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Memory dysfunction is prevalent in temporal lobe epilepsy, but little is known about the underlying pathophysiological etiologies. Here, we use spatial quantitation to examine differential expression of targeted proteins and transcripts in four brain regions essential for episodic memory (dentate gyrus, CA3, CA1, neocortex) between temporal lobe epilepsy patients with and without episodic memory impairment. Brain tissues were obtained from dominant temporal lobectomies in 16 adults with pharmacoresistant temporal lobe epilepsy associated with hippocampal sclerosis. Verbal memory tests from routine pre-operative clinical care were used to classify episodic memory as impaired or intact. Digital spatial profiling of a targeted protein panel and the whole transcriptome was performed using tissue sections from the temporal neocortex and hippocampus. We performed differential expression and pathway enrichment analysis between the memory groups within each temporal lobe region. Several proteins associated with neurodegenerative disease were overexpressed in the neocortex of patients with impaired memory, corroborating our prior findings using bulk transcriptomics. Spatial transcriptomics identified numerous differentially expressed transcripts in both neocortical and hippocampal subregions between memory groups, with little overlap across subregions. The strongest molecular signal was observed in the CA3 hippocampal subregion, known to play an essential role in memory encoding. Enrichment analyses revealed BDNF as a central hub in CA3-related networks regulating phenotype-relevant processes such as cognition, memory, long-term potentiation and neuritogenesis (Padj < 0.05). Results suggest memory impairment in temporal lobe epilepsy with hippocampal sclerosis is associated with molecular alterations within temporal lobe subregions that are independent from hippocampal cell loss, demographic variables and disease characteristics. Importantly, each temporal subregion shows a unique molecular signature associated with memory impairment. While many differentially expressed transcripts and proteins in the neocortex have been associated with neurodegenerative disorders/processes, differentially expressed transcripts in hippocampal subregions involve genes associated with neuritogenesis and long-term potentiation, processes essential for new memory formation.

Focal cortical dysplasia (FCD) is associated with blood-brain barrier (BBB) dysfunction in patients with difficult-to-treat epilepsy. However, the underlying cellular and molecular factors in cortical dysplasia (CD) associated with progressive neurovascular challenges during the pro-epileptic phase, post-seizure, and during epileptogenesis remain unclear. We studied the BBB function in a rat model of congenital (in utero radiation-induced, first hit) CD and longitudinally examined the cortical brain tissues at baseline and the progressive neurovascular alterations, glucose transporter-1 (GLUT1) expression, and glucose metabolic activity at 2, 15, and 30 days following a second hit using pentylenetetrazole-induced seizure. Our study revealed through immunoblotting, immunohistochemistry, and biochemical analysis that (1) altered vascular density and prolongation of BBB albumin leakages in CD rats continued through 30 days post-seizure; (2) CD brain tissues showed elevated matrix metalloproteinase-9 levels at 2 days post-seizure and microglial overactivation through 30 days post-seizure; (3) BBB tight junction protein and GLUT1 levels were decreased and neuronal monocarboxylate transporter-2 (MCT2) and mammalian target of rapamycin (mTOR) levels were increased in the CD rat brain: (4) ATPase activity is elevated and a low glucose/high lactate imbalance exists in CD rats; and (5) the mTOR pathway is activated and MCT2 levels are elevated in the presence of high lactate during glucose starvation in vitro. Together, this study suggests that BBB dysfunction, including decreased GLUT1 expression and metabolic disturbance, may contribute to epileptogenesis in this CD rat model through multiple mechanisms that could be translated to FCD therapy in medically refractory epilepsy.

