DOCSLIB.ORG

Apraxia of Speech and Nonverbal School-Aged Children with Autism I

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Apraxia of Speech and Nonverbal School-Aged Children with Autism I Topics Apraxia of Speech and Nonverbal School-Aged Children with Autism I. Introduction A. Apraxia of Speech Lawrence D. Shriberg B. The CAS/ASD Hypothesis II. Overviews Waisman Center A. Speech Sound Disorders (SSD) University of Wisconsin-Madison B. Childhood Apraxia of Speech (CAS) III. Speech Research in ASD Nonverbal School-aged Children with Autism A. Verbal ASD: Findings NIH Workshop, Bethesda, MD, April 13-14, 2010 B. Nonverbal ASD: Perspectives Locus of Apraxia of Speech in a Four-Phase Speech Processing Frameworka Apraxia of Speech in an Adolescent with Classic Galactosemia Encoding (auditory-perceptual) Memorial (storage, retrieval) Transcoding (planning-programming) Execution (neuromotor) aAfter Van der Merwe (2009) Multisyllabic Words Task 2 (MWT2) What is Apraxia of Speech? 1. emphasis 11. consciousness 2. probably 12. suspicious Say the following as quickly as you can: 3. sympathize 13. municipal 4. terminal 14. orchestra 5. synthesis 15. specific Six thick thistle sticks 6. especially 16. statistics Six thick thistle sticks 7. peculiar 17. fire extinguisher Six thick thistle sticks 8. skeptical 18. Episcopal church 9. fudgesicle 19. statistician 10. vulnerable 20. Nicaragua 1 Topics The CAS/ASD Hypothesisa I. Introduction CAS is a sufficient cause for: A. Apraxia of Speech B. The CAS/ASD Hypothesis Weak version: speech and prosody- II. Overviews voice deficits in persons with verbal ASD A. Speech Sound Disorders (SSD) B. Childhood Apraxia of Speech (CAS) Strong version: failure to acquire speech in III. Speech Research in ASD persons with nonverbal ASD A. Verbal ASD: Findings aChildhood Apraxia of Speech (CAS) is the term adopted in the ASHA (2007) report; Developmental Verbal Dyspraxia (DVD) continues to be B. Nonverbal ASD: Perspectives used in medical literatures and in most other countries Motivation for the Motivation for the CAS/ASD Hypothesis CAS/ASD Hypothesis Persons with ASD reportedly have praxic movement disorders Persons with ASD reportedly have significantly reduced (see elsewhere this workshop), implicating planning/programming early nonverbal oral behaviors presumed to share deficits, the presumed speech processing locus of CAS neural substrates with speech and reported to predict speech fluency (Gernsbacher et al., 2008; Iverson & Speech acquisition and performance researchers argue Wozniak, 2007; Page & Boucher, 1998; Seal & Bonvillion, from a number of perspectives that speech is domain 1997; see elsewhere this workshop) specific (e.g., Kent, 2000, 2004, 2010; McCauley et al., 2009; Potter et al., 2009; Weismer, 2006; Ziegler, 2002, 2008) CAS is the only subtype of speech disorder in which the onset of speech (compared to speech precision or Persons with ASD reportedly have imitative deficits (see stability) is delayed (Shriberg, 2010a; however, see IIA) elsewhere this workshop), with implications for motor processes in speech acquisition CAS and ASD were both implicated in recent genomic findings linking FOXP2 to CNTNAP2 (Poot et al., 2010; Vernes et al., Imitation deficits are not a core speech-processing 2008); CAS and ASD overlaps also reported for other candidate feature of CAS in frameworks such as in the widely genes and regions of interest accepted van der Merwe framework (2009); see also Kappes et al. (2009) and Terband and Maassen (2010) History of Classification Terms for SSD Topics of Known and Idiopathic Origins I. Introduction PHONOLOGY PHONOLOGY PHONOLOGICAL A. Apraxia of Speech AWARENESS MEMORY ARTICULATION ? PHONOLOGY SPEECH