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51. Viral manipulation of functionally distinct neurons from mice to humans

Author: Guoping Feng, Emilia Favuzzi, Vergara J, Sakopoulos S, Vormstein-Schneider D, Qing Xu, Sabri E, Jordane Dimidschstein, Sanchez, Jared B. Smith, Kenneth A. Pelkey, Mastro K, Qiangge Zhang, Devinsky O, Allaway K, Stevenson O, John V. Reynolds, Zhanyan Fu, Renata Batista-Brito, Gord Fishell, Kareem A. Zaghloul, Baolin Guo, Jessica Lin, Vogel I, Schneider G, Bernardo L. Sabatini, Chris J. McBain, Tom P. Franken, Lihua Guo, Saldi G, Burbridge T, Xiaoqing Yuan, Jitendra Sharma, Leena A. Ibrahim, Shuhan Huang, Ramesh Chittajallu, and Garcia Ma
Subjects: 0303 health sciences, biology, Vasoactive intestinal peptide, Cell, Context (language use), 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Cerebral cortex, Gene expression, medicine, biology.protein, Enhancer, Gene, Neuroscience, 030217 neurology & neurosurgery, Parvalbumin, 030304 developmental biology
Abstract: Recent success in identifying gene regulatory elements in the context of recombinant adeno-associated virus vectors have enabled cell type-restricted gene expression. However, within the cerebral cortex these tools are presently limited to broad classes of neurons. To overcome this limitation, we developed a strategy that led to the identification of multiple novel enhancers to target functionally distinct neuronal subtypes. By investigating the regulatory landscape of the disease gene Scn1a, we identified enhancers that target the breadth of its expression, including two that are selective for parvalbumin and vasoactive intestinal peptide cortical interneurons. Demonstrating the functional utility of these elements, we found that the PV-specific enhancer allowed for the selective targeting and manipulation of these neurons across species, from mice to humans. Finally, we demonstrate that our selection method is generalizable to other genes and characterize four additional PV-specific enhancers with exquisite specificity for distinct regions of the brain. Altogether, these viral tools can be used for cell-type specific circuit manipulation and hold considerable promise for use in therapeutic interventions.
Published: 2019
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52. Cortical abnormalities in epilepsy revealed by local EEG synchrony

Author: Schevon, C. A., Cappell, J., Emerson, R., Isler, J., Grieve, P., Goodman, R., Mckhann, G., Jr., Weiner, H., Doyle, W., Kuzniecky, R., Devinsky, O., and Gilliam, F.
Published: 2007
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53. Agreement between self reports and proxy reports of quality of life in epilepsy patients

Author: Hays, R. D., Vickrey, B. G., Hermann, B. P., Perrine, K., Cramer, J., Meador, K., Spritzer, K., and Devinsky, O.
Published: 1995
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54. Coarse behavioral context decoding

Author: Daniel Friedman, Lucia Melloni, Xi Jiang, David D. Gonda, Isaac Shamie, Eric Halgren, Devinsky O, Werner Doyle, Patricia Dugan, Abdulwahab Alasfour, Paolo Gabriel, Sonya Wang, Shifteh Sattar, Thomas Thesen, and Vikash Gilja
Subjects: Adult, Male, Multiple days, Adolescent, Computer science, Speech recognition, 0206 medical engineering, Biomedical Engineering, 02 engineering and technology, 03 medical and health sciences, Cellular and Molecular Neuroscience, Neural activity, Young Adult, 0302 clinical medicine, Humans, Cortical surface, Brain–computer interface, Cerebral Cortex, Behavior, Electroencephalography, 020601 biomedical engineering, Electrodes, Implanted, Support vector machine, Brain-Computer Interfaces, Female, Electrocorticography, Classifier (UML), 030217 neurology & neurosurgery, Decoding methods, Psychomotor Performance, Neural decoding
Abstract: Objective Current brain-computer interface (BCI) studies demonstrate the potential to decode neural signals obtained from structured and trial-based tasks to drive actuators with high performance within the context of these tasks. Ideally, to maximize utility, such systems will be applied to a wide range of behavioral settings or contexts. Thus, we explore the potential to augment such systems with the ability to decode abstract behavioral contextual states from neural activity. Approach To demonstrate the feasibility of such context decoding, we used electrocorticography (ECoG) and stereo-electroencephalography (sEEG) data recorded from the cortical surface and deeper brain structures, respectively, continuously across multiple days from three subjects. During this time, the subjects were engaged in a range of naturalistic behaviors in a hospital environment. Behavioral contexts were labeled manually from video and audio recordings; four states were considered: engaging in dialogue, rest, using electronics, and watching television. We decode these behaviors using a factor analysis and support vector machine (SVM) approach. Main results We demonstrate that these general behaviors can be decoded with high accuracies of 73% for a four-class classifier for one subject and 71% and 62% for a three-class classifier for two subjects. Significance To our knowledge, this is the first demonstration of the potential to disambiguate abstract naturalistic behavioral contexts from neural activity recorded throughout the day from implanted electrodes. This work motivates further study of context decoding for BCI applications using continuously recorded naturalistic activity in the clinical setting.
Published: 2018

55. List of Contributors

Author: Anand, K.J.S., primary, Bakshi, V.P., additional, Bandler, R., additional, Barrell, J.J., additional, Chang, L., additional, Clerc, N., additional, Devinsky, O., additional, Devroede, G., additional, Diehl, D.L., additional, Eisenberg, D., additional, Ericsson, A., additional, Felten, D.L., additional, Fields, H.L., additional, Foreman, R.D., additional, Furness, J.B., additional, Fuster, J.M., additional, Gruenewald, T.L., additional, Häbler, H.-J., additional, Huot, R.L., additional, Jänig, W., additional, Jessum, R., additional, Johnson, D.H., additional, Kalin, N.H., additional, Keay, K.A., additional, Kemeny, M.E., additional, Khasar, S.G., additional, Ladd, C.O., additional, Levine, J.D., additional, Li, H.-Y., additional, Maher, T.J., additional, Mayer, D.J., additional, Mayer, E.A., additional, McEwen, B.S., additional, Meaney, M.J., additional, Miao, F.J.-P., additional, Mittleman, M.A., additional, Munakata, J., additional, Musselman, D.L., additional, Naliboff, B.D., additional, Nemeroff, C.B., additional, Plotsky, P.M., additional, Price, D.D., additional, Price, J.L., additional, Rapgay, L., additional, Read, N.W., additional, Rinpoche, V.L., additional, Saper, C.B., additional, Sawchenko, P.E., additional, Shelton, S.E., additional, Sikes, R.W., additional, Smith, G.P., additional, Sobel, D.S., additional, Sovik, R., additional, Sternberg, E.M., additional, Thrivikraman, K.V., additional, Tranel, D., additional, Verrier, R.L., additional, and Vogt, B.A., additional
Published: 2000
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56. Use of the Brief Visuospatial Memory Test—Revised (BVMT-R) in neuropsychological evaluation of epilepsy surgery candidates

Author: Barr, W., Morrison, C., Zaroff, C., and Devinsky, O.
Published: 2004
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57. Quantitative analysis of phenotypic elements augments traditional electroclinical classification of common familial epilepsies

Author: Abou-Khalil, B, Afawi, Z, Allen, AS, Bautista, JF, Bellows, ST, Berkovic, SF, Bluvstein, J, Burgess, R, Cascino, G, Cossette, P, Cristofaro, S, Crompton, DE, Delanty, N, Devinsky, O, Dlugos, D, Ellis, CA, Epstein, MP, Fountain, NB, Freyer, C, Geller, EB, Glauser, T, Glynn, S, Goldberg-Stern, H, Goldstein, DB, Gravel, M, Haas, K, Haut, S, Heinzen, EL, Kirsch, HE, Kivity, S, Knowlton, R, Korczyn, AD, Kossoff, E, Kuzniecky, R, Loeb, R, Lowenstein, DH, Marson, AG, McCormack, M, McKenna, K, Mefford, HC, Motika, P, Mullen, SA, O'Brien, TJ, Ottman, R, Paolicchi, J, Parent, JM, Paterson, S, Petrou, S, Petrovski, S, Pickrell, WO, Poduri, A, Rees, MI, Sadleir, LG, Scheffer, IE, Shih, J, Singh, R, Sirven, J, Smith, M, Smith, PEM, Thio, LL, Thomas, RH, Venkat, A, Vining, E, Von Allmen, G, Weisenberg, J, Widdess-Walsh, P, Winawer, MR, Abou-Khalil, B, Afawi, Z, Allen, AS, Bautista, JF, Bellows, ST, Berkovic, SF, Bluvstein, J, Burgess, R, Cascino, G, Cossette, P, Cristofaro, S, Crompton, DE, Delanty, N, Devinsky, O, Dlugos, D, Ellis, CA, Epstein, MP, Fountain, NB, Freyer, C, Geller, EB, Glauser, T, Glynn, S, Goldberg-Stern, H, Goldstein, DB, Gravel, M, Haas, K, Haut, S, Heinzen, EL, Kirsch, HE, Kivity, S, Knowlton, R, Korczyn, AD, Kossoff, E, Kuzniecky, R, Loeb, R, Lowenstein, DH, Marson, AG, McCormack, M, McKenna, K, Mefford, HC, Motika, P, Mullen, SA, O'Brien, TJ, Ottman, R, Paolicchi, J, Parent, JM, Paterson, S, Petrou, S, Petrovski, S, Pickrell, WO, Poduri, A, Rees, MI, Sadleir, LG, Scheffer, IE, Shih, J, Singh, R, Sirven, J, Smith, M, Smith, PEM, Thio, LL, Thomas, RH, Venkat, A, Vining, E, Von Allmen, G, Weisenberg, J, Widdess-Walsh, P, and Winawer, MR
Abstract: OBJECTIVE: Classification of epilepsy into types and subtypes is important for both clinical care and research into underlying disease mechanisms. A quantitative, data-driven approach may augment traditional electroclinical classification and shed new light on existing classification frameworks. METHODS: We used latent class analysis, a statistical method that assigns subjects into groups called latent classes based on phenotypic elements, to classify individuals with common familial epilepsies from the Epi4K Multiplex Families study. Phenotypic elements included seizure types, seizure symptoms, and other elements of the medical history. We compared class assignments to traditional electroclinical classifications and assessed familial aggregation of latent classes. RESULTS: A total of 1120 subjects with epilepsy were assigned to five latent classes. Classes 1 and 2 contained subjects with generalized epilepsy, largely reflecting the distinction between absence epilepsies and younger onset (class 1) versus myoclonic epilepsies and older onset (class 2). Classes 3 and 4 contained subjects with focal epilepsies, and in contrast to classes 1 and 2, these did not adhere as closely to clinically defined focal epilepsy subtypes. Class 5 contained nearly all subjects with febrile seizures plus or unknown epilepsy type, as well as a few subjects with generalized epilepsy and a few with focal epilepsy. Family concordance of latent classes was similar to or greater than concordance of clinically defined epilepsy types. SIGNIFICANCE: Quantitative classification of epilepsy has the potential to augment traditional electroclinical classification by (1) combining some syndromes into a single class, (2) splitting some syndromes into different classes, (3) helping to classify subjects who could not be classified clinically, and (4) defining the boundaries of clinically defined classifications. This approach can guide future research, including molecular genetic studies, by identifyi
Published: 2019

58. Standardized Brain MRI Acquisition Protocols Improve Statistical Power in Multicenter Quantitative Morphometry Studies