Background and ObjectivesWe aim to provide detailed imaging-electroclinicopathologic characterization of the black line sign, a novel MRI marker for focal cortical dysplasia (FCD) IIB.Methods7T T2*-weighted gradient-echo (T2*w-GRE) images were retrospectively reviewed in a consecutive cohort of patients with medically intractable epilepsy with pathology-proven FCD II, for the occurrence of the black line sign. We examined the overlap between the black line region and the seizure-onset zone (SOZ) defined by intracranial EEG (ICEEG) and additionally assessed whether complete inclusion of the black line region in the surgical resection was associated with postoperative seizure freedom. The histopathologic specimen was aligned with the MRI to investigate the pathologic underpinning of the black line sign. Region-of-interest–based quantitative MRI (qMRI) analysis on the 7T T1 map was performed in the black line region, entire lesional gray matter (GM), and contralateral/ipsilateral normal gray and white matter (WM).ResultsWe included 20 patients with FCD II (14 IIB and 6 IIA). The black line sign was identified in 12/14 (85.7%) of FCD IIB and 0/6 of FCD IIA on 7T T2*w-GRE. The black line region was highly concordant with the ICEEG-defined SOZ (5/7 complete and 2/7 partial overlap). Seizure freedom was seen in 8/8 patients whose black line region was completely included in the surgical resection; in the 2 patients whose resection did not completely include the black line region, both had recurring seizures. Inclusion of the black line region in the surgical resection was significantly associated with seizure freedom (p= 0.02). QMRI analyses showed that the T1 mean value of the black line region was significantly different from the WM (p< 0.001), but similar to the GM. Well-matched histopathologic slices in one case revealed accumulated dysmorphic neurons and balloon cells in the black line region.DiscussionThe black line sign may serve as a noninvasive marker for FCD IIB. Both MRI-pathology and qMRI analyses suggest that the black line region was an abnormal GM component within the FCD. Being highly concordant with ICEEG-defined SOZ and significantly associated with seizure freedom when included in resection, the black line sign may contribute to the planning of ICEEG/surgery of patients with medically intractable epilepsy with FCD IIB.Classification of EvidenceThis study provides Class II evidence that in individuals with intractable focal epilepsy undergoing resection who have a 7T MRI with adequate image quality, the presence of the black line sign may suggest FCD IIB, be concordant with SOZ from ICEEG, and be associated with more seizure freedom if fully included in resection.

Summary Both mild and severe epilepsies are influenced by variants in the same genes, yet an explanation for the resulting phenotypic variation is unknown. As part of the ongoing Epi25 Collaboration, we performed a whole-exome sequencing analysis of 13,487 epilepsy-affected individuals and 15,678 control individuals. While prior Epi25 studies focused on gene-based collapsing analyses, we asked how the pattern of variation within genes differs by epilepsy type. Specifically, we compared the genetic architectures of severe developmental and epileptic encephalopathies (DEEs) and two generally less severe epilepsies, genetic generalized epilepsy and non-acquired focal epilepsy (NAFE). Our gene-based rare variant collapsing analysis used geographic ancestry-based clustering that included broader ancestries than previously possible and revealed novel associations. Using the missense intolerance ratio (MTR), we found that variants in DEE-affected individuals are in significantly more intolerant genic sub-regions than those in NAFE-affected individuals. Only previously reported pathogenic variants absent in available genomic datasets showed a significant burden in epilepsy-affected individuals compared with control individuals, and the ultra-rare pathogenic variants associated with DEE were located in more intolerant genic sub-regions than variants associated with non-DEE epilepsies. MTR filtering improved the yield of ultra-rare pathogenic variants in affected individuals compared with control individuals. Finally, analysis of variants in genes without a disease association revealed a significant burden of loss-of-function variants in the genes most intolerant to such variation, indicating additional epilepsy-risk genes yet to be discovered. Taken together, our study suggests that genic and sub-genic intolerance are critical characteristics for interpreting the effects of variation in genes that influence epilepsy.

Objective To investigate the neuroimaging and clinical features associated with sleep-related epilepsy (SRE) in patients with focal cortical dysplasia (FCD) type II. Methods Patients with histopathologically proven FCD type II were included from three epilepsy centers. SRE was defined according to the video EEG findings and seizure history. Cortical surface reconstruction and volume calculation were performed using FreeSurfer. The lesions were manually delineated on T1 volumetric MRI using the ITK-SNAP software. The lesion volumes were normalized by the intracranial volume of each patient. The lesions were classified as small or large by placing a threshold based on quantitative (whether the lesion was detected on MRI report) and qualitative (volume) criteria. Results A total of 77 consecutive patients were included. Of them, 36 had SRE and 41 had non-SRE. An earlier age of epilepsy onset, high seizure frequency, regional interictal EEG findings, and favorable surgical outcome were characteristic in both groups. Small lesions were defined as those having a volume

