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1. Evolution of white matter damage in amyotrophic lateral sclerosis

Author

Matt C. Gabel, Rebecca J. Broad, Alexandra L. Young, Sharon Abrahams, Mark E. Bastin, Ricarda A. L. Menke, Ammar Al‐Chalabi, Laura H. Goldstein, Stella Tsermentseli, Daniel C. Alexander, Martin R. Turner, P. Nigel Leigh, and Mara Cercignani

Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Objective To characterize disease evolution in amyotrophic lateral sclerosis using an event‐based model designed to extract temporal information from cross‐sectional data. Conventional methods for understanding mechanisms of rapidly progressive neurodegenerative disorders are limited by the subjectivity inherent in the selection of a limited range of measurements, and the need to acquire longitudinal data. Methods The event‐based model characterizes a disease as a series of events, each comprising a significant change in subject state. The model was applied to data from 154 patients and 128 healthy controls selected from five independent diffusion MRI datasets acquired in four different imaging laboratories between 1999 and 2016. The biomarkers modeled were mean fractional anisotropy values of white matter tracts implicated in amyotrophic lateral sclerosis. The cerebral portion of the corticospinal tract was divided into three segments. Results Application of the model to the pooled datasets revealed that the corticospinal tracts were involved before other white matter tracts. Distal corticospinal tract segments were involved earlier than more proximal (i.e., cephalad) segments. In addition, the model revealed early ordering of fractional anisotropy change in the corpus callosum and subsequently in long association fibers. Interpretation These findings represent data‐driven evidence for early involvement of the corticospinal tracts and body of the corpus callosum in keeping with conventional approaches to image analysis, while providing new evidence to inform directional degeneration of the corticospinal tracts. This data‐driven model provides new insight into the dynamics of neuronal damage in amyotrophic lateral sclerosis.

Published
2020
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3. Emerging Magnetic Resonance Imaging Techniques and Analysis Methods in Amyotrophic Lateral Sclerosis

Author

Andrew W. Barritt, Matt C. Gabel, Mara Cercignani, and P. Nigel Leigh

Subjects
motor neuron disease, MRI—magnetic resonance imaging, event-based model, quantitative magnetization transfer imaging, neurite orientation dispersion and density imaging (NODDI), Neurology. Diseases of the nervous system, RC346-429
Abstract

Objective markers of disease sensitive to the clinical activity, symptomatic progression, and underlying substrates of neurodegeneration are highly coveted in amyotrophic lateral sclerosis in order to more eloquently stratify the highly heterogeneous phenotype and facilitate the discovery of effective disease modifying treatments for patients. Magnetic resonance imaging (MRI) is a promising, non-invasive biomarker candidate whose acquisition techniques and analysis methods are undergoing constant evolution in the pursuit of parameters which more closely represent biologically-applicable tissue changes. Neurite Orientation Dispersion and Density Imaging (NODDI; a form of diffusion imaging), and quantitative Magnetization Transfer Imaging (qMTi) are two such emerging modalities which have each broadened the understanding of other neurological disorders and have the potential to provide new insights into structural alterations initiated by the disease process in ALS. Furthermore, novel neuroimaging data analysis approaches such as Event-Based Modeling (EBM) may be able to circumvent the requirement for longitudinal scanning as a means to comprehend the dynamic stages of neurodegeneration in vivo. Combining these and other innovative imaging protocols with more sophisticated techniques to analyse ever-increasing datasets holds the exciting prospect of transforming understanding of the biological processes and temporal evolution of the ALS syndrome, and can only benefit from multicentre collaboration across the entire ALS research community.

Published
2018
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4. Comparing multiband and singleband EPI in NODDI at 3 T: what are the implications for reproducibility and study sample sizes?

Author

Nicholas G. Dowell, Matt C. Gabel, Samira Bouyagoub, and Mara Cercignani

Subjects
Adult, Male, Intraclass correlation, Biophysics, Diffusion MRI, 030218 nuclear medicine & medical imaging, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Group differences, Power calculations, Neurites, Humans, Radiology, Nuclear Medicine and imaging, Statistical dispersion, Cerebrospinal Fluid, Mathematics, NODDI, Reproducibility, Multiband EPI, Radiological and Ultrasound Technology, Healthy subjects, Reproducibility of Results, Diffusion Magnetic Resonance Imaging, Sample size determination, Sample Size, Female, 030217 neurology & neurosurgery, Research Article, Biomedical engineering
Abstract

Objective The reproducibility of Neurite orientation dispersion and density imaging (NODDI) metrics from time-saving multiband (MB) EPI compared with singleband (SB) has not been considered. This study aims to evaluate the reproducibility of NODDI parameters from SB and MB acquisitions, determine the agreement between acquisitions and estimate the sample sizes required to detect between-group change. Methods Brain diffusion MRI data were acquired using SB and MB (acceleration factors 2 (MB2) and 3 (MB3)) on 8 healthy subjects on 2 separate visits. NODDI maps of isotropic volume fraction (FISO), neurite density (NDI) and orientation dispersion index (ODI) were estimated. Region-of-interest analysis was performed; variability across subjects and visits was measured using coefficients of variation (CoV). Intraclass correlation coefficient and Bland–Altman analysis were performed to assess reproducibility and detect any systematic bias between SB, MB2 and MB3. Power calculations were used to determine sample sizes required to detect group differences. Results Both NDI and ODI were reproducible between visits; however, FISO was variable. All parameters were not reproducible across methods; a systematic bias was observed with the derived values decreasing as the MB factor increases. The number of subjects needed to detect a between-group change is not significantly different between methods; however, ODI needs considerably higher sample sizes than NDI. Conclusions Both SB and MB yield highly reproducible NDI and ODI measures, but direct comparison of these parameters between methods is complicated by systematic differences that exist between the two approaches.

