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Objective: To identify early structural alterations preceding the development of drug‐resistance in mild mesial temporal lobe epilepsy (mMTLE), a drug‐responsive syndrome ideal for investigating epilepsy pathophysiology and potential prognostic markers of long‐term clinical outcome, using magnetic resonance imaging (MRI) at baseline and after 12‐year follow‐up. Methods: Since 2002, a total of 55 participants with a baseline diagnosis of mMTLE underwent three‐dimensional (3D) T1 1.5T MRI. Based on long‐term outcome (follow‐up 12 ± 3 years), we identified 39 patients with stable mMTLE (smMTLE) and 16 patients who had developed drug‐resistance overtime (refractory MTLE [rMTLE]). At follow‐up, 21 smMTLE and 13 rMTLE patients underwent 3T‐MRI including diffusion‐weighted scans. Structural images were processed using longitudinal voxel‐based morphometry and standard Freesurfer analysis. Statistical analyses were carried out accounting for age, age at onset, gender, hippocampal volume, and hippocampal sclerosis (Hs). Results: Patients presented similar demographic, clinical, and Hs features. White matter volume of the arcuate fasciculi, corticospinal tracts, left retrosplenial cingulum, and left inferior longitudinal fasciculus was reduced only in rMTLE patients before the development of drug‐resistance. At follow‐up, rMTLE showed decreased fractional anisotropy in the corpus callosum, superior longitudinal fasciculi, and major bundles of the right hemisphere. Significance: White matter temporal and extratemporal abnormalities are preexisting in patients with mild MTLE who will develop drug‐resistance, independently from the presence of Hs. Thus, these changes might be due to an inherited genetic alteration rather than a subordinate worsening after repeated seizures, multiple antiepileptic drugs, or initial precipitating factors. [ABSTRACT FROM AUTHOR]

Objective Seizures may occur in close temporal association with a stroke or after a variable interval. Moreover, epilepsy is often encountered in patients with leukoaraiosis. Although early post-stroke seizures have been studied extensively, less attention has been paid to post-stroke epilepsy ( PSE) and to epilepsy associated with leukoaraiosis ( EAL). The aim of this paper is to review data concerning pathophysiology, prognosis, and treatment of PSE and EAL. Methods We performed an extensive literature search to identify experimental and clinical articles on PSE and EAL. We also conducted a systematic review of risk factors for PSE and EAL among eligible studies. Results PSE is caused by enhanced neuronal excitability within and near the scar. The role played by white matter changes in EAL remains to be elucidated. Meta-analysis showed that cortical involvement (odds ratio [ OR] 3.71, 95% confidence interval [ CI] 2.34-5.90, p < 0.001), cerebral hemorrhage ( OR 2.41, 95% CI 1.57-3.70, p < 0.001), and early seizures ( OR 4.43, 95% CI 2.36-8.32, p < 0.001) are associated with an increased risk of PSE. As regards EAL, no prospective, population-based studies evaluated the role of different variables on seizure risk. Studies about the management of PSE are limited. PSE is generally well controlled by drugs. Data about risk factors, prognosis, and treatment of EAL are lacking. Significance Pathophysiology and risk factors are well defined for PSE but need to be elucidated for EAL. Management of PSE and EAL relies on the clinician's judgment and should be tailored on an individual basis. [ABSTRACT FROM AUTHOR]

Objective Corpus callosum ( CC) abnormalities are frequently reported in patients with refractory mesial temporal lobe epilepsy ( rMTLE). However, whether CC structural alterations are related to the epileptic syndrome itself or to refractoriness is still unknown. Thus, we aimed to compare patterns of CC change in patients with rMTLE and benign MTLE ( bMTLE), the latter of which represents a useful resource to better disentangle factors that contribute to refractoriness. Methods The study group included 79 patients with bMTLE (mean age 43.2 ± 14. 8 years), 61 with rMTLE (mean age 45.2 ± 12.4 years) and 134 healthy volunteers. Structural magnetic resonance imaging ( MRI) and diffusion tensor imaging ( DTI) were performed to measure thickness, mean diffusivity ( MD), and fractional anisotropy ( FA) over 50 regions of interest along the cross-sectional CC profile. Statistical analysis comprised analysis of variance (ANOVA) followed by post hoc Tukey's Honest Significant Difference test. Results We found that all imaging metrics of the CC splenium were altered in rMTLE patients compared to bMTLE and controls. We also found significantly reduced thickness and FA of the anterior CC in rMTLE compared to controls and that FA was reduced only in rMTLE compared to bMTLE. Patients with bMTLE did not differ from controls. Differences between disease subgroups were found in the midbody composed of sensorimotor fibers. Significance We found altered multimodal imaging metrics of the CC in rMTLE but not in bMTLE. These findings were independent of the radiologic presence of hippocampal sclerosis, suggesting that differences in the distribution of such alterations might be related to refractoriness. [ABSTRACT FROM AUTHOR]

