Memory Care: Best Practice Documentation

Total Page:16

File Type:pdf, Size:1020Kb

Memory Care: Best Practice Documentation Memory Care: Best Practice Documentation 1. SOC Homebound Status: a. If Mini-Cog score is 0-3, SELECT nervous system involvement under “Body Structure Impairment.” (See 4b note regarding consideration of reversible deliriums.) b. If Mini-Cog score is 0-2, SELECT Mental Function Impairment (Movement related, Sensory, Mental, Voice and Speech) under “Body Function Impairment.” (Note: Be as specific as possible; also, there can be multiple body function impairments related to the nervous system structural impairment.) c. Do not forget to assess for other Body Structure/Function impairments that may be independent of cognitive impairment. 2. Pain: If Mini-Cog score is 0-2, PAID-AD scale should be used to measure pain. If patient has impaired executive function, they are not likely able to adequately recall and quantify pain over a 24 hour period. Use of this tool helps to support skill and medical necessity. a. Document in “O” (Observation) section of nursing note or in “A” (Assessment) section of therapy note OR free-texted in physical assessment section under “other”. b. Keep in mind: in conditions such as Parkinson’s Disease where visuospatial awareness/perceptual awareness skill deficits are highly common in disease process (even in patients with seemingly WNL memory and problem solving): these deficits impact a patient’s ability to adequately quantify pain, even if cognition seems completely normal. c. “Vision” deficits in Parkinson’s sometimes mask deficits in visuospatial/perceptual awareness. Example: If a patient is wanting to sit in a trash bin vs chair, consider possible impairment of relationship between self and environment. 3. M1700: If Mini-Cog Score is 0-2, M1700 score should likely be 2,3,4, but should be individually assessed. a. Remember that a score of “4” refers to cognitive function that is totally dependent due to disturbances such as constant disorientation OR coma OR persistent vegetative state OR delirium. Consider: Does this patient have the ability to improve their cognitive function and functional scores, considering the disease process? Is patient disoriented to their own deficits, i.e. time, situations, CGs, current environment? Will the patient continue to need constant supervision ongoing due to their cognitive status/diagnosis? b. Consider reversible deliriums, i.e, post-op confusion due to anesthesia and opioid pain meds. This should be noted in the assessment portion of the EMR, and would not “count against” the audit score. However, if it is not clearly noted, the clinician may benefit from education here. The point is for all of us to get in the habit of doing a “5 (more or less) Why” process. Why is the Mini-Cog score less than 4? Our POC can then reflect appropriate interventions. 4. PHQ-2 Depression Screening: If Mini-Cog Score is 0-3, answer to question “Is the patient physically and cognitively able to be screened for depression using PHQ-2” is likely to be “No.” Consider executive function impairments and ability to adequately recall and quantify responses to screening questions of PHQ-2 “Over the last two weeks, how often have you been bothered by any of the following problems?” If the patient cannot remember 3 words in 3 minutes, how can they accurately recall the last 2 weeks to report on the PHQ-2? 5. Add-On Evaluations: If Mini-Cog score is 3 or less, physician should be contacted with results of Mini-Cog and request for referral to OT or ST. 6. Cognitive Staging: If Mini-Cog score is 3 or less, patient should be staged with CATG, ALLEN, RTI, GDS or other standardized tool. Stage should be based upon results of two different assessment tools. a. Mini-cog score of 3 indicates possible mild cognitive impairment. Further assessment needed. Recommend assessment with the MoCA, which has higher sensitivity and specificity for MCI. b. Add Snapshot note to reflect stage and which tool was used. 7. Memory Care Pathways: Should be used by both NURSING and THERAPY. a. TAKE CREDIT if you have to modify how you teach your patient Consider: use of spaced retrieval, how you approach patient, need for CG education regarding dementia medication/disease process. Example: Do you need to joke with patient first or pretend that you just so happened to run into them and they just so happen to be your favorite person in the world, before you can walk them? This is all part of a memory care approach!!! b. SLPs-Remember that “executive function” pathways may be selected only for Mild Cognitive Impairment, or Allen Level 5/GDS 2 or 3. Use of executive function implies cognitive rehabilitation, which Medicare and other payors consider to be unproven . 