DOCSLIB.ORG

Primary and Secondary Prevention Interventions for Cognitive Decline

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

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 overview of reviews? 21 METHODS 22 Objectives 22 Inclusion criteria 22 Exclusion criteria 23 Literature search 23 Selection of reviews 24 Data extraction 24 Data synthesis 25 Grading of the evidence 25 3 Table of contents Ethics 26 RESULTS 27 Description of included reviews 27 Primary prevention interventions 31 Secondary prevention interventions 37 Certainty of the evidence 40 Effects of interventions 41 Ethics 50 DISCUSSION 52 Main results 52 Certainty of the evidence 52 Strengths and weaknesses 53 Potential biases in the overview process 54 Overall completeness and applicability of the evidence 54 Agreements or disagreements with other overviews of reviews 57 Applications for practice 57 Need for further research 57 CONCLUSION 59 REFERENCES 60 APPENDICES 71 1 Glossary 71 2 Search strategy 77 3 Excluded reviews and reasons for exclusion 88 4 Assessment of methodological quality 90 5 Ongoing reviews 92 6 Description of included reviews 93 7 GRADE evidence profiles 97 4 Table of contents Key messages Dementia is a syndrome characterised by deterioration in memory, Title: thinking, behaviour, and the ability to perform everyday activities, Primary and secondary which ultimately may lead to total dependence and death. Since the prevention interventions for cognitive decline and dementia world’s population is steadily growing older, the number of people with ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ dementia is also increasing. It is therefore of utmost importance to Type of publication: identify effective strategies to prevent or delay its onset. Overview of reviews ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ The key findings of this overview of reviews are based on evidence Doesn’t answer everything: from eight systematic reviews. The results for the single interventions No interventions targeting people with dementia. targeting cognitively healthy people suggest that compared to control: No health economic Antihypertensive drugs may lead to a slight decrease in incidence of evaluation. dementia in people with hypertension (low certainty of evidence). ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ Statin therapy probably leads to little or no difference on incidence Who is responsible for this publication? of dementia in people with, or at risk of, cardiovascular disease The Norwegian Institute of (moderate certainty). Public Health completed this Omega‐3 Fatty Acids (FAs) probably lead to little or no effect on assignment which was com‐ cognitive test scores (moderate to high certainty). missioned by the National Association of Public Health. Computerised cognitive training probably leads to a slight ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ improvement in cognitive test scores directly after the training When were the literature (moderate certainty). searched? Literature searches were Aerobic exercise may lead to little or no effect on cognitive test conducted in January 2016. scores (low certainty). ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ Peer referees: The results for the interventions targeting people with mild cognitive Øyvind Kirkevold, professor impairment suggest that compared to control: Seksjon for sykepleie Avdeling Cholinesterase inhibitors probably lead to a slight decrease in for helse, omsorg og sykepleie, dementia incidence, but to significantly more adverse events Norges Teknisk‐Naturviten‐ skaplige Universitet. (moderate certainty). Vitamin E probably leads to little or no difference in incidence of Veslemøy Egede‐Nissen, førs‐ Alzheimer’s dementia (moderate certainty). telektor, Institutt for sykepleie Omega‐3 FAs probably lead to little or no difference in cognitive og helsefremmende arbeid, Høgskolen i Oslo og Akershus test scores (moderate to high certainty). We did not find any reviews that evaluated the effects of interventions targeting more than one risk factor, and we can therefore not say anything about the combined effects of these interventions. 5 Key messages Executive summary Background Dementia is a chronic syndrome characterised by deterioration in memory, thinking, behaviour, and the ability to perform everyday activities, which often leads to total de‐ pendence and death. The world’s population is steadily growing older, and as dementia is more prevalent in people over 70, and increases with increasing age, the number of people with dementia is also increasing. In 2012, around 71, 000 people in Norway had a dementia diagnosis, which represents 1.6% of the total population. Objectives The aim of this overview of reviews was to answer the following two questions: 1) What is the documented effectiveness of interventions to prevent cognitive decline or incidence of dementia in cognitively healthy people (primary prevention), 2) What is the documented effectiveness of interventions to prevent (further) cognitive decline or progression to dementia in people with mild cognitive impairment (MCI) or other early symptoms or signs of dementia (secondary prevention)? Methods We conducted an overview of reviews in accordance with the Knowledge Centre’s handbook. We searched in eight databases up to February 2016 for reviews evaluating the effects of interventions to prevent or delay cognitive decline or dementia in people with or without MCI. Two people independently screened all titles and abstracts, re‐ viewed full texts, assessed review quality, and graded the certainty of the evidence us‐ ing the GRADE (Grading of Recommendations Assessment, Development and Evalua‐ tion) tool. One author extracted data, and another checked that it was correct. Results We included eight high quality reviews published between 2009 and 2016. Five of the reviews involved primary prevention interventions for cognitively healthy people. Three reviews included secondary prevention interventions for people with MCI or memory complaints. The reviews evaluated the effects of pharmacological therapies (3 reviews), dietary supplements (3 reviews), aerobic training (one review), and cognitive training (one review). The comparator in the latter two was either another active inter‐ vention or no intervention, and placebo in all the others. 6 Executive summary Primary prevention interventions Pharmacological therapies Antihypertensive drugs. We included one review (4 trials; n=15,936) concerned with the effects of antihypertensive drugs on dementia incidence in older people with hyperten‐ sion. The participants were recruited in Europe, North America, China, Australasia and Tunisia. The pooled result (Odds Ratio [OR]: 0.89 [0.74 to 1.07]) indicates that antihy‐ pertensive drugs may lead to a slight decrease in incidence of dementia, as compared to placebo, at 1.8 to 4.5 years follow up. Cholesterol lowering drugs (Statins). We included one review (2 trials; n=26,340) con‐ cerned with the effects of statins on incidence of dementia in cognitively healthy older people with evidence of, or at high risk of, cerebrovascular disease. The studies were conducted in the UK, Ireland, and the Netherlands. The result of one trial (OR: 1.00 [0.61 to 1.65], n=20,536) indicates that statin therapy may lead to little or no difference in incidence of dementia, as compared to placebo. The other trial (n= 5,804) reported no difference in cognitive test scores between groups at mean 3.2 years follow up. Dietary supplements Omega‐3 Fatty Acids (FAs). We included one review (3 trials; n= 4,080) which evaluated the effects of Omega‐3 FAs on cognitive decline in cognitively healthy participants. The pooled results (Standardised Mean Difference [SMD] [4 tests]: 0.06 higher to 0.04 lower scores; Mean Difference [MD] [2 tests]: 0.12 higher to 0.07 lower scores) suggest that Omega‐3 FA supplementation probably leads to little or no difference in overall cognitive function, as compared to placebo, at 6 to 40 months follow up. Aerobic exercise We included one review (12 trials; n= 754) which evaluated the effects of supervised aerobic exercise on cognitive function in cognitively healthy older people. The studies were conducted in the USA, Canada and France. The pooled
Recommended publications
  • Psychogenic and Organic Amnesia. a Multidimensional Assessment of Clinical, Neuroradiological, Neuropsychological and Psychopathological Features