Objective Temporal and extratemporal white matter abnormalities have been identified frequently in patients with refractory mesial temporal lobe epilepsy ( rMTLE). However, the identification of potential water diffusion abnormalities in patients with drug-responsive, benign MTLE ( bMTLE) is still missing. The aim of this study was to identify markers of refractoriness in MTLE. Methods The study group included 48 patients with bMTLE (mean age 42.8 + 13.5 years), 38 with rMTLE (mean age 41.7 + 14.1 years) and 54 healthy volunteers. Diffusion tensor imaging ( DTI) was performed to measure mean diffusivity ( MD) and fractional anisotropy ( FA) in a regions-of-interest analysis comprising hippocampi and temporal lobe gray and white matter regions. The presence of hippocampal sclerosis ( Hs) was assessed using automated magnetic resonance imaging ( MRI) evaluation. For statistics we used chi-square test; two-tailed, two-sample t-test; and stratified linear regression. Results The significant demographic differences between the two patient groups were sex (p = 0.003), duration of epilepsy (p = 0.003) and complex febrile convulsions (p = 0.0001). In rMTLE, temporal white matter MD was higher and FA lower, as compared to bMTLE. The analysis of diagnostic accuracy (area under the receiver operator characteristic [ ROC] curve [ AUC]) showed that FA had an AUC for discriminating patients affected from those unaffected by refractory MTLE of 74.0% (p < 0.001), a value that was higher than that of temporal MD (64.0%), hippocampus volume (65.0%), and Hs (66.0%). Significance We performed DTI measurements in MTLE and found a significant reduction of FA along the white matter of the temporal lobes in rMTLE, suggesting it as a valuable measure of refractoriness in MTLE. [ABSTRACT FROM AUTHOR]

Genetic factors play a major role in the etiology of juvenile myoclonic epilepsy ( JME), a common form of idiopathic generalized epilepsy, but so far, genes related to JME remain largely unknown. JME shares electroclinical features with Unverricht-Lundborg disease (progressive myoclonic epilepsy type 1; EPM1), a form of progressive myoclonus epilepsy characterized by myoclonus, epilepsy, and gradual neurologic deterioration. EPM1 is caused by mutations in the gene that codes for cystatin B ( CSTB), an inhibitor of cysteine protease. In the present study, we wished to investigate the role of the CSTB gene in patients with JME. Fifty-seven unrelated patients (35 women; mean age ± standard deviation [SD], 24.1 ± 7.7; mean age ± SD at onset, 15.3 ± 2.4) with JME were enrolled. Twenty-three of 57 patients were the probands of families with JME. The molecular diagnosis was carried out to identify the common dodecamer repeat expansion mutation or other disease-causing mutations in the CSTB gene. The molecular analysis did not depict mutations in any of the 57 patients with JME. Our study did not support a role for the CSTB gene in patients with familial or sporadic JME. [ABSTRACT FROM AUTHOR]

