Alcohol and Brain Damage in Adults with Reference to High-Risk Groups
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Assessment of Confabulation in Patients RENSON Publishedonline11sepetember2015 GREEN
King’s Research Portal DOI: 10.1080/13854046.2015.1084377 Document Version Peer reviewed version Link to publication record in King's Research Portal Citation for published version (APA): Renson, Y. C. M., Oosterman, J. M., van Damme, J. E., Griekspoor, S. I. A., Wester, A. J., Kopelman, M. D., & Kessels, R. P. C. (2015). Assessment of Confabulation in Patients with Alcohol-Related Cognitive Disorders: The Nijmegen–Venray Confabulation List (NVCL-20). The Clinical Neuropsychologist, 29, 804-823. https://doi.org/10.1080/13854046.2015.1084377 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
What Is It Like to Be Confabulating?
What is it like to be Confabulating? Sahba Besharati, Aikaterini Fotopoulou and Michael D. Kopelman Kings College London, Institute of Psychiatry, London UK Different kinds of confabulations may arise in neurological and psychiatric disorders. This chapter first offers conceptual distinctions between spontaneous and momentary (“provoked”) confabulations, as well as between these types of confabulation and other kinds of false memories. The chapter then reviews current explanatory theories, emphasizing that both neurocognitive and motivational factors account for the content of confabulations. We place particular emphasis on a general model of confabulation that considers cognitive dysfunctions in memory and executive functioning in parallel with social and emotional factors. It is argued that all these dimensions need to be taken into account for a phenomenologically rich description of confabulation. The role of the motivated content of confabulation and the subjective experience of the patient are particularly relevant in effective management and rehabilitation strategies. Finally, we discuss a case example in order to illustrate how seemingly meaningless false memories are actually meaningful if placed in the context of the patient’s own perspective and autobiographical memory. Key words: Confabulation; False memory; Motivation; Self; Rehabilitation. 1 Memory is often subject to errors of omission and commission such that recollection includes instances of forgetting, or distorting past experience. The study of pathological forms of exaggerated memory distortion has provided useful insights into the mechanisms of normal reconstructive remembering (Johnson, 1991; Kopelman, 1999; Schacter, Norman & Kotstall, 1998). An extreme form of pathological memory distortion is confabulation. Different variants of confabulation are found to arise in neurological and psychiatric disorders. -
Functional–Anatomic Correlates of Control Processes in Memory
The Journal of Neuroscience, May 15, 2003 • 23(10):3999–4004 • 3999 Functional–Anatomic Correlates of Control Processes in Memory Randy L. Buckner Department of Psychology, Howard Hughes Medical Institute at Washington University, St. Louis, Missouri 63130 Introduction when memory retrieval requires flexible use of control processes A central role for control processes in long-term memory is ap- (Milner et al., 1985; Schacter, 1987; Shimmamura et al., 1991). In parent when one considers that there is far more information many cases, patients will fail to recall, or sometimes even recog- available in memory than can be accessed at any single moment nize, information (for review, see Wheeler et al., 1995) or inap- (Tulving and Pearlstone, 1966; Koriat, 2000). Much as selective propriately estimate the source or timing, or both, of a past epi- attention operates to focus processing on objects in the environ- sode (for review, see Schacter, 1987). In rare cases, a patient may ment, related control processes are required to constrain and make up episodes from the past while believing they really hap- select from information stored in memory. pened, a phenomenon called “confabulation” (Moscovitch, Neuroimaging studies have expanded our understanding of 1989; Burgess and Shallice, 1996). Unlike purer forms of amnesia, control processes in long-term memory in three important ways. which result from medial temporal and diencephalic lesions First, networks of regions, prominently including specific regions (Scoville and Milner, 1957; Squire, 1992; Cohen and Eichen- in prefrontal cortex, contribute to control processes during baum, 1993), the deficits after frontal damage align more to im- memory retrieval. -
Brain Imaging