    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?

    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

    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.
  • Alzheimer's Disease Prevention: from Risk Factors to Early Intervention

    Alzheimer's Disease Prevention: from Risk Factors to Early Intervention

    Crous-Bou et al. Alzheimer's Research & Therapy (2017) 9:71 DOI 10.1186/s13195-017-0297-z REVIEW Open Access Alzheimer’s disease prevention: from risk factors to early intervention Marta Crous-Bou1, Carolina Minguillón1, Nina Gramunt1,2 and José Luis Molinuevo1,2* Abstract Due to the progressive aging of the population, Alzheimer’s disease (AD) is becoming a healthcare burden of epidemic proportions for which there is currently no cure. Disappointing results from clinical trials performed in mild–moderate AD dementia combined with clear epidemiological evidence on AD risk factors are contributing to the development of primary prevention initiatives. In addition, the characterization of the long asymptomatic stage of AD is allowing the development of intervention studies and secondary prevention programmes on asymptomatic at-risk individuals, before substantial irreversible neuronal dysfunction and loss have occurred, an approach that emerges as highly relevant. In this manuscript, we review current strategies for AD prevention, from primary prevention strategies based on identifying risk factors and risk reduction, to secondary prevention initiatives based on the early detection of the pathophysiological hallmarks and intervention at the preclinical stage of the disease. Firstly, we summarize the evidence on several AD risk factors, which are the rationale for the establishment of primary prevention programmes as well as revising current primary prevention strategies. Secondly, we review the development of public–private partnerships for disease prevention that aim to characterize the AD continuum as well as serving as platforms for secondary prevention trials. Finally, we summarize currently ongoing clinical trials recruiting participants with preclinical AD or a higher risk for the onset of AD-related cognitive impairment.
  • Electrophysiological Studies of Cognitive Reappraisal Success and Failure in Amci