8. Diagnosis: Document dementia related dx: Carefully probe family/facility/MD if specific diagnosis has ever been documented or investigated. Symptom codes may be used. See coding information below. 9. HH Utilization: Be sure that nursing and therapy visit numbers are appropriate based on C/F scores, PLOF, and medical record. Consider staggering disciplines as appropriate to optimize utilization but also allow success of meeting each discipline’s goals – who really needs to be in there first? Should all disciplines be in simultaneously? In patients with cognitive impairment, these codes are acceptable to support medical necessity. 1. Verify through discipline-specific Local Coverage Determination as applicable available at cms.gov 2. Supporting documentation required for all (H and P, etc. for diagnoses; collaboration with physician for symptom codes) F01.xx Vascular dementia (Code 169.31 first, followed by F01.5+) F02.xx Dementia in other diseases classified elsewhere. Must code underlying pathology first, i.e. Alzheimers, Creutzfeldt-Jakob disease, DLB, Dementia with Parkinsonism F03.xx Dementia unspecified F03.90 Unspecified dementia without behavioral disturbances F03.91 Unspecified dementia with behavioral disturbances. G30.x Alzheimer’s disease G31.x G31.1 Senile degeneration, non-alcohol related G31.0 Picks disease G31.2 Degeneration of N.S. due to alcohol G31.83 DLB G31.84 MCI R41.0 Confusion (with no current diagnosis) R41.3 Memory loss (with no current diagnosis) R41.81 Cognitive decline (with no current diagnosis) R41.84 Other specified cognitive deficit, i.e., R41.848 Attention and concentration deficit R41.841 Cognitive communication deficit R41.842 Visuospatial deficit R41.843 Psychomotor deficit R41.844 Frontal lobe and executive function deficit Only code a specific pathology, i.e., Alzheimer’s, Vascular, Lewy Body, etc., with supporting documentation from physician included in EMR. Symptom codes, such as R41.84, can be used with supporting therapist assessment documentation. As always, coordinate with referring physician. These are guidelines only. Specific questions should be directed to your PRQI or BD. .
Recommended publications
  • Neuroinflammation and Functional Connectivity in Alzheimer's Disease: Interactive Influences on Cognitive Performance
    Research Articles: Neurobiology of Disease Neuroinflammation and functional connectivity in Alzheimer's disease: interactive influences on cognitive performance https://doi.org/10.1523/JNEUROSCI.2574-18.2019 Cite as: J. Neurosci 2019; 10.1523/JNEUROSCI.2574-18.2019 Received: 5 October 2018 Revised: 25 March 2019 Accepted: 11 April 2019 This Early Release article has been peer-reviewed and accepted, but has not been through the composition and copyediting processes. The final version may differ slightly in style or formatting and will contain links to any extended data. Alerts: Sign up at www.jneurosci.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Copyright © 2019 Passamonti et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. 1 Neuroinflammation and functional connectivity in Alzheimer’s disease: 2 interactive influences on cognitive performance 3 4 L. Passamonti1*, K.A. Tsvetanov1*, P.S. Jones1, W.R. Bevan-Jones2, R. Arnold2, R.J. Borchert1, 5 E. Mak2, L. Su2, J.T. O’Brien2#, J.B. Rowe1,3# 6 7 Joint *first and #last authorship 8 9 10 Authors’ addresses 11 1Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 12 2Department of Psychiatry, University of Cambridge, Cambridge, UK 13 3Cognition and Brain Sciences Unit, Medical Research Council, Cambridge,
    [Show full text]
  • Neurocognitive and Functional Impairment in Adult and Paediatric Tuberculous Meningitis [Version 1; Peer Review: 2 Approved]