Published
2020

5. Evolution of white matter damage in amyotrophic lateral sclerosis

Author

Rebecca Broad, Matt C. Gabel, Sharon Abrahams, Ammar Al-Chalabi, Ricarda A. L. Menke, Daniel C. Alexander, Stella Tsermentseli, Mara Cercignani, Alexandra L. Young, Martin R Turner, Laura H. Goldstein, P. Nigel Leigh, and Mark E. Bastin

Subjects
0301 basic medicine, Neurosciences. Biological psychiatry. Neuropsychiatry, Corpus callosum, White matter, 03 medical and health sciences, 0302 clinical medicine, Neuronal damage, Fractional anisotropy, medicine, Amyotrophic lateral sclerosis, RC346-429, Research Articles, business.industry, General Neuroscience, medicine.disease, 030104 developmental biology, Disease evolution, medicine.anatomical_structure, Corticospinal tract, Neurology. Diseases of the nervous system, Neurology (clinical), business, Neuroscience, 030217 neurology & neurosurgery, RC321-571, Research Article, Diffusion MRI
Abstract

Objective To characterize disease evolution in amyotrophic lateral sclerosis using an event‐based model designed to extract temporal information from cross‐sectional data. Conventional methods for understanding mechanisms of rapidly progressive neurodegenerative disorders are limited by the subjectivity inherent in the selection of a limited range of measurements, and the need to acquire longitudinal data. Methods The event‐based model characterizes a disease as a series of events, each comprising a significant change in subject state. The model was applied to data from 154 patients and 128 healthy controls selected from five independent diffusion MRI datasets acquired in four different imaging laboratories between 1999 and 2016. The biomarkers modeled were mean fractional anisotropy values of white matter tracts implicated in amyotrophic lateral sclerosis. The cerebral portion of the corticospinal tract was divided into three segments. Results Application of the model to the pooled datasets revealed that the corticospinal tracts were involved before other white matter tracts. Distal corticospinal tract segments were involved earlier than more proximal (i.e., cephalad) segments. In addition, the model revealed early ordering of fractional anisotropy change in the corpus callosum and subsequently in long association fibers. Interpretation These findings represent data‐driven evidence for early involvement of the corticospinal tracts and body of the corpus callosum in keeping with conventional approaches to image analysis, while providing new evidence to inform directional degeneration of the corticospinal tracts. This data‐driven model provides new insight into the dynamics of neuronal damage in amyotrophic lateral sclerosis.

Published
2020

6. Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets

Author

Dirk J. Heslenfeld, Merel Postema, Paul M. Thompson, Sarah Baumeister, Tiffany M. Chaim-Avancini, Catharina A. Hartman, Sara Lera-Miguel, Patrick de Zeeuw, Sara Ambrosino, Neil A. Harrison, Marcus V. Zanetti, Philip Asherson, Joel T. Nigg, Liesbeth Reneman, David Coghill, Gustavo Sudre, Alysa E. Doyle, Francisco X. Castellanos, Tobias Banaschewski, Oscar Vilarroya, Mario Rodrigues Louzã, Kaylita Chantiluke, Annette Conzelmann, Georg G. von Polier, Lizanne J. S. Schweren, Anastasia Christakou, Klaus-Peter Lesch, Sarah Durston, Simon E. Fisher, Yuliya N. Yoncheva, Jochen Seitz, David C. Glahn, Timothy J. Silk, Norbert Skokauskas, Mark A. Bellgrove, Damien A. Fair, Geraldo F. Busatto, Georg C. Ziegler, Eric Earl, Yannis Paloyelis, Jeffery N. Epstein, Jaap Oosterlaan, Clare Kelly, Paulo Mattos, Gregor Kohls, Jan Haavik, Joseph Biederman, Janita Bralten, Neda Jahanshad, Claiton H.D. Bau, Thomas Ethofer, Paul Pauli, Cibele Edom Bandeira, Andreas Reif, Pieter J. Hoekstra, Theo G.M. van Erp, Susanne Walitza, Marie F. Høvik, Sarah Hohmann, Barbara Franke, Luisa Lázaro, Thomas Frodl, Tinatin Gogberashvili, Jonna Kuntsi, J. Antoni Ramos-Quiroga, Daniel Brandeis, Stephanie E. Novotny, Martine Hoogman, Juan Carlos Soliva Vila, Anouk Schrantee, Rosa Nicolau, Kerstin Konrad, Eileen Oberwelland Weiss, Ruth O'Gorman Tuura, Bernd Kardatzki, Felipe Almeida Picon, Hazel McCarthy, Yolanda Vives-Gilabert, Ana Cubillo, Charles B Malpas, Mara Cercignani, Astri J. Lundervold, Michael C. Stevens, Eugenio H. Grevet, Katya Rubia, Renata B. Cupertino, Philip Shaw, Georgii Karkashadze, Fernanda Tovar-Moll, Bob Oranje, Leyla Namazova-Baranova, A.A. Baranov, Andreas J. Fallgatter, Leanne Tamm, Terry L. Jernigan, Matt C. Gabel, Clyde Francks, Pedro G.P. Rosa, Stephen V. Faraone, Jan K. Buitelaar, Kerstin J. Plessen, Silvia Brem, Sarah E. Medland, Alasdair Vance, Ramona Baur-Streubel, ENIGMA ADHD Working Group, General Paediatrics, ARD - Amsterdam Reproduction and Development, Radiology and Nuclear Medicine, APH - Mental Health, APH - Personalized Medicine, ANS - Brain Imaging, ANS - Compulsivity, Impulsivity & Attention, Institut Català de la Salut, [Postema MC] Language and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands. [Hoogman M] Department of Human Genetics, Radboud University Medical Center, Nijmegen, Netherlands. Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands. [Ambrosino S] NICHE lab, Department of Psychiatry, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands. [Asherson P] Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK. [Banaschewski T] Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany. [Bandeira CE] Adulthood ADHD Outpatient Program (ProDAH), Clinical Research Center, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil. Department of Genetics, Institute of Biosciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. [Ramos-Quiroga JA] Servei de Psiquiatria, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Grup de Recerca en Psiquiatria, Salut Mental i Addiccions, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Biomedical Network Research Centre on Mental Health (CIBERSAM), Barcelona, Catalonia, Spain. Departament de Psiquiatria i Medicina Legal, Universitat Autònoma de Barcelona, Bellaterra, Spain, Vall d'Hebron Barcelona Hospital Campus, Cognitive Psychology, IBBA, Clinical Neuropsychology, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Pediatric surgery, and Radiology and nuclear medicine