B. The CAS/ASD Hypothesis SOUND PHONOLOGICAL ARTICULATION PRODUCTION II. Overviews ARTICULATION A. Speech Sound Disorders (SSD) “PHONOLOGY” “ARTICULATION” “ARTICULATION “ARTICULATION “ARTICULATION- “PHONOLOGY” “SPEECH SOUND” AND OR PHONOLOGY” B. Childhood Apraxia of Speech (CAS) PHONOLOGY” PHONOLOGY” 1920-1970 1970-1980 1980-1990 1990-2004 2005 III. Speech Research in ASD A. Verbal ASD: Findings B. Nonverbal ASD: Perspectives 2 Eight Putative Etiological Subtypes of SSD of Currently Unknown Origin Genomic Research in Speech Delay No. Type Subtype Abbreviation Risk Factors Processes Affected 1 Speech Delay Speech Delay–Genetic SD-GEN Polygenic/ Cognitive-Linguistic Environmental There have been no genes identified to date 2 Speech Delay– SD-OME Polygenic/ Auditory-Perceptual that code specifically for Speech Delay Otitis Media with Effusion Environmental 3 Speech Delay– Developmental SD-DPI Polygenic/ Affective- Psychosocial Involvement Environmental Temperamental Several candidate genes for Speech Delay 4 Motor Speech Motor Speech Disorder– MSD-AOS Monogenic? Speech-Motor Control have been associated with language Disorder Apraxia of Speech Oligogenic? impairment and dyslexia, including 5 Motor Speech Disorder– MSD-DYS Monogenic? Speech-Motor Control Dysarthria Oligogenic? regions of interest reported on 5 of the 6 Motor Speech Disorder- MSD-NOS Monogenic? Speech-Motor Control Not Otherwise Specified Polygenic? Oligogenic? 22 autosomes: 1, 3, 6, 15, 16 Environmental? 7 Speech Errors Speech Errors-Sibilants SE-/s/ Environmental Phonological Attunement 8 Speech Errors-Rhotics SE-/r/ Environmental Phonological Attunement Topics Research in CAS Genomic I. Introduction Phenotype A. Apraxia of Speech Neuroimaging B. The CAS/ASD Hypothesis e.g., Lewis (2008); Robin (2008) II. Overviews Speech Motor Control and Computational A. Speech Sound Disorders (SSD) Neural Modeling; e.g., Maas, Robin, Wright, et al. (2008); B. Childhood Apraxia of Speech (CAS) Terband et al. (2009); Terband and III. Speech Research in ASD Maassen (2010); Wright et al. (2009) A. Verbal ASD: Findings Treatment B. Nonverbal ASD: Perspectives e.g., Maas, Robin, Austermann Hula, et al. (2008) Genomic Research in CAS: Genomic Research in CAS: The Iconic Pedigree Some FOXP2 Highlights Molecular genetic and neurocognitive publications on the London ‘KE’ family beginning with Hurst et al. (1990) catalyzed worldwide interest from many disciplines in the possibility of speech-language genes Lai et al. (2001) identified FOXP2 as the gene segregating in affected members of the family FOXP2 disruptions and motor speech disorder consistent with CAS reported in four other families (MacDermot et al., 2005; Shriberg et al., 2006; Shriberg, 2010b; Zeesman et al., 2006) Continuing functional analyses of FOXP2; knockout, knockdown, and knockin Foxp2 orthologs in vertebrate species including rodents, birds, reptiles, and fish Zebra finch genome sequenced; parrot genome next 3 Genomic Research in CAS: Alternative Neural Circuit Proposals for Foxp2 Expression in Mouse Vocalizationsa Madison Group CAS documented in three siblings with an unbalanced chromosome 4q;16q translocation (Shriberg, Jakielski, & El-Shanti, 2008) Phenotype studies of a mother and son in a new family with a FOXP2 disruption, including possible ASD in the son Array Comparative Genomic Hybridization (aCGH; copy number) studies of children with idiopathic CAS Resequencing studies of five children with idiopathic CAS; exome analyses covering > 90% of the protein coding subset of the genome aCampbell et al. (2009) Phenotype Research in CAS Phenotype Research in CAS: The Phenotype Constraint “…lack of a definition and an agreed-upon set of criteria for subject