    Electrophysiological Studies of Cognitive Reappraisal Success and Failure in Amci

    brain sciences Article Electrophysiological Studies of Cognitive Reappraisal Success and Failure in aMCI Shasha Xiao 1, Yingjie Li 1,*, Meng Liu 2 and Yunxia Li 2,* 1 School of Communication and Information Engineering, Shanghai Institute for Advanced Communication and Data Science, Shanghai University, Shanghai 200444, China; [email protected] 2 Department of Neurology, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China; [email protected] * Correspondence: [email protected] (Y.L.); [email protected] (Y.L.) Abstract: Background: Although successful reappraisal relies on cognitive resources, how cogni- tive impairment affects brain processes related to cognitive reappraisal is not yet clear. Methods: Forty-four amnestic mild cognitive impairment (aMCI) subjects and 72 healthy elderly controls (HECs) were divided into the MCI-Failure (n = 23), MCI-Success (n = 21), HEC-Failure (n = 26), and HEC-Success (n = 46) groups according to changes in self-reported affect using reappraisal. All participants viewed 30 negative and 30 neutral images preceded by straightforward descriptions of these images and 30 negative images preceded by more neutral descriptions. Results: Reappraisal failure was found to be more common in people with MCI. Reappraisal failure is associated with altered neurophysiological indices of negative-reappraisal stimuli processing that are reflected in smaller theta responsivity to negative-reappraisal stimuli between 350–550 ms. The MCI-Success group showed enhanced LPP for negative-reappraisal stimuli from 1200 to 3500 ms, reflecting com- pensatory effort to complete the reappraisal task, while subjects in other groups showed reduced LPP for negative-reappraisal stimuli from 550 to 1200 ms. Conclusions: These findings deepen Citation: Xiao, S.; Li, Y.; Liu, M.; Li, Y.
  • The Role of Statins in Both Cognitive Impairment and Protection Against Dementia: a Tale of Two Mechanisms Bob G

    The Role of Statins in Both Cognitive Impairment and Protection Against Dementia: a Tale of Two Mechanisms Bob G

    Schultz et al. Translational Neurodegeneration (2018) 7:5 https://doi.org/10.1186/s40035-018-0110-3 REVIEW Open Access The role of statins in both cognitive impairment and protection against dementia: a tale of two mechanisms Bob G. Schultz, Denise K. Patten and Daniel J. Berlau* Abstract Nearly 30% of adults 40 years and older in the United States are on a statin. Their widespread use heightens the importance of careful consideration of their varied effects on the body. Although randomized controlled trials have not confirmed cognitive impairing effects with statins, continuing evidence suggests statins have the ability to cause reversible cognitive impairment in some patients. Paradoxically, statins have also been shown to decrease the risk of dementia, Alzheimer’s disease, and improve cognitive impairment in some cases. However, randomized controlled trials have similarly failed to find the beneficial effect. Supporting evidence for both claims is compelling whereas known limitations of the clinical trials may explain the lack of findings. This narrative review aims to explain why there is still controversy and how both effects can, and may, be possible. The mechanisms that have been hypothesized for each effect are seemingly independent from one another and may explain the contradicting results. Being mindful of the complex effects of statins, health care providers need to be able to identify patients who are at risk for or already experiencing cognitive impairment from statin use while also identifying those who could potentially decrease their risk of dementia with statins. Keywords: Statin, Cognition, Dementia, Memory, Cholesterol, Alzheimer’s disease, Vascular dementia, Neuroprotection Background people in the United States (10% of Americans) are cur- Cardiovascular disease (CVD) is the leading cause of rently on a statin with an estimated 56 million people morbidity and mortality in the United States and ele- (24% of Americans) eligible to consider a statin.
  • Cognitive Behavioral Therapy (CBT)