Author: George, A, Kuzniecky, R, Rusinek, H, Pardoe, HR, French, J, Lowenstein, D, Cristofaro, S, McKenna, K, Mays, V, Shack, D, Barnard, S, Burke, C, Hegde, M, Glauser, T, O'Brien, T, Pollard, J, Ting, T, Meador, K, Darby, D, Morrison, C, Penovich, P, Schembri, A, Kanner, A, Altilab, HH, Barry, J, Hesdorffer, D, Hope, O, Nadkarni, S, Sperling, M, Winawer, M, Dlugos, D, Beal, J, Boro, A, Herman, S, Singh, R, Halford, J, Thio, LL, Pardoe, H, Cascino, G, Glynn, S, Jackson, G, Knowlton, R, Gidal, B, Abou-Khalil, B, Alldredge, B, Faught, E, Ficker, D, Klein, P, Mintzer, S, Detyniecki, K, Haut, S, Hixson, J, Holmes, M, Kalviainen, R, Widdess-Walsh, P, Krishnamurthy, K, Park, K, Gelfand, M, Kang, J, Krauss, G, Cole, A, Atkinson, P, Trinka, E, Kirschner, M, Schmid, E, Somerville, E, Zentner, C, Laue-Gizzi, H, Rodriguez, A, Devinsky, O, Nadkarni, M, Cook, M, Berkovic, S, Bebin, M, Szaflarsk, J, Szabo, C, Burneo, J, Abou-Khalil, BW, Weisenberg, J, Altilab, H, George, A, Kuzniecky, R, Rusinek, H, Pardoe, HR, French, J, Lowenstein, D, Cristofaro, S, McKenna, K, Mays, V, Shack, D, Barnard, S, Burke, C, Hegde, M, Glauser, T, O'Brien, T, Pollard, J, Ting, T, Meador, K, Darby, D, Morrison, C, Penovich, P, Schembri, A, Kanner, A, Altilab, HH, Barry, J, Hesdorffer, D, Hope, O, Nadkarni, S, Sperling, M, Winawer, M, Dlugos, D, Beal, J, Boro, A, Herman, S, Singh, R, Halford, J, Thio, LL, Pardoe, H, Cascino, G, Glynn, S, Jackson, G, Knowlton, R, Gidal, B, Abou-Khalil, B, Alldredge, B, Faught, E, Ficker, D, Klein, P, Mintzer, S, Detyniecki, K, Haut, S, Hixson, J, Holmes, M, Kalviainen, R, Widdess-Walsh, P, Krishnamurthy, K, Park, K, Gelfand, M, Kang, J, Krauss, G, Cole, A, Atkinson, P, Trinka, E, Kirschner, M, Schmid, E, Somerville, E, Zentner, C, Laue-Gizzi, H, Rodriguez, A, Devinsky, O, Nadkarni, M, Cook, M, Berkovic, S, Bebin, M, Szaflarsk, J, Szabo, C, Burneo, J, Abou-Khalil, BW, Weisenberg, J, and Altilab, H
Abstract: BACKGROUND AND PURPOSE: In this study, we used power analysis to calculate required sample sizes to detect group-level changes in quantitative neuroanatomical estimates derived from MRI scans obtained from multiple imaging centers. Sample size estimates were derived from (i) standardized 3T image acquisition protocols and (ii) nonstandardized clinically acquired images obtained at both 1.5 and 3T as part of the multicenter Human Epilepsy Project. Sample size estimates were compared to assess the benefit of standardizing acquisition protocols. METHODS: Cortical thickness, hippocampal volume, and whole brain volume were estimated from whole brain T1-weighted MRI scans processed using Freesurfer v6.0. Sample sizes required to detect a range of effect sizes were calculated using (i) standard t-test based power analysis methods and (ii) a nonparametric bootstrap approach. RESULTS: A total of 32 participants were included in our analyses, aged 29.9 ± 12.62 years. Standard deviation estimates were lower for all quantitative neuroanatomical metrics when assessed using standardized protocols. Required sample sizes per group to detect a given effect size were markedly reduced when using standardized protocols, particularly for cortical thickness changes <.2 mm and hippocampal volume changes <10%. CONCLUSIONS: The use of standardized protocols yielded up to a five-fold reduction in required sample sizes to detect disease-related neuroanatomical changes, and is particularly beneficial for detecting subtle effects. Standardizing image acquisition protocols across scanners prior to commencing a study is a valuable approach to increase the statistical power of multicenter MRI studies.
Published: 2019

59. The Epilepsy Genetics Initiative: Systematic reanalysis of diagnostic exomes increases yield

Author: Berkovic, SF, Goldstein, DB, Heinzen, EL, Laughlin, BL, Lowenstein, DH, Lubbers, L, Stewart, R, Whittemore, V, Angione, K, Bazil, CW, Bier, L, Bluvstein, J, Brimble, E, Campbell, C, Cavalleri, G, Chambers, C, Choi, H, Cilio, MR, Ciliberto, M, Cornes, S, Delanty, N, Demarest, S, Devinsky, O, Dlugos, D, Dubbs, H, Dugan, P, Ernst, ME, Gibbons, M, Goodkin, HP, Helbig, I, Jansen, L, Johnson, K, Joshi, C, Lippa, NC, Marsh, E, Martinez, A, Millichap, J, Mulhern, MS, Numis, A, Park, K, Pippucci, T, Poduri, A, Porter, B, Regan, B, Sands, TT, Scheffer, IE, Schreiber, JM, Sheidley, B, Singhal, N, Smith, L, Sullivan, J, Taylor, A, Tolete, P, Afgani, TM, Aggarwal, V, Burgess, R, Dixon-Salazar, T, Hemati, P, Milder, J, Petrovski, S, Revah-Politi, A, Stong, N, Berkovic, SF, Goldstein, DB, Heinzen, EL, Laughlin, BL, Lowenstein, DH, Lubbers, L, Stewart, R, Whittemore, V, Angione, K, Bazil, CW, Bier, L, Bluvstein, J, Brimble, E, Campbell, C, Cavalleri, G, Chambers, C, Choi, H, Cilio, MR, Ciliberto, M, Cornes, S, Delanty, N, Demarest, S, Devinsky, O, Dlugos, D, Dubbs, H, Dugan, P, Ernst, ME, Gibbons, M, Goodkin, HP, Helbig, I, Jansen, L, Johnson, K, Joshi, C, Lippa, NC, Marsh, E, Martinez, A, Millichap, J, Mulhern, MS, Numis, A, Park, K, Pippucci, T, Poduri, A, Porter, B, Regan, B, Sands, TT, Scheffer, IE, Schreiber, JM, Sheidley, B, Singhal, N, Smith, L, Sullivan, J, Taylor, A, Tolete, P, Afgani, TM, Aggarwal, V, Burgess, R, Dixon-Salazar, T, Hemati, P, Milder, J, Petrovski, S, Revah-Politi, A, and Stong, N
Abstract: OBJECTIVE: The Epilepsy Genetics Initiative (EGI) was formed in 2014 to create a centrally managed database of clinically generated exome sequence data. EGI performs systematic research-based reanalysis to identify new molecular diagnoses that were not possible at the time of initial sequencing and to aid in novel gene discovery. Herein we report on the efficacy of this approach 3 years after inception. METHODS: One hundred sixty-six individuals with epilepsy who underwent diagnostic whole exome sequencing (WES) were enrolled, including 139 who had not received a genetic diagnosis. Sequence data were transferred to the EGI and periodically reevaluated on a research basis. RESULTS: Eight new diagnoses were made as a result of updated annotations or the discovery of novel epilepsy genes after the initial diagnostic analysis was performed. In five additional cases, we provided new evidence to support or contradict the likelihood of variant pathogenicity reported by the laboratory. One novel epilepsy gene was discovered through dual interrogation of research and clinically generated WES. SIGNIFICANCE: EGI's diagnosis rate of 5.8% represents a considerable increase in diagnostic yield and demonstrates the value of periodic reinterrogation of whole exome data. The initiative's contributions to gene discovery underscore the importance of data sharing and the value of collaborative enterprises.
Published: 2019

60. Decrease of sympathetic cardiovascular modulation after temporal lobe epilepsy surgery

Author: Hilz, M. J., Devinsky, O., Doyle, W., Mauerer, A., and Dütsch, M.
Published: 2002

61. Anatomic and Physiological Considerations in Pallidotomy for Parkinson’s Disease

Author: Dogali, M., primary, Berić, A., additional, Sterio, D., additional, Eidelberg, D., additional, Fazzini, E., additional, Takikawa, S., additional, Samelson, D. R., additional, Devinsky, O., additional, and Kolodny, E. H., additional
Published: 1995
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62. Not all predictions are equal: 'What' and 'When' predictions modulate activity in auditory cortex through different mechanisms

Author: Auksztulewicz, R, Schwiedrzik, C, Thesen, T, Doyle, W, Devinsky, O, De Ozorio Nobre, A, Schroeder, C, Friston, K, and Melloni, L
Subjects: Adult, Male, Time Factors, Computer science, Auditory area, Models, Neurological, Prefrontal Cortex, Stimulus (physiology), Auditory cortex, 050105 experimental psychology, 03 medical and health sciences, Superior temporal gyrus, Young Adult, 0302 clinical medicine, Neural Pathways, Reaction Time, Humans, 0501 psychology and cognitive sciences, Predictability, Research Articles, Auditory Cortex, General Neuroscience, 05 social sciences, Motor Cortex, Neurophysiology, Middle Aged, Anticipation, Psychological, Associative learning, Electrophysiology, Acoustic Stimulation, Evoked Potentials, Auditory, Visual Perception, Female, Electrocorticography, Neuroscience, 030217 neurology & neurosurgery
Abstract: Using predictions based on environmental regularities is fundamental for adaptive behavior. While it is widely accepted that predictions across different stimulus attributes (e.g., time and content) facilitate sensory processing, it is unknown whether predictions across these attributes rely on the same neural mechanism. Here, to elucidate the neural mechanisms of predictions, we combine invasive electrophysiological recordings (human electrocorticography in 4 females and 2 males) with computational modeling while manipulating predictions about content (“what”) and time (“when”). We found that “when” predictions increased evoked activity over motor and prefrontal regions both at early (∼180 ms) and late (430–450 ms) latencies. “What” predictability, however, increased evoked activity only over prefrontal areas late in time (420–460 ms). Beyond these dissociable influences, we found that “what” and “when” predictability interactively modulated the amplitude of early (165 ms) evoked responses in the superior temporal gyrus. We modeled the observed neural responses using biophysically realistic neural mass models, to better understand whether “what” and “when” predictions tap into similar or different neurophysiological mechanisms. Our modeling results suggest that “what” and “when” predictability rely on complementary neural processes: “what” predictions increased short-term plasticity in auditory areas, whereas “when” predictability increased synaptic gain in motor areas. Thus, content and temporal predictions engage complementary neural mechanisms in different regions, suggesting domain-specific prediction signaling along the cortical hierarchy. Encoding predictions through different mechanisms may endow the brain with the flexibility to efficiently signal different sources of predictions, weight them by their reliability, and allow for their encoding without mutual interference.SIGNIFICANCE STATEMENTPredictions of different stimulus features facilitate sensory processing. However, it is unclear whether predictions of different attributes rely on similar or different neural mechanisms. By combining invasive electrophysiological recordings of cortical activity with experimental manipulations of participants' predictions about content and time of acoustic events, we found that the two types of predictions had dissociable influences on cortical activity, both in terms of the regions involved and the timing of the observed effects. Further, our biophysical modeling analysis suggests that predictability of content and time rely on complementary neural processes: short-term plasticity in auditory areas and synaptic gain in motor areas, respectively. This suggests that predictions of different features are encoded with complementary neural mechanisms in different brain regions.
Published: 2018