selection [is the] single most No biomarker for CAS important impediment to theoretical and clinical advancement in AOS.” No one behavioral marker McNeil (2001) pathognomonic for CAS “…the problem lies not so much in defining the No set of behavioral markers with underlying impairment of AOS as in a lack of clear operational definitions or procedural criteria for the high diagnostic accuracy for CAS differential diagnosis of AOS.” Maassen (2002) Phenotype Research in CAS: CAS Research: Phenotype Constraints in FOXP2 Studies Madison Phenotype Research CAS in Complex CAS as an Adult CAS as a Sequelae of Clinical assessment of affected KE family members not Neurodevelopmental Idiopathic reported to date. The measures identifying affected AOS Neurological Disorder Disorders Disorder 1 from unaffected KE family members were speech services, and performances on non-standardized Foxp2 avian Core Speech Features Pathognomonic and mammal Core Non-Speech Features 2 Signs/Markers nonsense word repetition tasks and oral motor tasks. knock-o/d/i Relevant Age Issues genotypes Relevant Severity Issues 3 Speech data from KE family and from family members in two other FOXP2 families are consistent with Genetic Substrates dysarthria, as well as apraxia of speech (Morgan Neural Substrates et al., 2005; Shriberg, 2010b; Shriberg et al., 2006). 4 Assessment FOXP2 has low attributable risk for CAS. Treatment Prevention 4 Competence, Precision, Complex Neurodevelopmental Disorders Reporting ‘Significant Speech Delay’/CAS Stability Analytics (CPSA)a Autism Competence Chromosome Translocations (Normative; Down syndrome (Trisomy 21) Mastery) Rolandic Epilepsy Fragile X syndrome (FMR1) Joubert syndrome (CEP290; AHI1) Precision Stability Galactosemia (Spatiotemporal (Spatiotemporal Accuracy) Consistency) Rett syndrome (MeCP2) Russell-Silver syndrome (FOXP2) Velocardiofacial syndrome (22q11.2 deletion) aShriberg, Fourakis, et al. (2010) Identifying Markers of CAS in Neurogenetic Contexts Can Inform Markers of Idiopathic CAS Topics I. Introduction Findings to date are interpreted as support for the premise that an operationalized and standardized set A. Apraxia of Speech of perceptual and acoustic markers of CAS can be B. The CAS/ASD Hypothesis identified from and cross
Load more

Recommended publications
  • A Sub-Acute Case of Resolving Acquired Apraxia of Speech and Aphasia Shannon C
    hysical M f P ed l o ic a in n r e u & o R J International Journal of Physical l e a h n a o b i Mauszycki et al., Int J Phys Med Rehabil 2014, 2:2 t i l a ISSN: 2329-9096i t a n r t i e o t n 10.4172/2329-9096.1000188 n I Medicine & Rehabilitation DOI: Research Article Open Access A Sub-Acute Case of Resolving Acquired Apraxia of Speech and Aphasia Shannon C. Mauszycki1,2*, Sandra Wright1 and Julie L. Wambaugh1,2 ¹VA Salt Lake City Healthcare System, Salt Lake City, UT, USA ²University of Utah, Salt Lake City, UT, USA *Corresponding author: Shannon C. Mauszycki, Aphasia/Apraxia Research Lab, 151-A, Building 2, 500 Foothill Drive, Salt Lake City, UT 84148, USA, Tel: 801-582-1565, Ext: 2182; Fax: 801-584-5621; E-mail: [email protected] Rec date: 20 Feb 2014; Acc date:21 March 2014; Pub date: 23 March 2014 Copyright: © 2014 Mauszycki SC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Apraxia of speech (AOS) is a neurogenic, motor speech disorder that disrupts the planning for speech production. However, there are only a few reports that have described the evolution of stroke-induced AOS symptoms in the acute or sub-acute phase of recovery. The purpose of this report was to provide a data-based description of an individual with sub-acute AOS and aphasia followed from 1 month post-onset a stroke to 8 months post-stroke.