    Cognitive Behavioral Therapy (CBT)

    University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Educational Psychology Papers and Publications Educational Psychology, Department of 2010 Cognitive Behavioral Therapy (CBT) Rhonda Turner University of Nebraska-Lincoln Susan M. Swearer Napolitano University of Nebraska-Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/edpsychpapers Part of the Educational Psychology Commons Turner, Rhonda and Swearer Napolitano, Susan M., "Cognitive Behavioral Therapy (CBT)" (2010). Educational Psychology Papers and Publications. 147. https://digitalcommons.unl.edu/edpsychpapers/147 This Article is brought to you for free and open access by the Educational Psychology, Department of at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Educational Psychology Papers and Publications by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Published in Encyclopedia of Cross-Cultural School Psychology (2010), p. 226-229. Copyright 2010, Springer. Used by permission. Cognitive Behavioral Therapy (CBT) Therapy, Rational Living Therapy, Schema Focused Therapy and Dialectical Behavior Rhonda Turner and Susan M. Swearer Therapy. Department of Educational Psychology, Uni- History of CBT versity of Nebraska-Lincoln, Lincoln, Nebraska, A precursor to the development of CBT U.S.A. was the emergence of Albert Bandura’s So- cial Learning Theory. Unlike the prevail- Cognitive Behavioral Therapy (CBT) is a ing psychodynamic or behavioral views form of psychotherapy that focuses on the of psychological disturbance, Bandura role of cognition in the expression of emo- viewed people as consciously and actively tions and behaviors. CBT assumes that mal- interacting cognitively with their environ- adaptive feelings and behaviors develop ments. He introduced the notion that cog- through cognitive processes which evolve nitive mediation occurs in the stimulus-re- from interactions with others and experi- sponse cycle of human behavior.
  • Can the Treatment of Hypertension in the Middle-Aged Prevent Dementia in the Elderly?

    Can the Treatment of Hypertension in the Middle-Aged Prevent Dementia in the Elderly?

    High Blood Press Cardiovasc Prev DOI 10.1007/s40292-016-0144-5 REVIEW ARTICLE Can the Treatment of Hypertension in the Middle-Aged Prevent Dementia in the Elderly? 1 1 1 1 Antonio Coca • Eila Monteagudo • Mo´nica Dome´nech • Miguel Camafort • Cristina Sierra1 Received: 16 February 2016 / Accepted: 28 March 2016 Ó Springer International Publishing Switzerland 2016 Abstract Hypertension, one of the main risk factors for 1 Introduction cardiovascular disease, is thought to play a crucial role in the pathophysiology of cognitive impairment. Studies have Cardiovascular disease (CVD) remains the leading cause of associated hypertension with subjective cognitive failures death worldwide. The Global Burden of Disease study and objective cognitive decline. Subjective cognitive fail- estimated that 29.6 % of all deaths were caused by CVD in ures may reflect the early phase of a long pathological 2010, more than all communicable, maternal, neonatal and process leading to cognitive decline and dementia that has nutritional disorders combined, and twice the number of been associated with hypertension and other cardiovascular deaths caused by cancer [1]. The burden of CVD in Europe risk factors. The underlying cerebral structural change remains heavy, although the prevalence varies dramatically associated with cognitive decline may be a consequence of among countries. More than four million Europeans die of the cerebral small-vessel disease induced by high blood CVD every year, and many more are hospitalized after pressure and may be detected on magnetic resonance acute episodes or are treated for chronic CVD [2]. The imaging as white matter hyperintensities, cerebral percentage of the population affected by hypertension, one microbleeds, lacunar infarcts or enlarged perivascular of the main risk factors for CVD, is remarkably high and, spaces.
  • Effect of Phosphatidylserine Administration on Symptoms of Attention-Deficit/Hyperactivity Disorder in Children S