63. Electrocorticographic responses to time-compressed speech vary across the cortical auditory hierarchy

Author: Oded Ghitza, David Poeppel, Thomas Thesen, Ido Davidesco, Uri Hasson, Devinsky O, Charles E. Schroeder, Werner Doyle, Christopher J. Honey, and Lucia Melloni
Subjects: medicine.medical_specialty, 05 social sciences, Auditory area, Information processing, Inferior frontal gyrus, Audiology, Intelligibility (communication), 050105 experimental psychology, Angular gyrus, 03 medical and health sciences, Superior temporal gyrus, 0302 clinical medicine, medicine, otorhinolaryngologic diseases, 0501 psychology and cognitive sciences, Psychology, 030217 neurology & neurosurgery, Sentence, Spoken language
Abstract: Human listeners understand spoken language across a variety of rates, but when speech is presented three times or more faster than its usual rate, it becomes unintelligible. How the brain achieves such tolerance and why speech becomes unintelligible above certain rates is still unclear. We addressed these questions using electrocorticography (ECoG) recordings in 7 epileptic patients (two female). Patients rated the intelligibility of sentences presented at the original rate (100%), speeded rates (33% or 66% of the original sentence duration) and a slowed rate (150%). We then examined which parameters of the neural response covary with the transition from intelligible to unintelligible speech. Specifically, we asked whether neural responses: 1) track the acoustic envelope of the incoming speech; 2) “scale” with speech rate, i.e. whether neural responses elicited by slowed and speeded sentences can be linearly scaled to match the responses to the original sentence. Behaviorally, intelligibility was at ceiling for speech rates of 66% and above, but dropped significantly for the 33% rate. At the neural level, Superior Temporal Gyrus regions (STG) in close proximity to A1 (‘low-level’) tracked the acoustic envelope and linearly scaled with the input across all speech rates, irrespective of intelligibility. In contrast, secondary auditory areas in the STG as well as the inferior frontal gyrus and angular gyrus (‘high-level’) tracked the acoustic envelope and linearly scaled with input only for intelligible speech. These results help reconcile seemingly contradictory previous findings and provide better understanding of how information processing unfolds along the cortical auditory hierarchy.
Published: 2018
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64. The past, present and future challenges in epilepsy related and sudden deaths and biobanking

Author: Thom, M, Boldrini, M, Bundock, E, Sheppard, MN, and Devinsky, O
Abstract: Awareness and research on epilepsy-related deaths (ERD), in particular Sudden Unexpected Death in Epilepsy (SUDEP), have exponentially increased over the last two decades. Most publications have focused on guidelines that inform clinicians dealing with these deaths, educating patients, potential risk factors and mechanisms. There is a relative paucity of information available for pathologists who conduct these autopsies regarding appropriate post-mortem practice and investigations. As we move from recognizing SUDEP as the most common form of ERD toward in-depth investigations into its causes and prevention, health professionals involved with these autopsies and post-mortem procedure must remain fully informed. Systematizing a more comprehensive and consistent practice of examining these cases will facilitate 1) more precise determination of cause of death, 2) identification of SUDEP for improved epidemiological surveillance (the first step for an intervention study), and 3) bio-banking and cell-based research. This article reviews how pathologists and healthcare professionals have approached ERD, current practices, logistical problems and areas to improve and harmonize. The main neuropathology, cardiac and genetic findings in SUDEP are outlined, providing a framework for best practices, integration of clinical, pathologic and molecular genetic investigations in SUDEP, and ultimately prevention.
Published: 2018

65. Short-term safety of mTOR inhibitors in infants and very young children with tuberous sclerosis complex (TSC): Multicentre clinical experience

Author: Krueger DA, Capal JK, Curatolo P, Devinsky O, Ess K, Tzadok M, Koenig MK, Narayanan V, Ramos F, Jozwiak S, de Vries P, Jansen AC, Wong M, Mowat D, Lawson J, Bruns S, Franz DN, and TSCure Research Group
Subjects: Sirolimus, Tuberous sclerosis complex, mTOR, Infant, Everolimus, Safety
Abstract: OBJECTIVE: To evaluate the safety of mTOR inhibitors (sirolimus or everolimus) in infants and very young children with tuberous sclerosis complex (TSC) under two years of age. METHODS: Study design was retrospective to capture medical record data from 52 international TSC Centres who initiated treatment with sirolimus or everolimus in TSC children before the age of two years. Data collection included demographic and clinical information including reason(s) for initiating treatment with mTOR inhibitors, treatment duration, dosing, and corresponding serum trough levels, response to treatment, and adverse events (AE). RESULTS: 19 of 52 (37%) TSC Centres reported treatment of at least one child with TSC under the age of two years with everolimus or sirolimus. Treatment-related data were provided for 45 patients meeting inclusion criteria. Everolimus was utilised 87% of the time, compared to 24% for sirolimus (5 subjects, 11%, were treated separately with both). Refractory epilepsy (45%) was the most common primary reason for initiating treatment and treatment was initiated on average at 11.6 ± 7.6 months of age. At least one AE, suspected or definitely treatment-related, occurred in 35 of 45 (78%) treated subjects. Most AEs were mild (Grade 1) or moderate (Grade 2) in severity and most commonly related to infections. Severe AE (Grade 3) was reported in 7 subjects (20%) and no life-threatening AE (Grade 4) or death/disability (Grade 5) was reported. Treatment was discontinued due to an AE in 9 of 45 (20%). CONCLUSIONS: Everolimus, and to a lesser extent sirolimus, are increasingly being used to treat TSC infants and very young children for multiple TSC-associated clinical indications. While AEs were common, most were not severe and did not prevent continued treatment in the majority of this younger population.
Published: 2018

66. Structural brain abnormalities in the common epilepsies assessed in a worldwide ENIGMA study

Author: Whelan, Cd, Altmann, A, Botía, Ja, Jahanshad, N, Hibar, Dp, Absil, J, Alhusaini, S, Alvim, Mkm, Auvinen, P, Bartolini, E, Bergo, Fpg, Bernardes, T, Blackmon, K, Braga, B, Caligiuri, Me, Calvo, A, Carr, Sj, Chen, J, Chen, S, Cherubini, A, David, P, Domin, M, Foley, S, França, W, Haaker, G, Isaev, D, Keller, Ss, Kotikalapudi, R, Kowalczyk, Ma, Kuzniecky, R, Langner, S, Lenge, M, Leyden, Km, Liu, M, Loi, Rq, Martin, P, Mascalchi, M, Morita, Me, Pariente, Jc, Rodríguez-Cruces, R, Rummel, C, Saavalainen, T, Semmelroch, Mk, Severino, M, Thomas, Rh, Tondelli, M, Tortora, D, Vaudano, AE39, Vivash, L40, von Podewils F42, Wagner, J43, Weber, B43, Yao, Y46, Yasuda, CL7, Zhang, G47, Bargalló, N15, Bender, B26, Bernasconi, N, Bernasconi, A, Bernhardt, Bc, Blümcke, I, Carlson, C, Cavalleri, Gl, Cendes, F, Concha, L, Delanty, N, Depondt, C, Devinsky, O, Doherty, CP51, Focke, Nk, Gambardella, A, Guerrini, R, Hamandi, K, Jackson, Gd, Kälviäinen, R, Kochunov, P, Kwan, P, Labate, A, McDonald, Cr, Meletti, S, O'Brien, Tj, Ourselin, S, Richardson MP Striano, P, Thesen, T, Wiest, R, Zhang, J, Vezzani, A, Ryten, M, Thompson, Pm, and Sisodiya, Sm.
Subjects: MRI, epilepsy, precentral gyrus, thalamus
Published: 2018

67. Effect of Cannabidiol on Drop Seizures in the Lennox-Gastaut Syndrome

Author: Devinsky, O, Patel, AD, Cross, JH, Villanueva, V, Wirrell, EC, Privitera, M, Greenwood, SM, Roberts, C, Checketts, D, VanLandingham, KE, Zuberi, SM, and GWPCARE3 Study Grp
Abstract: BACKGROUND Cannabidiol has been used for treatment-resistant seizures in patients with severe early-onset epilepsy. We investigated the efficacy and safety of cannabidiol added to a regimen of conventional antiepileptic medication to treat drop seizures in patients with the Lennox-Gastaut syndrome, a severe developmental epileptic encephalopathy. METHODS In this double-blind, placebo-controlled trial conducted at 30 clinical centers, we randomly assigned patients with the Lennox-Gastaut syndrome (age range, 2 to 55 years) who had had two or more drop seizures per week during a 28-day baseline period to receive cannabidiol oral solution at a dose of either 20 mg per kilogram of body weight (20-mg cannabidiol group) or 10 mg per kilogram (10-mg cannabidiol group) or matching placebo, administered in two equally divided doses daily for 14 weeks. The primary outcome was the percentage change from baseline in the frequency of drop seizures (average per 28 days) during the treatment period. RESULTS A total of 225 patients were enrolled; 76 patients were assigned to the 20-mg cannabidiol group, 73 to the 10-mg cannabidiol group, and 76 to the placebo group. During the 28-day baseline period, the median number of drop seizures was 85 in all trial groups combined. The median percent reduction from baseline in drop-seizure frequency during the treatment period was 41.9% in the 20-mg cannabidiol group, 37.2% in the 10-mg cannabidiol group, and 17.2% in the placebo group (P = 0.005 for the 20-mg cannabidiol group vs. placebo group, and P = 0.002 for the 10-mg cannabidiol group vs. placebo group). The most common adverse events among the patients in the cannabidiol groups were somnolence, decreased appetite, and diarrhea; these events occurred more frequently in the higher-dose group. Six patients in the 20-mg cannabidiol group and 1 patient in the 10-mg cannabidiol group discontinued the trial medication because of adverse events and were withdrawn from the trial. Fourteen patients who received cannabidiol (9%) had elevated liver aminotransferase concentrations. CONCLUSIONS Among children and adults with the Lennox-Gastaut syndrome, the addition of cannabidiol at a dose of 10 mg or 20 mg per kilogram per day to a conventional antiepileptic regimen resulted in greater reductions in the frequency of drop seizures than placebo. Adverse events with cannabidiol included elevated liver aminotransferase concentrations.
Published: 2018

68. Neural correlates of unstructured motor behaviors

Author: Gabriel, Paolo G, primary, Chen, K J, additional, Alasfour, A, additional, Pailla, T, additional, Doyle, W K, additional, Devinsky, O, additional, Friedman, D, additional, Dugan, P, additional, Melloni, L, additional, Thesen, T, additional, Gonda, D, additional, Sattar, S, additional, Wang, S G, additional, and Gilja, V, additional
Published: 2019
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69. 3T MRI Whole-Brain Microscopy Discrimination of Subcortical Anatomy, Part 2: Basal Forebrain

Author: Hoch, M.J., primary, Bruno, M.T., additional, Faustin, A., additional, Cruz, N., additional, Mogilner, A.Y., additional, Crandall, L., additional, Wisniewski, T., additional, Devinsky, O., additional, and Shepherd, T.M., additional
Published: 2019
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70. Simulating human sleep spindle MEG and EEG from ion channel and circuit level dynamics

