Post-Stroke Language Disorders
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Phonological Activation in Pure Alexia
Cognitive Neuropsychology ISSN: 0264-3294 (Print) 1464-0627 (Online) Journal homepage: http://www.tandfonline.com/loi/pcgn20 Phonological Activation in Pure Alexia Marie Montant & Marlene Behrmann To cite this article: Marie Montant & Marlene Behrmann (2001) Phonological Activation in Pure Alexia, Cognitive Neuropsychology, 18:8, 697-727, DOI: 10.1080/02643290143000042 To link to this article: http://dx.doi.org/10.1080/02643290143000042 Published online: 09 Sep 2010. Submit your article to this journal Article views: 47 View related articles Citing articles: 15 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=pcgn20 Download by: [Carnegie Mellon University] Date: 13 May 2016, At: 08:41 COGNITIVE NEUROPSYCHOLOGY, 2001, 18 (8), 697–727 PHONOLOGICAL ACTIVATION IN PURE ALEXIA Marie Montant CNRS, Marseille, France and Carnegie Mellon University, Pittsburgh, USA Marlene Behrmann Carnegie Mellon University and Center for the Neural Basis of Cognition, Pittsburgh, USA Pure alexia is a reading impairment in which patients appear to read letter-by-letter. This disorder is typically accounted for in terms of a peripheral deficit that occurs early on in the reading system, prior to the activation of orthographic word representations. The peripheral interpretation of pure alexia has recently been challenged by the phonological deficit hypothesis, which claims that a postlexical discon- nection between orthographic and phonological information contributes to or is responsible for the dis- order. Because this hypothesis was mainly supported by data from a single patient (IH), who also has surface dyslexia, the present study re-examined this hypothesis with another pure alexic patient (EL). -
Case Study 1 & 2
CASE Courtesy of: STUDY Mitchell S.V. Elkind, MD, Columbia University 1 & 2 and Shadi Yaghi, MD. Brown University CASE 1 CASE 1 A 20 year old man with no past medical history presented to a primary stroke center with sudden left sided weakness and imbalance followed by decreased level of consciousness. Head CT showed no hemorrhage, no acute ischemic changes, and a hyper-dense basilar artery. CT angiography showed a mid-basilar occlusion. CASE 1 CONTINUED Head CT showed no hemorrhage, no acute ischemic changes, and a hyper-dense basilar artery (Figure 1, arrow). CT angiography showed a mid-basilar occlusion (Figure 2, arrow). INFORMATION FOR PATIENTS Fig. 1 AND FAMILIESFig. 2 CASE 1 CONTINUED He received Alteplase intravenous tPA and was transferred to a comprehensive stroke center where angiography confirmed mid-basilar occlusion (Figure 3, arrow ). He underwent mechanical thrombectomy (Figure 4) with recanalization of the basilar artery. His neurological exam improved and he was discharged to home after 2 days. At his 3 month follow up, he was back to normal and returned to college. Fig. 3 Fig. 4 CASE 2 CASE 2 A 62 year old woman with a history of hypertension and hyperlipidemia presented to a primary stroke center with sudden onset of weakness of the right side. On examination, she had a global aphasia, left gaze preference, right homonymous hemianopsia (field cut), right facial droop, dysarthria, and right hemiplegia (NIH Stroke Scale = 22). Head CT showed only equivocal hypodensity in the left middle cerebral artery territory (Figure 1 on next slide). CT angiography showed a left middle cerebral artery occlusion (Figure 2 on next slide, arrow). -
Classification of Aphasic Phenomena
LE JOURNAL CANAD1EN DES SCIENCES NEUROLOG1QUES Classification of Aphasic Phenomena ANDREW KERTESZ SUMMARY: A brief but comprehensive Most clinicians will agree that al tions cover the same phenomenon. survey of classifying aphasia reveals though aphasic disability is complex, In Table I the various terms are that most investigators describe at least many patients are clinically similar shown to overlap and those describ four major groups, conveniently labelled and may be classified into identifi ing the same disturbance appear un Broca's, Wernicke's, anomic and global. able groups. There are many classi derneath each other. Four columns Conduction and transcortical aphasias fications indicating that none is al appear to represent the entities that are less generally described and mod ality specific syndromes rarely, if ever, together satisfactory. Nevertheless, almost everybody identifies: exist purely. The controversy between this effort is useful and even neces 1. What Broca (1861) described as unifiers and splitters continues but ob sary to diagnose and treat aphasics aphemia, Wernicke (1874) called jective numerical taxonomy may solve and to understand the phenomena. motor aphasia. Marie (1906) did not some of the problems of classification. The opponents of classification consider Broca's aphemia true point out the numerous disagree aphasia. Pick (1913) labelled it ex ments among observers, the many pressive aphasia with agrammatism RESUME: Line etude breve, mais com exceptions that cannot be fitted into and Weisenburg & McBride (1935) prehensive, de la classification de categories and the frequent evolu popularized "expressive aphasia" I'aphasic revile que la plupart des cher- cheurs decrivent au moins 4 groupes tion of certain types into others. -