    Wellcome Open Research 2019, 4:178 Last updated: 20 MAY 2021 REVIEW Neurocognitive and functional impairment in adult and paediatric tuberculous meningitis [version 1; peer review: 2 approved] Angharad G. Davis 1-3, Sam Nightingale4, Priscilla E. Springer 5, Regan Solomons 5, Ana Arenivas6,7, Robert J. Wilkinson 2,8,9, Suzanne T. Anderson10,11*, Felicia C. Chow 12*, Tuberculous Meningitis International Research Consortium 1University College London, Gower Street, London, WC1E 6BT, UK 2Francis Crick Institute, Midland Road, London, NW1 1AT, UK 3Institute of Infectious Diseases and Molecular Medicine. Department of Medicine, University of Cape Town, Observatory, 7925, South Africa 4HIV Mental Health Research Unit, University of Cape Town,, Observatory, 7925, South Africa 5Department of Paediatrics and Child Health, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa 6The Institute for Rehabilitation and Research Memorial Hermann, Department of Rehabilitation Psychology and Neuropsychology,, Houston, Texas, USA 7Baylor College of Medicine, Department of Physical Medicine and Rehabilitation, Houston, Texas, USA 8Department of Infectious Diseases, Imperial College London, London, W2 1PG, UK 9Wellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Diseases and Molecular Medicine at Department of Medicine, University of Cape Town, Observatory, 7925, South Africa 10MRC Clinical Trials Unit at UCL, University College London, London, WC1E 6BT, UK 11Evelina Community, Guys and St Thomas’
    [Show full text]
  • Cognitive Impairment/Dementia – Summary
    Cognitive Impairment/Dementia Care Guide December 2014 SUMMARY GOALS Early identification of affected patients Prevention of victimization Reduce symptom severity Improve quality of life ALERTS Victimized patients Increase in rules violation behaviors Worsening personal hygiene Anxiety and agitation, especially at night Complete Advance Directive-Durable Power of Attorney for Health Care (DPAHC) early in course of disease Prison environment may mask symptoms DIAGNOSTIC CRITERIA/EVALUATION Definition - Mild Cognitive Impairment (MCI) Cognitive decline greater than expected for age and education level without significantly interfering with activities of daily life. Evidence of memory impairment Preservation of general cognitive and functional abilities Absence of diagnosed dementia Definition - Dementia Cognitive impairment with: significant decline from previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, social cognition, perceptual motor) interference with independence in daily activities Not occurring exclusively with delirium Not better explained by another disorder Neurobehavioral abnormalities History - MCI and Dementia patients may have similar historical findings which contribute to the ultimate diagnosis: Poor adherence to rules and routines Personal hygiene problems Impaired comprehension History of head injury, substance abuse, or other medical contributors Differential Diagnosis – Mild Cognitive Impairment (MCI) Medication
    [Show full text]
  • The Cognitive Basis of Dyslexia in School-Aged Children: a Multiple Case
    The cognitive basis of dyslexia The cognitive basis of dyslexia in school-aged children: a multiple case study in a transparent orthography Agnieszka Dębska1*, Magdalena Łuniewska1,2*, Julian Zubek2, Katarzyna Chyl1, Agnieszka Dynak1,2, Gabriela Dzięgiel-Fivet1, Joanna Plewko1, Katarzyna Jednoróg1, Anna Grabowska3 * these authors contributed equally to the paper 1Laboratory of Language Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland 2 Faculty of Psychology, University of Warsaw, Warsaw, Poland 3Faculty of Psychology, SWPS University of Social Sciences and Humanities, Warsaw, Poland Laboratory of Language Neurobiology Nencki Institute of Experimental Biology, Polish Academy of Sciences ul. Pasteura 3, 02-093 Warszawa, Poland Conflict of Interest Statement None of the authors has to declare a conflict of interest. Supplementary materials 1. Tables and Figures 2. Supplementary materials S1, S2, S3 and S4 1 The cognitive basis of dyslexia The cognitive basis of dyslexia in school-aged children: a multiple case study in a transparent orthography Research highlights ● This study tested the (co)existence of cognitive deficits in dyslexia in phonological awareness, rapid naming, visual and selective attention, auditory skills, and implicit learning. ● The most frequent deficits in Polish children with dyslexia included a phonological (51%) and a rapid naming deficit (26%), which coexisted in 14% of children. ● Despite the severe reading impairment, 26% of children with dyslexia presented no deficits in measured cognitive abilities. ● RAN explains reading skills variability across the whole spectrum of reading ability; phonological skills explain variability best among average and good readers but not poor readers. Abstract This study focused on the role of numerous cognitive skills such as phonological awareness (PA), rapid automatized naming (RAN), visual and selective attention, auditory skills, and implicit learning in developmental dyslexia.