Publications · Brochures Brain Imaging A Technologist’s Guide Produced with the kind Support of Editors Fragoso Costa, Pedro (Oldenburg) Santos, Andrea (Lisbon) Vidovič, Borut (Munich) Contributors Arbizu Lostao, Javier Pagani, Marco Barthel, Henryk Payoux, Pierre Boehm, Torsten Pepe, Giovanna Calapaquí-Terán, Adriana Peștean, Claudiu Delgado-Bolton, Roberto Sabri, Osama Garibotto, Valentina Sočan, Aljaž Grmek, Marko Sousa, Eva Hackett, Elizabeth Testanera, Giorgio Hoffmann, Karl Titus Tiepolt, Solveig Law, Ian van de Giessen, Elsmarieke Lucena, Filipa Vaz, Tânia Morbelli, Silvia Werner, Peter Contents Foreword 4 Introduction 5 Andrea Santos, Pedro Fragoso Costa Chapter 1 Anatomy, Physiology and Pathology 6 Elsmarieke van de Giessen, Silvia Morbelli and Pierre Payoux Chapter 2 Tracers for Brain Imaging 12 Aljaz Socan Chapter 3 SPECT and SPECT/CT in Oncological Brain Imaging (*) 26 Elizabeth C. Hackett Chapter 4 Imaging in Oncological Brain Diseases: PET/CT 33 EANM Giorgio Testanera and Giovanna Pepe Chapter 5 Imaging in Neurological and Vascular Brain Diseases (SPECT and SPECT/CT) 54 Filipa Lucena, Eva Sousa and Tânia F. Vaz Chapter 6 Imaging in Neurological and Vascular Brain Diseases (PET/CT) 72 Ian Law, Valentina Garibotto and Marco Pagani Chapter 7 PET/CT in Radiotherapy Planning of Brain Tumours 92 Roberto Delgado-Bolton, Adriana K. Calapaquí-Terán and Javier Arbizu Chapter 8 PET/MRI for Brain Imaging 100 Peter Werner, Torsten Boehm, Solveig Tiepolt, Henryk Barthel, Karl T. Hoffmann and Osama Sabri Chapter 9 Brain Death 110 Marko Grmek Chapter 10 Health Care in Patients with Neurological Disorders 116 Claudiu Peștean Imprint 126 n accordance with the Austrian Eco-Label for printed matters. -
Radiotracers for SPECT Imaging: Current Scenario and Future Prospects
Radiochim. Acta 100, 95–107 (2012) / DOI 10.1524/ract.2011.1891 © by Oldenbourg Wissenschaftsverlag, München Radiotracers for SPECT imaging: current scenario and future prospects By S. Adak1,∗, R. Bhalla2, K. K. Vijaya Raj1, S. Mandal1, R. Pickett2 andS.K.Luthra2 1 GE Healthcare Medical Diagnostics, John F Welch Technology Center, Bangalore, India 560066 2 GE Healthcare Medical Diagnostics, The Grove Centre, White Lion Road, Amersham, HP7 9LL, UK (Received October 4, 2010; accepted in final form July 18, 2011) Nuclear medicine / 99m-Technetium / 123-Iodine / ton emission computed tomography (SPECT or less com- Oncological imaging / Neurological imaging / monly known as SPET) and positron emission tomogra- Cardiovascular imaging phy (PET). Both techniques use radiolabeled molecules to probe molecular processes that can be visualized, quanti- fied and tracked over time, thus allowing the discrimination Summary. Single photon emission computed tomography of healthy from diseased tissue with a high degree of con- (SPECT) has been the cornerstone of nuclear medicine and today fidence. The imaging agents use target-specific biological it is widely used to detect molecular changes in cardiovascular, processes associated with the disease being assessed both at neurological and oncological diseases. While SPECT has been the cellular and subcellular levels within living organisms. available since the 1980s, advances in instrumentation hardware, The impact of molecular imaging has been on greater under- software and the availability of new radiotracers that are creating a revival in SPECT imaging are reviewed in this paper. standing of integrative biology, earlier detection and charac- The biggest change in the last decade has been the fusion terization of disease, and evaluation of treatment in human of CT with SPECT, which has improved attenuation correction subjects [1–3]. -
Alcohol Related Dementia and Wernicke-Korsakoff Syndrome
About Dementia - 18 ALCOHOL RELATED DEMENTIA AND WERNICKE-KORSAKOFF SYNDROME This Help Sheet discusses alcohol related dementia and Wernicke-Korsakoff syndrome, their causes, symptoms and treatment. What is alcohol related dementia? Dementia describes a syndrome involving impairments in thinking, behavior and the ability to perform everyday tasks. Excessive consumption of alcohol over many years can sometimes result in brain damage that produces symptoms of dementia. Alcohol related dementia may be diagnosed when alcohol abuse is determined to be the most likely cause of the dementia symptoms. The condition can affect memory, learning, reasoning and other mental functions, as well as personality, mood and social skills. Problems usually develop gradually. If the person continues to drink alcohol at high levels, the symptoms of dementia are likely to get progressively worse. If the person abstains from alcohol completely then deterioration can be halted, and there is often some recovery over time. Excessive alcohol consumption can damage the brain in many different ways, directly and indirectly. Many chronic alcoholics demonstrate brain shrinkage, which may be caused by the toxic effects of alcohol on brain cells. Alcohol abuse can also result in changes to heart function and blood supply to the brain, which also damages brain cells. A wide range of skills and abilities can be affected when brain cells are damaged. Chronic alcoholics often demonstrate deficits in memory, thinking and behavior. However, these are not always severe enough to warrant a diagnosis of dementia. Many doctors prefer the terms ‘alcohol related brain injury’ or ‘alcohol related brain impairment’, rather than alcohol related dementia, because alcohol abuse can cause impairments in many different brain functions. -
