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												  Psychophysiology of AggressionCHAPTER 5 Psychophysiology of Aggression SUSAN BRANJE and HANS M. KOOT Brief Introduction In this chapter we review psychophysiological studies of the development and main- tenance of aggression in childhood and adolescence. As aggression is likely to be a function of a complex interplay between individual and social factors, this review is concerned with the role of psychophysiological or neurobiological systems in aggressive behavior of children and adolescents, as well as with the interactions of these systems with social factors. The autonomic nervous system (ANS) and the hypothalamic–pituitary–adrenal (HPA) axis both play important roles in the regulation of stress and decision making, and these stress-regulating mechanisms are thought to be important in understanding individual differences in aggressive behavior (Van Goozen, Fairchild, Snoek, & Harold, 2007). Therefore, we focus on the roles of the ANS and the HPA axis in particular. Main Issues Although a large body of literature has addressed psychophysiological correlates of aggressive behavior, the results of these studies are at times quite inconsistent. Contributing to this inconsistency in findings is the heterogeneity in studies in terms of methodological and theoretical issues. We pay attention to a number of these issues, which include the heterogeneity in behavioral constructs and the roles of sex and age. 84 Book_Malti.indb 84 5/10/2018 3:24:42 PM Psychophysiology of Aggression 85 Different Forms of Antisocial and Aggressive Behavior Regarding heterogeneity in behavioral constructs, many studies focus on antisocial behavior more generally and do not distinguish aggressive behaviors from other antisocial or externalizing behaviors. Although externalizing behaviors are often significantly and strongly correlated, failing to distinguish them might obscure research findings and interpretations.
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												  What to Expect After Having a Subarachnoid Hemorrhage (SAH) Information for Patients and Families Table of ContentsWhat to expect after having a subarachnoid hemorrhage (SAH) Information for patients and families Table of contents What is a subarachnoid hemorrhage (SAH)? .......................................... 3 What are the signs that I may have had an SAH? .................................. 4 How did I get this aneurysm? ..................................................................... 4 Why do aneurysms need to be treated?.................................................... 4 What is an angiogram? .................................................................................. 5 How are aneurysms repaired? ..................................................................... 6 What are common complications after having an SAH? ..................... 8 What is vasospasm? ...................................................................................... 8 What is hydrocephalus? ............................................................................... 10 What is hyponatremia? ................................................................................ 12 What happens as I begin to get better? .................................................... 13 What can I expect after I leave the hospital? .......................................... 13 How will the SAH change my health? ........................................................ 14 Will the SAH cause any long-term effects? ............................................. 14 How will my emotions be affected? .......................................................... 15 When should