    [Show full text]
  • Common Disorders of Speech in Children by T
    Arch Dis Child: first published as 10.1136/adc.34.177.444 on 1 October 1959. Downloaded from A DESCRIPTION AND CLASSIFICATION OF THE COMMON DISORDERS OF SPEECH IN CHILDREN BY T. T. S. INGRAM From the Department of Child Life and Health, University of Edinburgh and the Royal Hospitalfor Sick Children, Edinburgh (RECEIVED FOR PUBLICATION MARCH 9, 1959) The full assessment of children suffering from speech defects, speech therapy is rarely provided. speech defects requires a team consisting of speech Children with speech defects attending these schools therapist, paediatrician, psychologist and otologist. were frequently referred to the Speech Clinic in the The additional services of a phonetician, neurologist, Hospital. orthodontist, plastic surgeon, radiologist, social Detailed family, birth and developmental histories worker or psychiatric social worker and child were taken, with particular emphasis on the rate, and psychiatrist are often helpful. any abnormalities, of speech development. The Unfortunately the majority of descriptions and children were subjected to a detailed paediatric and classifications of speech disorders in childhood are neurological examination, and behaviour in play by speech therapists working without much medical was observed for as long as possible in each case. co-operation and advice. With honourable excep- The child's speech was studied jointly by the by copyright. tions, they tend to regard speech disorders as rather paediatrician and the speech therapist, and detailed isolated phenomena, dissociated from the other notes were made of its intelligibility and of the behavioural and psychological characteristics of the particular defects which were observed. In many child. In the present paper an attempt is made to cases tape recordings were made, though it is always describe and classify the disorders of speech most easier, in fact, to examine speech for defects of frequently encountered in a hospital speech clinic articulation in the presence of the patient.
    [Show full text]
  • Evaluation of Ideomotor Apraxia in Patients with Stroke: a Study of Reliability and Validity
    J Rehabil Med 2006; 38: 108Á/112 EVALUATION OF IDEOMOTOR APRAXIA IN PATIENTS WITH STROKE: A STUDY OF RELIABILITY AND VALIDITY Kurtulus Kaya, MD1, Sibel Unsal-Delialioglu, MD1, Murat Kurt, PhD2, Nermin Altinok3 and Sumru Ozel, MD1 From the 1Physical Medicine and Rehabilitation Clinic, 2Department of Neuropsychology Rehabilitation and 3Department of Speech Therapy, Ankara Physical Medicine and Rehabilitation Education and Research Hospital, Ankara, Turkey Objective: This aim of this study was to determine the define it verbally, but fail to perform it when given a verbal reliability and validity of an established ideomotor apraxia command (6). For example, a patient with ideomotor apraxia test when applied to a Turkish stroke patient population and may be able to close his or her eyes spontaneously, but may fail to healthy controls. to do so when instructed verbally. These patients are able to Subjects: The study group comprised 50 patients with right perform simple, spontaneous and automatic movements per- hemiplegia and 36 with left hemiplegia, who had developed the fectly. Ideomotor apraxia can be defined, in brief, as a move- condition as a result of a cerebrovascular accident, and 33 age- matched healthy subjects. ment disorder arising from damage to the parietofrontal Methods: The subjects were evaluated for apraxia using an connections that control deliberate movements (7). established ideomotor apraxia test. The cut-off value of the Successful maintenance of a rehabilitation program for test and the reliability coefficient between observers were patients with stroke depends on the patient’s fulfilment of given determined. instructions as well as their performance of prescribed exercise.
    [Show full text]
  • 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.
    [Show full text]
  • THE CLINICAL ASSESSMENT of the PATIENT with EARLY DEMENTIA S Cooper, J D W Greene V15
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2005.081133 on 16 November 2005. Downloaded from THE CLINICAL ASSESSMENT OF THE PATIENT WITH EARLY DEMENTIA S Cooper, J D W Greene v15 J Neurol Neurosurg Psychiatry 2005;76(Suppl V):v15–v24. doi: 10.1136/jnnp.2005.081133 ementia is a clinical state characterised by a loss of function in at least two cognitive domains. When making a diagnosis of dementia, features to look for include memory Dimpairment and at least one of the following: aphasia, apraxia, agnosia and/or disturbances in executive functioning. To be significant the impairments should be severe enough to cause problems with social and occupational functioning and the decline must have occurred from a previously higher level. It is important to exclude delirium when considering such a diagnosis. When approaching the patient with a possible dementia, taking a careful history is paramount. Clues to the nature and aetiology of the disorder are often found following careful consultation with the patient and carer. A focused cognitive and physical examination is useful and the presence of specific features may aid in diagnosis. Certain investigations are mandatory and additional tests are recommended if the history and examination indicate particular aetiologies. It is useful when assessing a patient with cognitive impairment in the clinic to consider the following straightforward questions: c Is the patient demented? c If so, does the loss of function conform to a characteristic pattern? c Does the pattern of dementia conform to a particular pattern? c What is the likely disease process responsible for the dementia? An understanding of cognitive function and its anatomical correlates is necessary in order to ascertain which brain areas are affected.