    [Show full text]
  • Mild Cognitive Impairment (Mci) and Dementia February 2017
    CareCare Process Process Model Model FEBRUARY MONTH 2015 2017 DIAGNOSIS AND MANAGEMENT OF Mild Cognitive Impairment (MCI) and Dementia minor update - 12 / 2020 The Intermountain Cognitive Care Development Team developed this care process model (CPM) to improve the diagnosis and treatment of patients with cognitive impairment across the staging continuum from mild impairment to advanced dementia. It is primarily intended as a tool to assist primary care teams in making the diagnosis of dementia and in providing optimal treatment and support to patients and their loved ones. This CPM is based on existing guidelines, where available, and expert opinion. WHAT’S INSIDE? Why Focus ON DIAGNOSIS AND MANAGEMENT ALGORITHMS OF DEMENTIA? Algorithm 1: Diagnosing Dementia and MCI . 6 • Prevalence, trend, and morbidity. In 2016, one in nine people age 65 and Algorithm 2: Dementia Treatment . .. 11 older (11%) has Alzheimer’s, the most common dementia. By 2050, that Algorithm 3: Driving Assessment . 13 number may nearly triple, and Utah is expected to experience one of the Algorithm 4: Managing Behavioral and greatest increases of any state in the nation.HER,WEU One in three seniors dies with Psychological Symptoms . 14 a diagnosis of some form of dementia.ALZ MCI AND DEMENTIA SCREENING • Costs and burdens of care. In 2016, total payments for healthcare, long-term AND DIAGNOSIS ...............2 care, and hospice were estimated to be $236 billion for people with Alzheimer’s MCI TREATMENT AND CARE ....... HUR and other dementias. Just under half of those costs were borne by Medicare. MANAGEMENT .................8 The emotional stress of dementia caregiving is rated as high or very high by nearly DEMENTIA TREATMENT AND PIN, ALZ 60% of caregivers, about 40% of whom suffer from depression.
    [Show full text]
  • Impacts of Cognitive Impairment for Different Levels and Causes of Traumatic Brain Injury, and Education Status in TBI Patients
    Dement Neuropsychol 2018 December;12(4):415-420 Original Article http://dx.doi.org/10.1590/1980-57642018dn12-040012 Impacts of cognitive impairment for different levels and causes of traumatic brain injury, and education status in TBI patients Minoo Sharbafshaaer1 ABSTRACT. Traumatic brain injury (TBI) is one of main causes of death and disability among many young and old populations in different countries. Objective: The aim of this study were to consider and predict the cognitive impairments according to different levels and causes of TBI, and education status. Methods: The study was performed using the Mini-Mental State Examination (MMSE) to estimate cognitive impairment in patients at a trauma center in Zahedan city. Individuals were considered eligible if 18 years of age or older. This investigation assessed a subset of patients from a 6-month pilot study. Results: The study participants comprised 66% males and 34% females. Patient mean age was 32.5 years and SD was 12.924 years. One-way analysis of variance between groups indicated cognitive impairment related to different levels and causes of TBI, and education status in patients. There was a significant difference in the dimensions of cognitive impairments for different levels and causes of TBI, and education status. A regression test showed that levels of traumatic brain injury (β=.615, p=.001) and education status (β=.426, p=.001) predicted cognitive impairment. Conclusion: Different levels of TBI and education status were useful for predicting cognitive impairment in patients. Severe TBI and no education were associated with worse cognitive performance and higher disability. These data are essential in terms of helping patients understand their needs.