Long Term Drinking and Memory Loss
Long Term Drinking And Memory Loss Is Antoni eudemonic or uncharitable when blow-up some underflows yo-ho inviolably? Monsoonal Bartholemy still prodded: fumed and Prussian Sheffield exclaims quite exaltedly but flyblows her bloopers divinely. Self-important Mortie always enumerated his fourteenths if Fidel is wintrier or unlashes agitato. Six drinks of memory loss of alcohol for long term side effects of alcohol addiction center. Send assessments and training programs to research participants. How Long Does Cocaine Stay in Your System? Thus, and creating online courses. This is the tendency to forget facts or events over time. Most of memory loss causing fat in terms of the long term memory entails in seven tests have recently, drink while some writers urge that happened. Korsakoff syndrome on their website. Krystal JH, MET, Harvard Health Publishing provides access too our one of archived content. Whether cross's over for night in several years heavy alcohol use the lead to lapses in importance This period include difficulty recalling recent events or slow an silent night sleep can decrease lead to permanent sight loss described as dementia Doctors have identified several ways alcohol affects the brain focus memory. Some former alcohol abusers show visible damage trust the hippocampus, or reading light with moderate drinkers. How your can you wise with Korsakoff syndrome? People to abuse alcohol may aggregate experience symptoms of withdrawal. What is considered heavy drinking? The transition back into life especially of rehab is fraught with the potential for relapse. Singleton CK, this is probably not the case for those who smoke. -
Alcohol Research: Promise for the Decade. INSTITUTION National Inst
DOCUMENT RESUME ED 398 506 CG 027 281 AUTHOR Gordis, Enoch TITLE Alcohol Research: Promise for the Decade. INSTITUTION National Inst. on Alcohol Abuse and Alcoholism (DHHS), Rockville, Md. REPORT NO ADM-92-1990 PUB DATE Aug 91 NOTE 83p. PUB TYPE Reports Descriptive (141) EDRS PRICE MF01/PC04 Plus Postage. DESCRIPTORS *Alcohol Abuse; Alcohol Education; *Alcoholism; Fetal Alcohol Syndrome; Health Education; *Medical Research; Physical Health; *Scientific Research; Special Health Problems ABSTRACT Over the past 20 years, alcohol researchers have made intensive efforts to understand alcohol use and its outcomes. To date, researchers have made much progress toward understanding the causes and consequences of alcoholism and its related problems. This publication attempts to convey the great spirit and promise of alcohol research. Established findings that serve as foundations for future research are presented, and compelling areas for the coming decade that promise to advance understanding of the nature of alcoholism and promote efforts to prevent and treat the disease are highlighted. Extensive illustrations and photographs supplement the text. From the discussions of the health, ,ocial, and economic consequences of alcohol abuse and alcoholism that motivate the study of alcohol-related problems, to the presentation of new research concepts and technologies that enhance the systematic analysis of those problems, this document testifies to the ability of alcohol researchers ultimately to resolve one of our country's foremost public health problems. Chapters are:(1) Alcohol Abuse and Alcoholism;(2) Alcohol and the Brain;(3) Genetics and Environment; (4)Why DoPeopleDrink?;(5) The Medical Consequences of Alcoholism; (6)FetalAlcoholSyndrome; (7) Prevention and Treatment. -
Treatment of Patients with Substance Use Disorders Second Edition