Subjects
Dominància cerebral, trastornos mentales::trastornos del desarrollo neurológico::trastornos generalizados del desarrollo del niño::trastorno del espectro del autismo [PSIQUIATRÍA Y PSICOLOGÍA], Autism Spectrum Disorder, Caudate nucleus, Attention-deficit, Audiology, sistema nervioso::sistema nervioso central::encéfalo [ANATOMÍA], 0302 clinical medicine, Mental Disorders::Neurodevelopmental Disorders::Attention Deficit and Disruptive Behavior Disorders::Attention Deficit Disorder with Hyperactivity [PSYCHIATRY AND PSYCHOLOGY], 130 000 Cognitive Neurology & Memory, Developmental and Educational Psychology, Brain asymmetry, Child, media_common, large-scale data, brain laterality, 05 social sciences, scale data, Brain, hyperactivity disorder, brain asymmetry, structural MRI, Mental Disorders::Neurodevelopmental Disorders::Child Development Disorders, Pervasive::Autism Spectrum Disorder [PSYCHIATRY AND PSYCHOLOGY], Magnetic Resonance Imaging, Psychiatry and Mental health, Globus pallidus, Attention&#8208, Autism spectrum disorder, Psychology, 050104 developmental & child psychology, Neuroinformatics, Adult, medicine.medical_specialty, Adolescent, media_common.quotation_subject, deficit, Nervous System::Central Nervous System::Brain [ANATOMY], Asymmetry, behavioral disciplines and activities, Article, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Age groups, mental disorders, medicine, Humans, Attention deficit hyperactivity disorder, 0501 psychology and cognitive sciences, ddc:610, large&#8208, Other subheadings::Other subheadings::/diagnostic imaging [Other subheadings], Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Otros calificadores::Otros calificadores::/diagnóstico por imagen [Otros calificadores], Cervell - Imatgeria, medicine.disease, Trastorn per dèficit d'atenció amb hiperactivitat, Attention Deficit Disorder with Hyperactivity, Pediatrics, Perinatology and Child Health, Orbitofrontal cortex, Caudate Nucleus, trastornos mentales::trastornos del desarrollo neurológico::trastornos conductuales disruptivos y déficit de atención::trastornos de déficit de atención con hiperactividad [PSIQUIATRÍA Y PSICOLOGÍA], 030217 neurology & neurosurgery
Abstract

Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from −0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait., Journal of Child Psychology and Psychiatry, 62 (10), ISSN:0021-9630, ISSN:1469-7610

Published
2021

7. Subcortical brain volume, regional cortical thickness, and cortical surface area across disorders:Findings from the ENIGMA ADHD, ASD, and OCD working groups

