Amnesia and Crime: a Neuropsychiatric Response
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Memory Part 1: Overview
FUNCTIONAL VIGNETTE Memory Part 1: Overview F.D. Raslau, A.P. Klein, J.L. Ulmer, V. Mathews, and L.P. Mark common layman’s conception of memory is the simple stor- Aage and retrieval of learned information that often evokes comparison to a filing system. Our everyday experience of mem- ory, however, is in fact a complicated multifactorial process that consists of both conscious and unconscious components, and de- pends on the integration of a variety of information from distinct functional systems, each processing different types of information by different areas of the brain (substrates), while working in a concerted fashion.1-4 In other words, memory is not a singular process. It represents an integrated network of neurologic tasks and connections. In this light, memory may evoke comparison with an orchestra composed of many different instruments, each making different sounds and responsible for different parts of the score, but when played together in the proper coordinated fash- ion, making an integrated musical experience that is greater than the simple sum of the individual instruments. Memory consists of 2 broad categories (Fig 1): short- and long-term memory.5 Short-term memory is also called work- ing memory. Long-term memory can be further divided into FIG 1. Classification of memory. declarative and nondeclarative memory. These are also re- ferred to as explicit/conscious and implicit/unconscious mem- heard (priming), and salivating when you see a favorite food ory, respectively. Declarative or explicit memory consists of (conditioning). episodic (events) and semantic (facts) memory. Nondeclara- The process of memory is dynamic with continual change over tive or implicit memory consists of priming, skill learning, and time.5 Memory traces are initially formed as a series of connections conditioning. -
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]. -
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. -
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. -
Does Amnesia Specifically Predict Alzheimer's Pathology?
Does amnesia specifically predict Alzheimer’s pathology? A neuropathological study Maxime Bertoux, Pascaline Cassagnaud, Thibaud Lebouvier, Florence Lebert, Marie Sarazin, Isabelle Le Ber, Bruno Dubois, Brain Bank, Sophie Auriacombe, Didier Hannequin, et al. To cite this version: Maxime Bertoux, Pascaline Cassagnaud, Thibaud Lebouvier, Florence Lebert, Marie Sarazin, et al.. Does amnesia specifically predict Alzheimer’s pathology? A neuropathological study. Neurobiology of Aging, Elsevier, In press. hal-02898941 HAL Id: hal-02898941 https://hal.archives-ouvertes.fr/hal-02898941 Submitted on 14 Jul 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Amnesia/AD pathology 1 Does amnesia specifically predict Alzheimer’s pathology? A neuropathological study. Maxime Bertoux*1a, Pascaline Cassagnaud*b, Thibaud Lebouvier*c, Florence Leberta, Marie Sarazinde, Isabelle Le Berfg, Bruno Duboisfg, NeuroCEB Brain Bank, Sophie Auriacombeh, Didier Hannequini, David Walloni, Mathieu Ceccaldij, Claude-Alain Mauragek, Vincent Deramecourtc, Florence Pasquiera a Univ Lille, Lille Neuroscience & Cognition (Inserm UMRS1172) Degenerative and vascular cognitive disorders, CHU Lille, Laboratory of Excellence Distalz (Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer’s disease). F-59000, Lille, France.F-59000, Lille, France. b Univ Lille, CHU Lille, Laboratory of Excellence Distalz (Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer’s disease). -
When the Mind Falters: Cognitive Losses in Dementia
T L C When the Mind Falters: Cognitive Losses in Dementia by L Joel Streim, MD T Associate Professor of Psychiatry C Director, Geriatric Psychiatry Fellowship Program University of Pennsylvania VISN 4 Mental Illness Research Education and Clinical Center Philadelphia VA Medical Center Delaware Valley Geriatric Education Center The goal of this module is to teach direct staff about the syndrome of dementia and its clinical effects on residents. It focuses on the ways that the symptoms of dementia affect persons’ functional ability and behavior. We begin with an overview of the symptoms of cognitive impairment. We continue with a description of the causes, epidemiology, and clinical course (stages) of dementia. We then turn to a closer look at the specific areas of cognitive impairment, and examine how deficits in different areas of cognitive function can interfere with the person’s daily functioning, causing disability. The accompanying videotape illustrates these principles, using the example of a nursing home resident whose cognitive impairment interferes in various ways with her eating behavior and ability to feed herself. 