Memory Disorders Associated with Consumption Of
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Psychogenic and Organic Amnesia. a Multidimensional Assessment of Clinical, Neuroradiological, Neuropsychological and Psychopathological Features
Behavioural Neurology 18 (2007) 53–64 53 IOS Press Psychogenic and organic amnesia. A multidimensional assessment of clinical, neuroradiological, neuropsychological and psychopathological features Laura Serraa,∗, Lucia Faddaa,b, Ivana Buccionea, Carlo Caltagironea,b and Giovanni A. Carlesimoa,b aFondazione IRCCS Santa Lucia, Roma, Italy bClinica Neurologica, Universita` Tor Vergata, Roma, Italy Abstract. Psychogenic amnesia is a complex disorder characterised by a wide variety of symptoms. Consequently, in a number of cases it is difficult distinguish it from organic memory impairment. The present study reports a new case of global psychogenic amnesia compared with two patients with amnesia underlain by organic brain damage. Our aim was to identify features useful for distinguishing between psychogenic and organic forms of memory impairment. The findings show the usefulness of a multidimensional evaluation of clinical, neuroradiological, neuropsychological and psychopathological aspects, to provide convergent findings useful for differentiating the two forms of memory disorder. Keywords: Amnesia, psychogenic origin, organic origin 1. Introduction ness of the self – and a period of wandering. According to Kopelman [33], there are three main predisposing Psychogenic or dissociative amnesia (DSM-IV- factors for global psychogenic amnesia: i) a history of TR) [1] is a clinical syndrome characterised by a mem- transient, organic amnesia due to epilepsy [52], head ory disorder of nonorganic origin. Following Kopel- injury [4] or alcoholic blackouts [20]; ii) a history of man [31,33], psychogenic amnesia can either be sit- psychiatric disorders such as depressed mood, and iii) uation specific or global. Situation specific amnesia a severe precipitating stress, such as marital or emo- refers to memory loss for a particular incident or part tional discord [23], bereavement [49], financial prob- of an incident and can arise in a variety of circum- lems [23] or war [21,48]. -
Novel Approaches for the Treatment of Alzheimer's and Parkinson's Disease
International Journal of Molecular Sciences Review Novel Approaches for the Treatment of Alzheimer’s and Parkinson’s Disease Michiel Van Bulck 1,2 , Ana Sierra-Magro 1,2, Jesus Alarcon-Gil 1, Ana Perez-Castillo 1,2 and Jose A. Morales-Garcia 1,2,3,* 1 Instituto de Investigaciones Biomédicas (CSIC-UAM), Arturo Duperier, 4. 28029 Madrid, Spain; [email protected] (M.V.B.); [email protected] (A.S.-M.); [email protected] (J.A.-G.); [email protected] (A.P.-C.) 2 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo, 5, 28031 Madrid, Spain 3 Departamento de Biología Celular, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Plaza Ramón y Cajal s/n, 28040 Madrid, Spain * Correspondence: [email protected] Received: 31 December 2018; Accepted: 3 February 2019; Published: 8 February 2019 Abstract: Neurodegenerative disorders affect around one billion people worldwide. They can arise from a combination of genomic, epigenomic, metabolic, and environmental factors. Aging is the leading risk factor for most chronic illnesses of old age, including Alzheimer’s and Parkinson’s diseases. A progressive neurodegenerative process and neuroinflammation occur, and no current therapies can prevent, slow, or halt disease progression. To date, no novel disease-modifying therapies have been shown to provide significant benefit for patients who suffer from these devastating disorders. Therefore, early diagnosis and the discovery of new targets and novel therapies are of upmost importance. Neurodegenerative diseases, like in other age-related disorders, the progression of pathology begins many years before the onset of symptoms. Many efforts in this field have led to the conclusion that exits some similar events among these diseases that can explain why the aging brain is so vulnerable to suffer neurodegenerative diseases. -
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. -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
How the Brain and Memory Works 10
Caring For A Loved One With Dementia 10 How the Brain and Memory Works Introduction The way our brain stores memories is a complex process across many areas of the brain. Luckily, memories are not all stored in one place. They are spread out across different brain regions, or lobes, and allow us to keep and recall memories even if one area of the brain is damaged. Although the brain’s process for storing memories is sometimes compared to a filing cabinet, the processes are extremely complex and still not fully understood. 2 Creating memories 3. Store information The human brain is made up of neurons. Neurons are nerve cells that talk to each other through a synapse- a connection This is the process of retaining the information in short term, or between cells that sends information. Neurons receive and more permanently in long term memory. An area of the brain carry information to the parts of the brain to process or store called the Hippocampus plays an important role in storing long information. The brain has approximately 100 billion nerve term memories. cells, give or take 15 billion. 4. Recall To create memories, the brain must accomplish the following processes: Memories that are frequently recalled become stronger than those accessed less frequently. The neurons linked to this 1. Encode information information create a neural pathway- a road to that memory. Think of it as walking along a path. The more frequently you This process allows something of interest to be stored in the walk on the same path, the more defined the trail becomes. -
PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names INN which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service CAS registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. -
Primary and Secondary Prevention Interventions for Cognitive Decline
2016 Primary and secondary prevention interventions for cognitive decline and dementia Overview of reviews Published by The Norwegian Institute of Public Health Section for evidence summaries in the Knowledge Centre Title Primary and secondary prevention interventions for cognitive decline and dementia Norwegian title Primær‐ og sekundærforebyggende tiltak for kognitiv svikt og demens Responsible Camilla Stoltenberg, direktør Authors Gerd M Flodgren, project leader, researcher, the Knowledge Centre Rigmor C Berg, Head of Unit, for Social Welfare Research at the Knowledge Centre ISBN 978‐82‐8082‐745‐6 Projectnumber 798 Type of publication Overview of reviews No of pages 69 (110 inklusiv vedlegg) Client Nasjonalforeningen for folkehelsen MeSH terms Alzheimer’s disease, dementia, cognition, cognitive impairment, cognitive disorders, memory complaints, primary prevention, secondary prevention Citation Flodgren GM, Berg RC. Primary and secondary prevention interventions for cognitive decline and dementia. [Primær‐ og sekundærforebyggende tiltak for kognitiv svikt og demens] Rapport −2016. Oslo: Folkehelseinstituttet, 2016. 2 Table of contents Table of contents TABLE OF CONTENTS 3 KEY MESSAGES 5 EXECUTIVE SUMMARY 6 Background 6 Objectives 6 Methods 6 Results 6 Discussion 8 Conclusions 8 HOVEDFUNN (NORSK) 9 SAMMENDRAG (NORSK) 10 Bakgrunn 10 Problemstillinger 10 Metoder 10 Resultat 10 Diskusjon 12 Konklusjon 12 PREFACE 13 OBJECTIVES 15 BACKGROUND 16 Description of the condition 16 How the interventions may work 18 Why is it important to do this -
Effect of Phosphatidylserine Administration on Symptoms of Attention-Deficit/Hyperactivity Disorder in Children S
AGRO SET_OTT_06.qxp 27-10-2006 10:14 Pagina 16 Effect of phosphatidylserine administration on symptoms of attention-deficit/hyperactivity disorder in children S. HIRAYAMA1*,Y. MASUDA2,R. RABELER3 *Corresponding author 1. Department of Early Childhood Education and Care, Kurashiki City College, 160 Hieda, Kurashikishi, Okayama, Japan 2. Kojima first High School, Okayama, Japan 3. Cargill Food Ingredients GmbH, Freising, Germany PURPOSE the emotional response in the frontal lobe, due to a problem of disinhibition (1). Disinhibition consists of disinhibition of To clarify whether the administration of phosphatidylserine attention (inattention) and that of behaviour (hyperactivity ("PS") can improve the attention-deficit ("AD") and and impulsiveness). hyperactivity disorder ("HD") symptoms in children. with AD/HD patients are classified into inattention-predominant Infant nutrition AD/HD. type, hyperactivity and impulsiveness -dominant type and mixed type. Each symptom causes problems in learning and relation between family members. Though the cause of STUDY DESIGN AND SUBJECTS disorders has yet to be identified (2), central stimulants (a type of psycho stimulant) are used in the treatment. These A pilot study in 15 AD/HD children 6 to 12 years old (including drugs can alleviate the AD/HD symptoms to some extent (3, 6 suspected to have AD/HD) who had rarely received 4). However, there is no consensus on the long term use of medication before. These 15 children took 200 mg/day of PS these drugs and adverse events (adverse reactions) may in a capsule every day for 2 months. The following items were occur during or years after the treatment (5). Accordingly, investigated at the start of study ("pre-study") and upon supplementary and substitute medication is frequently completion of study ("post-study): 1) AD/HD symptoms advised. -
The Importance of Sleep in Fear Conditioning and Posttraumatic Stress Disorder
Biological Psychiatry: Commentary CNNI The Importance of Sleep in Fear Conditioning and Posttraumatic Stress Disorder Robert Stickgold and Dara S. Manoach Abnormal sleep is a prominent feature of Axis I neuropsychia- fear and distress are extinguished. Based on a compelling tric disorders and is often included in their DSM-5 diagnostic body of work from human and rodent studies, fear extinction criteria. While often viewed as secondary, because these reflects not the erasure of the fear memory but the develop- disorders may themselves diminish sleep quality, there is ment of a new safety or “extinction memory” that inhibits the growing evidence that sleep disorders can aggravate, trigger, fear memory and its associated emotional response. and even cause a range of neuropsychiatric conditions. In this issue, Straus et al. (3 ) report that total sleep Moreover, as has been shown in major depression and deprivation can impair the retention of such extinction mem- attention-deficit/hyperactivity disorder, treating sleep can ories. In their study, healthy human participants in three improve symptoms, suggesting that disrupted sleep contri- groups successfully learned to associate a blue circle (condi- butes to the clinical syndrome and is an appropriate target for tioned stimulus) with the occurrence of an electric shock treatment. In addition to its effects on symptoms, sleep (unconditioned stimulus) during a fear acquisition session. disturbance, which is known to impair emotional regulation The following day, during extinction learning, the blue circle and cognition in otherwise healthy individuals, may contribute was repeatedly presented without the shock. The day after to or cause disabling cognitive deficits. For sleep to be a target that, extinction recall was tested by again repeatedly present- for treatment of symptoms and cognitive deficits in neurop- ing the blue circle without the shock. -