Author: Rosen, B.Q., primary, Krishnan, G.P., additional, Sanda, P., additional, Komarov, M., additional, Sejnowski, T., additional, Rulkov, N., additional, Ulbert, I., additional, Eross, L., additional, Madsen, J., additional, Devinsky, O., additional, Doyle, W., additional, Fabo, D., additional, Cash, S., additional, Bazhenov, M., additional, and Halgren, E., additional
Published: 2019
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71. 3T MRI Whole-Brain Microscopy Discrimination of Subcortical Anatomy, Part 1: Brain Stem

Author: Hoch, M.J., primary, Bruno, M.T., additional, Faustin, A., additional, Cruz, N., additional, Crandall, L., additional, Wisniewski, T., additional, Devinsky, O., additional, and Shepherd, T.M., additional
Published: 2019
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72. A double-blind, placebo-controlled study of remacemide hydrochloride in patients with refractory epilepsy following pre-surgical assessment

Author: Devinsky, O, Vazquez, B, Faught, E, Leppik, I.E, Pellock, J.M, Schachter, S, Alderfer, V, and Holdich, T.A.H
Published: 2002
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73. De novo variants in the alternative exon 5 of SCN8A cause epileptic encephalopathy

Author: Berkovic, SF, Dixon-Salazar, T, Goldstein, DB, Heinzen, EL, Laughlin, BL, Lowenstein, DH, Lubbers, L, Milder, J, Stewart, R, Whittemore, V, Angione, K, Bazil, CW, Bier, L, Bluvstein, J, Brimble, E, Campbell, C, Chambers, C, Choi, H, Cilio, MR, Ciliberto, M, Cornes, S, Delanty, N, Demarest, S, Devinsky, O, Dlugos, D, Dubbs, H, Dugan, P, Ernst, ME, Gallentine, W, Gibbons, M, Goodkin, H, Grinton, B, Helbig, I, Jansen, L, Johnson, K, Joshi, C, Lippa, NC, Makati, MA, Marsh, E, Martinez, A, Millichap, J, Moskovich, Y, Mulhern, MS, Numis, A, Park, K, Poduri, A, Porter, B, Sands, TT, Scheffer, IE, Sheidley, B, Singhal, N, Smith, L, Sullivan, J, Riviello, JJ, Taylor, A, Tolete, P, Berkovic, SF, Dixon-Salazar, T, Goldstein, DB, Heinzen, EL, Laughlin, BL, Lowenstein, DH, Lubbers, L, Milder, J, Stewart, R, Whittemore, V, Angione, K, Bazil, CW, Bier, L, Bluvstein, J, Brimble, E, Campbell, C, Chambers, C, Choi, H, Cilio, MR, Ciliberto, M, Cornes, S, Delanty, N, Demarest, S, Devinsky, O, Dlugos, D, Dubbs, H, Dugan, P, Ernst, ME, Gallentine, W, Gibbons, M, Goodkin, H, Grinton, B, Helbig, I, Jansen, L, Johnson, K, Joshi, C, Lippa, NC, Makati, MA, Marsh, E, Martinez, A, Millichap, J, Moskovich, Y, Mulhern, MS, Numis, A, Park, K, Poduri, A, Porter, B, Sands, TT, Scheffer, IE, Sheidley, B, Singhal, N, Smith, L, Sullivan, J, Riviello, JJ, Taylor, A, and Tolete, P
Abstract: PurposeAs part of the Epilepsy Genetics Initiative, we re-evaluated clinically generated exome sequence data from 54 epilepsy patients and their unaffected parents to identify molecular diagnoses not provided in the initial diagnostic interpretation.MethodsWe compiled and analyzed exome sequence data from 54 genetically undiagnosed trios using a validated analysis pipeline. We evaluated the significance of the genetic findings by reanalyzing sequence data generated at Ambry Genetics, and from a number of additional case and control cohorts.ResultsIn 54 previously undiagnosed trios, we identified two de novo missense variants in SCN8A in the highly expressed alternative exon 5 A-an exon only recently added to the Consensus Coding Sequence database. One additional undiagnosed epilepsy patient harboring a de novo variant in exon 5 A was found in the Ambry Genetics cohort. Missense variants in SCN8A exon 5 A are extremely rare in the population, further supporting the pathogenicity of the de novo alterations identified.ConclusionThese results expand the range of SCN8A variants in epileptic encephalopathy patients and illustrate the necessity of ongoing reanalysis of negative exome sequences, as advances in the knowledge of disease genes and their annotations will permit new diagnoses to be made.
Published: 2018

74. Genome-wide mega-analysis identifies 16 loci and highlights diverse biological mechanisms in the common epilepsies

Author: Abou-Khalil, B, Auce, P, Avbersek, A, Bahlo, M, Balding, DJ, Bast, T, Baum, L, Becker, AJ, Becker, F, Berghuis, B, Berkovic, SF, Boysen, KE, Bradfield, JP, Brody, LC, Buono, RJ, Campbell, E, Cascino, GD, Catarino, CB, Cavalleri, GL, Cherny, SS, Chinthapalli, K, Coffey, AJ, Compston, A, Coppola, A, Cossette, P, Craig, JJ, de Haan, G-J, De Jonghe, P, de Kovel, CGF, Delanty, N, Depondt, C, Devinsky, O, Dlugos, DJ, Doherty, CP, Elger, CE, Eriksson, JG, Ferraro, TN, Feucht, M, Francis, B, Franke, A, French, JA, Freytag, S, Gaus, V, Geller, EB, Gieger, C, Glauser, T, Glynn, S, Goldstein, DB, Gui, H, Guo, Y, Haas, KF, Hakonarson, H, Hallmann, K, Haut, S, Heinzen, EL, Helbig, I, Hengsbach, C, Hjalgrim, H, Iacomino, M, Ingason, A, Jamnadas-Khoda, J, Johnson, MR, Kalviainen, R, Kantanen, A-M, Kasperaviciute, D, Trenite, DK-N, Kirsch, HE, Knowlton, RC, Koeleman, BPC, Krause, R, Krenn, M, Kunz, WS, Kuzniecky, R, Kwan, P, Lal, D, Lau, Y-L, Lehesjoki, A-E, Lerche, H, Leu, C, Lieb, W, Lindhout, D, Lo, WD, Lopes-Cendes, I, Lowenstein, DH, Malovini, A, Marson, AG, Mayer, T, McCormack, M, Mills, JL, Mirza, N, Moerzinger, M, Moller, RS, Molloy, AM, Muhle, H, Newton, M, Ng, P-W, Noethen, MM, Nuernberg, P, O'Brien, TJ, Oliver, KL, Palotie, A, Pangilinan, F, Peter, S, Petrovski, S, Poduri, A, Privitera, M, Radtke, R, Rau, S, Reif, PS, Reinthaler, EM, Rosenow, F, Sander, JW, Sander, T, Scattergood, T, Schachter, SC, Schankin, CJ, Scheffer, IE, Schmitz, B, Schoch, S, Sham, PC, Shih, JJ, Sills, GJ, Sisodiya, SM, Slattery, L, Smith, A, Smith, DF, Smith, MC, Smith, PE, Sonsma, ACM, Speed, D, Sperling, MR, Steinhoff, BJ, Stephani, U, Stevelink, R, Strauch, K, Striano, P, Stroink, H, Surges, R, Tan, KM, Thio, LL, Thomas, GN, Todaro, M, Tozzi, R, Vari, MS, Vining, EPG, Visscher, F, von Spiczak, S, Walley, NM, Weber, YG, Wei, Z, Weisenberg, J, Whelan, CD, Widdess-Walsh, P, Wolff, M, Wolking, S, Yang, W, Zara, F, Zimprich, F, Abou-Khalil, B, Auce, P, Avbersek, A, Bahlo, M, Balding, DJ, Bast, T, Baum, L, Becker, AJ, Becker, F, Berghuis, B, Berkovic, SF, Boysen, KE, Bradfield, JP, Brody, LC, Buono, RJ, Campbell, E, Cascino, GD, Catarino, CB, Cavalleri, GL, Cherny, SS, Chinthapalli, K, Coffey, AJ, Compston, A, Coppola, A, Cossette, P, Craig, JJ, de Haan, G-J, De Jonghe, P, de Kovel, CGF, Delanty, N, Depondt, C, Devinsky, O, Dlugos, DJ, Doherty, CP, Elger, CE, Eriksson, JG, Ferraro, TN, Feucht, M, Francis, B, Franke, A, French, JA, Freytag, S, Gaus, V, Geller, EB, Gieger, C, Glauser, T, Glynn, S, Goldstein, DB, Gui, H, Guo, Y, Haas, KF, Hakonarson, H, Hallmann, K, Haut, S, Heinzen, EL, Helbig, I, Hengsbach, C, Hjalgrim, H, Iacomino, M, Ingason, A, Jamnadas-Khoda, J, Johnson, MR, Kalviainen, R, Kantanen, A-M, Kasperaviciute, D, Trenite, DK-N, Kirsch, HE, Knowlton, RC, Koeleman, BPC, Krause, R, Krenn, M, Kunz, WS, Kuzniecky, R, Kwan, P, Lal, D, Lau, Y-L, Lehesjoki, A-E, Lerche, H, Leu, C, Lieb, W, Lindhout, D, Lo, WD, Lopes-Cendes, I, Lowenstein, DH, Malovini, A, Marson, AG, Mayer, T, McCormack, M, Mills, JL, Mirza, N, Moerzinger, M, Moller, RS, Molloy, AM, Muhle, H, Newton, M, Ng, P-W, Noethen, MM, Nuernberg, P, O'Brien, TJ, Oliver, KL, Palotie, A, Pangilinan, F, Peter, S, Petrovski, S, Poduri, A, Privitera, M, Radtke, R, Rau, S, Reif, PS, Reinthaler, EM, Rosenow, F, Sander, JW, Sander, T, Scattergood, T, Schachter, SC, Schankin, CJ, Scheffer, IE, Schmitz, B, Schoch, S, Sham, PC, Shih, JJ, Sills, GJ, Sisodiya, SM, Slattery, L, Smith, A, Smith, DF, Smith, MC, Smith, PE, Sonsma, ACM, Speed, D, Sperling, MR, Steinhoff, BJ, Stephani, U, Stevelink, R, Strauch, K, Striano, P, Stroink, H, Surges, R, Tan, KM, Thio, LL, Thomas, GN, Todaro, M, Tozzi, R, Vari, MS, Vining, EPG, Visscher, F, von Spiczak, S, Walley, NM, Weber, YG, Wei, Z, Weisenberg, J, Whelan, CD, Widdess-Walsh, P, Wolff, M, Wolking, S, Yang, W, Zara, F, and Zimprich, F
Abstract: The epilepsies affect around 65 million people worldwide and have a substantial missing heritability component. We report a genome-wide mega-analysis involving 15,212 individuals with epilepsy and 29,677 controls, which reveals 16 genome-wide significant loci, of which 11 are novel. Using various prioritization criteria, we pinpoint the 21 most likely epilepsy genes at these loci, with the majority in genetic generalized epilepsies. These genes have diverse biological functions, including coding for ion-channel subunits, transcription factors and a vitamin-B6 metabolism enzyme. Converging evidence shows that the common variants associated with epilepsy play a role in epigenetic regulation of gene expression in the brain. The results show an enrichment for monogenic epilepsy genes as well as known targets of antiepileptic drugs. Using SNP-based heritability analyses we disentangle both the unique and overlapping genetic basis to seven different epilepsy subtypes. Together, these findings provide leads for epilepsy therapies based on underlying pathophysiology.
Published: 2018