    [Show full text]
  • Chronic Anxiety and Stammering Ashley Craig & Yvonne Tran
    Advances in PsychiatricChronic Treatment anxiety (2006), and vol. stammering 12, 63–68 Fear of speaking: chronic anxiety and stammering Ashley Craig & Yvonne Tran Abstract Stammering results in involuntary disruption of a person’s capacity to speak. It begins at an early age and can persist for life for at least 20% of those stammering at 2 years old. Although the aetiological role of anxiety in stammering has not been determined, evidence is emerging that suggests people who stammer are more chronically and socially anxious than those who do not. This is not surprising, given that the symptoms of stammering can be socially embarrassing and personally frustrating, and have the potential to impede vocational and social growth. Implications for DSM–IV diagnostic criteria for stammering and current treatments of stammering are discussed. We hope that this article will encourage a better understanding of the consequences of living with a speech or fluency disorder as well as motivate the development of treatment protocols that directly target the social fears associated with stammering. Stammering (also called stuttering) is a fluency childhood, many recover naturally in early disorder that results in involuntary disruptions of adulthood (Bloodstein, 1995). We found a higher a person’s verbal utterances when, for example, prevalence rate (of up to 1.4%) in children and they are speaking or reading aloud (American adolescents (2–19 years of age), with males in this Psychiatric Association, 1994). The primary symptoms of the disorder are shown in Box 1. If the symptoms are untreated in early childhood, Box 1 Symptoms of stammering there is a risk that the concomitant behaviours will become more pronounced (Bloodstein, 1995; Craig Behavioural symptoms • et al, 2003a).
    [Show full text]
  • Evidence-Based Physical Therapy for Individuals with Rett Syndrome: a Systematic Review
    brain sciences Review Evidence-Based Physical Therapy for Individuals with Rett Syndrome: A Systematic Review Marta Fonzo, Felice Sirico and Bruno Corrado * Department of Public Health, University of Naples “Federico II”, 80131 Naples, Italy; [email protected] (M.F.); [email protected] (F.S.) * Correspondence: [email protected]; Tel.: +39-081-7462795 Received: 14 June 2020; Accepted: 29 June 2020; Published: 30 June 2020 Abstract: Rett syndrome is a rare genetic disorder that affects brain development and causes severe mental and physical disability. This systematic review analyzes the most recent evidence concerning the role of physical therapy in the management of individuals with Rett syndrome. The review was carried out in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses. A total of 17319 studies were found in the main scientific databases. Applying the inclusion/exclusion criteria, 22 studies were admitted to the final phase of the review. Level of evidence of the included studies was assessed using the Oxford Centre for Evidence-Based Medicine—Levels of Evidence guide. Nine approaches to physical therapy for patients with Rett syndrome were identified: applied behavior analysis, conductive education, environmental enrichment, traditional physiotherapy with or without aids, hydrotherapy, treadmill, music therapy, computerized systems, and sensory-based treatment. It has been reported that patients had clinically benefited from the analysed approaches despite the fact that they did not have strong research evidence. According to the results, a multimodal individualized physical therapy program should be regularly recommended to patients with Rett syndrome in order to preserve autonomy and to improve quality of life.