MRI-negative (MRI-) pharmacoresistant focal epilepsy (PFE) patients are most challenging for epilepsy surgical management. This study utilizes a voxel-based MRI postprocessing technique, implemented using a morphometric analysis program (MAP), aiming to facilitate detection of subtle focal cortical dysplasia (FCD) in MRI- patients. Furthermore, the study examines the concordance between MAP-identified regions and localization from magnetic source imaging (MSI).Included in this retrospective study were 25 MRI- surgical patients. MAP was performed on T1-weighted MRI, with comparison to a normal database. The pertinence of MAP+ areas was confirmed by MSI, surgical outcome and pathology. Analyses of MAP and MSI were performed blindly from patients' clinical information and independently from each other.The detection rate of subtle changes by MAP was 48% (12/25). Once MAP+ areas were resected, patients were more likely to be seizure-free (p=0.02). There were no false positives in the 25 age-matched normal controls. Seven patients had a concordant MSI correlate. Patients in whom a concordant area was identified by both MAP and MSI had a significantly higher chance of achieving a seizure-free outcome following complete resection of this area (p=0.008). In the 9 resected MAP+ areas, pathology revealed FCD type IA in 7 and type IIB in 2.MAP shows promise in identifying subtle FCD abnormalities and increasing the diagnostic yield of conventional MRI visual analysis in presurgical evaluation of PFE. Concordant MRI postprocessing and MSI analyses may lead to the noninvasive identification of a structurally and electrically abnormal subtle lesion that can be surgically targeted.

Fast ripples are reported to be highly localizing to the epileptogenic or seizure-onset zone (SOZ) but may not be readily found in neocortical epilepsy, whereas ripples are insufficiently localizing. Herein we classified interictal neocortical ripples by associated characteristics to identify a subtype that may help to localize the SOZ in neocortical epilepsy. We hypothesize that ripples associated with an interictal epileptiform discharge (IED) are more pathologic, since the IED is not a normal physiologic event.We studied 35 patients with epilepsy with neocortical epilepsy who underwent invasive electroencephalography (EEG) evaluation by stereotactic EEG (SEEG) or subdural grid electrodes. Interictal fast ripples and ripples were visually marked during slow-wave sleep lasting 10-30 min. Neocortical ripples were classified as type I when superimposed on epileptiform discharges such as paroxysmal fast, spike, or sharp wave, and as type II when independent of epileptiform discharges.In 21 patients with a defined SOZ, neocortical fast ripples were detected in the SOZ of only four patients. Type I ripples were detected in 14 cases almost exclusively in the SOZ or primary propagation area (PP) and marked the SOZ with higher specificity than interictal spikes. In contrast, type II ripples were not correlated with the SOZ. In 14 patients with two or more presumed SOZs or nonlocalizable onset pattern, type I but not type II ripples also occurred in the SOZs. We found the areas with only type II ripples outside of the SOZ (type II-O ripples) in SEEG that localized to the primary motor cortex and primary visual cortex.Neocortical fast ripples and type I ripples are specific markers of the SOZ, whereas type II ripples are not. Type I ripples are found more readily than fast ripples in human neocortical epilepsy. Type II-O ripples may represent spontaneous physiologic ripples in the human neocortex.

To investigate the utility of magnetic source imaging (MSI) and ictal single photon emission computed tomography (SPECT), each compared with intracranial electroencephalography (EEG) (ICEEG), to localize the epileptogenic zone (EZ) and predict epilepsy surgery outcome in patients with nonlesional neocortical focal epilepsy.Studied were 14 consecutive patients with nonlesional neocortical epilepsy who underwent presurgical evaluation including ICEEG, positive MSI, and localizing subtraction Ictal SPECT coregistered to MRI (SISCOM) analysis. Follow-up after epilepsy surgery was ≥ 24 months. ICEEG, MSI, and SPECT results were classified using a sublobar classification.Of 14 patients, 6 (42.9%) became seizure-free after surgery. Sublobar ICEEG focus was completely resected in 11 patients; 5 (45.5%) of them became seizure- free. Concordance of ICEEG and MSI and complete focus resection was found in 5 (35.7%) patients; 80% of them became seizure-free. Sublobar ICEEG-MSI concordance and complete focus resection significantly increased the chance of seizure freedom after epilepsy surgery (p = 0.038). In contrast, of the 6 patients (42.9%) with concordant ICEEG and SISCOM and complete focus resection, only 66.7% became seizure-free (p = 0.138). Assuming concordant results, the additive value to ICEEG alone for localizing the EZ is higher with ICEEG-MSI (odds ratio 14) compared to ICEEG-SISCOM (odds ratio 6).This study shows that combination of MSI and/or SISCOM with ICEEG is useful in the presurgical evaluation of patients with nonlesional neocortical epilepsy. Concordant test results of either MSI or SISCOM with ICEEG provide useful additive information for that provided by ICEEG alone to localize the EZ in this most challenging group of patients. When sublobar concordance with ICEEG is observed, MSI is more advantageous compared to SISCOM in predicting seizure-free epilepsy surgery outcome.

