.doi.org/10.4103/1673-5374.379048.

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Abstract JOURNAL/nrgr/04.03/01300535-202402000-00037/inline-graphic1/v/2023-07-19T141749Z/r/image-tiff Temporal lobe epilepsy is a multifactorial neurological dysfunction syndrome that is refractory, resistant to antiepileptic drugs, and has a high recurrence rate. The pathogenesis of temporal lobe epilepsy is complex and is not fully understood. Intracellular calcium dynamics have been implicated in temporal lobe epilepsy. However, the effect of fluctuating calcium activity in CA1 pyramidal neurons on temporal lobe epilepsy is unknown, and no longitudinal studies have investigated calcium activity in pyramidal neurons in the hippocampal CA1 and primary motor cortex M1 of freely moving mice. In this study, we used a multi-channel fiber photometry system to continuously record calcium signals in CA1 and M1 during the temporal lobe epilepsy process. We found that calcium signals varied according to the grade of temporal lobe epilepsy episodes. In particular, cortical spreading depression, which has recently been frequently used to represent the continuously and substantially increased calcium signals, was found to correspond to complex and severe behavioral characteristics of temporal lobe epilepsy ranging from grade II to grade V. However, vigorous calcium oscillations and highly synchronized calcium signals in CA1 and M1 were strongly related to convulsive motor seizures. Chemogenetic inhibition of pyramidal neurons in CA1 significantly attenuated the amplitudes of the calcium signals corresponding to grade I episodes. In addition, the latency of cortical spreading depression was prolonged, and the above-mentioned abnormal calcium signals in CA1 and M1 were also significantly reduced. Intriguingly, it was possible to rescue the altered intracellular calcium dynamics. Via simultaneous analysis of calcium signals and epileptic behaviors, we found that the progression of temporal lobe epilepsy was alleviated when specific calcium signals were reduced, and that the end-point behaviors of temporal lobe epilepsy were improved. Our results indicate that the calcium dynamic between CA1 and M1 may reflect specific epileptic behaviors corresponding to different grades. Furthermore, the selective regulation of abnormal calcium signals in CA1 pyramidal neurons appears to effectively alleviate temporal lobe epilepsy, thereby providing a potential molecular mechanism for a new temporal lobe epilepsy diagnosis and treatment strategy.

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HERMANN, BRUCE, MICHAEL SEIDENBERG, BRIAN BELL, PAUL RUTECKI, RAJ D. SHETH, GARY WENDT, DANIEL O'LEARY, and VINCE MAGNOTTA. "Extratemporal quantitative MR volumetrics and neuropsychological status in temporal lobe epilepsy." Journal of the International Neuropsychological Society 9, no. 3 (February 25, 2003): 353–62. http://dx.doi.org/10.1017/s1355617703930013.

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Neuropsychological studies of temporal lobe epilepsy have focused heavily on the nature and extent of memory dysfunction and its relationship to the neuropathological status of the hippocampus and related mesial temporal lobe structures. In this study, we examined whole brain and lobar quantitative MRI volumes and comprehensive neuropsychological performance in 58 patients with temporal lobe epilepsy and 62 healthy controls in order to determine (1) the nature and degree of extratemporal structural abnormalities in localization-related temporal lobe epilepsy; (2) the nature and degree of cognitive abnormalities outside of anterograde memory function; and (3) the relationship of volumetric abnormalities to neuropsychological status. Temporal lobe epilepsy patients exhibited significant reduction in the volume of adjusted (age, gender, height) total cerebral tissue (−5.8%), more evident in white (−9.8%) compared to gray matter (−3.0%) tissue volumes. Significant volumetric reductions were evident across frontal, temporal and parietal but not occipital lobe regions. Subarachnoid but not total ventricular CSF was significantly increased in epilepsy patients. Neuropsychological abnormality was generalized in nature, consistent with the generalized nature of the morphometric abnormalities, and reductions in cerebral tissue volumes were directly associated with poorer cognitive performance. In summary, patients with temporal lobe epilepsy exhibited clinically significant structural and functional abnormalities that extended outside the epileptogenic temporal lobe. The degree to which these structural and cognitive abnormalities are due to factors that cause the epilepsy, as opposed to reflecting the consequences of chronic epilepsy (e.g., duration and severity of epilepsy), remain to be determined. (JINS, 2003, 9, 353–362.)

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Choi, Hyunmi, Randall L. Sell, Leslie Lenert, Peter Muennig, Robert R. Goodman, Frank G. Gilliam, and John B. Wong. "Epilepsy Surgery for Pharmacoresistant Temporal Lobe Epilepsy." JAMA 300, no. 21 (December 3, 2008): 2497. http://dx.doi.org/10.1001/jama.2008.771.

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Kanner, Andres M. "Negative Symptoms in Temporal Lobe Epilepsy." Epilepsy Currents 2, no. 5 (September 2002): 168–69. http://dx.doi.org/10.1111/j.1535-7597.2002.00063.x.