75. STAG1 mutations cause a novel cohesinopathy characterised by unspecific syndromic intellectual disability

Author: Lehalle, D., Mosca-Boidron, A.L., Begtrup, A., Boute-Benejean, O., Charles, P., Cho, M.T., Clarkson, A., Devinsky, O., Duffourd, Y., Duplomb-Jego, L., Gerard, B., Jacquette, A., Kuentz, P., Masurel-Paulet, A., McDougall, C., Moutton, S., Olivie, H., Park, S.M., Rauch, A., Revencu, N., Riviere, J.B., Rubin, K., Simonic, I., Shears, D.J., Smol, T., Tavares, A.L.T., Terhal, P., Thevenon, J., Gassen, K. van, Vincent-Delorme, C., Willemsen, M.H., Wilson, G.N., Zackai, E., Zweier, C., Callier, P., Thauvin-Robinet, C., Faivre, L., Lehalle, D., Mosca-Boidron, A.L., Begtrup, A., Boute-Benejean, O., Charles, P., Cho, M.T., Clarkson, A., Devinsky, O., Duffourd, Y., Duplomb-Jego, L., Gerard, B., Jacquette, A., Kuentz, P., Masurel-Paulet, A., McDougall, C., Moutton, S., Olivie, H., Park, S.M., Rauch, A., Revencu, N., Riviere, J.B., Rubin, K., Simonic, I., Shears, D.J., Smol, T., Tavares, A.L.T., Terhal, P., Thevenon, J., Gassen, K. van, Vincent-Delorme, C., Willemsen, M.H., Wilson, G.N., Zackai, E., Zweier, C., Callier, P., Thauvin-Robinet, C., and Faivre, L.
Abstract: Item does not contain fulltext, BACKGROUND: Cohesinopathies are rare neurodevelopmental disorders arising from a dysfunction in the cohesin pathway, which enables chromosome segregation and regulates gene transcription. So far, eight genes from this pathway have been reported in human disease. STAG1 belongs to the STAG subunit of the core cohesin complex, along with five other subunits. This work aimed to identify the phenotype ascribed to STAG1 mutations. METHODS: Among patients referred for intellectual disability (ID) in genetics departments worldwide, array-comparative genomic hybridisation (CGH), gene panel, whole-exome sequencing or whole-genome sequencing were performed following the local diagnostic standards. RESULTS: A mutation in STAG1 was identified in 17 individuals from 16 families, 9 males and 8 females aged 2-33 years. Four individuals harboured a small microdeletion encompassing STAG1; three individuals from two families had an intragenic STAG1 deletion. Six deletions were identified by array-CGH, one by whole-exome sequencing. Whole-exome sequencing found de novo heterozygous missense or frameshift STAG1 variants in eight patients, a panel of genes involved in ID identified a missense and a frameshift variant in two individuals. The 17 patients shared common facial features, with wide mouth and deep-set eyes. Four individuals had mild microcephaly, seven had epilepsy. CONCLUSIONS: We report an international series of 17 individuals from 16 families presenting with syndromic unspecific ID that could be attributed to a STAG1 deletion or point mutation. This first series reporting the phenotype ascribed to mutation in STAG1 highlights the importance of data sharing in the field of rare disorders.
Published: 2017

76. Simulating human sleep spindle MEG and EEG from ion channel and circuit level dynamics

Author: Rosen, B.Q., primary, Krishnan, G.P., additional, Sanda, P., additional, Komarov, M., additional, Sejnowski, T., additional, Rulkov, N., additional, Ulbert, I., additional, Eross, L., additional, Madsen, J., additional, Devinsky, O., additional, Doyle, W., additional, Fabo, D., additional, Cash, S., additional, Bazhenov, M., additional, and Halgren, E., additional
Published: 2017
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77. Beeinträchtigung der Baroreflexfunktion bei Patienten mit Temporallappenepilepsien

Author: Dütsch, M, Devinsky, O, and Hilz, M.J
Published: 2024
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78. Periventricular white matter abnormalities and restricted repetitive behavior in autism spectrum disorder

Author: Blackmon, K, Ben-Avi, E, Wang, X, Pardoe, HR, Di Martino, A, Halgren, E, Devinsky, O, Thesen, T, Kuzniecky, R, Blackmon, K, Ben-Avi, E, Wang, X, Pardoe, HR, Di Martino, A, Halgren, E, Devinsky, O, Thesen, T, and Kuzniecky, R
Abstract: Malformations of cortical development are found at higher rates in autism spectrum disorder (ASD) than in healthy controls on postmortem neuropathological evaluation but are more variably observed on visual review of in-vivo MRI brain scans. This may be due to the visually elusive nature of many malformations on MRI. Here, we utilize a quantitative approach to determine whether a volumetric measure of heterotopic gray matter in the white matter is elevated in people with ASD, relative to typically developing controls (TDC). Data from a primary sample of 48 children/young adults with ASD and 48 age-, and gender-matched TDCs, selected from the Autism Brain Imaging Data Exchange (ABIDE) open-access database, were analyzed to compare groups on (1) blinded review of high-resolution T1-weighted research sequences; and (2) quantitative measurement of white matter hypointensity (WMH) volume calculated from the same T1-weighted scans. Groupwise WMH volume comparisons were repeated in an independent, multi-site sample (80 ASD/80 TDC), also selected from ABIDE. Visual review resulted in equivalent proportions of imaging abnormalities in the ASD and TDC group. However, quantitative analysis revealed elevated periventricular and deep subcortical WMH volumes in ASD. This finding was replicated in the independent, multi-site sample. Periventricular WMH volume was not associated with age but was associated with greater restricted repetitive behaviors on both parent-reported and clinician-rated assessment inventories. Thus, findings demonstrate that periventricular WMH volume is elevated in ASD and associated with a higher degree of repetitive behaviors and restricted interests. Although the etiology of focal WMH clusters is unknown, the absence of age effects suggests that they may reflect a static anomaly.
Published: 2016

79. De novo loss of function mutations in KIAA2022 are associated with epilepsy and neurodevelopmental delay in females

Author: Webster, R., primary, Cho, M.T., additional, Retterer, K., additional, Millan, F., additional, Nowak, C., additional, Douglas, J., additional, Ahmad, A., additional, Raymond, G.V., additional, Johnson, M.R., additional, Pujol, A., additional, Begtrup, A., additional, McKnight, D., additional, Devinsky, O., additional, and Chung, W.K., additional
Published: 2016
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80. Human Dorsolateral Prefrontal Cortex Is Not Necessary for Spatial Working Memory

Author: Mackey, W. E., primary, Devinsky, O., additional, Doyle, W. K., additional, Meager, M. R., additional, and Curtis, C. E., additional
Published: 2016
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81. Copy number variant analysis from exome data in 349 patients with epileptic encephalopathy

Author: Abou-Khalil, B, Alldredge, BK, Allen, AS, Andermann, E, Andermann, F, Amrom, D, Bautista, JF, Berkovic, SF, Boro, A, Cascino, G, Coe, BP, Consalvo, D, Cook, J, Cossette, P, Crumrine, P, Delanty, N, Devinsky, O, Dlugos, D, Eichler, EE, Epstein, MP, Fiol, M, Fountain, NB, French, J, Friedman, D, Geller, EB, Glauser, T, Glynn, S, Goldstein, DB, Haut, SR, Hayward, J, Heinzen, EL, Helmers, SL, Johnson, MR, Joshi, S, Kanner, A, Kirsch, HE, Knowlton, RC, Kossoff, EH, Krumm, N, Kuperman, R, Kuzniecky, R, Lowenstein, DH, Marson, AG, McGuire, SM, Mefford, HC, Motika, PV, Nelson, B, Nieh, SE, Novotny, EJ, O'Brien, TJ, Ottman, R, Paolicchi, JM, Parent, J, Park, K, Petrou, S, Petrovski, S, Poduri, A, Raja, A, Ruzzo, EK, Scheffer, IE, Shellhaas, RA, Sherr, E, Shih, JJ, Singh, R, Sirven, J, Smith, MC, Sullivan, J, Liu, LT, Venkat, A, Vining, EPG, Von Allmen, GK, Weisenberg, JL, Widdess-Walsh, P, Winawer, MR, Abou-Khalil, B, Alldredge, BK, Allen, AS, Andermann, E, Andermann, F, Amrom, D, Bautista, JF, Berkovic, SF, Boro, A, Cascino, G, Coe, BP, Consalvo, D, Cook, J, Cossette, P, Crumrine, P, Delanty, N, Devinsky, O, Dlugos, D, Eichler, EE, Epstein, MP, Fiol, M, Fountain, NB, French, J, Friedman, D, Geller, EB, Glauser, T, Glynn, S, Goldstein, DB, Haut, SR, Hayward, J, Heinzen, EL, Helmers, SL, Johnson, MR, Joshi, S, Kanner, A, Kirsch, HE, Knowlton, RC, Kossoff, EH, Krumm, N, Kuperman, R, Kuzniecky, R, Lowenstein, DH, Marson, AG, McGuire, SM, Mefford, HC, Motika, PV, Nelson, B, Nieh, SE, Novotny, EJ, O'Brien, TJ, Ottman, R, Paolicchi, JM, Parent, J, Park, K, Petrou, S, Petrovski, S, Poduri, A, Raja, A, Ruzzo, EK, Scheffer, IE, Shellhaas, RA, Sherr, E, Shih, JJ, Singh, R, Sirven, J, Smith, MC, Sullivan, J, Liu, LT, Venkat, A, Vining, EPG, Von Allmen, GK, Weisenberg, JL, Widdess-Walsh, P, and Winawer, MR
Abstract: Infantile spasms (IS) and Lennox-Gastaut syndrome (LGS) are epileptic encephalopathies characterized by early onset, intractable seizures, and poor developmental outcomes. De novo sequence mutations and copy number variants (CNVs) are causative in a subset of cases. We used exome sequence data in 349 trios with IS or LGS to identify putative de novo CNVs. We confirm 18 de novo CNVs in 17 patients (4.8%), 10 of which are likely pathogenic, giving a firm genetic diagnosis for 2.9% of patients. Confirmation of exome-predicted CNVs by array-based methods is still required due to false-positive rates of prediction algorithms. Our exome-based results are consistent with recent array-based studies in similar cohorts and highlight novel candidate genes for IS and LGS.
Published: 2015

82. Cortical thickness abnormalities associated with dyslexia, independent of remediation status

Author: Ma, Y, Koyama, MS, Milham, MP, Castellanos, FX, Quinn, BT, Pardoe, H, Wang, X, Kuzniecky, R, Devinsky, O, Thesen, T, Blackmon, K, Ma, Y, Koyama, MS, Milham, MP, Castellanos, FX, Quinn, BT, Pardoe, H, Wang, X, Kuzniecky, R, Devinsky, O, Thesen, T, and Blackmon, K
Abstract: Abnormalities in cortical structure are commonly observed in children with dyslexia in key regions of the "reading network." Whether alteration in cortical features reflects pathology inherent to dyslexia or environmental influence (e.g., impoverished reading experience) remains unclear. To address this question, we compared MRI-derived metrics of cortical thickness (CT), surface area (SA), gray matter volume (GMV), and their lateralization across three different groups of children with a historical diagnosis of dyslexia, who varied in current reading level. We compared three dyslexia subgroups with: (1) persistent reading and spelling impairment; (2) remediated reading impairment (normal reading scores), and (3) remediated reading and spelling impairments (normal reading and spelling scores); and a control group of (4) typically developing children. All groups were matched for age, gender, handedness, and IQ. We hypothesized that the dyslexia group would show cortical abnormalities in regions of the reading network relative to controls, irrespective of remediation status. Such a finding would support that cortical abnormalities are inherent to dyslexia and are not a consequence of abnormal reading experience. Results revealed increased CT of the left fusiform gyrus in the dyslexia group relative to controls. Similarly, the dyslexia group showed CT increase of the right superior temporal gyrus, extending into the planum temporale, which resulted in a rightward CT asymmetry on lateralization indices. There were no group differences in SA, GMV, or their lateralization. These findings held true regardless of remediation status. Each reading level group showed the same "double hit" of atypically increased left fusiform CT and rightward superior temporal CT asymmetry. Thus, findings provide evidence that a developmental history of dyslexia is associated with CT abnormalities, independent of remediation status.
Published: 2015