    [Show full text]
  • Processing of Degraded Speech in Brain Disorders
    brain sciences Review Processing of Degraded Speech in Brain Disorders Jessica Jiang 1, Elia Benhamou 1, Sheena Waters 2 , Jeremy C. S. Johnson 1, Anna Volkmer 3, Rimona S. Weil 1 , Charles R. Marshall 1,2, Jason D. Warren 1,† and Chris J. D. Hardy 1,*,† 1 Dementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London WC1N 3BG, UK; [email protected] (J.J.); [email protected] (E.B.); [email protected] (J.C.S.J.); [email protected] (R.S.W.); [email protected] (C.R.M.); [email protected] (J.D.W.) 2 Preventive Neurology Unit, Wolfson Institute of Preventive Medicine, Queen Mary University of London, London EC1M 6BQ, UK; [email protected] 3 Division of Psychology and Language Sciences, University College London, London WC1H 0AP, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-203-448-3676 † These authors contributed equally to this work. Abstract: The speech we hear every day is typically “degraded” by competing sounds and the idiosyncratic vocal characteristics of individual speakers. While the comprehension of “degraded” speech is normally automatic, it depends on dynamic and adaptive processing across distributed neural networks. This presents the brain with an immense computational challenge, making de- graded speech processing vulnerable to a range of brain disorders. Therefore, it is likely to be a sensitive marker of neural circuit dysfunction and an index of retained neural plasticity. Consid- ering experimental methods for studying degraded speech and factors that affect its processing in healthy individuals, we review the evidence for altered degraded speech processing in major Citation: Jiang, J.; Benhamou, E.; neurodegenerative diseases, traumatic brain injury and stroke.
    [Show full text]
  • Social Anxiety Disorder and Stuttering: Current Status And
    G Model JFD-5535; No. of Pages 14 ARTICLE IN PRESS Journal of Fluency Disorders xxx (2013) xxx–xxx Contents lists available at ScienceDirect Journal of Fluency Disorders Social anxiety disorder and stuttering: Current status and future directions ∗ Lisa Iverach , Ronald M. Rapee Centre for Emotional Health, Department of Psychology, Macquarie University, Australia a r t i c l e i n f o a b s t r a c t Article history: Anxiety is one of the most widely observed and extensively studied psychological concomi- Received 17 March 2013 tants of stuttering. Research conducted prior to the turn of the century produced evidence Received in revised form 11 August 2013 of heightened anxiety in people who stutter, yet findings were inconsistent and ambiguous. Accepted 20 August 2013 Failure to detect a clear and systematic relationship between anxiety and stuttering was Available online xxx attributed to methodological flaws, including use of small sample sizes and unidimensional measures of anxiety. More recent research, however, has generated far less equivocal find- Keywords: ings when using social anxiety questionnaires and psychiatric diagnostic assessments in Stuttering larger samples of people who stutter. In particular, a growing body of research has demon- Anxiety strated an alarmingly high rate of social anxiety disorder among adults who stutter. Social Social anxiety disorder anxiety disorder is a prevalent and chronic anxiety disorder characterised by significant fear Social phobia of humiliation, embarrassment, and negative evaluation in social or performance-based Cognitive Behaviour Therapy situations. In light of the debilitating nature of social anxiety disorder, and the impact of stuttering on quality of life and personal functioning, collaboration between speech pathol- ogists and psychologists is required to develop and implement comprehensive assessment and treatment programmes for social anxiety among people who stutter.
    [Show full text]
  • Parental Questions About Developmental Coordination Disorder: a Synopsis of Current Evidence
    missiuna_9757.qxd 10/6/2006 3:40 PM Page 507 ORIGINAL ARTICLE Parental questions about developmental coordination disorder: A synopsis of current evidence Cheryl Missiuna PhD OTReg(Ont)1, Robin Gaines PhD SLP(C) CASLPO CCC-SLP2, Helen Soucie PhD3, Jennifer McLean MD FRCPC4 C Missiuna, R Gaines, H Soucie, J McLean. Parental questions Les questions des parents sur le trouble de about developmental coordination disorder: A synopsis of l’acquisition de la coordination : Un synopsis current evidence. Paediatr Child Health 2006;11(8):507-512. des données probantes courantes In recent years, knowledge about developmental coordination disor- der (DCD) has accumulated very rapidly. Considerable progress has Ces dernières années, les connaissances sur le trouble de l’acquisition de la coordination (TAC) se sont accumulées très rapidement. Des progrès been made in the understanding of DCD, but recent studies have not considérables ont été réalisés dans la compréhension du TAC, mais les been compiled in a way that makes them easily accessible to practic- études récentes n’ont pas été compilées de manière à les rendre facilement ing paediatricians. In the present paper, the literature is reviewed and accessibles aux pédiatres en exercice. Dans le présent article, on analyse organized around the questions commonly raised by parents of chil- les publications et on les organise selon les questions que posent souvent dren with DCD when they meet with their paediatrician. Parents les parents d’enfants atteints d’un TAC lorsqu’ils rencontrent leur express concern and seek information about their child’s movement pédiatre. Les parents sont préoccupés et cherchent à obtenir de difficulties.