This study aims to investigate seizure worsening and its predictors after epilepsy surgery.A retrospective chart review of patients who underwent unilobar epilepsy surgery between 1990 and 2007 and had recurrence of at least one seizure was performed. Seizure worsening was defined as an increase in total average monthly seizure frequency, average monthly generalized tonic-clonic seizures (GTCS), new-onset GTCS, or new-onset status epilepticus. The occurrence of sudden unexpected death in epilepsy (SUDEP) was captured. Multivariate logistic regression analysis was used to identify predictors of worsening.A total of 276 patients with postoperative seizure recurrence were identified. Monthly average seizure frequency worsening occurred in 9.8%, GTC worsening in 8.0%, new-onset GTCs in 1.4%, new-onset status epilepticus in 2.2%, and death from SUDEP in 1.4%. A higher risk of worsening was seen with extratemporal resections as compared to temporal lobe surgeries (odds ratio [OR] 3.11, 95% confidence interval [CI] 1.21-7.95; p = 0.018), and in patients with low preoperative seizure frequency30 seizures/month (OR 14.82, 95% CI 2.81-275.41; p = 0.0003). Predictors of increased GTCs included an incomplete resection (OR 3.98, 95% CI 1.39-12.59; p = 0.010) and multiple recorded ictal patterns (OR 5.91, 95% CI 1.20-26.96; p = 0.030). Multiple seizure semiologies correlated with worsening after temporal lobe resections.The most vulnerable patients for seizure worsening following epilepsy surgery include those with extratemporal resections, incomplete resections, and multiple recorded ictal patterns.

Outcomes following unilobar surgeries for refractory epilepsy have been well described. However, little is known about long-term seizure outcomes following multilobar resections. The aim of the current study was to identify long-term seizure control and predictors of seizure recurrence in this patient population.Records of patients who underwent multilobar epilepsy surgery at the Cleveland Clinic between 1994 and 2010 were retrospectively reviewed. A postoperative follow-up of at least 6 months was required. Patients were classified as seizure free if they achieved an Engel class I at last follow-up. Long-term chances of seizure freedom were illustrated using a survival analysis, and predictors of recurrence were identified using Cox proportional hazard modeling.Sixty-three patients with medically intractable epilepsy underwent multilobar surgical resections during the study period (mean follow-up of 4.6 years). Predominant resection types included extended occipital (temporoparietooccipital, parietooccipital, temporooccipital: 57%), frontotemporal (21%), and temporoparietal (17%). Mean age at surgery was 21.4 years and mean age at seizure onset was 10.1 years. Fifty-six percent of the patients underwent extraoperative invasive electroencephalography (EEG) evaluations. At 6 postoperative months, 71% (95% confidence interval (CI) 65-77) were seizure-free (SF), 64% (CI 58-70) were SF at 1 year, 52% (CI 46-59) were SF at 5 years, and 41% (CI 32-50) remained SF at 10 years. Forty-one patients had at least one breakthrough seizure after surgery (median timing of recurrence 6.1 months), with an Engel class 1 achieved again by last follow-up in 12 of these 41 cases. Nine patients required a reoperation. Patients who underwent extended occipital/posterior quadrant resections had more favorable outcomes as compared to the other groups. With multivariate analysis, the type of resection (p = 0.03), preoperative auras (p = 0.03), an incomplete resection (0.03), and the presence of postoperative spikes (p = 0.0003) correlated with seizure recurrence. The risk of seizure recurrence for an incomplete resection was 2.3 (CI 1.53-3.36), preoperative aura 2.3 (CI 1.34-3.87), and postoperative spikes on surface EEG 2.5 (CI 1.29-4.71).A favorable outcome can be achieved in 41% of patients undergoing multilobar resections for epilepsy surgery at 10 years of follow-up. Close to one-third of patients who have breakthrough seizures after surgery are able to regain seizure freedom by last follow-up. Predictors of recurrence include resection type (frontotemporal and parietotemporal resections did worse), presence of preoperative aura, an incomplete surgical resection, and the presence of postoperative interictal discharges on EEG.