1 T L Objectives C At the end of this module you should be able to: Describe the stages of dementia Distinguish among specific cognitive impairments from dementia L Link specific cognitive impairments with the T disabilities they cause C Give examples of cognitive impairments and disabilities Describe what to do when there is an acute change in cognitive or functional status Delaware Valley Geriatric Education Center At the end of this module you should be able to • Describe the stages of dementia. These are early, middle and late, and we discuss them in more detail. -
PAVOL JOZEF ŠAFARIK UNIVERSITY in KOŠICE Dissociative Amnesia: a Clinical and Theoretical Reconsideration DEGREE THESIS
PAVOL JOZEF ŠAFARIK UNIVERSITY IN KOŠICE FACULTY OF MEDICINE Dissociative amnesia: a clinical and theoretical reconsideration Paulo Alexandre Rocha Simão DEGREE THESIS Košice 2017 PAVOL JOZEF ŠAFARIK UNIVERSITY IN KOŠICE FACULTY OF MEDICINE FIRST DEPARTMENT OF PSYCHIATRY Dissociative amnesia: a clinical and theoretical reconsideration Paulo Alexandre Rocha Simão DEGREE THESIS Thesis supervisor: Mgr. MUDr. Jozef Dragašek, PhD., MHA Košice 2017 Analytical sheet Author Paulo Alexandre Rocha Simão Thesis title Dissociative amnesia: a clinical and theoretical reconsideration Language of the thesis English Type of thesis Degree thesis Number of pages 89 Academic degree M.D. University Pavol Jozef Šafárik University in Košice Faculty Faculty of Medicine Department/Institute Department of Psychiatry Study branch General Medicine Study programme General Medicine City Košice Thesis supervisor Mgr. MUDr. Jozef Dragašek, PhD., MHA Date of submission 06/2017 Date of defence 09/2017 Key words Dissociative amnesia, dissociative fugue, dissociative identity disorder Thesis title in the Disociatívna amnézia: klinické a teoretické prehodnotenie Slovak language Key words in the Disociatívna amnézia, disociatívna fuga, disociatívna porucha identity Slovak language Abstract in the English language Dissociative amnesia is a one of the most intriguing, misdiagnosed conditions in the psychiatric world. Dissociative amnesia is related to other dissociative disorders, such as dissociative identity disorder and dissociative fugue. Its clinical features are 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. -
Mild Cognitive Impairment Douglas W
Mild Cognitive Normal Impairment (MCI) Mild Cognitive Impairment Douglas W. Scharre, MD Director, Division of Cognitive Neurology Ohio State University Dementia Dementia Definition • Syndrome of acquired persistent intellectual impairment • Persistent deficits in at least three of the following: Definitions 9 Memory 9 Language 9 Visuospatial 9 Personality or emotional state 9 Cognition • Resulting in impairment in Activities of Daily Living (ADL) 1 Mild Cognitive Impairment MCI Related (MCI) Definition Conditions • Definitions vary - be careful! AAMI: Age-Associated Memory Impairment • Petersen criteria • Non-disease, aging-related decline in – Memory complaint memory – Memory loss on testing greater that 1.5 standard • Diagnostic criteria are ambiguous deviations below normal for age • Complaints of memory loss more related – Other non-memory cognitive domains normal or to affect/personality than test scores mild deficits (language, visuospatial, executive, personality or emotional state) • Prevalence in the elderly varies from 18% up to 38% depending on the study – Mostly normal activities of daily living Barker et al. Br J Psychiatry 1995;167:642-8 Arch Neurol 1999;56:303-8 Hanninen et al. Age and Aging 1996;25:201-5 MCI Related MCI Related Conditions Conditions • Age-Associated Memory Impairment Benign Senescent Forgetfulness or Mild (AAMI) Memory Impairment (MMI) • Memory tests > 2 s.d. below normal age and • Benign Senile Forgetfulness or Mild education matched individuals Memory Impairment (MMI) • Normal non-memory cognitive domains -
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.