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												  Neuroinflammation and Functional Connectivity in Alzheimer's Disease: Interactive Influences on Cognitive PerformanceResearch Articles: Neurobiology of Disease Neuroinflammation and functional connectivity in Alzheimer's disease: interactive influences on cognitive performance https://doi.org/10.1523/JNEUROSCI.2574-18.2019 Cite as: J. Neurosci 2019; 10.1523/JNEUROSCI.2574-18.2019 Received: 5 October 2018 Revised: 25 March 2019 Accepted: 11 April 2019 This Early Release article has been peer-reviewed and accepted, but has not been through the composition and copyediting processes. The final version may differ slightly in style or formatting and will contain links to any extended data. Alerts: Sign up at www.jneurosci.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Copyright © 2019 Passamonti et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. 1 Neuroinflammation and functional connectivity in Alzheimer’s disease: 2 interactive influences on cognitive performance 3 4 L. Passamonti1*, K.A. Tsvetanov1*, P.S. Jones1, W.R. Bevan-Jones2, R. Arnold2, R.J. Borchert1, 5 E. Mak2, L. Su2, J.T. O’Brien2#, J.B. Rowe1,3# 6 7 Joint *first and #last authorship 8 9 10 Authors’ addresses 11 1Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 12 2Department of Psychiatry, University of Cambridge, Cambridge, UK 13 3Cognition and Brain Sciences Unit, Medical Research Council, Cambridge,
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												![Neurocognitive and Functional Impairment in Adult and Paediatric Tuberculous Meningitis [Version 1; Peer Review: 2 Approved]](https://docslib.b-cdn.net/cover/2973/neurocognitive-and-functional-impairment-in-adult-and-paediatric-tuberculous-meningitis-version-1-peer-review-2-approved-412973.webp)  Neurocognitive and Functional Impairment in Adult and Paediatric Tuberculous Meningitis [Version 1; Peer Review: 2 Approved]Wellcome Open Research 2019, 4:178 Last updated: 20 MAY 2021 REVIEW Neurocognitive and functional impairment in adult and paediatric tuberculous meningitis [version 1; peer review: 2 approved] Angharad G. Davis 1-3, Sam Nightingale4, Priscilla E. Springer 5, Regan Solomons 5, Ana Arenivas6,7, Robert J. Wilkinson 2,8,9, Suzanne T. Anderson10,11*, Felicia C. Chow 12*, Tuberculous Meningitis International Research Consortium 1University College London, Gower Street, London, WC1E 6BT, UK 2Francis Crick Institute, Midland Road, London, NW1 1AT, UK 3Institute of Infectious Diseases and Molecular Medicine. Department of Medicine, University of Cape Town, Observatory, 7925, South Africa 4HIV Mental Health Research Unit, University of Cape Town,, Observatory, 7925, South Africa 5Department of Paediatrics and Child Health, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa 6The Institute for Rehabilitation and Research Memorial Hermann, Department of Rehabilitation Psychology and Neuropsychology,, Houston, Texas, USA 7Baylor College of Medicine, Department of Physical Medicine and Rehabilitation, Houston, Texas, USA 8Department of Infectious Diseases, Imperial College London, London, W2 1PG, UK 9Wellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Diseases and Molecular Medicine at Department of Medicine, University of Cape Town, Observatory, 7925, South Africa 10MRC Clinical Trials Unit at UCL, University College London, London, WC1E 6BT, UK 11Evelina Community, Guys and St Thomas’
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												  What%Is%Epilepsy?%What%is%Epilepsy?% Epilepsy(is(a(brain(disorder(in(which(a(person(has(repeated(seizures((convulsions)(over(time.(Seizures(are( episodes(of(disturbed(brain(activity(that(cause(changes(in(attention(or(behavior.( Causes( Epilepsy(occurs(when(permanent(changes(in(brain(tissue(cause(the(brain(to(be(too(excitable(or(jumpy.( The(brain(sends(out(abnormal(signals.(This(results(in(repeated,(unpredictable(seizures.((A(single(seizure( that(does(not(happen(again(is(not(epilepsy.)( Epilepsy(may(be(due(to(a(medical(condition(or(injury(that(affects(the(brain,(or(the(cause(may(be( unknown((idiopathic).( Common(causes(of(epilepsy(include:( •Stroke(or(transient(ischemic(attack((TIA)( •Dementia,(such(as(Alzheimer's(disease( •Traumatic(brain(injury( •Infections,(including(brain(abscess,(meningitis,(encephalitis,(and(AIDS( •Brain(problems(that(are(present(at(birth((congenital(brain(defect)( •Brain(injury(that(occurs(during(or(near(birth( •Metabolism(disorders(present(at(birth((such(as(phenylketonuria)( •Brain(tumor( •Abnormal(blood(vessels(in(the(brain( •Other(illness(that(damage(or(destroy(brain(tissue( •Use(of(certain(medications,(including(antidepressants,(tramadol,(cocaine,(and(amphetamines( Epilepsy(seizures(usually(begin(between(ages(5(and(20,(but(they(can(happen(at(any(age.(There(may(be(a( family(history(of(seizures(or(epilepsy.( Symptoms( Symptoms(vary(from(person(to(person.(Some(people(may(have(simple(staring(spells,(while(others(have( violent(shaking(and(loss(of(alertness.(The(type(of(seizure(depends(on(the(part(of(the(brain(affected(and( cause(of(epilepsy.(