Objective To evaluate whether vagus nerve stimulation (VNS) as adjunct to best medical practice (VNS + BMP) is superior to BMP alone in improving long-term health-related quality of life (HRQoL). Methods PuLsE (Open Prospective Randomized Long-term Effectiveness) was a prospective, randomized, parallel-group, open-label, and long-term effectiveness study (conducted at 28 sites in Europe and Canada). Adults with pharmacoresistant focal seizures (n = 112) received VNS + BMP or BMP (1:1 ratio). Medications and VNS parameters could be adjusted as clinically indicated for optimal seizure control while minimizing adverse effects. Primary endpoint was mean change from baseline HRQoL (using Quality of Life in Epilepsy Inventory-89 total score; QOLIE-89). Secondary endpoints included changes in seizure frequency, responder rate (≥50% decrease in seizure frequency), Centre for Epidemiologic Studies Depression scale (CES-D), Neurological Disorders Depression Inventory-Epilepsy scale (NDDI-E), Clinical Global Impression-Improvement scale (CGI-I), Adverse Event Profile (AEP), and antiepileptic drug (AED) load. The study was prematurely terminated due to recruitment difficulties prior to completing the planned enrollment of n = 362. Results for n = 96 who had baseline and at least one follow-up QOLIE-89 assessment (from months 3-12) were included in this analysis. Mixed model repeated measures (MMRM) analysis of variance was performed on change from baseline for the primary and secondary endpoints. Results Significant between-group differences in favor of VNS + BMP were observed regarding improvement in HRQoL, seizure frequency, and CGI-I score (respective p-values < 0.05, 0.03, and 0.01). More patients in the VNS + BMP group (43%) reported adverse events (AEs) versus BMP group (21%) (p = 0.01), a difference reflecting primarily mostly transient AEs related to VNS implantation or stimulation. No significant difference between treatment groups was observed for changes in CES-D, NDDI-E, AEP, and AED load. Significance VNS therapy as a treatment adjunct to BMP in patients with pharmacoresistant focal seizures was associated with a significant improvement in HRQoL compared with BMP alone. A PowerPoint slide summarizing this article is available for download in the Supporting Information section . [ABSTRACT FROM AUTHOR]

Summary Purpose: Psychogenic nonepileptic seizures (PNES) are among the most common clinical manifestations of conversion disorder and consist of paroxysmal behavior that resembles epileptic seizures. Preliminary data from functional neuroimaging studies gave plausible evidence that limbic circuits and sensorimotor cortex might be engaged in conversion disorder. Nonetheless, no advanced magnetic resonance imaging (MRI) studies have focused on patients with PNES. Methods: We enrolled 20 consecutive patients in whom the diagnosis of PNES was based on ictal video-electroencephalography (EEG) of the habitual episodes and 40 healthy subjects matched for age and sex All patients underwent a formal neuropsychological investigation and a neuropsychiatric assessment. All of the patients also underwent two distinct morphologic whole-brain MR measurements, voxel-based morphometry (VBM), and cortical thickness analysis, in a multimethod approach. Key Findings: None of the patients had serious medical or neurologic illness, substance abuse, or psychotic disorder, or were taking antipsychotic drugs. VBM and cortical thickness analyses in the patients with PNES revealed abnormal cortical atrophy of the motor and premotor regions in the right hemisphere and the cerebellum bilaterally. We also observed a significant association between increasing depression scores and atrophy involving the premotor regions. Significance: The results of this study illustrate that motor and premotor regions in the right hemisphere and the cerebellum bilaterally play an important role in the pathogenesis of PNES and that these structures are correlated with depressive symptoms. Our findings suggest a multistep model in the pathogenesis of PNES, in which the phenomenology is driven by psychological factors interacting with specific biologic abnormalities. [ABSTRACT FROM AUTHOR]

A splice site variation (c.603-91G>A or rs3812718) in the SCN1A gene has been claimed to influence efficacy and dose requirements of carbamazepine and phenytoin. We investigated the relationship between c.603-91G>A polymorphism and response to antiepileptic drugs (AEDs) in 482 patients with drug-resistant and 401 patients with drug-responsive focal epilepsy. Most commonly used AEDs were carbamazepine and oxcarbazepine. The distribution of c.603-91G>A genotypes was similar among drug-resistant and drug-responsive subjects, both in the entire population and in the groups treated with carbamazepine or oxcarbazepine. There was no association between the c.603-91G>A genotype and dosages of carbamazepine or oxcarbazepine. These findings rule out a major role of the SCN1A polymorphism as a determinant of AED response. [ABSTRACT FROM AUTHOR]