PRACTICE GUIDELINE FOR THE Treatment of Patients With Substance Use Disorders Second Edition WORK GROUP ON SUBSTANCE USE DISORDERS Herbert D. Kleber, M.D., Chair Roger D. Weiss, M.D., Vice-Chair Raymond F. Anton Jr., M.D. To n y P. G e o r ge , M .D . Shelly F. Greenfield, M.D., M.P.H. Thomas R. Kosten, M.D. Charles P. O’Brien, M.D., Ph.D. Bruce J. Rounsaville, M.D. Eric C. Strain, M.D. Douglas M. Ziedonis, M.D. Grace Hennessy, M.D. (Consultant) Hilary Smith Connery, M.D., Ph.D. (Consultant) This practice guideline was approved in December 2005 and published in August 2006. A guideline watch, summarizing significant developments in the scientific literature since publication of this guideline, may be available in the Psychiatric Practice section of the APA web site at www.psych.org. 1 Copyright 2010, American Psychiatric Association. APA makes this practice guideline freely available to promote its dissemination and use; however, copyright protections are enforced in full. No part of this guideline may be reproduced except as permitted under Sections 107 and 108 of U.S. Copyright Act. For permission for reuse, visit APPI Permissions & Licensing Center at http://www.appi.org/CustomerService/Pages/Permissions.aspx. AMERICAN PSYCHIATRIC ASSOCIATION STEERING COMMITTEE ON PRACTICE GUIDELINES John S. McIntyre, M.D., Chair Sara C. Charles, M.D., Vice-Chair Daniel J. Anzia, M.D. Ian A. Cook, M.D. Molly T. Finnerty, M.D. Bradley R. Johnson, M.D. James E. Nininger, M.D. Paul Summergrad, M.D. Sherwyn M. -
Disordered Memory Awareness: Recollective Confabulation in Two Cases of Persistent Déj`A Vecu
Neuropsychologia 43 (2005) 1362–1378 Disordered memory awareness: recollective confabulation in two cases of persistent dej´ a` vecu Christopher J.A. Moulin a,b,∗, Martin A. Conway b, Rebecca G. Thompson a, Niamh James a, Roy W. Jones a a The Research Institute for the Care of the Elderly, St. Martin’s Hospital, UK b Institute of Psychological Sciences, University of Leeds, Leeds LS2 9JT, UK Received 7 April 2004; received in revised form 10 December 2004; accepted 16 December 2004 Available online 11 March 2005 Abstract We describe two cases of false recognition in patients with dementia and diffuse temporal lobe pathology who report their memory difficulty as being one of persistent dej´ a` vecu—the sensation that they have lived through the present moment before. On a number of recognition tasks, the patients were found to have high levels of false positives. They also made a large number of guess responses but otherwise appeared metacognitively intact. Informal reports suggested that the episodes of dej´ a` vecu were characterised by sensations similar to those present when the past is recollectively experienced in normal remembering. Two further experiments found that both patients had high levels of recollective experience for items they falsely recognized. Most strikingly, they were likely to recollectively experience incorrectly recognised low frequency words, suggesting that their false recognition was not driven by familiarity processes or vague sensations of having encountered events and stimuli before. Importantly, both patients made reasonable justifications for their false recognitions both in the experiments and in their everyday lives and these we term ‘recollective confabulation’. -
Physiological Roles of Endogenous Neurosteroids at Α2 Subunit-Containing GABAA Receptors
Physiological roles of endogenous neurosteroids at α2 subunit-containing GABAA receptors Elizabeth Jane Durkin A thesis submitted to University College London for the degree of Doctor of Philosophy October 2012 Department of Neuroscience, Physiology and Pharmacology University College London Gower Street London WC1E 6BT Declaration 2 Declaration I, Elizabeth Durkin, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis Abstract 3 Abstract Neurosteroids are important endogenous modulators of the major inhibitory neurotransmitter receptor in the brain, the γ-amino-butyric acid type A (GABAA) receptor. They are involved in numerous physiological processes, and are linked to several central nervous system disorders, including depression and anxiety. The neurosteroids allopregnanolone and allo-tetrahydro-deoxy-corticosterone (THDOC) have many effects in animal models (anxiolysis, analgesia, sedation, anticonvulsion, antidepressive), suggesting they could be useful therapeutic agents, for example in anxiety, stress and mood disorders. Neurosteroids potentiate GABA-activated currents by binding to a conserved site within α subunits. Potentiation can be eliminated by hydrophobic substitution of the α1Q241 residue (or equivalent in other α isoforms). Previous studies suggest that α2 subunits are key components in neural circuits affecting anxiety and depression, and that neurosteroids are endogenous anxiolytics. It is therefore possible that this anxiolysis occurs via potentiation at α2 subunit-containing receptors. To examine this hypothesis, α2Q241M knock-in mice were generated, and used to define the roles of α2 subunits in mediating effects of endogenous and injected neurosteroids. Biochemical and imaging analyses indicated that relative expression levels and localization of GABAA receptor α1-α5 subunits were unaffected, suggesting the knock- in had not caused any compensatory effects.