Author

Pedro Moreira, Ruth O'Gorman Tuura, Mara Cercignani, Philip Aherson, Maria Jalbrzikowski, Kate D. Fitzgerald, Declan G. Murphy, Bernd Kardatzki, Christine Ecker, David F. Tolin, Fern Jaspers-Fayer, Pedro Morgado, Juan Carlos Soliva Vila, Kang Ik K. Cho, Kathrin Koch, Timothy J. Silk, Philip R. Szeszko, Thomas Frodl, Mara Parellada, Shlomi Haar, Eileen Daly, Bob Oranje, Anouk Schrantee, Leyla Namazova-Baranova, Joseph A. King, Beatriz Luna, Silvia Brem, Eric Earl, Alasdair Vance, Michela Tosetti, Christine Deruelle, Ramona Baur-Streubel, Jackie Fitzgerald, Kirsten O'Hearn, Michael C. Stevens, Yoshiyuki Hirano, J. Antoni Ramos-Quiroga, Erika L. Nurmi, Kaylita Chantiluke, Joseph O'Neill, Kerstin Kohls, Olga Puig, Devon Shook, Clodagh M. Murphy, Gustavo Sudre, Marlene Behrmann, Jaap Oosterlaan, Tinatin Gogberashvili, Lianne Schmaal, Carles Soriano-Mas, Liesbeth Hoekstra, Ignacio Martínez-Zalacaín, Noam Soreni, Marcel P. Zwiers, Paulo Mattos, Gregor Kohls, Andreas J. Fallgatter, Tiffany M. Chaim-Avancini, Alexander Baranov, S. Evelyn Stewart, Sara Dallaspezia, Gianfranco Spalletta, Jonna Kuntsi, Lizanne J. S. Schweren, Joel T. Nigg, Leanne Tamm, Premika S.W. Boedhoe, Adriana Di Martino, Jane McGrath, Marcelo C. Batistuzzo, Norbert Skokauskas, Filippo Muratori, John Piacentini, Jean-Paul Fouche, Sarah Baumeister, Alan Anticevic, Neil A. Harrison, Christine M. Freitag, Pedro G.P. Rosa, Stephen V. Faraone, Ana Cubillo, David Mataix-Cols, Yuki Sakai, Stefan Ehrlich, Eileen Oberwelland Weiss, Fabrizio Piras, Dirk J. Heslenfeld, Je-Yeon Yun, Paul Pauli, Catharina A. Hartman, Ganesan Venkatasubramanian, Janardhanan C. Narayanaswamy, Charles B Malpas, Jan C. Beucke, José M. Menchón, Egill A. Fridgeirsson, Margot J. Taylor, Mauricio Moller Martinho, H. Blair Simpson, Jan K. Buitelaar, Gerd Kvale, Ivanei E. Bramati, Aki Tsuchiyagaito, Susanne Walitza, Irene Bollettini, Jeffery N. Epstein, Anders M. Dale, Thomas Ethofer, Terry L. Jernigan, David Coghill, Rachel Marsh, Andreas Reif, Astri J. Lundervold, Pieter J. Hoekstra, Oana Georgiana Rus, Damiaan Denys, Gregory L. Wallace, Matt C. Gabel, Hazel McCarthy, Sarah Hohmann, Rosa Nicolau, Stephanie H. Ameis, Neda Jahanshad, Takashi Nakamae, Xin Feng, Emily R. Stern, Georg G. von Polier, Yanni Liu, Paulo Marques, Anushree Bose, Hao Hu, Sara Lera-Miguel, Deniz A. Gürsel, Jochen Seitz, Jos W. R. Twisk, Mario Rodrigues Louzã, Clare Kelly, Annette Conzelmann, Alysa E. Doyle, Odile A. van den Heuvel, Anthony A. James, Chris Perriello, Joost Janssen, Damien A. Fair, Norbert Kathmann, Francisco X. Castellanos, Paul D. Arnold, Oscar Vilarroya, Geraldo F. Busatto, Federica Piras, Pino Alonso, Akiko Nakagawa, Sarah Durston, Lena Schwarz, Mitul A. Mehta, Dan J. Stein, Celso Arango, Daan van Rooij, Ilan Dinstein, Anastasia Christakou, Klaus-Peter Lesch, Kerstin J. Plessen, Jennifer Fedor, Yolanda Vives-Gilabert, Ilaria Gori, Louise Gallagher, Brian P. Brennan, Yuqi Cheng, Barbara Franke, Sabin Khadka, Stephanie E. Novotny, Martine Hoogman, Georgii Karkashadze, Georg C. Ziegler, Yuliya N. Yoncheva, Rosa Calvo, Thomas Wolfers, Marcelo Q. Hoexter, Benjamin A. Ely, Masaru Kuno, Alessandra Retico, Yoshinari Abe, Geoffrey B. Hall, Tobias Banaschewski, Anatoly Anikin, Christine Lochner, Astrid Morer, Guido van Wingen, Jan Haavik, Joseph Biederman, Luisa Lázaro, Francesco Benedetti, Fengfeng Zhou, Guillaume Auzias, Daniel Brandeis, Dmitry Kapilushniy, Katya Rubia, Philip Shaw, Christian Kaufmann, Sara Calderoni, Marcus V. Zanetti, Anastasia Solovieva, Zhen Wang, Francesca Assogna, Jamie D. Feusner, Chaim Huyser, Fernanda Tovar-Moll, Theo G.M. van Erp, Y.C. Janardhan Reddy, Jun Soo Kwon, Yannis Paloyelis, Anna Calvo, Patricia Gruner, Kathrin C. Zierhut, Liesbeth Reneman, Tomohiro Nakao, Janita Bralten, Marie F. Høvik, Mark A. Bellgrove, Maarten Mennes, Paul M. Thompson, Institut de Neurosciences de la Timone (INT), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Epidemiology and Data Science, Pediatric surgery, Radiology and nuclear medicine, Amsterdam Neuroscience - Compulsivity, Impulsivity & Attention, Psychiatry, APH - Methodology, APH - Health Behaviors & Chronic Diseases, Boedhoe, Premika S W, van Rooij, Daan, Hoogman, Martine, Twisk, Jos W R, Schmaal, Lianne, Abe, Yoshinari, Alonso, Pino, Ameis, Stephanie H, Anikin, Anatoly, Anticevic, Alan, Arango, Celso, Arnold, Paul D, Asherson, Philip, Assogna, Francesca, Auzias, Guillaume, Banaschewski, Tobia, Baranov, Alexander, Batistuzzo, Marcelo C, Baumeister, Sarah, Baur-Streubel, Ramona, Behrmann, Marlene, Bellgrove, Mark A, Benedetti, Francesco, Beucke, Jan C, Biederman, Joseph, Bollettini, Irene, Bose, Anushree, Bralten, Janita, Bramati, Ivanei E, Brandeis, Daniel, Brem, Silvia, Brennan, Brian P, Busatto, Geraldo F, Calderoni, Sara, Calvo, Anna, Calvo, Rosa, Castellanos, Francisco X, Cercignani, Mara, Chaim-Avancini, Tiffany M, Chantiluke, Kaylita C, Cheng, Yuqi, Cho, Kang Ik K, Christakou, Anastasia, Coghill, David, Conzelmann, Annette, Cubillo, Ana I, Dale, Anders M, Dallaspezia, Sara, Daly, Eileen, Denys, Damiaan, Deruelle, Christine, Di Martino, Adriana, Dinstein, Ilan, Doyle, Alysa E, Durston, Sarah, Earl, Eric A, Ecker, Christine, Ehrlich, Stefan, Ely, Benjamin A, Epstein, Jeffrey N, Ethofer, Thoma, Fair, Damien A, Fallgatter, Andreas J, Faraone, Stephen V, Fedor, Jennifer, Feng, Xin, Feusner, Jamie D, Fitzgerald, Jackie, Fitzgerald, Kate D, Fouche, Jean-Paul, Freitag, Christine M, Fridgeirsson, Egill A, Frodl, Thoma, Gabel, Matt C, Gallagher, Louise, Gogberashvili, Tinatin, Gori, Ilaria, Gruner, Patricia, Gürsel, Deniz A, Haar, Shlomi, Haavik, Jan, Hall, Geoffrey B, Harrison, Neil A, Hartman, Catharina A, Heslenfeld, Dirk J, Hirano, Yoshiyuki, Hoekstra, Pieter J, Hoexter, Marcelo Q, Hohmann, Sarah, Høvik, Marie F, Hu, Hao, Huyser, Chaim, Jahanshad, Neda, Jalbrzikowski, Maria, James, Anthony, Janssen, Joost, Jaspers-Fayer, Fern, Jernigan, Terry L, Kapilushniy, Dmitry, Kardatzki, Bernd, Karkashadze, Georgii, Kathmann, Norbert, Kaufmann, Christian, Kelly, Clare, Khadka, Sabin, King, Joseph A, Koch, Kathrin, Kohls, Gregor, Konrad, Kerstin, Kuno, Masaru, Kuntsi, Jonna, Kvale, Gerd, Kwon, Jun Soo, Lázaro, Luisa, Lera-Miguel, Sara, Lesch, Klaus-Peter, Hoekstra, Liesbeth, Liu, Yanni, Lochner, Christine, Louza, Mario R, Luna, Beatriz, Lundervold, Astri J, Malpas, Charles B, Marques, Paulo, Marsh, Rachel, Martínez-Zalacaín, Ignacio, Mataix-Cols, David, Mattos, Paulo, Mccarthy, Hazel, Mcgrath, Jane, Mehta, Mitul A, Menchón, José M, Mennes, Maarten, Martinho, Mauricio Moller, Moreira, Pedro S, Morer, Astrid, Morgado, Pedro, Muratori, Filippo, Murphy, Clodagh M, Murphy, Declan G M, Nakagawa, Akiko, Nakamae, Takashi, Nakao, Tomohiro, Namazova-Baranova, Leyla, Narayanaswamy, Janardhanan C, Nicolau, Rosa, Nigg, Joel T, Novotny, Stephanie E, Nurmi, Erika L, Weiss, Eileen Oberwelland, O'Gorman Tuura, Ruth L, O'Hearn, Kirsten, O'Neill, Joseph, Oosterlaan, Jaap, Oranje, Bob, Paloyelis, Yanni, Parellada, Mara, Pauli, Paul, Perriello, Chri, Piacentini, John, Piras, Fabrizio, Piras, Federica, Plessen, Kerstin J, Puig, Olga, Ramos-Quiroga, J Antoni, Reddy, Y C Janardhan, Reif, Andrea, Reneman, Liesbeth, Retico, Alessandra, Rosa, Pedro G P, Rubia, Katya, Rus, Oana Georgiana, Sakai, Yuki, Schrantee, Anouk, Schwarz, Lena, Schweren, Lizanne J S, Seitz, Jochen, Shaw, Philip, Shook, Devon, Silk, Tim J, Simpson, H Blair, Skokauskas, Norbert, Soliva Vila, Juan Carlo, Solovieva, Anastasia, Soreni, Noam, Soriano-Mas, Carle, Spalletta, Gianfranco, Stern, Emily R, Stevens, Michael C, Stewart, S Evelyn, Sudre, Gustavo, Szeszko, Philip R, Tamm, Leanne, Taylor, Margot J, Tolin, David F, Tosetti, Michela, Tovar-Moll, Fernanda, Tsuchiyagaito, Aki, van Erp, Theo G M, van Wingen, Guido A, Vance, Alasdair, Venkatasubramanian, Ganesan, Vilarroya, Oscar, Vives-Gilabert, Yolanda, von Polier, Georg G, Walitza, Susanne, Wallace, Gregory L, Wang, Zhen, Wolfers, Thoma, Yoncheva, Yuliya N, Yun, Je-Yeon, Zanetti, Marcus V, Zhou, Fengfeng, Ziegler, Georg C, Zierhut, Kathrin C, Zwiers, Marcel P, Thompson, Paul M, Stein, Dan J, Buitelaar, Jan, Franke, Barbara, van den Heuvel, Odile A, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Adult Psychiatry, ANS - Compulsivity, Impulsivity & Attention, Graduate School, Child Psychiatry, General Paediatrics, ARD - Amsterdam Reproduction and Development, Radiology and Nuclear Medicine, APH - Personalized Medicine, and APH - Mental Health