: In refractory temporal lobe epilepsy (rTLE), gray matter (GM) abnormalities are not confined to the hippocampus but also are found in extrahippocampal structures. Very recently we observed in mild TLE (mTLE) with or without mesiotemporal sclerosis (MTS), GM reductions in regions outside the presumed epileptogenic focus. To date, there are no studies that directly investigate whether whole-brain GM volume differs between rTLE and mTLE. Herein, we used optimized voxel-based morphometry (VBM) to identify GM abnormalities beyond the hippocampus in both rTLE and mTLE with evidence of MTS. : Brain magnetic resonance imaging (MRI) and optimized VBM were performed in 19 unrelated patients with mTLE, 19 patients with rTLE, and 37 healthy controls. MRI diagnosis of MTS was based on the atrophy of the hippocampal formation and/or mesiotemporal hyperintensity on fluid-attenuated inversion recovery (FLAIR) or T2 images, or both. : No patients (rTLE and mTLE) had generalized tonic–clonic or complex partial seizures for at least 3 weeks before scanning. Both mTLE and rTLE patients showed GM volume reduction of the bilateral thalamus, left hippocampus, and sensorimotor cortex compared with controls. No significant GM difference was found between rTLE and mTLE groups. : In both rTLE and mTLE, VBM shows GM reductions not confined to the hippocampus involving mainly the thalamus bilaterally. This finding together with the lack of significant GM differences between the two TLE groups supports the hypothesis that mTLE and rTLE might lie along a biologic continuum, suggesting a pathophysiologic role of the thalamus in partial epilepsy. [ABSTRACT FROM AUTHOR]

: Older enzyme-inducing antiepileptic drugs (AEDs) may induce supraphysiologic plasma concentrations of total (t) homocysteine (Hcy). The aim of the present study was to investigate the effect of new AEDs on plasma tHcy levels. : Patients 18–50 years of age, on AEDs monotherapy, with no other known cause of hyper-tHcy were enrolled. Plasma tHcy, folate, vitamin B12, and AEDs levels were determined by standard high-performance liquid chromatography (HPLC) methods. Methylenetetrahydrofolate-reductase ( MTHFR) polymorphisms were checked using Puregene genomic DNA purification system (Gentra, Celbio, Italy). A group of healthy volunteers matched for age and sex was taken as control. : Two hundred fifty-nine patients (151 on newer and 108 on older AEDs) and 231 controls were enrolled. Plasma tHcy levels were significantly higher [mean values, standard error (SE) 16.8, 0.4 vs. 9.1, 0.2 μm; physiologic range 5–13 μm] and folate lower (6.3, 0.1 vs. 9.3, 0.1 nm; normal > 6.8 nm) in patients compared to controls. Patients treated with oxcarbazepine, topiramate, carbamazepine, and phenobarbital exhibited mean plasma tHcy levels above the physiologic range [mean values (SE) 16 (0.8), 19.1 (0.8), 20.5 (1.0), and 18.5 (1.5) μm, respectively]. Conversely, normal tHcy concentrations were observed in the lamotrigine and levetiracetam groups [both 11.1 (0.5) μm]. : Oxcarbazepine and topiramate might cause hyper-tHcy, most likely because of the capacity of these agents to induce the hepatic enzymes. Because literature data suggest that hyper-tHcy may contribute to the development of cerebrovascular diseases and brain atrophy, a supplement of folate can be considered in these patients to normalize plasma tHcy. [ABSTRACT FROM AUTHOR]

To facilitate an integrated and rational approach to the care of women with epilepsy of childbearing potential, a group of experts appointed by Italian scientific societies in the fields of epileptology, neonatology, pediatrics, neuropediatrics, child neuropsychiatry, obstetrics, and gynecology held a joint meeting in Santa Trada di Cannitello, Reggio Calabria, Italy, on October 15–16, 2004, with the aim of reaching consensus on the optimal management of these women. An ad hoc system for the classification of available published evidence and the opinions of experts was developed and used to grade recommendations on different aspects related to counseling, diagnostic, and treatment issues. The present document summarizes available evidence on the reciprocal interactions between epilepsy, antiepileptic drugs, fertility, contraception, pregnancy, delivery, breastfeeding, and the offspring. Recommendations are made concerning the information and counseling that should be provided to women with epilepsy with respect to issues related to contraception, conception, pregnancy, labour, and puerperium. More detailed recommendations on the same issues are provided to physicians and other healthcare professionals involved in the care of these women, with special reference to choice of effective contraception, optimization of antiepileptic drug therapy, use of prenatal diagnostic tests and other monitoring procedures, and appropriate management practices in relation to childbirth, puerperium, and the care of the child. [ABSTRACT FROM AUTHOR]