    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

    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.
  • FAP) in Ibero-America: Review of Current Status and Some Proposals

    FAP) in Ibero-America: Review of Current Status and Some Proposals

    INTERNATIONAL JOURNAL OF BEHAVIORAL CONSULTATION AND THERAPY ©2012, ALL RIGHTS RESERVED 2012, VOL. 7, NO. 2–3 ISSN: 1555–7855 Functional Analytic Psychotherapy (FAP) in Ibero-America: Review of current status and some proposals Amanda Muñoz-Martínez, Mónica Novoa-Gómez, & Rochy Vargas Gutiérrez H Abstract Functional Analytic Psychotherapy (FAP) has been making an important rise in Ibero-America in recent years. This paper presents a review of different contributions, problems and some proposals Three principal topics are reviewed: (a) general characteristics and theoretical bases of FAP, (b) the uses of FAP and its relationship with other therapies, and (c) FAP´s empirical research. A number V in Ibero-America emphasize epistemological and conceptual aspects of FAP and its relationship with other interventions from Third Wave Behavior Therapies, especially Acceptance and Commitment Therapy (ACT). With regard to the third topic, FAP is an effective therapeutic perspective, but it is important to increase the research in this area. Keywords Functional Analytic Psicotherapy, Third Wave Behavior Therapy, Behavioral Analysis and Clinical Psychology n recent years, the Third Wave Behavior Therapies have made ciples and therapeutic rules described by Kohlenberg and Tsai Ian important impact on the field of clinical psychology, becom- (1991). ing an alternative to treating clients with personality disorders As indicated by Parada, Sarmiento and Urbina (2008), FAP is or serious behavioral problems, difficulties not as frequently based on the findings of the Experimental Analysis of Behavior, focused on by cognitive-behavioral therapists (Rodríguez- from which established the principles of radical behaviorism and Naranjo, 1998). The third generation behavior therapies provide based on which they derived both as Applied Behavioral Analy- contextual explanations for clinical problems, fostering more sis and Clinical Behavioral Analysis (Dougher & Hayes, 1999).

  • Chapter 8 Neuropsychiatric Disorders, Including Dementia – Prevention Is Better Than Cure

    Chapter 8 Neuropsychiatric disorders, including dementia – prevention is better than cure I look up to the hills, but where will my help really come from? My help will come from the Lord, the Creator of heaven and earth. He will not let you fall. Your Protector will not fall asleep. Israel’s Protector does not get tired. He never sleeps. The Lord is your Protector. The Lord stands by your side, shading and protecting you. The sun cannot harm you during the day, and the moon cannot harm you at night. The Lord will protect you from every danger. He will protect your soul. The Lord will protect you as you come and go, both now and forever. Psalms 121: 1-8 ERV Chapter 8 Neuropsychiatric disorders, including dementia – prevention is better page 197 than cure Figure 8-1 Relationships between autoimmune diseases and dementia Autoimmune conditions and genetic factors can cause vascular dementia Chronic inflammation of brain cells due to Autoimmune conditions various autoimmune conditions leads to Lewy Vascular Multi- dementia Body Infarct Rheumatoid Arthritis dementia Consequences Underactive thyroid Look after yourself Systemic Lupus Immune system attacking central nervous system (CNS) Adrenal insufficiency Exercise, healthy diet and avoiding stress reduces inflammation of brain cells Brain cell death, plaque formation, leading to Type 1 and 2 diabetes SACD / MS-like presentation Less chance of developing dementia due to routine use of anti-inflammatories. Psoriasis CVD risks higher For example:aspirin and non steroidal anti- inflammatories Chapter 8 Neuropsychiatric disorders, including dementia – prevention is better page 198 than cure Vitamin B12 deficiency and neuropsychiatric symptoms – an overview Neuropsychiatric symptoms are among the most common presenting signs of vitamin B12 deficiency yet the diagnosis is often missed because of lack of awareness of this condition among clinicians (Lachner et al., 2012).