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												  Leveraging Insights and Approaches from Social and Affective Neuroscience to Promote Adaptive Aging: a WorkshopLeveraging Insights and Approaches from Social and Affective Neuroscience to Promote Adaptive Aging: A Workshop National Academies of Sciences, Engineering, and Medicine Division of Behavioral and Social Sciences and Education in collaboration with the National Institute on Aging November 18-19, 2019 Keck Center of the National Academies 500 Fifth Street NW, Washington, DC 20001 Final April 10, 2020 This meeting summary was prepared by Bethany Stokes, Rose Li and Associates, Inc., under contract to the National Institute on Aging (NIA). The views expressed in this document reflect both individual and collective opinions of the meeting participants and not necessarily those of the NIA. Review of earlier versions of this meeting summary by the following individuals is gratefully acknowledged: Kelly Beazley, Natalie Ebner, Derek Isaacowitz, Janice Kiecolt-Glaser, Anne Krendl, Rose Maria Li, Beatriz Luna, Mara Mather, Ulrich Mayr, Meghan Meyer, Judith Moskowitz, Lisbeth Nielsen, Marc Schulz, Rebecca Spencer, Luke Stoeckel, Ann Thompson, Nancy Tuvesson. Leveraging Insights from Social and Affective Neuroscience November 18-19, 2019 Table of Contents Acronym Definitions ............................................................................................................. iii Meeting Summary ................................................................................................................. 1 Introduction ..................................................................................................................................1
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												  Social Neuroscience and Psychopathology: Identifying the Relationship Between Neural Function, Social Cognition, and Social BehaHooker, C.I. (2014). Social Neuroscience and Psychopathology, Chapter to appear in Social Neuroscience: Mind, Brain, and Society Social Neuroscience and Psychopathology: Identifying the relationship between neural function, social cognition, and social behavior Christine I. Hooker, Ph.D. ***************************** Learning Goals: 1. Identify main categories of social and emotional processing and primary neural regions supporting each process. 2. Identify main methodological challenges of research on the neural basis of social behavior in psychopathology and strategies for addressing these challenges. 3. Identify how research in the three social processes discussed in detail – social learning, self-regulation, and theory of mind – inform our understanding of psychopathology. Summary Points: 1. Several psychiatric disorders, such as schizophrenia and autism, are characterized by social functioning deficits, but there are few interventions that effectively address social problems. 2. Treatment development is hindered by research challenges that limit knowledge about the neural systems that support social behavior, how those neural systems and associated social behaviors are compromised in psychopathology, and how the social environment influences neural function, social behavior, and symptoms of psychopathology. 3. These research challenges can be addressed by tailoring experimental design to optimize sensitivity of both neural and social measures as well as reduce confounds associated with psychopathology. 4. Investigations on the neural mechanisms of social learning, self-regulation, and Theory of Mind provide examples of methodological approaches that can inform our understanding of psychopathology. 5. High-levels of neuroticism, which is a vulnerability for anxiety disorders, is related to hypersensitivity of the amygdala during social fear learning. 6. High-levels of social anhedonia, which is a vulnerability for schizophrenia- spectrum disorders, is related to reduced lateral prefrontal cortex (LPFC) activity 1 Hooker, C.I.