Purpose: Photosensitivity can represent a serious problem in epilepsy patients, also because pharmacologic treatment is often ineffective. Nonpharmacologic treatment using blue sunglasses is effective and safe in controlling photosensitivity, but large series of patients have never been studied. Methods: This multicenter study was conducted in 12 epilepsy centers in northern, central, southern, and insular Italy. A commercially available lens, named Z1, obtained in a previous trial, was used to test consecutively enrolled pediatric and adult epilepsy patients with photosensitivity. Only type 4 photosensitivity (photoparoxysmal response, PPR) was considered in the study. A standardized method was used for photostimulation. Results: Six hundred ten epilepsy patients were tested. Four hundred (66%) were female patients; 396 (65%) were younger than 14 years. Three hundred eighty-one (62%) subjects were pharmacologically treated at the time of investigation. Z1 lenses made PPR disappear in 463 (75.9%) patients, and PPR was considerably reduced in an additional 109 (17.9%) of them. PPR remained unchanged only in the remaining 38 (6.2%) patients. The response of PPR to Z1 lenses was not significantly influenced by the patients' age, sex, or type of epilepsy. No difference was found between pharmacologically treated and untreated patients. Conclusions: The Z1 lens is highly effective in controlling PPR in a very large number of photosensitive epilepsy patients irrespective of their epilepsy or antiepileptic drug treatment. The lens might become a valid resource in the daily activity of any clinician who cares for patients with epilepsy. [ABSTRACT FROM AUTHOR]

Purpose:To clarify the possible role of other factors including the ApoEℇ4 allele for memory decline in temporal lobe epilepsy (TLE).Methods:We conducted a neuropsychological and molecular study in 138 consecutive patients (78 female patients; mean age, 50.2 years, SD± 17.9; range, 14 to 87 years) with mild nonlesional TLE, who rarely or never had seizures at long-term follow-up. The mean age at seizure onset was 33.0 years (SD,±21.7), and the mean duration of epilepsy was 17.1 years (SD,±15.7).Results:Thirty-four (25%) of 138 patients had test scores indicating verbal learning deficit (VLD). The presence of an ApoEℇ4 allele was associated with an increased risk of VLD (OR, 4.18; 95% CI, 1.66–10.55). The effect of the ApoE genotype was independent of both the age at epilepsy onset and disease duration as well as of a low educational level, which were separately associated with VLD (p values= 0.045, 0.001, and 0.001, respectively). A significant linear trend (p= 0.005) was seen in the relation between disease duration and cognitive impairment, with the highest risk being in patients with an epilepsy duration≥25.5 years (OR, 7.06; 95% CI, 1.67–29.85), especially if they carried theℇ4 allele (OR, 32.29; 95% CI, 5.23–195.72).Conclusions:These results provide evidence for an alteration in cognitive performance as a function of the presence of the ApoEℇ4 allele and point to the critical role of disease duration itself for cognitive impairment in TLE. [ABSTRACT FROM AUTHOR]

Familial mesial temporal lobe epilepsy (FMTLE) was first described as a benign syndrome with prominent psychic and autonomic seizures and no association with hippocampal sclerosis (HS) or febrile seizures (FS). Better definition of the syndrome allowed identification of more heterogeneous phenotypes with mild to severe epileptic disorders, and a variable association with HS and FS. The genetics of these conditions is largely unknown and the hope for the future is that the identification of FMTLE genes will lead to more appropriate approaches for the diagnosis and treatment of TLE. [ABSTRACT FROM AUTHOR]

Summary: Purpose: To evaluate how many patients with a clinical picture of idiopathic childhood localization-related epilepsies may also have silent celiac disease (CD). This will help determine whether investigation for CD should be restricted to those patients with childhood partial epilepsy with occipital paroxysms (CPEO) or should be extended to all patients with childhood partial epilepsy (CPE) regardless of seizure type and electroencephalographic (EEG) paroxysms. Methods: The study group consisted of 72 patients (31 girls and 41 boys; mean age, 12.6 ± 4.28 years; age at onset, 6.4 ± 3.7 years) who were observed consecutively over a 5-year period and who received an initial diagnosis of idiopathic CPE. A diagnosis of CD was confirmed by using enzyme-linked immunosorbent assay (ELISA) to assess the presence of antigliadin antibodies and the immunofluorescent undirected test to assess the presence of antiendomysium antibodies. Results: Twenty-five patients had CPEO, whereas the remaining 47 had CPE with centrotemporal spikes (CPEC). None of the patients with CPEC had positive antibody tests. Of the 25 patients with CPEO, two (8%) had antiendomysium immunoglobulin (Ig) A antibodies. In both of these patients, the jejunal biopsy showed atrophy of the villi and hyperplasia of the crypts, consistent with a diagnosis of CD. Brain computed tomography (CT) was normal in one of these patients and revealed occipital corticosubcortical calcifications in the other. Conclusions: Our study indicates that CD screening should be performed routinely only in patients with CPEO. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "A definition and classification of status epilepticus-Report of the ILAE Task Force on Classification of Status Epilepticus" that was published in the previous issue.