Nitric oxide has been associated with epileptogenesis. Previous studies have shown increased expression of N-methyl-d-aspartate (NMDA) subunit NR2B receptors in epileptic dysplastic human neocortex. The expression of neuronal nitric oxide synthase (nNOS), and its relation to this subunit NR2B in epileptic dysplastic tissue has never been addressed.Ten patients with medically intractable epilepsy caused by focal cortical dysplasia (CD), and 2 patients with mesial temporal sclerosis (control group) underwent pre- and/or intraoperative invasive monitoring evaluations. Cortical samples from epileptogenic and nonepileptogenic areas were collected from each patient intraoperatively. Samples were processed for cresyl violet staining, immunocytochemical tests with nNOS, NeuN, and NR2B, and immunofluorescence analyses to evaluate colocalized immunoreactivity between nNOS and NR2B.All samples obtained in the patients with epilepsy revealed CD in various degrees. In the nonepileptic sample group, cresyl violet staining revealed normal cortical architecture in 9 samples, but a mild degree of CD in 3. The density and intensity of nNOS-stained neurons was remarkably increased in the epileptic tissue compared with nonepileptic samples (p0.05). Two types of nNOS-stained neurons were identified: Type I, expressing strong nNOS immunoreactivity in larger neurons; and Type II, expressing weak nNOS immunoreactivity in slightly smaller neurons. Different from Type I neurons, Type II nNOS-stained neurons revealed immunoreactivity colocalized with NR2B antibody.The overexpression of nNOS in the epileptic samples and the immunoreactivity colocalization between nNOS and NR2B may suggest a possible role of nNOS and NO in the pathophysiological mechanisms related to in situ epileptogenicity.

Occipital resections for epilepsy are rare. Reasons for this are the relative infrequency of occipital epilepsy, difficulty in localizing epilepsy originating in the occipital lobe, imprecisely defined seizure outcome in patients treated with focal occipital resections in the MR imaging era, and concerns about producing visual deficits. The impact of lesion location on vision and seizure biology, the management decision-making process, and the outcomes following resection need elaboration.The authors studied 21 consecutive patients who underwent focal occipital resections for epilepsy at Cleveland Clinic Epilepsy Center over a 13-year period during which MR imaging was used. Demographics, imaging, and data relating to the epilepsy and its surgical management were collected. The collateral sulcus, the border between the medial surface and the lateral convexity, and the inferior temporal sulcus were used to subdivide the occipital lobe into medial, lateral, and basal zones. Lesions that did not involve most or all of the occipital lobe (sublobar) were spatially categorized into these zones. Visual function, semiology, and scalp electroencephalography were evaluated in relation to these spatial categories. Preresection and postresection visual function and seizure frequency were evaluated and compared. Lastly, an exhaustive review and discussion of the published literature on occipital resections for epilepsy was carried out.Five lesions were lobar and 16 were sublobar. Patients with medial or lobar lesions had a much greater likelihood of preoperative visual field defects. Those with basal or lateral lesions had a greater likelihood of having a visual aura preceding some or all of their seizures and a trend (not significant) toward having a concordant lateralized onset by scalp electroencephalography. Invasive recordings were used in 8 cases. All patients had lesions (malformations of cortical development, tumors, or gliosis) that were completely resected, as evaluated on postoperative MR imaging. At last follow-up, 17 patients (81%) were seizure free or had only occasional auras (Wieser Class 1 or 2). The remaining 4 patients (19%) had a worthwhile improvement in seizure control (Class 3 or 4). Of the patients for whom both pre- and postoperative visual testing data were available, 50% suffered no new visual deficits, and 17% each developed a new quadrantanopia or a hemianopia.Lesional occipital lobe epilepsy can be successfully managed with resection to obtain excellent seizure-free rates. Individually tailored resections (in lateral occipital lesions, for example) may help preserve intact vision in a subset of cases (38% in this series). Invasive recordings may further guide surgical decision-making as delineated by an algorithm generated by the authors. The authors' results suggest that the spatial location of the lesion correlates both with the semiology of the seizure and with the presence of visual deficit.

Studies have shown a lower risk for verbal memory decline following dominant anterior temporal lobectomy (ATL) among patients with poor, presurgical verbal memory scores. It is unclear however, if the risk of decline is increased in patients who also have reduced visual memory. Objective and subjective memory outcome following left ATL was examined in twelve patients with reduced presurgical visual and verbal memory scores. Only one patient demonstrated a meaningful decline in memory scores, with a decline in visual memory following surgery. Presurgically, this patient demonstrated poor memory bilaterally on Wada testing and small discrepancy in hippocampal volumes. She was also one of two patients who continued to have seizures post-surgery. This preliminary study suggests that patients with unilateral, left TLE and poor verbal and visual memory are unlikely to show meaningful memory declines following left ATL, particularly if they demonstrate expected patterns on Wada testing, hippocampal volume discrepancy (leftright), and postsurgical seizure-freedom.