Memory Dysfunction in Neurological Practice Andrew E Budson, Bruce H Price
Downloaded from pn.bmj.com on 5 February 2007 42 Practical Neurology HOW TO UNDERSTAND IT Pract Neurol 2007; 7: 42–47 Memory dysfunction in neurological practice Andrew E Budson, Bruce H Price A E Budson Geriatric Research Educational Clinical Center, Edith Nourse Rogers Memorial Veterans Hospital, Bedford, MA; Boston University Alzheimer’s Disease Center, Boston University, Boston, MA; Division of Cognitive and Behavioral Neurology, Department of Neurology, Brigham and Women’s Hospital, Boston, MA; Harvard Medical School, Boston, MA, USA B H Price Department of Neurology, McLean Hospital, Belmont, MA and Harvard Medical School, Boston, MA, USA Correspondence to: Dr A E Budson Building 62, Room B30, Edith Nourse Rogers Memorial Veterans Hospital, 200 Springs Road, Bedford, MA 01730, USA; [email protected] Downloaded from pn.bmj.com on 5 February 2007 Budson, Price 43 omplaints of impaired memory are Episodic memory is the explicit and declarative among the most common symptoms reported to neurologists. Moreover, memory system that we all use to recall our C impairment of memory is one of the personal experience most disabling aspects of many neurological disorders, including neurodegenerative dis- eases, strokes, tumours, head trauma, collection of mental abilities that use hypoxia, cardiac surgery, malnutrition, atten- different systems within the brain. A memory tion deficit disorder, depression, anxiety, system is a way that the brain processes medication adverse effects, and just normal information in order to make it available for aging. This memory loss often impairs the use at a later time. Some systems are patient’s daily activities, profoundly affecting associated with conscious awareness (explicit) not just them but also their families. -
The Three Amnesias
The Three Amnesias Russell M. Bauer, Ph.D. Department of Clinical and Health Psychology College of Public Health and Health Professions Evelyn F. and William L. McKnight Brain Institute University of Florida PO Box 100165 HSC Gainesville, FL 32610-0165 USA Bauer, R.M. (in press). The Three Amnesias. In J. Morgan and J.E. Ricker (Eds.), Textbook of Clinical Neuropsychology. Philadelphia: Taylor & Francis/Psychology Press. The Three Amnesias - 2 During the past five decades, our understanding of memory and its disorders has increased dramatically. In 1950, very little was known about the localization of brain lesions causing amnesia. Despite a few clues in earlier literature, it came as a complete surprise in the early 1950’s that bilateral medial temporal resection caused amnesia. The importance of the thalamus in memory was hardly suspected until the 1970’s and the basal forebrain was an area virtually unknown to clinicians before the 1980’s. An animal model of the amnesic syndrome was not developed until the 1970’s. The famous case of Henry M. (H.M.), published by Scoville and Milner (1957), marked the beginning of what has been called the “golden age of memory”. Since that time, experimental analyses of amnesic patients, coupled with meticulous clinical description, pathological analysis, and, more recently, structural and functional imaging, has led to a clearer understanding of the nature and characteristics of the human amnesic syndrome. The amnesic syndrome does not affect all kinds of memory, and, conversely, memory disordered patients without full-blown amnesia (e.g., patients with frontal lesions) may have impairment in those cognitive processes that normally support remembering. -
Disordered Recognition Memory: Recollective Confabulation
cortex xxx (2013) 1e12 Available online at www.sciencedirect.com Journal homepage: www.elsevier.com/locate/cortex Special issue: Research report Disordered recognition memory: Recollective confabulation Chris J.A. Moulin* Laboratoire d’Etude de l’Apprentissage et du De´veloppement, CNRS UMR 5022, Universite´ de Bourgogne, Dijon, France article info abstract Article history: Recollective confabulation (RC) is encountered as a conviction that a present moment is a Received 31 January 2012 repetition of one experienced previously, combined with the retrieval of confabulated Reviewed 12 April 2012 specifics to support that assertion. It is often described as persistent de´ja` vu by family Revised 24 September 2012 members and caregivers. On formal testing, patients with RC tend to produce a very high Accepted 24 January 2013 level of false positive errors. In this paper, a new case series of 11 people with dementia or Published online xxx mild cognitive impairment (MCI) and with de´ja` vu-like experiences is presented. In two experiments the nature of the recognition memory deficit is explored. The results from Keywords: these two experiments suggest e contrary to our hypothesis in earlier published case re- Dementia ports e that recollection mechanisms are relatively spared in this group, and that patients De´ja` vu experience familiarity for non-presented items. The RC patients tended to be overconfident Reduplicative paramnesia in their assessment of recognition memory, and produce inaccurate assessments of their Familiarity performance. These findings are discussed with reference to delusions more generally, and Metacognition point to a combined memory and metacognitive deficit, possibly arising from damage to temporal and right frontal regions.