83. Thalamic functional connectivity predicts seizure laterality in individual TLE patients: Application of a biomarker development strategy

Author: Barron, DS, Fox, PT, Pardoe, H, Lancaster, J, Price, LR, Blackmon, K, Berry, K, Cavazos, JE, Kuzniecky, R, Devinsky, O, Thesen, T, Barron, DS, Fox, PT, Pardoe, H, Lancaster, J, Price, LR, Blackmon, K, Berry, K, Cavazos, JE, Kuzniecky, R, Devinsky, O, and Thesen, T
Abstract: Noninvasive markers of brain function could yield biomarkers in many neurological disorders. Disease models constrained by coordinate-based meta-analysis are likely to increase this yield. Here, we evaluate a thalamic model of temporal lobe epilepsy that we proposed in a coordinate-based meta-analysis and extended in a diffusion tractography study of an independent patient population. Specifically, we evaluated whether thalamic functional connectivity (resting-state fMRI-BOLD) with temporal lobe areas can predict seizure onset laterality, as established with intracranial EEG. Twenty-four lesional and non-lesional temporal lobe epilepsy patients were studied. No significant differences in functional connection strength in patient and control groups were observed with Mann-Whitney Tests (corrected for multiple comparisons). Notwithstanding the lack of group differences, individual patient difference scores (from control mean connection strength) successfully predicted seizure onset zone as shown in ROC curves: discriminant analysis (two-dimensional) predicted seizure onset zone with 85% sensitivity and 91% specificity; logistic regression (four-dimensional) achieved 86% sensitivity and 100% specificity. The strongest markers in both analyses were left thalamo-hippocampal and right thalamo-entorhinal cortex functional connection strength. Thus, this study shows that thalamic functional connections are sensitive and specific markers of seizure onset laterality in individual temporal lobe epilepsy patients. This study also advances an overall strategy for the programmatic development of neuroimaging biomarkers in clinical and genetic populations: a disease model informed by coordinate-based meta-analysis was used to anatomically constrain individual patient analyses.
Published: 2015

84. Estimating brain's functional graph from the structural graph's Laplacian

Author: Abdelnour, F., additional, Dayan, M., additional, Devinsky, O., additional, Thesen, T., additional, and Raj, A., additional
Published: 2015
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85. Estimating function from structure in epileptics using graph diffusion model

Author: Abdelnour, F, primary, Raj, A, additional, Dayan, M, additional, Devinsky, O, additional, and Thesen, T, additional
Published: 2015
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86. Functional neuroimaging abnormalities in idiopathic generalized epilepsy

Author: McGill, ML, Devinsky, O, Wang, X, Quinn, BT, Pardoe, H, Carlson, C, Butler, T, Kuzniecky, R, Thesen, T, McGill, ML, Devinsky, O, Wang, X, Quinn, BT, Pardoe, H, Carlson, C, Butler, T, Kuzniecky, R, and Thesen, T
Abstract: Magnetic resonance imaging (MRI) techniques have been used to quantitatively assess focal and network abnormalities. Idiopathic generalized epilepsy (IGE) is characterized by bilateral synchronous spike-wave discharges on electroencephalography (EEG) but normal clinical MRI. Dysfunctions involving the neocortex, particularly the prefrontal cortex, and thalamus likely contribute to seizure activity. To identify possible morphometric and functional differences in the brains of IGE patients and normal controls, we employed measures of thalamic volumes, cortical thickness, gray-white blurring, fractional anisotropy (FA) measures from diffusion tensor imaging (DTI) and fractional amplitude of low frequency fluctuations (fALFF) in thalamic subregions from resting state functional MRI. Data from 27 patients with IGE and 27 age- and sex-matched controls showed similar thalamic volumes, cortical thickness and gray-white contrast. There were no differences in FA values on DTI in tracts connecting the thalamus and prefrontal cortex. Functional analysis revealed decreased fALFF in the prefrontal cortex (PFC) subregion of the thalamus in patients with IGE. We provide minimum detectable effect sizes for each measure used in the study. Our analysis indicates that fMRI-based methods are more sensitive than quantitative structural techniques for characterizing brain abnormalities in IGE.
Published: 2014

87. De novo loss of function mutations in KIAA2022 are associated with epilepsy and neurodevelopmental delay in females.

Author: Webster, R., Cho, M.T., Retterer, K., Millan, F., Nowak, C., Douglas, J., Ahmad, A., Raymond, G.V., Johnson, M.R., Pujol, A., Begtrup, A., McKnight, D., Devinsky, O., and Chung, W.K.
Subjects: GENETIC mutation, EPILEPSY, BRAIN diseases, INTELLECTUAL disabilities, AUTISM
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Published: 2017
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88. Efficacy of tDCS for Treating Working Memory Dysfunction and Depression in Patients with Temporal Lobe Epilepsy

Author: Jefferson, A., primary, Byant, A., additional, Devinsky, O., additional, Fusco, H., additional, Shafi, M., additional, Barr, W., additional, Friedman, D., additional, Press, D., additional, Herman, S., additional, O'Connor, M., additional, Schachter, S.S., additional, Pascual-Leone, A., additional, and Liu, A.A., additional
Published: 2014
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89. Major depressive disorder and neurovascular unit dysfunction with blood–brain barrier hyperpermeability: A critical analysis of human and experimental data

Author: Najjar, S., primary, Pearlman, D.M., additional, Devinsky, O., additional, Najjar, A., additional, and Zagzag, D., additional
Published: 2014
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90. Mood, anxiety, and incomplete seizure control affect quality of life after epilepsy surgery

Author: Hamid, H., primary, Blackmon, K., additional, Cong, X., additional, Dziura, J., additional, Atlas, L. Y., additional, Vickrey, B. G., additional, Berg, A. T., additional, Bazil, C. W., additional, Langfitt, J. T., additional, Walczak, T. S., additional, Sperling, M. R., additional, Shinnar, S., additional, and Devinsky, O., additional
Published: 2014
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91. De novo mutations in epileptic encephalopathies

Author: Allen, AS, Berkovic, SF, Cossette, P, Delanty, N, Dlugos, D, Eichler, EE, Epstein, MP, Glauser, T, Goldstein, DB, Han, Y, Heinzen, EL, Hitomi, Y, Howell, KB, Johnson, MR, Kuzniecky, R, Lowenstein, DH, Lu, Y-F, Madou, MRZ, Marson, AG, Mefford, HC, Nieh, SE, O'Brien, TJ, Ottman, R, Petrovski, S, Poduri, A, Ruzzo, EK, Scheffer, IE, Sherr, EH, Yuskaitis, CJ, Abou-Khalil, B, Alldredge, BK, Bautista, JF, Boro, A, Cascino, GD, Consalvo, D, Crumrine, P, Devinsky, O, Fiol, M, Fountain, NB, French, J, Friedman, D, Geller, EB, Glynn, S, Haut, SR, Hayward, J, Helmers, SL, Joshi, S, Kanner, A, Kirsch, HE, Knowlton, RC, Kossoff, E, Kuperman, R, McGuire, SM, Motika, PV, Novotny, EJ, Paolicchi, JM, Parent, JM, Park, K, Shellhaas, RA, Shih, JJ, Singh, R, Sirven, J, Smith, MC, Sullivan, J, Thio, LL, Venkat, A, Vining, EPG, Von Allmen, GK, Weisenberg, JL, Widdess-Walsh, P, Winawer, MR, Allen, AS, Berkovic, SF, Cossette, P, Delanty, N, Dlugos, D, Eichler, EE, Epstein, MP, Glauser, T, Goldstein, DB, Han, Y, Heinzen, EL, Hitomi, Y, Howell, KB, Johnson, MR, Kuzniecky, R, Lowenstein, DH, Lu, Y-F, Madou, MRZ, Marson, AG, Mefford, HC, Nieh, SE, O'Brien, TJ, Ottman, R, Petrovski, S, Poduri, A, Ruzzo, EK, Scheffer, IE, Sherr, EH, Yuskaitis, CJ, Abou-Khalil, B, Alldredge, BK, Bautista, JF, Boro, A, Cascino, GD, Consalvo, D, Crumrine, P, Devinsky, O, Fiol, M, Fountain, NB, French, J, Friedman, D, Geller, EB, Glynn, S, Haut, SR, Hayward, J, Helmers, SL, Joshi, S, Kanner, A, Kirsch, HE, Knowlton, RC, Kossoff, E, Kuperman, R, McGuire, SM, Motika, PV, Novotny, EJ, Paolicchi, JM, Parent, JM, Park, K, Shellhaas, RA, Shih, JJ, Singh, R, Sirven, J, Smith, MC, Sullivan, J, Thio, LL, Venkat, A, Vining, EPG, Von Allmen, GK, Weisenberg, JL, Widdess-Walsh, P, and Winawer, MR
Abstract: Epileptic encephalopathies are a devastating group of severe childhood epilepsy disorders for which the cause is often unknown. Here we report a screen for de novo mutations in patients with two classical epileptic encephalopathies: infantile spasms (n = 149) and Lennox-Gastaut syndrome (n = 115). We sequenced the exomes of 264 probands, and their parents, and confirmed 329 de novo mutations. A likelihood analysis showed a significant excess of de novo mutations in the ∼4,000 genes that are the most intolerant to functional genetic variation in the human population (P = 2.9 × 10(-3)). Among these are GABRB3, with de novo mutations in four patients, and ALG13, with the same de novo mutation in two patients; both genes show clear statistical evidence of association with epileptic encephalopathy. Given the relevant site-specific mutation rates, the probabilities of these outcomes occurring by chance are P = 4.1 × 10(-10) and P = 7.8 × 10(-12), respectively. Other genes with de novo mutations in this cohort include CACNA1A, CHD2, FLNA, GABRA1, GRIN1, GRIN2B, HNRNPU, IQSEC2, MTOR and NEDD4L. Finally, we show that the de novo mutations observed are enriched in specific gene sets including genes regulated by the fragile X protein (P < 10(-8)), as has been reported previously for autism spectrum disorders.
Published: 2013

92. Intracranial Cortical Responses during Visual-Tactile Integration in Humans

Author: Quinn, B. T., primary, Carlson, C., additional, Doyle, W., additional, Cash, S. S., additional, Devinsky, O., additional, Spence, C., additional, Halgren, E., additional, and Thesen, T., additional
Published: 2013
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93. Expectations prior to epilepsy surgery: An exploratory comparison of men and women

Author: Bower, C.M., Hays, R.D., Devinsky, O., Spencer, S.S., Sperling, M.R., Haut, S., Vassar, S., and Vickrey, B.G.
Published: 2009
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94. Detection of Epileptogenic Cortical Malformations with Surface-Based MRI Morphometry