Subjects
Male, Research Report, Obsessive-Compulsive Disorder, Frontal cortex, Systems Analysis, Attention Deficit Hyperactivity Disorder, Autism Spectrum Disorder, [SDV]Life Sciences [q-bio], Hippocampal formation, Audiology, 0302 clinical medicine, 130 000 Cognitive Neurology & Memory, Child, Obsessive-compulsive disorder (OCD), ComputingMilieux_MISCELLANEOUS, Intelligence quotient, Psychopathology, ATTENTION-DEFICIT/HYPERACTIVITY DISORDER, ABNORMALITIES, ENIGMA, Organ Size, 3. Good health, Psychiatry and Mental health, Autism spectrum disorder, Brain size, Cohort, Female, MRI, Adult, medicine.medical_specialty, CORTEX, Adolescent, DEFICIT HYPERACTIVITY DISORDER, Human Development, Neuroimaging, behavioral disciplines and activities, Article, 03 medical and health sciences, FIELD-STRENGTH, mental disorders, medicine, MEGA-ANALYSIS, Attention deficit hyperactivity disorder, Humans, Cortical surface, Structural MRI, Attention Deficit Disorder with Hyperactivity, Cerebrum, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], business.industry, medicine.disease, 030227 psychiatry, VOXEL, Autism, business, 030217 neurology & neurosurgery
Abstract