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												  Cognitive Impairment/Dementia – SummaryCognitive Impairment/Dementia Care Guide December 2014 SUMMARY GOALS Early identification of affected patients Prevention of victimization Reduce symptom severity Improve quality of life ALERTS Victimized patients Increase in rules violation behaviors Worsening personal hygiene Anxiety and agitation, especially at night Complete Advance Directive-Durable Power of Attorney for Health Care (DPAHC) early in course of disease Prison environment may mask symptoms DIAGNOSTIC CRITERIA/EVALUATION Definition - Mild Cognitive Impairment (MCI) Cognitive decline greater than expected for age and education level without significantly interfering with activities of daily life. Evidence of memory impairment Preservation of general cognitive and functional abilities Absence of diagnosed dementia Definition - Dementia Cognitive impairment with: significant decline from previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, social cognition, perceptual motor) interference with independence in daily activities Not occurring exclusively with delirium Not better explained by another disorder Neurobehavioral abnormalities History - MCI and Dementia patients may have similar historical findings which contribute to the ultimate diagnosis: Poor adherence to rules and routines Personal hygiene problems Impaired comprehension History of head injury, substance abuse, or other medical contributors Differential Diagnosis – Mild Cognitive Impairment (MCI) Medication
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												  Adenomatous Polyposis Coli Heterozygous Knockout Mice Display Hypoactivity and Age-Dependent Working Memory DeficitsView metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central ORIGINAL RESEARCH ARTICLE published: 21 December 2011 BEHAVIORAL NEUROSCIENCE doi: 10.3389/fnbeh.2011.00085 Adenomatous polyposis coli heterozygous knockout mice display hypoactivity and age-dependent working memory deficits Hisatsugu Koshimizu1,2, Yasuyuki Fukui 3, Keizo Takao 2,4, Koji Ohira 1,2, Koichi Tanda 3,5, Kazuo Nakanishi 3, Keiko Toyama 1,2, Masanobu Oshima 6, Makoto Mark Taketo 7 and Tsuyoshi Miyakawa 1,2,4* 1 Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan 2 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi, Japan 3 Genetic Engineering and Functional Genomics Group, Frontier Technology Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan 4 Section of Behavior Patterns, Center for Genetic Analysis of Behavior, National Institute for Physiological Sciences, Okazaki, Japan 5 Department of Pediatrics, Kyoto Prefectural University of Medicine, Kyoto, Japan 6 Division of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan 7 Department of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto, Japan Edited by: A tumor suppressor gene, Adenomatous polyposis coli (Apc), is expressed in the nervous Jeff Dalley, University of system from embryonic to adulthood stages, and transmits the Wnt signaling pathway in Cambridge, UK which schizophrenia susceptibility genes, including T-cell factor 4 (TCF4) and calcineurin Reviewed by: (CN), are involved. However, the functions of Apc in the nervous system are largely Jeff Dalley, University of Cambridge, UK unknown. In this study, as the first evaluation of Apc function in the nervous system, Adam C.
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												  The Cognitive Basis of Dyslexia in School-Aged Children: a Multiple CaseThe cognitive basis of dyslexia The cognitive basis of dyslexia in school-aged children: a multiple case study in a transparent orthography Agnieszka Dębska1*, Magdalena Łuniewska1,2*, Julian Zubek2, Katarzyna Chyl1, Agnieszka Dynak1,2, Gabriela Dzięgiel-Fivet1, Joanna Plewko1, Katarzyna Jednoróg1, Anna Grabowska3 * these authors contributed equally to the paper 1Laboratory of Language Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland 2 Faculty of Psychology, University of Warsaw, Warsaw, Poland 3Faculty of Psychology, SWPS University of Social Sciences and Humanities, Warsaw, Poland Laboratory of Language Neurobiology Nencki Institute of Experimental Biology, Polish Academy of Sciences ul. Pasteura 3, 02-093 Warszawa, Poland Conflict of Interest Statement None of the authors has to declare a conflict of interest. Supplementary materials 1. Tables and Figures 2. Supplementary materials S1, S2, S3 and S4 1 The cognitive basis of dyslexia The cognitive basis of dyslexia in school-aged children: a multiple case study in a transparent orthography Research highlights ● This study tested the (co)existence of cognitive deficits in dyslexia in phonological awareness, rapid naming, visual and selective attention, auditory skills, and implicit learning. ● The most frequent deficits in Polish children with dyslexia included a phonological (51%) and a rapid naming deficit (26%), which coexisted in 14% of children. ● Despite the severe reading impairment, 26% of children with dyslexia presented no deficits in measured cognitive abilities. ● RAN explains reading skills variability across the whole spectrum of reading ability; phonological skills explain variability best among average and good readers but not poor readers. Abstract This study focused on the role of numerous cognitive skills such as phonological awareness (PA), rapid automatized naming (RAN), visual and selective attention, auditory skills, and implicit learning in developmental dyslexia.