A letter to the editor is presented on a quantitative assessment of psychogenic nonepileptic seizures.

A response from the author to the letter regarding the study on epilepsy on cerebrovascular disease is presented.

A letter to the editor is presented in response to the article Mind the gap: Multiple events and lengthy delays before presentation with a "first seizure" published in a previous issue of 2015.

Researchers screened nine Italian families with generalized epilepsy with febrile seizures plus (GEFS+) for mutations in SCN1A, SCN1B, and GABRG2 genes. Probands were ascertained from the clinical practice in three epilepsy centers in southern Italy. Detailed family pedigrees were constructed, including maternal and paternal lines extending as far back as possible. In nine families, researchers investigated 110 members of whom 37 individuals were determined to be affected. Most patients had febrile seizures (FSs) or FS plus (FS+) alone. A consistent number of patients also had only a febrile generalized seizures. Few patients had myoclonic seizures. One patient had a clinical picture of severe myoclonic epilepsy at infancy (SMEI). In two of the nine GEFS+ families, researchers identified two novel mutations of the SCN1A gene that cosegregated with the disorder. Neither mutation was observed in any of the 100 control individuals matched for ethnicity. Both these mutations changed highly conserved amino acids. Researchers have provided evidence of two novel disease mutations of the SCN1A gene in patients with GEFS+, whereas no mutation was found within the SCN1B or GABGR2 genes.

A study illustrated an association between temporal lobe epilepsy (TLE) and low-expression promoter alleles of the prodynorphin gene (PDYN) in familial-risk patients. Furthermore, irrespective of their family history, L-homozygotes had an increased risk of febrile convulsions (FCs) or a more severe phenotype. A second study, however, failed to replicate any of these associations. None of the observed genotype counts deviated significantly from those expected according to Hardy-Weinberg equilibrium. No allelic or genotypic association was found in the sample including either all patients or only familial-risk TLE patients. Moreover, no effect of L-alleles was found on the age at onset, severity of TLE phenotype, or previous FCs. Although PDYN may be a plausible candidate gene for TLE, it does not seem to play a major role in its pathogenesis, in patients with mild non-lesional TLE.

In refractory mesial temporal lobe epilepsy (MTLE) extrahippocampal and neocortical abnormalities have been described in patients with or without mesial temporal sclerosis (MTS). Recently we observed gray matter reductions in regions outside the hippocampus in benign MTLE with or without MTS. Cortical thickness has been proposed as a viable methodologic alternative for assessment of neuropathologic changes in extratemporal regions. Herein, we aimed to use this technique to describe cortical abnormalities in patients with benign TLE. Whole-brain cortical thickness analysis (FreeSurfer) was performed in 32 unrelated patients with benign TLE [16 patients with signs of MTS on magnetic resonance imaging (MRI), pMTLE; 16 without, nMTLE] and 44 healthy controls. In the pMTLE group, the most significant thinning was found in the sensorimotor cortex bilaterally but was more extensive in the left hemisphere (false discovery rate, p < 0.05). Other areas were localized in the occipital cortex, left supramarginal gyrus, left superior parietal gyrus, left paracentral sulcus, left inferior/middle/superior frontal gyrus, left inferior frontal sulcus, right cingulate cortex, right superior frontal gyrus, right inferior parietal gyrus, right fusiform gyrus, and cuneus/precuneus. In the nMTLE, a similar neurodegenerative pattern was detected, although not surviving correction for multiple comparisons. Direct comparison between pMTLE and nMTLE did not reveal significant changes. Patients with either benign pMTLE or nMTLE showed comparable cortical thinning, mainly confined to the sensorimotor cortex. This finding that is not appreciated on routine MRI supports the hypothesis that similar to refractory MTLE, even in benign MTLE, pathology in neocortical regions maybe implicated in the pathophysiology of this syndrome. [ABSTRACT FROM AUTHOR]