ObjectiveAttention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and obsessive-compulsive disorder (OCD) are common neurodevelopmental disorders that frequently co-occur. We aimed to directly compare all three disorders. The ENIGMA consortium is ideally positioned to investigate structural brain alterations across these disorders.MethodsStructural T1-weighted whole-brain MRI of controls (n=5,827) and patients with ADHD (n=2,271), ASD (n=1,777), and OCD (n=2,323) from 151 cohorts worldwide were analyzed using standardized processing protocols. We examined subcortical volume, cortical thickness and surface area differences within a mega-analytical framework, pooling measures extracted from each cohort. Analyses were performed separately for children, adolescents, and adults using linear mixed-effects models adjusting for age, sex and site (and ICV for subcortical and surface area measures).ResultsWe found no shared alterations among all three disorders, while shared alterations between any two disorders did not survive multiple comparisons correction. Children with ADHD compared to those with OCD had smaller hippocampal volumes, possibly influenced by IQ. Children and adolescents with ADHD also had smaller ICV than controls and those with OCD or ASD. Adults with ASD showed thicker frontal cortices compared to adult controls and other clinical groups. No OCD-specific alterations across different age-groups and surface area alterations among all disorders in childhood and adulthood were observed.ConclusionOur findings suggest robust but subtle alterations across different age-groups among ADHD, ASD, and OCD. ADHD-specific ICV and hippocampal alterations in children and adolescents, and ASD-specific cortical thickness alterations in the frontal cortex in adults support previous work emphasizing neurodevelopmental alterations in these disorders.

Published
2020

8. Neurite orientation and dispersion density imaging (NODDI) detects cortical and corticospinal tract degeneration in ALS

Author

Nicholas G. Dowell, Anil K. Seth, P. Nigel Leigh, Mara Cercignani, Rebecca Broad, Matt C. Gabel, Daniel C. Alexander, David J. Schwartzman, and Hui Zhang

Subjects
Male, Internal capsule, Neurite, Pyramidal Tracts, Axonal loss, Corpus callosum, 03 medical and health sciences, 0302 clinical medicine, Neurites, Humans, Medicine, Neurodegeneration, Amyotrophic lateral sclerosis, Aged, Cerebral Cortex, business.industry, Amyotrophic Lateral Sclerosis, Precentral gyrus, Anatomy, Middle Aged, medicine.disease, Axons, Frontal Lobe, Psychiatry and Mental health, Diffusion Magnetic Resonance Imaging, RC0346, Case-Control Studies, Corticospinal tract, Female, Surgery, Neurology (clinical), business, 030217 neurology & neurosurgery, Diffusion MRI
Abstract

BackgroundCorticospinal tract (CST) degeneration and cortical atrophy are consistent features of amyotrophic lateral sclerosis (ALS). We hypothesised that neurite orientation dispersion and density imaging (NODDI), a multicompartment model of diffusion MRI, would reveal microstructural changes associated with ALS within the CST and precentral gyrus (PCG) ‘in vivo’.Methods23 participants with sporadic ALS and 23 healthy controls underwent diffusion MRI. Neurite density index (NDI), orientation dispersion index (ODI) and free water fraction (isotropic compartment (ISO)) were derived. Whole brain voxel-wise analysis was performed to assess for group differences. Standard diffusion tensor imaging (DTI) parameters were computed for comparison. Subgroup analysis was performed to investigate for NODDI parameter differences relating to bulbar involvement. Correlation of NODDI parameters with clinical variables were also explored. The results were accepted as significant where pResultsIn the ALS group NDI was reduced in the extensive regions of the CST, the corpus callosum and the right PCG. ODI was reduced in the right anterior internal capsule and the right PCG. Significant differences in NDI were detected between subgroups stratified according to the presence or absence of bulbar involvement. ODI and ISO correlated with disease duration.ConclusionsNODDI demonstrates that axonal loss within the CST is a core feature of degeneration in ALS. This is the main factor contributing to the altered diffusivity profile detected using DTI. NODDI also identified dendritic alterations within the PCG, suggesting microstructural cortical dendritic changes occur together with CST axonal damage.