    [Show full text]
  • Clinical Treatment Guidelines for Alcohol and Drug Clinicians
    Clinical Treatment Guidelines for Alcohol and Drug Clinicians Co-occurring acquired brain injury / cognitive impairment and alcohol and other drug use disorders Richard Cash Amanda Philactides 2006 State of Victoria. Produced with permission. This work is copyright. Apart from any use as permitted under the Copyright Act 1968, no part may be reproduced by any process without permission. Copyright enquiries can be made to the Communications and Publications Unit, Turning Point Alcohol and Drug Centre, 54-62 Gertrude St, Fitzroy, Victoria, 3065, Australia. Published by Turning Point Alcohol and Drug Centre under funding provided by the Drug Treatment Services Unit, Department of Human Services, Victoria. The views expressed in this material are not necessarily those of the Victorian Government. The correct citation for this publication is: Cash, R. & Philactides, A. (2006). Clinical Treatment Guidelines for Alcohol and Drug Clinicians. No. 14: Co-occurring acquired brain injury / cognitive impairment and alcohol and other drug use disorders. Fitzroy, Victoria: Turning Point Alcohol and Drug Centre Inc. ISBN: ?? Introduction In late 2005 The Department Of Human Services Drug Policy Branch commissioned Turning Point Alcohol and Drug Centre to develop a set of clinical treatment guidelines for clinicians working with clients with comorbid acquired brain injury (ABI) and alcohol and drug use disorder. The process of development for these guidelines has involved a widespread literature review, consultation with a key-informant group comprising brain injury and alcohol and drug specialists from a variety of backgrounds, and consultation with the state-wide group of alcohol and drug and ABI clinicians and consultants. This clinical treatment guideline is made up of four parts: a literature review, a key informants issues paper, an assessment guide and a set of treatment resources.
    [Show full text]
  • Negative Symptom and Cognitive Deficit Treatment Response In
    Negative Symptom and Cognitive Deficit Treatment Response in Schizophrenia This page intentionally left blank Negative Symptom and Cognitive Deficit Treatment Response in Schizophrenia Edited by RICHARD S. E. KEEFE, PH.D. JOSEPH P. M CEVOY, M.D. Washington, DC London, England Note: The authors have worked to ensure that all information in this book concerning drug dosages, schedules, and routes of administration is accurate as of the time of publication and consistent with standards set by the U.S. Food and Drug Administration and the general medical community. As medical research and practice advance, how- ever, therapeutic standards may change. For this reason and because human and me- chanical errors sometimes occur, we recommend that readers follow the advice of a physician who is directly involved in their care or the care of a member of their family. Books published by the American Psychiatric Press, Inc., represent the views and opinions of the individual authors and do not necessarily represent the policies and opinions of the Press or the American Psychiatric Association. Copyright © 2001 American Psychiatric Press, Inc. ALL RIGHTS RESERVED Manufactured in the United States of America on acid-free paper 040302014321 First Edition American Psychiatric Press, Inc. 1400 K Street, N.W., Washington, DC20005 www.appi.org Library of Congress Cataloging-in-Publication Data Negative symptom and cognitive deficit treatment response in schizophrenia / edited by Richard S. E. Keefe, Joseph P. McEvoy. — 1st ed. p. ; cm. Includes bibliographic references and index. ISBN 0-88048-785-2 (alk. paper) 1. Schizophrenia—Diagnosis. 2. Schizophrenia—Chemotherapy. 3. Cognition disorders—Chemotherapy.