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												  Utility for Candidate Gene Studies in Human Attention-Deficit HyperactivityJournal of Neuroscience Methods 166 (2007) 294–305 Rodent models: Utility for candidate gene studies in human attention-deficit hyperactivity disorder (ADHD) Jonathan Mill a,b,∗ a Centre for Addiction and Mental Health, Toronto, Canada b Toronto Western Research Institute, Toronto, Canada Received 6 September 2006; received in revised form 30 November 2006; accepted 30 November 2006 Abstract Attention-deficit hyperactivity disorder (ADHD) is a common neurobehavioral disorder defined by symptoms of developmentally inappropriate inattention, impulsivity and hyperactivity. Behavioral genetic studies provide overwhelming evidence for a significant genetic role in the patho- genesis of the disorder. Rodent models have proven extremely useful in helping understand more about the genetic basis of ADHD in humans. A number of well-characterized rodent models have been proposed, consisting of inbred strains, selected lines, genetic knockouts, and transgenic animals, which have been used to inform candidate gene studies in ADHD. In addition to providing information about the dysregulation of known candidate genes, rodents are excellent tools for the identification of novel ADHD candidate genes. While not yet widely used to identify genes for ADHD-like behaviors in rodents, quantitative trait loci (QTL) mapping approaches using recombinant inbred strains, heterogeneous stock mice, and chemically mutated animals have the potential to revolutionize our understanding of the genetic basis of ADHD. © 2006 Elsevier B.V. All rights reserved. Keywords: Attention-deficit hyperactivity disorder (ADHD); Genetics; Animal model; Quantitative trait loci (QTL); Rodents; Behavior; Candidate gene 1. Introduction is likely that susceptibility is mediated by the effect of numer- ous genes of small effect, interacting both epistatically and with Attention-deficit hyperactivity disorder (ADHD) is a com- the environment.
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												  Brain Injury and Opioid OverdoseBrain Injury and Opioid Overdose: Acquired Brain Injury is damage to the brain 2.8 million brain injury related occurring after birth and is not related to congenital or degenerative disease. This includes anoxia and hospital stays/deaths in 2013 hypoxia, impairment (lack of oxygen), a condition consistent with drug overdose. 70-80% of hospitalized patients are discharged with an opioid Rx Opioid Use Disorder, as defined in DSM 5, is a problematic pattern of opioid use leading to clinically significant impairment, manifested by meaningful risk 63,000+ drug overdose-related factors occurring within a 12-month period. deaths in 2016 Overdose is injury to the body (poisoning) that happens when a drug is taken in excessive amounts “As the number of drug overdoses continues to rise, and can be fatal. Opioid overdose induces respiratory doctors are struggling to cope with the increasing number depression that can lead to anoxic or hypoxic brain of patients facing irreversible brain damage and other long injury. term health issues.” Substance Use and Misuse is: The frontal lobe is • Often a contributing factor to brain injury. History of highly susceptible abuse/misuse is common among individuals who to brain oxygen have sustained a brain injury. loss, and damage • Likely to increase for individuals who have misused leads to potential substances prior to and post-injury. loss of executive Acute or chronic pain is a common result after brain function. injury due to: • Headaches, back or neck pain and other musculo- Sources: Stojanovic et al 2016; Melton, C. Nov. 15,2017; Devi E. skeletal conditions commonly reported by veterans Nampiaparampil, M.D., 2008; Seal K.H., Bertenthal D., Barnes D.E., et al 2017; with a history of brain injury.