    [Show full text]
  • Apraxia in Mild Cognitive Impairment and Alzheimer's Disease
    2.4 Apraxia in Mild Cognitive Impairment and Alzheimer’s disease: validity and reliability of the Van Heugten test for apraxia Dementia and Geriatric Cognitive Disorders, 2014 Lieke L. Smits1, Marinke Flapper1, Nicole Sistermans1, Yolande A.L. Pijnenburg1, Philip Scheltens1 1,2 and Wiesje M. van der Flier Alzheimer Center and departments of 1 Neurology and 2 Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, the Netherlands. Abstract Objective: To assess reliability and validity of Van Heugten test for apraxia (VHA), developed for and used in stroke patients, in a memory clinic population. To assess presence and severity of apraxia in Mild Cognitive Impairment (MCI) and Alzheimer’s disease (AD) and to investigate which AD patients were likely to have apraxia. Methods: We included 90 controls (age:609 years,MMSE:282), 90 MCI patients (age:657 years,MMSE:262) and 158 AD patients (age:668 years,MMSE:205). Apraxia was evaluated by VHA assessing ideational and ideomotor praxis. We retested 20 patients to assess reliability. Results: Intrarater reliability was 0.88 and interrater reliability was 0.73. AD patients performed worse on VHA (median:88;range:51-90) than controls (median:90;range:88-90) and MCI patients (median:89;range:84-90) (both p<0.001). Apraxia was prevalent in 35% of AD patients, 10% of MCI and not in controls (0%;p<0.001). In AD, dementia severity was the main risk for apraxia; 15% of mildly versus 52% of moderately demented patients had apraxia (OR(95%CI)=6.7(2.9-15.6)). The second risk factor was APOE genotype; APOE Ɛ4 non-carriers (47%) were at increased risk compared to carriers (30%) (OR(95%CI)=2.1(1-4.7)).
    [Show full text]
  • II./2.9. Language and Higher Cerebral Functions II./2.9.1. Disorders Of
    II./2.9. Language and higher cerebral functions II./2.9.1. Disorders of language Disorders of language include disturbance of speech, writing and reading. II./2.9.1.1. Disorders of speech (aphasias) Aphasia is a speech disorder caused by lesion of cortical speech centers and their connections, characterized by the disturbance in the use and production of verbal symbols. Dysarthria is a disturbance of phonation (voice production), articulation, pronunciation and prosody (intonation, rhythm). Dysarthria may be caused by the lesion of cortical centers of innervating the muscles of speech, bilateral lesion of corticobulbar fibers, bulbar motoneuron disorders, myasthenia gravis, myopathies, and cerebellar What is the difference disorders. between aphasia and dysarthria? Anatomy Brain regions related to speech are in most people located in the dominant (left) hemisphere: the Wernicke’s speech center (Br22 and a small part of Br39 and Br40), responsible for the comprehension of speech, lies adjacent to the primary auditory cortex in the posterior two-thirds of the superior temporal gyrus. Its connection with the angular gyrus ensures the coupling of perceptual and learned memories with speech. The angular and the supramarginal gyri are associative areas at the border of the auditory, sensory and visual cortices. The Broca’s motor speech center is in the middle and inferior frontal gyrus, and the lower part of the precentral gyrus (Br44). The motor speech area is connected by the arcuate bundle with the angular and the supramarginal gyri, and the Wernicke area. The occipitofrontal bundle connects the angular and the supramarginal gyri with the frontal opercular areas.
    [Show full text]