Published
2018

9. Brain Imaging of the Cortex in ADHD: A Coordinated Analysis of Large-Scale Clinical and Population-Based Samples

Author

Luisa Lázaro, Dmitry Kapilushniy, Elena Shumskaya, Katya Rubia, Ana Cubillo, Philip Shaw, Marcus V. Zanetti, Anders M. Dale, Thomas Ethofer, Andreas Reif, Pieter J. Hoekstra, Mariam Zentis, Sarah Baumeister, Sara Lera-Miguel, Kerstin J. Plessen, Anastasia Solovieva, Catharina A. Hartman, João P.O.F.T. Guimarães, Tonya White, Hazel McCarthy, Thomas Frodl, Stephanie E. Novotny, Martine Hoogman, Mara Cercignani, Gustavo Sudre, Patrick de Zeeuw, Tiffany M. Chaim-Avancini, Ivanei E. Bramati, Yolanda Vives-Gilabert, J. Antoni Ramos-Quiroga, Jonna Kuntsi, Clare Kelly, Joel T. Nigg, Dirk J. Heslenfeld, Tinatin Gogberashvili, Mark A. Bellgrove, Susanne Walitza, Sarah Hohmann, Jan Haavik, Kaylita Chantiluke, Joseph Biederman, Marcel P. Zwiers, Maarten Mennes, Neil A. Harrison, Hanan El Marroun, Norbert Skokauskas, Mitul A. Mehta, Annette Conzelmann, Fernanda Tovar-Moll, Rosa Nicolau, Juan Carlos Soliva Vila, Mario Rodrigues Louzã, Ruth O'Gorman Tuura, Anastasia Christakou, Barbara Franke, Charles B Malpas, Theo G.M. van Erp, Eileen Oberwelland Weiss, Terry L. Jernigan, Alysa E. Doyle, Daniel Brandeis, David Coghill, L. Reneman, Tobias Banaschewski, Geraldo F. Busatto, Sarah Durston, Anouk Schrantee, Philip Asherson, Lena Schwarz, Georgii Karkashadze, Kerstin Konrad, Anatoly Anikin, Neda Jahanshad, Paul M. Thompson, Georg C. Ziegler, Paulo Mattos, Michael C. Stevens, Janita Bralten, Matt C. Gabel, Thomas Wolfers, Alasdair Vance, Leanne Tamm, Georg G. von Polier, Timothy J. Silk, Bernd Kardatzki, Jochen Seitz, Sabin Khadka, Ryan L. Muetzel, Marie F. Høvik, Damien A. Fair, Astri J. Lundervold, Eric Earl, Jeffery N. Epstein, Ramona Baur-Streubel, Paul Pauli, Yuliya N. Yoncheva, Jaap Oosterlaan, Gregor Kohls, Henning Tiemeier, Francisco X. Castellanos, Silvia Brem, Oscar Vilarroya, Pedro G.P. Rosa, Stephen V. Faraone, Klaus-Peter Lesch, Jan K. Buitelaar, Bob Oranje, Leyla Namazova-Baranova, A.A. Baranov, Andreas J. Fallgatter, Anna Calvo, Sara Ambrosino, Kathrin C. Zierhut, Yannis Paloyelis, Lizanne J. S. Schweren, APH - Personalized Medicine, ANS - Compulsivity, Impulsivity & Attention, Radiology and Nuclear Medicine, General Paediatrics, ARD - Amsterdam Reproduction and Development, APH - Mental Health, Child and Adolescent Psychiatry / Psychology, Department of Psychology, Education and Child Studies, Erasmus MC other, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Psychiatrie & Neuropsychologie, RS: MHeNs - R3 - Neuroscience, and Pediatric surgery

Subjects
Male, SYMPTOMS, CHILDREN, Audiology, physiopathology [Cerebral Cortex], 0302 clinical medicine, CONNECTIVITY, 130 000 Cognitive Neurology & Memory, diagnostic imaging [Cerebral Cortex], physiopathology [Attention Deficit Disorder with Hyperactivity], PARTICIPANTS, Young adult, Child, Child Behavior Checklist, Cerebral Cortex, education.field_of_study, ATTENTION-DEFICIT/HYPERACTIVITY DISORDER, Age Factors, 220 Statistical Imaging Neuroscience, Brain, Middle Aged, Magnetic Resonance Imaging, Psychiatry and Mental health, medicine.anatomical_structure, Cerebral cortex, Child, Preschool, Female, MRI, Adult, medicine.medical_specialty, Adolescent, DEFICIT HYPERACTIVITY DISORDER, Population, Neuroimaging, behavioral disciplines and activities, 150 000 MR Techniques in Brain Function, Article, Young Adult, 03 medical and health sciences, Sex Factors, All institutes and research themes of the Radboud University Medical Center, mental disorders, medicine, Journal Article, Attention deficit hyperactivity disorder, Humans, ddc:610, education, METAANALYSIS, Psychiatric Status Rating Scales, Fusiform gyrus, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], business.industry, ADULTS, pathology [Attention Deficit Disorder with Hyperactivity], medicine.disease, 030227 psychiatry, SIZE, Attention Deficit Disorder with Hyperactivity, Case-Control Studies, Endophenotype, RC0321, diagnostic imaging [Attention Deficit Disorder with Hyperactivity], pathology [Cerebral Cortex], business, 030217 neurology & neurosurgery
Abstract

Contains fulltext : 204879pub.pdf (Publisher’s version ) (Open Access) Contains fulltext : 204879pos.pdf (Author’s version postprint ) (Open Access) OBJECTIVE: Neuroimaging studies show structural alterations of various brain regions in children and adults with attention deficit hyperactivity disorder (ADHD), although nonreplications are frequent. The authors sought to identify cortical characteristics related to ADHD using large-scale studies. METHODS: Cortical thickness and surface area (based on the Desikan-Killiany atlas) were compared between case subjects with ADHD (N=2,246) and control subjects (N=1,934) for children, adolescents, and adults separately in ENIGMA-ADHD, a consortium of 36 centers. To assess familial effects on cortical measures, case subjects, unaffected siblings, and control subjects in the NeuroIMAGE study (N=506) were compared. Associations of the attention scale from the Child Behavior Checklist with cortical measures were determined in a pediatric population sample (Generation-R, N=2,707). RESULTS: In the ENIGMA-ADHD sample, lower surface area values were found in children with ADHD, mainly in frontal, cingulate, and temporal regions; the largest significant effect was for total surface area (Cohen's d=-0.21). Fusiform gyrus and temporal pole cortical thickness was also lower in children with ADHD. Neither surface area nor thickness differences were found in the adolescent or adult groups. Familial effects were seen for surface area in several regions. In an overlapping set of regions, surface area, but not thickness, was associated with attention problems in the Generation-R sample. CONCLUSIONS: Subtle differences in cortical surface area are widespread in children but not adolescents and adults with ADHD, confirming involvement of the frontal cortex and highlighting regions deserving further attention. Notably, the alterations behave like endophenotypes in families and are linked to ADHD symptoms in the population, extending evidence that ADHD behaves as a continuous trait in the population. Future longitudinal studies should clarify individual lifespan trajectories that lead to nonsignificant findings in adolescent and adult groups despite the presence of an ADHD diagnosis.