    [Show full text]
  • Cognitive Deficits in Myopathies
    International Journal of Molecular Sciences Review Cognitive Deficits in Myopathies Eleni Peristeri 1, Athina-Maria Aloizou 1, Paraskevi Keramida 1, Zisis Tsouris 1, Vasileios Siokas 1, Alexios-Fotios A. Mentis 2,3 and Efthimios Dardiotis 1,* 1 Department of Neurology, Laboratory of Neurogenetics, Faculty of Medicine, University of Thessaly, University Hospital of Larissa, PC 41110 Larissa, Greece; [email protected] (E.P.); [email protected] (A.-M.A.); [email protected] (P.K.); [email protected] (Z.T.); [email protected] (V.S.) 2 Public Health Laboratories, Hellenic Pasteur Institute, PC 11521 Athens, Greece; [email protected] 3 Department of Microbiology, Faculty of Medicine, University of Thessaly, University Hospital of Larissa, PC 41110 Larissa, Greece * Correspondence: [email protected]; Tel.: +30-241-350-1137 Received: 7 April 2020; Accepted: 25 May 2020; Published: 27 May 2020 Abstract: Myopathies represent a wide spectrum of heterogeneous diseases mainly characterized by the abnormal structure or functioning of skeletal muscle. The current paper provides a comprehensive overview of cognitive deficits observed in various myopathies by consulting the main libraries (Pubmed, Scopus and Google Scholar). This review focuses on the causal classification of myopathies and concomitant cognitive deficits. In most studies, cognitive deficits have been found after clinical observations while lesions were also present in brain imaging. Most studies refer to hereditary myopathies, mainly Duchenne muscular dystrophy (DMD), and myotonic dystrophies (MDs); therefore, most of the overview will focus on these subtypes of myopathies. Most recent bibliographical sources have been preferred. Keywords: myopathies; dystrophies; cognitive deficits; behavioral indices; brain imaging indices 1. Introduction Myopathies represent a wide spectrum of heterogeneous diseases mainly characterized by the abnormal structure or functioning of skeletal muscle [1]; they can be hereditary or acquired, and can also manifest during the course of endocrine, autoimmune or metabolic disorders.
    [Show full text]
  • Cognitive Deficits and Alcohol Dependence Syndrome – a Paradigm Relationship
    RESEARCH ARTICLE COGNITIVE DEFICITS AND ALCOHOL DEPENDENCE SYNDROME – A PARADIGM RELATIONSHIP Madhusudhan S, Anitha A, Sharon Ruth Associate Professor, Department of Psychiatry, BMCRI, Bangalore, India. Junior Resident, Department of Psychiatry, BMCRI, Bangalore, India. Clinical Psychologist, Department of Psychiatry, BMCRI, Bangalore, India. Abstract Objectives: Background- Chronic alcohol use causes not only physical consequences but causes cognitive deficits also. 50 and 80% of the Alcohol dependent syndrome patients present with cognitive deficits. These cognitive deficits will significantly contribute to poor functional outcomes which lead to reduced health related quality of life. Objectives- To assess Cognitive deficits in Alcohol Dependent syndrome (ADS). To find the relationship between early onset of alcohol use, duration of Alcohol use and large quantity of alcohol use with Cognitive deficit pattern. Method- A cross sectional study was done on 38 patients with ADS, aged 18- 45 years, education ≥7th std, with no major psychiatric or medical co- morbidities. AUDIT scale was administered to look for dependence pattern, CIWA scale was applied to look for withdrawal symptoms. MoCA scale was applied to screen for cognitive impairment in patient with MMSE score (25 and above). In subjects with cognitive impairment on MoCA scale (25 and below), neuropsychological assessment was done using neuropsychological battery of test from NIMHANS Neuropsych battery standardised on Indian Population. Results- There was impairment in the Cognitive domains as follows, speed of processing (BACS - 100%), attention (DF- 97%) working memory (DF-97%, DB-100%, LNS - 84%), visual memory (100%), visuo- spatial memory (78%), executive functions (CT2 -92%), reasoning and problem solving (maze- 81%) in majority and a significant relation between early onset of alcohol use, duration of Alcohol use.