Pharmacoresistant epilepsy arising from the dominant temporal region in patients with intact memory and normal anatomical imaging, presents major challenges in the preoperative definition of the epileptogenic zone, and the planning of the extent of the surgical resection. We report on the case of a 42-year-old, right-handed male who presented with recurrent daily seizures that were resistant to antiepileptic drugs. Multiple, non-invasive (scalp) video-EEG evaluations revealed focal epilepsy arising from the left fronto-temporal region. Multiple high resolution MRIs that were performed at multiple Epilepsy Centers failed to show any abnormality. Fluoro-deoxyglucose PET scan showed extensive, left antero-mesial temporal hypometabolism, and ictal SPECT showed increased perfusion in the left insula in addition to the left mesial and anterior temporal pole. Neuropsychological testing and intracarotid methohexital testing revealed excellent memory to the left, dominant side. A two-stage invasive evaluation with subdural grid electrodes followed by depth electrode recordings allowed the localization of the epileptogenic region to the temporal pole. A selective resection of the left temporal pole (that spared the hippocampal formation) resulted in a seizure-free outcome (one year follow-up) with no significant consequences on memory function. We conclude that targeted, invasive recording techniques should be used for the accurate localization and delineation of the extent of the epileptogenic zone in cases of suspected, non-lesional, dominant hemisphere, temporal lobe epilepsy with preserved memory function. The use of the staged invasive approach may increase the chances for memory (function) sparing through tailored, temporal resection.

Malformations of cortical development are frequent causes of human refractory epilepsy. The freeze-lesion model in rats shows histopathological features similar to those found in human polymicrogyria. Previous studies reported in vitro hyperexcitability in this model, but in vivo epileptogenicity has not been confirmed.Neocortical freeze lesions were induced in Sprague-Dawley rat pups (n = 10) on postnatal day 0 or 1 (P0/P1). Sham-operated animals served as controls (n = 10). On P60, animals were implanted with epidural electrodes for long-term video-EEG monitoring (4 weeks). The threshold for pentylenetetrazol-induced seizures was determined. Animals were sacrificed and brain sections processed for histological staining and in vitro electrophysiological recordings. Epileptiform field potential repetition rate, amplitude and integral were compared between slices containing a cortical freeze lesion, and slices from sham-operated rats.No interictal spikes and no electrographic or clinical seizures occurred in either group. The median threshold for pentylenetetrazol-induced seizures was 60 mg/kg for lesioned, and 45 mg/kg for control animals (difference not significant). No spontaneous epileptiform field potentials were recorded from either freeze-lesion or control slices bathed in normal, artificial cerebrospinal fluid (ACSF). Upon omission of Mg(2+) from the bath, epileptiform field potentials were elicited that showed a significantly higher burst integral in the freeze lesion slices compared to control slices.Neocortical freeze lesions induced in newborn rat pups show histological characteristics reminiscent of human cortical dysplasia. Brain slices containing neocortical freeze lesions display hyperexcitability in vitro, but the same lesion does not appear to show spontaneous epileptogenicity in vivo.

To identify the temporal lobe cortical dysplasia (CD) histopathology classification subtype and determine the seizure outcome of patients who underwent temporal lobectomy with coincident CD.We reviewed the data of 28 patients with temporal lobe epilepsy who underwent surgery with pathologically verified CD at our institution from 1990 to 2000. The seizure outcome was assessed at a minimum of 1 year after surgery according to Engel's classification.Of 28 patients who underwent surgery, nine (32.1%) had isolated CD, and 19 (67.9%) had CD and hippocampal sclerosis (CDHS). Twenty-six (92.9%) patients had histopathology subtype Ia (architectural abnormalities). Twenty (71.4%) patients were seizure free (Engel class I). Favorable seizure outcome (Engel class I, II) was achieved in 26 (92.9%) patients. No difference in seizure outcome was noted between patients with CD and CDHS.The most common histopathologic subtype in patients with temporal lobe CD is type Ia (architectural abnormalities). Temporal lobectomy in temporal lobe epilepsy patients with CD can achieve favorable seizure outcome.