Published
2019

10. Deficits in neurite density underlie white matter structure abnormalities in first-episode psychosis

Author

Nicholas G. Dowell, Sarah N. Garfinkel, Mara Cercignani, Matt C. Gabel, Kathryn Greenwood, Hugo D. Critchley, Geoff Davies, Nick Medford, Anil K. Seth, and Charlotte L. Rae

Subjects
Adult, Male, Psychosis, Neurite, Adolescent, Neuroimaging, White matter, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Fractional anisotropy, Neural Pathways, medicine, Neurites, Humans, Biological Psychiatry, medicine.diagnostic_test, Age Factors, Brain, Magnetic resonance imaging, Commissure, QM0531, medicine.disease, White Matter, 030227 psychiatry, medicine.anatomical_structure, Diffusion Magnetic Resonance Imaging, Diffusion Tensor Imaging, Psychotic Disorders, Case-Control Studies, Anisotropy, Female, Psychology, Neuroscience, 030217 neurology & neurosurgery, Diffusion MRI
Abstract

Background\udStructural abnormalities across multiple white matter tracts are recognized in people with early psychosis, consistent with dysconnectivity as a neuropathological account of symptom expression. We applied advanced neuroimaging techniques to characterize microstructural white matter abnormalities for a deeper understanding of the developmental etiology of psychosis.\udMethods\udThirty-five first-episode psychosis patients, and 19 healthy controls, participated in a quantitative neuroimaging study using neurite orientation dispersion and density imaging, a multishell diffusion-weighted magnetic resonance imaging technique that distinguishes white matter fiber arrangement and geometry from changes in neurite density. Fractional anisotropy (FA) and mean diffusivity images were also derived. Tract-based spatial statistics compared white matter structure between patients and control subjects and tested associations with age, symptom severity, and medication.\udResults\udPatients with first-episode psychosis had lower regional FA in multiple commissural, corticospinal, and association tracts. These abnormalities predominantly colocalized with regions of reduced neurite density, rather than aberrant fiber bundle arrangement (orientation dispersion index). There was no direct relationship with active symptoms. FA decreased and orientation dispersion index increased with age in patients, but not control subjects, suggesting accelerated effects of white matter geometry change.\udConclusions\udDeficits in neurite density appear fundamental to abnormalities in white matter integrity in early psychosis. In the first application of neurite orientation dispersion and density imaging in psychosis, we found that processes compromising axonal fiber number, density, and myelination, rather than processes leading to spatial disruption of fiber organization, are implicated in the etiology of psychosis. This accords with a neurodevelopmental origin of aberrant brain-wide structural connectivity predisposing individuals to psychosis.

Published
2017

11. PO117 Regional efficacy of fingolimod in multiple sclerosis

Author

Stephen Bremner, Matt C. Gabel, Waqar Rashid, Leonora Fisniku, Bettina Newell, Catherine Warren, Iulia Bogdan, Anna Koniotes, and Giles Ruffer

Subjects
medicine.medical_specialty, Expanded Disability Status Scale, business.industry, Patient demographics, Multiple sclerosis, Medical record, Mean age, medicine.disease, Fingolimod, Clinical trial, Psychiatry and Mental health, Internal medicine, Cohort, medicine, Surgery, Neurology (clinical), business, medicine.drug
Abstract

Background Fingolimod is approved in England as second-line treatment for highly active relapsing-remitting multiple sclerosis (RRMS). Objectives To evaluate the real world effects of fingolimod in a typical NHS clinical setting (relevant to justify cost, risk of therapies like fingolimod and appropriate prescribing). Methodology Retrospective reviewing of medical records and MRI scans of RRMS patients on fingolimod for minimum 1 year at BSUH NHS Trust. Patient demographics, disease duration, Expanded Disability Status Scale (EDSS) and no evidence of disease activity (NEDA) were used as covariates. Findings were compared with FREEDOMS and TRANSFORMS outcomes. Results 61 patients, followed-up for a mean of 2.7–years were included. The cohort was slightly older (mean age 43 vs. 36), included a higher proportion of females (85% vs. 65%–69%), had longer disease duration (12.5 vs 8) and was more disabled (median EDSS 4 vs 3) compared with trial data. At 1 year 81.35% were relapse-free, similar to trial data. For the whole follow-up period, NEDA was seen in 57.37% of patients, suggesting some expected waning effect. No patient covariates were found significant. 14.75% of patients discontinued treatment. Conclusion Our data shows similar efficacy for fingolimod is possible within an NHS setting with comparable retention to clinical trials.

Published
2017

12. COGNITIVE IMPAIRMENT OCCURS BEFORE LOSS OF FUNCTION IN ALS

Author

Daniel C. Alexander, Stella Tsermentseli, Mara Cercignani, Alexandra L. Young, Matt C. Gabel, P. Nigel Leigh, Ammar Al-Chalabi, and Laura H. Goldstein

Subjects
medicine.medical_specialty, Disease progression, Cognition, medicine.disease, Psychiatry and Mental health, Physical medicine and rehabilitation, medicine, Surgery, Neurology (clinical), Functional ability, Amyotrophic lateral sclerosis, Cognitive impairment, Psychology, Neuroscience, Loss function, Executive dysfunction, Event (probability theory)
Abstract

Objectives Using a historical amyotrophic lateral sclerosis (ALS) dataset comprising detailed cognitive and clinical assessments, we used a novel event-based model to analyse the likely ordering of these biomarkers in the progression of ALS. Methods The dataset was derived from a cross-sectional sample of 28 ALS patients who were not classified as having ALS-FTD and 26 matched controls (see1 regarding cognitive and clinical assessments). The event-based model was adapted for ALS from previous work in Alzheimer9s disease.23 Unlike traditional models of disease progression, event-based models do not rely on a priori staging of patients but extract the event ordering directly from the data, thus minimising subjective bias. Results The most likely order of progression showed that changes in executive function occur at an early stage of disease evolution. Language impairment tended to occur after executive dysfunction. Changes in functional ability assessed by rate of change of ALSFRS-R occurred after the changes in executive function. Conclusions These findings suggest that executive dysfunction occurs early in the evolution of ALS.

Published
2016

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