Author: Feany, M, Thesen, T, Quinn, BT, Carlson, C, Devinsky, O, DuBois, J, McDonald, CR, French, J, Leventer, R, Felsovalyi, O, Wang, X, Halgren, E, Kuzniecky, R, Feany, M, Thesen, T, Quinn, BT, Carlson, C, Devinsky, O, DuBois, J, McDonald, CR, French, J, Leventer, R, Felsovalyi, O, Wang, X, Halgren, E, and Kuzniecky, R
Abstract: Magnetic resonance imaging has revolutionized the detection of structural abnormalities in patients with epilepsy. However, many focal abnormalities remain undetected in routine visual inspection. Here we use an automated, surface-based method for quantifying morphometric features related to epileptogenic cortical malformations to detect abnormal cortical thickness and blurred gray-white matter boundaries. Using MRI morphometry at 3T with surface-based spherical averaging techniques that precisely align anatomical structures between individual brains, we compared single patients with known lesions to a large normal control group to detect clusters of abnormal cortical thickness, gray-white matter contrast, local gyrification, sulcal depth, jacobian distance and curvature. To assess the effects of threshold and smoothing on detection sensitivity and specificity, we systematically varied these parameters with different thresholds and smoothing levels. To test the effectiveness of the technique to detect lesions of epileptogenic character, we compared the detected structural abnormalities to expert-tracings, intracranial EEG, pathology and surgical outcome in a homogeneous patient sample. With optimal parameters and by combining thickness and GWC, the surface-based detection method identified 92% of cortical lesions (sensitivity) with few false positives (96% specificity), successfully discriminating patients from controls 94% of the time. The detected structural abnormalities were related to the seizure onset zones, abnormal histology and positive outcome in all surgical patients. However, the method failed to adequately describe lesion extent in most cases. Automated surface-based MRI morphometry, if used with optimized parameters, may be a valuable additional clinical tool to improve the detection of subtle or previously occult malformations and therefore could improve identification of patients with intractable focal epilepsy who may benefit from surgery.
Published: 2011

95. Long-term association between seizure outcome and depression after resective epilepsy surgery.

Author: Hamid H, Liu H, Cong X, Devinsky O, Berg AT, Vickrey BG, Sperling MR, Shinnar S, Langfitt JT, Walczak TS, Barr WB, Dziura J, Bazil CW, Spencer SS, Hamid, H, Liu, H, Cong, X, Devinsky, O, Berg, A T, and Vickrey, B G
Published: 2011
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96. Hyperfamiliarity for faces.

Author: Devinsky O, Davachi L, Santchi C, Quinn BT, Staresina BP, Thesen T, Devinsky, O, Davachi, L, Santchi, C, Quinn, B T, Staresina, B P, and Thesen, T
Published: 2010
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97. Septal nuclei enlargement in human temporal lobe epilepsy without mesial temporal sclerosis

Author: Butler, T., primary, Zaborszky, L., additional, Wang, X., additional, McDonald, C. R., additional, Blackmon, K., additional, Quinn, B. T., additional, DuBois, J., additional, Carlson, C., additional, Barr, W. B., additional, French, J., additional, Kuzniecky, R., additional, Halgren, E., additional, Devinsky, O., additional, and Thesen, T., additional
Published: 2013
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98. MRI Characterization and Longitudinal Study of Focal Cerebellar Lesions in a Young Tuberous Sclerosis Cohort

Author: Vaughn, J., primary, Hagiwara, M., additional, Katz, J., additional, Roth, J., additional, Devinsky, O., additional, Weiner, H., additional, and Milla, S., additional
Published: 2012
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99. Grand Rounds