    [Show full text]
  • The Cognitive Deficits Responsible for Developmental Dyslexia: Review of Evidence for a Visual Attentional Deficit Hypothesis
    The cognitive deficits responsible for developmental dyslexia: Review of evidence for a visual attentional deficit hypothesis. Sylviane Valdois, Marie-Line Bosse, Marie-Josèphe Tainturier To cite this version: Sylviane Valdois, Marie-Line Bosse, Marie-Josèphe Tainturier. The cognitive deficits responsible for developmental dyslexia: Review of evidence for a visual attentional deficit hypothesis.. Dyslexia, Wiley, 2004, 10, pp.339-363. hal-00826009 HAL Id: hal-00826009 https://hal.archives-ouvertes.fr/hal-00826009 Submitted on 25 May 2013 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. DYS : 284 PROD.TYPE: COM ED: UMA PAGN: SOLLY SCAN: XXX pp.1^25 (col.¢g.: NIL) 3B2 1 & 3 The Cognitive Deficits 5 Responsible for 7 Developmental Dyslexia: 9 Review of Evidence for a 11 Selective Visual Attentional 13 F Disorder 15 Sylviane Valdois1,*, Marie-Line Bosse1 and Marie-Joseephe" 17 Tainturier2 1 Laboratoire de Psychologie et Neuro-Cognition (UMR 5105 CNRS), Universite! Pierre 19 Mendees" France, Grenoble, France 2 School of Psychology, University of Wales, Bangor, UK 21 23 There is strong converging evidence suggesting that developmental dyslexia stems from a phonological processing deficit. However, 25 this hypothesis has been challenged by the widely admitted heterogeneity of the dyslexic population, and by several reports of 27 dyslexic individuals with no apparent phonological deficit.
    [Show full text]
  • Assessing and Measuring Cognitive Function in Major Depressive Disorder
    Downloaded from http://ebmh.bmj.com/ on July 14, 2017 - Published by group.bmj.com Assessing and measuring cognitive function in major depressive disorder Renee-Marie Ragguett,1 Danielle S Cha,1,2 Ron Kakar,1 Joshua D Rosenblat,1,3 Yena Lee,1 Roger S McIntyre1,3,4 1Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, Ontario, Canada; 2Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada; 3Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; 4Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada Correspondence to Dr Roger S McIntyre, Departments of Psychiatry and Pharmacology, University of Toronto, Toronto, Ontario, Canada; Mood Disorders Psychopharmacology Unit, University Health Network, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8; [email protected] ABSTRACT Cognitive dysfunction is a major component of major depressive disorder (MDD). No ‘gold-standard’ tool exists for the assessment of cognitive dysfunction for adults with MDD. The use of measurement-based care to improve treatment outcomes invites the need for a systematic screening, evaluation and measurement tool. The aim herein was to provide a succinct summary of literature documenting clinical implication of cognitive dysfunction in MDD, and a review of available screening, diagnostic and measurement tools for cognitive dysfunction in MDD is provided. We also take the opportunity to introduce a screening tool (ie, the THINC-it tool) targeted at addressing the unmet needs. We found that there are limitations to the current measurement scales; for example, many are not targeted for MDD and not all digitally available tests are free of charge. Furthermore, the spectrum of cognitive dysfunction in MDD is poorly represented by the existing tests and as such, there is a lack of sensitivity in the ability to screen a patient with MDD for a cognitive dysfunction.
    [Show full text]