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Negative Symptoms in Temporal Lobe Epilepsy Getz K, Hermann B, Seidenberg M, Bell B, Dow C, Jones J, Woodard A, Rutecki P, Sheth R, O'Leary D, Magnotta V. Am J Psychiatry 2002;159:644–651 Objective This study examined the frequency of negative and positive symptoms in nonpsychotic patients with temporal lobe epilepsy and the relationship of negative and positive symptoms to cognition, quantitative magnetic resonance imaging (MRI) volumetrics, and depression. Method Eighty-four patients with temporal lobe epilepsy and 74 healthy comparison subjects were evaluated for negative and positive symptoms and underwent comprehensive neuropsychological evaluation, quantitative MRI volumetrics, and assessment of mood state and depression. Results Negative symptoms were significantly more prevalent in the patients with temporal lobe epilepsy (31%) than in the comparison subjects (8%). There was no difference between groups in the rate of positive symptoms. Although the epilepsy patients as a group exhibited generalized cognitive impairment relative to the comparison subjects, the epilepsy patients with negative symptoms performed significantly worse than patients without negative symptoms and comparison subjects across measures of nonverbal intelligence, visuoperception, speeded visuomotor processing, and memory. The epilepsy patients with negative symptoms exhibited significantly greater diffuse atrophy than the healthy comparison subjects and higher CSF volumes than the epilepsy patients without negative symptoms. The epilepsy patients with and without negative symptoms had statistically equivalent Beck Depression Inventory scores and lifetime history of mood disorders, including major depression. Conclusions Negative but not positive symptoms were more prevalent in temporal lobe epilepsy patients than in healthy comparison subjects. Negative symptoms were independent of current and past depression and were associated with neuropsychological deficits exceeding the general cognitive morbidity associated with temporal lobe epilepsy and with quantitative MRI indices, suggesting greater cerebral atrophy.

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Trimmel, Karin, Andre L. van Graan, Lorenzo Caciagli, Anja Haag, Matthias J. Koepp, Pamela J. Thompson, and John S. Duncan. "Left temporal lobe language network connectivity in temporal lobe epilepsy." Brain 141, no. 8 (June 23, 2018): 2406–18. http://dx.doi.org/10.1093/brain/awy164.

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Lee, J. W., F. Andermann, F. Dubeau, A. Bernasconi, D. MacDonald, A. Evans, and D. C. Reutens. "Morphometric Analysis of the Temporal Lobe in Temporal Lobe Epilepsy." Epilepsia 39, no. 7 (July 1998): 727–36. http://dx.doi.org/10.1111/j.1528-1157.1998.tb01158.x.

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Uddin, F. J., C. Nogueira, and A. Sama. "An unusual presentation of epilepsy." Journal of Laryngology & Otology 125, no. 6 (March 28, 2011): 633–34. http://dx.doi.org/10.1017/s0022215110002847.

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AbstractObjective:To report a case of fluctuating hearing due to auditory aura, as an unusual presentation of temporal lobe epilepsy.Methods:Case report and review of English language literature on temporal lobe epilepsy and auditory aura.Results:A 31-year-old man presented with intermittent symptoms of bilateral fullness in the ears associated with deafness. He was subsequently diagnosed with temporal lobe epilepsy. Further enquiry revealed a family history of epilepsy.Conclusion:Auditory aura as a presentation of temporal lobe epilepsy is rarely encountered in otolaryngological practice. This case highlights the importance of obtaining detailed information on epilepsy, including any family history of epilepsy, as a routine part of history-taking in patients presenting with fluctuating hearing loss.

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Gourmaud, Sarah, Haochang Shou, David J. Irwin, Kimberly Sansalone, Leah M. Jacobs, Timothy H. Lucas, Eric D. Marsh, Kathryn A. Davis, Frances E. Jensen, and Delia M. Talos. "Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy." Brain 143, no. 1 (December 13, 2019): 191–209. http://dx.doi.org/10.1093/brain/awz381.

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Abstract 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.

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Teplyshova, A. M., and E. V. Shalimanova. "Cognitive impairment in temporal lobe epilepsy." Epilepsy and paroxysmal conditions 14, no. 4 (January 18, 2023): 355–61. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2022.134.

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Cognitive impairment (CI) is a common comorbid pathology in epilepsy patients that exerts profound negative impact on quality of life. The CI causes may be due to various factors related to etiology, clinical manifestations, and treatment of epilepsy. A typical disorder in temporal lobe epilepsy is memory impairment. However, neuropsychological impairments may be more extensive and involve other neuropsychological domains. The risk of CI in patients with temporal lobe epilepsy may increase in structural brain disorders such as hippocampal sclerosis as well as in frequent seizures, early onset and long course of the disease. Surgical treatment of epilepsy may positively or negatively impact the cognitive function. In recent years, due to development of neurosciences as well as advances in the field of medical technologies, particularly neuroimaging, genetics, immunology, and biochemistry, new data emerged regarding potential mechanisms for developing CI in patients with epilepsy. The aim of the review is to assess available ideas about neurophysiological mechanisms of CI development, cues influencing emergence of neuropsychological disorders in patients with temporal lobe epilepsy.

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Mani, Jayanti. "Temporal lobe epilepsy in children." Journal of Pediatric Neurosciences 3, no. 1 (2008): 2. http://dx.doi.org/10.4103/1817-1745.40584.

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Kalamangalam, GiridharP. "Hypergraphia in temporal lobe epilepsy." Annals of Indian Academy of Neurology 12, no. 3 (2009): 193. http://dx.doi.org/10.4103/0972-2327.56323.

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Millichap, J. Gordon. "Temporal Lobe Malformations and Epilepsy." Pediatric Neurology Briefs 12, no. 4 (April 1, 1998): 26. http://dx.doi.org/10.15844/pedneurbriefs-12-4-2.

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Millichap, J. Gordon. "Familial Mesial Temporal Lobe Epilepsy." Pediatric Neurology Briefs 15, no. 2 (February 1, 2001): 13. http://dx.doi.org/10.15844/pedneurbriefs-15-2-6.

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