Author: Fayolle, G., primary, Levick, W., additional, Lajiness-O'Neill, R., additional, Fastenau, P., additional, Briskin, S., additional, Bass, N., additional, Silva, M., additional, Critchfield, E., additional, Nakase-Richardson, R., additional, Hertza, J., additional, Loughan, A., additional, Perna, R., additional, Northington, S., additional, Boyd, S., additional, Anderson, A., additional, Peery, S., additional, Chafetz, M., additional, Maris, M., additional, Ramezani, A., additional, Sylvester, C., additional, Goldberg, K., additional, Constantinou, M., additional, Karekla, M., additional, Hall, J., additional, Edwards, M., additional, Balldin, V., additional, Strutt, A., additional, Pavlik, V., additional, Marquez de la Plata, C., additional, Cullum, M., additional, lacritz, l., additional, Reisch, J., additional, Massman, P., additional, Royall, D., additional, Barber, R., additional, Younes, S., additional, Wiechmann, A., additional, O'Bryant, S., additional, Patel, K., additional, Suhr, J., additional, Chari, S., additional, Yokoyama, J., additional, Bettcher, B., additional, Karydas, A., additional, Miller, B., additional, Kramer, J., additional, Zec, R., additional, Fritz, S., additional, Kohlrus, S., additional, Robbs, R., additional, Ala, T., additional, Gifford, K., additional, Cantwell, N., additional, Romano, R., additional, Jefferson, A., additional, Holland, A., additional, Newton, S., additional, Bunting, J., additional, Coe, M., additional, Carmona, J., additional, Harrison, D., additional, Puente, A., additional, Terry, D., additional, Faraco, C., additional, Brown, C., additional, Patel, A., additional, Watts, A., additional, Kent, A., additional, Siegel, J., additional, Miller, S., additional, Ernst, W., additional, Chelune, G., additional, Holdnack, J., additional, Sheehan, J., additional, Duff, K., additional, Pedraza, O., additional, Crawford, J., additional, Miller, L., additional, Hobson Balldin, V., additional, Benavides, H., additional, Johnson, L., additional, Tshuma, L., additional, Dezhkam, N., additional, Hayes, L., additional, Love, C., additional, Stephens, B., additional, Webbe, F., additional, Mulligan, K., additional, Dunham, K., additional, Shadi, S., additional, Sofko, C., additional, Denney, R., additional, Rolin, S., additional, Sibson, J., additional, Ogbeide, S., additional, Glover, M., additional, Warchol, A., additional, Hunter, B., additional, Nichols, C., additional, Riccio, C., additional, Cohen, M., additional, Dennison, A., additional, Wasserman, T., additional, Schleicher-Dilks, S., additional, Adler, M., additional, Golden, C., additional, Olivier, T., additional, LeMonda, B., additional, McGinley, J., additional, Pritchett, A., additional, Chang, L., additional, Cloak, C., additional, Cunningham, E., additional, Lohaugen, G., additional, Skranes, J., additional, Ernst, T., additional, Parke, E., additional, Thaler, N., additional, Etcoff, L., additional, Allen, D., additional, Andrews, P., additional, McGregor, S., additional, Daniels, R., additional, Hochsztein, N., additional, Miles-Mason, E., additional, Granader, Y., additional, Vasserman, M., additional, MacAllister, W., additional, Casto, B., additional, Patrick, K., additional, Hurewitz, F., additional, Chute, D., additional, Booth, A., additional, Koch, C., additional, Roid, G., additional, Balkema, N., additional, Kiefel, J., additional, Bell, L., additional, Maerlender, A., additional, Belkin, T., additional, Katzenstein, J., additional, Semerjian, C., additional, Culotta, V., additional, Band, E., additional, Yosick, R., additional, Burns, T., additional, Arenivas, A., additional, Bearden, D., additional, Olson, K., additional, Jacobson, K., additional, Ubogy, S., additional, Sterling, C., additional, Taub, E., additional, Griffin, A., additional, Rickards, T., additional, Uswatte, G., additional, Davis, D., additional, Sweeney, K., additional, Llorente, A., additional, Boettcher, A., additional, Hill, B., additional, Ploetz, D., additional, Kline, J., additional, Rohling, M., additional, O'Jile, J., additional, Holler, K., additional, Petrauskas, V., additional, Long, J., additional, Casey, J., additional, Duda, T., additional, Hodsman, S., additional, Stricker, S., additional, Martner, S., additional, Hansen, R., additional, Ferraro, F., additional, Tangen, R., additional, Hanratty, A., additional, Tanabe, M., additional, O'Callaghan, E., additional, Houskamp, B., additional, McDonald, L., additional, Pick, L., additional, Guardino, D., additional, Pietz, T., additional, Kayser, K., additional, Gray, R., additional, Letteri, A., additional, Crisologo, A., additional, Witkin, G., additional, Sanders, J., additional, Mrazik, M., additional, Harley, A., additional, Phoong, M., additional, Melville, T., additional, La, D., additional, Gomez, R., additional, Berthelson, L., additional, Robbins, J., additional, Lane, E., additional, Rahman, P., additional, Konopka, L., additional, Fasfous, A., additional, Zink, D., additional, Peralta-Ramirez, N., additional, Perez-Garcia, M., additional, Su, S., additional, Lin, G., additional, Kiely, T., additional, Schatzberg, A., additional, Keller, J., additional, Dykstra, J., additional, Feigon, M., additional, Renteria, L., additional, Fong, M., additional, Piper, L., additional, Lee, E., additional, Vordenberg, J., additional, Contardo, C., additional, Magnuson, S., additional, Doninger, N., additional, Luton, L., additional, Drane, D., additional, Phelan, A., additional, Stricker, W., additional, Poreh, A., additional, Wolkenberg, F., additional, Spira, J., additional, DeRight, J., additional, Jorgensen, R., additional, Fitzpatrick, L., additional, Crowe, S., additional, Woods, S., additional, Doyle, K., additional, Weber, E., additional, Cameron, M., additional, Cattie, J., additional, Cushman, C., additional, Grant, I., additional, Blackstone, K., additional, Moore, D., additional, Roberg, B., additional, Somogie, M., additional, Thelen, J., additional, Lovelace, C., additional, Bruce, J., additional, Gerstenecker, A., additional, Mast, B., additional, Litvan, I., additional, Hargrave, D., additional, Schroeder, R., additional, Buddin, W., additional, Baade, L., additional, Heinrichs, R., additional, Boseck, J., additional, Berry, K., additional, Koehn, E., additional, Davis, A., additional, Meyer, B., additional, Gelder, B., additional, Sussman, Z., additional, Espe-Pfeifer, P., additional, Musso, M., additional, Barker, A., additional, Jones, G., additional, Gouvier, W., additional, Johnson, V., additional, Zaytsev, L., additional, Freier-Randall, M., additional, Sutton, G., additional, Ringdahl, E., additional, Olsen, J., additional, Byrd, D., additional, Rivera-Mindt, M., additional, Fellows, R., additional, Morgello, S., additional, Wheaton, V., additional, Jaehnert, S., additional, Ellis, C., additional, Olavarria, H., additional, Loftis, J., additional, Huckans, M., additional, Pimental, P., additional, Frawley, J., additional, Welch, M., additional, Jennette, K., additional, Rinehardt, E., additional, Schoenberg, M., additional, Strober, L., additional, Genova, H., additional, Wylie, G., additional, DeLuca, J., additional, Chiaravalloti, N., additional, Ibrahim, E., additional, Seiam, A., additional, Bohlega, S., additional, Lloyd, H., additional, Goldberg, M., additional, Marceaux, J., additional, Fallows, R., additional, McCoy, K., additional, Yehyawi, N., additional, Luther, E., additional, Hilsabeck, R., additional, Fulton, R., additional, Stevens, P., additional, Erickson, S., additional, Dodzik, P., additional, Williams, R., additional, Dsurney, J., additional, Najafizadeh, L., additional, McGovern, J., additional, Chowdhry, F., additional, Acevedo, A., additional, Bakhtiar, A., additional, Karamzadeh, N., additional, Amyot, F., additional, Gandjbakhche, A., additional, Haddad, M., additional, Johnson, M., additional, Wade, J., additional, Harper, L., additional, Barghi, A., additional, Mark, V., additional, Christopher, G., additional, Marcus, D., additional, Spady, M., additional, Bloom, J., additional, Zimmer, A., additional, Miller, M., additional, Schuster, D., additional, Ebner, H., additional, Mortimer, B., additional, Palmer, G., additional, Happe, M., additional, Paxson, J., additional, Jurek, B., additional, Graca, J., additional, Meyers, J., additional, Lange, R., additional, Brickell, T., additional, French, L., additional, Iverson, G., additional, Shewchuk, J., additional, Madler, B., additional, Heran, M., additional, Brubacher, J., additional, Ivins, B., additional, Baldassarre, M., additional, Paper, T., additional, Herrold, A., additional, Chin, A., additional, Zgaljardic, D., additional, Oden, K., additional, Lambert, M., additional, Dickson, S., additional, Miller, R., additional, Plenger, P., additional, Sutherland, E., additional, Glatts, C., additional, Schatz, P., additional, Walker, K., additional, Philip, N., additional, McClaughlin, S., additional, Mooney, S., additional, Seats, E., additional, Carnell, V., additional, Raintree, J., additional, Brown, D., additional, Hodges, C., additional, Amerson, E., additional, Kennedy, C., additional, Moore, J., additional, Ferris, C., additional, Roebuck-Spencer, T., additional, Vincent, A., additional, Bryan, C., additional, Catalano, D., additional, Warren, A., additional, Monden, K., additional, Driver, S., additional, Chau, P., additional, Seegmiller, R., additional, Baker, M., additional, Malach, S., additional, Mintz, J., additional, Villarreal, R., additional, Peterson, A., additional, Leininger, S., additional, Strong, C., additional, Donders, J., additional, Merritt, V., additional, Vargas, G., additional, Rabinowitz, A., additional, Arnett, P., additional, Whipple, E., additional, Schultheis, M., additional, Robinson, K., additional, Iacovone, D., additional, Biester, R., additional, Alfano, D., additional, Nicholls, M., additional, Klas, P., additional, Jeffay, E., additional, Zakzanis, K., additional, Vandermeer, M., additional, Womble, M., additional, Corley, E., additional, Considine, C., additional, Fichtenberg, N., additional, Harrison, J., additional, Pollock, M., additional, Mouanoutoua, A., additional, Brimager, A., additional, Lebby, P., additional, Sullivan, K., additional, Edmed, S., additional, Kieffer, K., additional, McCarthy, M., additional, Wiegand, L., additional, Lindsey, H., additional, Hernandez, M., additional, Noniyeva, Y., additional, Lapis, Y., additional, Padua, M., additional, Poole, J., additional, Brooks, B., additional, McKay, C., additional, Meeuwisse, W., additional, Emery, C., additional, Mazur-Mosiewicz, A., additional, Sherman, E., additional, Kirkwood, M., additional, Gunner, J., additional, Miele, A., additional, Silk-Eglit, G., additional, Lynch, J., additional, McCaffrey, R., additional, Stewart, J., additional, Tsou, J., additional, Scarisbrick, D., additional, Chan, R., additional, Bure-Reyes, A., additional, Cortes, L., additional, Gindy, S., additional, Biddle, C., additional, Shah, D., additional, Jaberg, P., additional, Moss, R., additional, Horner, M., additional, VanKirk, K., additional, Dismuke, C., additional, Turner, T., additional, Muzzy, W., additional, Dunnam, M., additional, Warner, G., additional, Donnelly, K., additional, Donnelly, J., additional, Kittleson, J., additional, Bradshaw, C., additional, Alt, M., additional, Margolis, S., additional, Ostroy, E., additional, Higgins, K., additional, Eng, K., additional, Akeson, S., additional, Wall, J., additional, Davis, J., additional, Hansel, J., additional, Wang, B., additional, Gervais, R., additional, Greiffenstein, M., additional, Denning, J., additional, VonDran, E., additional, Campbell, E., additional, Brockman, C., additional, Teichner, G., additional, Waid, R., additional, Buican, B., additional, Armistead-Jehle, P., additional, Bailie, J., additional, Dilay, A., additional, Cottingham, M., additional, Boyd, C., additional, Asmussen, S., additional, Neff, J., additional, Schalk, S., additional, Jensen, L., additional, DenBoer, J., additional, Hall, S., additional, Holcomb, E., additional, Axelrod, B., additional, Demakis, G., additional, Rimland, C., additional, Ward, J., additional, Ross, M., additional, Bailey, M., additional, Stubblefield, A., additional, Smigielski, J., additional, Geske, J., additional, Karpyak, V., additional, Reese, C., additional, Larrabee, G., additional, Allen, L., additional, Celinski, M., additional, Gilman, J., additional, LaDuke, C., additional, DeMatteo, D., additional, Heilbrun, K., additional, Swirsky-Sacchetti, T., additional, Dedman, A., additional, Withers, K., additional, Deneen, T., additional, Fisher, J., additional, Spray, B., additional, Savage, R., additional, Wiener, H., additional, Tyer, J., additional, Ningaonkar, V., additional, Devlin, B., additional, Go, R., additional, Sharma, V., additional, Fontanetta, R., additional, Calderon, C., additional, Coad, S., additional, Fontaneta, R., additional, Vertinski, M., additional, Verbiest, R., additional, Snyder, J., additional, Kinney, J., additional, Rach, A., additional, Young, J., additional, Crouse, E., additional, Schretlen, D., additional, Weaver, J., additional, Buchholz, A., additional, Gordon, B., additional, Macciocchi, S., additional, Seel, R., additional, Godsall, R., additional, Brotsky, J., additional, DiRocco, A., additional, Houghton-Faryna, E., additional, Bolinger, E., additional, Hollenbeck, C., additional, Hart, J., additional, Lee, B., additional, Strauss, G., additional, Adams, J., additional, Martins, D., additional, Catalano, L., additional, Waltz, J., additional, Gold, J., additional, Haas, G., additional, Brown, L., additional, Luther, J., additional, Goldstein, G., additional, Kelley, E., additional, Raba, C., additional, Trettin, L., additional, Solvason, H., additional, Buchanan, R., additional, Baldock, D., additional, Etherton, J., additional, Phelps, T., additional, Richmond, S., additional, Tapscott, B., additional, Thomlinson, S., additional, Cordeiro, L., additional, Wilkening, G., additional, Parikh, M., additional, Graham, L., additional, Grosch, M., additional, Hynan, L., additional, Weiner, M., additional, Cullum, C., additional, Menon, C., additional, Lacritz, L., additional, Castro-Couch, M., additional, Irani, F., additional, Houshyarnejad, A., additional, Norman, M., additional, Fonseca, F., additional, Browne, B., additional, Alvarez, J., additional, Jiminez, Y., additional, Baez, V., additional, Resendiz, C., additional, Scott, B., additional, Farias, G., additional, York, M., additional, Lozano, V., additional, Mahoney, M., additional, Hernandez Mejia, M., additional, Pacheco, E., additional, Homs, A., additional, Ownby, R., additional, Nici, J., additional, Hom, J., additional, Lutz, J., additional, Dean, R., additional, Finch, H., additional, Pierce, S., additional, Moses, J., additional, Mann, S., additional, Feinberg, J., additional, Choi, A., additional, Kaminetskaya, M., additional, Pierce, C., additional, Zacharewicz, M., additional, Gavett, B., additional, Horwitz, J., additional, Ory, J., additional, Carbuccia, K., additional, Morra, L., additional, Garcon, S., additional, Lucas, M., additional, Donovick, P., additional, Whearty, K., additional, Campbell, K., additional, Camlic, S., additional, Brinckman, D., additional, Ehrhart, L., additional, Weisser, V., additional, Medaglia, J., additional, Merzagora, A., additional, Reckess, G., additional, Ho, T., additional, Testa, S., additional, Woolery, H., additional, Farcello, C., additional, Klimas, N., additional, Meyer, J., additional, Barwick, F., additional, Drayer, K., additional, Galusha, J., additional, Schmitt, A., additional, Livingston, R., additional, Stewart, R., additional, Quarles, L., additional, Pagitt, M., additional, Barke, C., additional, Baker, A., additional, Baker, N., additional, Cook, N., additional, Ahern, D., additional, Correia, S., additional, Resnik, L., additional, Barnabe, K., additional, Gnepp, D., additional, Benjamin, M., additional, Zlatar, Z., additional, Garcia, A., additional, Harnish, S., additional, Crosson, B., additional, Vaughan, L., additional, Fedio, A., additional, Sexton, J., additional, Cummings, S., additional, Logemann, A., additional, Lassiter, N., additional, Fedio, P., additional, Gremillion, A., additional, Nemeth, D., additional, Whittington, T., additional, Reckow, J., additional, Lewandowski, C., additional, Cole, J., additional, Lewandowski, A., additional, Spector, J., additional, Ford-Johnson, L., additional, Lengenfelder, J., additional, Sumowski, J., additional, Morse, C., additional, McKeever, J., additional, Zhao, L., additional, Leist, T., additional, Marcinak, J., additional, Piecora, K., additional, Al-Khalil, K., additional, Martin, P., additional, Thompson, L., additional, Kowalczyk, W., additional, Golub, S., additional, Lemann, E., additional, Piehl, J., additional, Rita, N., additional, Moss, L., additional, Nogin, R., additional, Drapeau, C., additional, Malm, S., additional, Armstrong, L., additional, Glidewell, R., additional, Orr, W., additional, Mears, G., additional, Allen, C., additional, Pierson, E., additional, Kavanaugh, B., additional, Tayim, F., additional, Llanes, S., additional, Poston, K., additional, Beathard, J., additional, Stolberg, P., additional, Jones, W., additional, Mayfield, J., additional, Weller, J., additional, Demireva, P., additional, McInerney, K., additional, Riddle, T., additional, Primus, M., additional, Highsmith, J., additional, Everhart, D., additional, Lehockey, K., additional, Sullivan, S., additional, Mandava, S., additional, Murphy, B., additional, Lalwani, L., additional, Rosselli, M., additional, Carrasco, R., additional, Zuckerman, S., additional, Brand, J., additional, Rivera Mindt, M., additional, Schaffer, S., additional, Alper, K., additional, Devinsky, O., additional, Barr, W., additional, Langer, K., additional, Fraiman, J., additional, Scagliola, J., additional, Roman, E., additional, Martinez, A., additional, Konopacki, K., additional, Juliano, A., additional, Whiteside, D., additional, Widmann, G., additional, Franzwa, M., additional, Sokal, B., additional, Morgan, E., additional, Bondi, M., additional, Delano-Wood, L., additional, Cormier, R., additional, Cumley, N., additional, Elek, M., additional, Green, M., additional, Kruger, A., additional, Pacheco, L., additional, Robinson, G., additional, Welch, H., additional, Parriott, D., additional, Loe, S., additional, Hughes, L., additional, Natta, L., additional, Quenicka, W., additional, McGoldirck, K., additional, Bennett, T., additional, Soper, H., additional, Collier, S., additional, Connolly, M., additional, Di Pinto, M., additional, Handel, E., additional, Davidson, K., additional, Livers, E., additional, Frantz, S., additional, Allen, J., additional, Jerard, T., additional, Sakhai, S., additional, Barney, S., additional, McGoldrick, K., additional, Sordahl, J., additional, Torrence, N., additional, and John, S., additional
Published: 2012
Full Text: View/download PDF

100. Suicide outcomes after resective epilepsy surgery

Author: Hamid⁎, H., primary, Devinsky, O., additional, Vickrey, B.G., additional, Berg, A.T., additional, Bazil, C.W., additional, and Pacia, J.T., additional
Published: 2012
Full Text: View/download PDF

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