Prospect for a Social Neuroscience
Levels of Analysis in the Behavioral Sciences Prospect for a • Psychological Social Neuroscience – Mental structures and processes • Sociocultural – Social, cultural structures and processes Berkeley Social Ontology Group • Biophysical Spring 2014 – Biological, physical structures and processes 1 2 Levels of Analysis On Terminology in the Behavioral Sciences • Physiological Psychology (1870s) Sociocultural – Animal Research Social Psychology • Neuropsychology (1955, 1963) Social Cognition – Behavioral Analysis – Brain Insult, Injury, or Disease Psychological • Neuroscience (1963) – Interdisciplinary Cognitive Psychology • Molecular/Cellular Cognitive Neuroscience Social Neuroscience •Systems • Behavioral Biophysical 3 4 Towards a Social Neuropsychology The Evolution of Klein & Kihlstrom (1998) Social Neuroscience Neurology NEUROSCIENCE • Beginnings with Phineas Gage (1848) Neuroanatomy Molecular – Phrenology, Frontal Lobe, and Personality Integrative and • Neuropsychological Methods, Concepts Neurophysiology Cellular Cognitive – Neurological Cases – Brain-Imaging Methods Systems Affective • But Neurology Doesn’t Solve Our Problems Behavioral Conative(?) – Requires Psychological Theory Social – Adequate Task Analysis at Behavioral Level 5 6 1 The Rhetoric of Constraint “Rethinking Social Intelligence” Goleman (2006), p. 324 “Knowledge of the body and brain can The new neuroscientific findings on social life have usefully constrain and inspire concepts the potential to reinvigorate the social and behavioral sciences. The basic assumptions -
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. -
Cognitive Performance Deficits and Dysgraphia in Alzheimer's Disease
Send Orders for Reprints to [email protected] 6 Open Medicine Journal, 2015, 2, 6-16 Open Access Cognitive Performance Deficits and Dysgraphia in Alzheimer’s Disease Patients Emanuela Onofri1, Marco Mercuri1, MariaLucia Salesi1, Max Rapp Ricciardi2 and Trevor Archer*,2 1Department of Anatomy, Histology, Legal Medicine and Orthopaedics, Sapienza University of Rome, Italy 2Department of Psychology, University of Gothenburg, Gothenburg, Sweden Abstract: Introduction: Agraphia or dysgraphia, observed often in early AD, encompasses a progressive disorganization and degeneration of the various components of handwriting. Methods: Deficits in writing ability, dysgraphia, and the relationship with other measures of cognitive decline were studied in a group of 30 patients, originating from the Lazio region, Rome, Italy, presenting a moderate to relatively severe stage of Alzheimer’s disease (AD). Extent of dysgraphia and cognitive performance was compared with a matched group of healthy controls selected from the same region. Results: Several markedly strong relationships between dysgraphia and several measures of cognitive performance in AD patients were observed concomitant with consistent deficits by this patient sample in comparison with the matched group of healthy control subjects were obtained. Additionally, several measures of loss of functional integrity, MMSE, ADL and IADL, were found to be associated with both dysgraphia and impairments in cognitive performance. Conclusion: The present results are discussed from the notion of -
A Young Woman with Sudden Hemiparesis
f Clin al o ica rn l & ISSN : 2376-0249 u o M J e l d a i c n International Journal of a o l i Vol 5 • Iss 3• 1000601 Mar, 2018 t I m a n a r g e t i n n I g DOI: 10.4172/2376-0249.1000601 ISSN: 2376-0249 Clinical & Medical Images Case Report A Young Woman with Sudden Hemiparesis Monique Boukobza* and Jean-Pierre Laissy Department of Radiology, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France (1) (2) (3) (4) (5) (6) Figure 1: Diffusion weighted imaging (DWI) shows hyperintensity indicative of core infarction on MRI within less than 3 h after onset. Figure 2: Fluid-attenuated inversion recuperation imaging-Hyperintense vessels proximal to the sylvian fissure. Figure 3: Fluid-attenuated inversion recuperation imaging-Hyperintense vessels distal to the sylvian fissure. Figure 4: Magnetic resonance angiography-Severe vasospasm of the left internal carotid artery (short arrow) and middle cerebral artery (M1 segment) (long arrow). Figure 5: Digital subtraction angiography-Severe vasospasm (long arrow) and small aneurysm of the left anterior choroidal artery of 10 mm of diameter (short arrow). Figure 6: Magnetic resonance angiography follow-up-Exclusion of the aneurysm and normal caliber of the cerebral arteries. Abstract Stroke related to cerebral vasospasm may have the same appearance that ischemic stroke of other causes. The correct diagnosis is critical to avoid inappropriate treatments as thombolysis and anticoaglant therapy. In this case, a previous young healthy woman presented with acute onset of right-sided hemiplegia and expressive aphasia. Interpretation of Magnetic Resonance Images was challenging: acute ischemia, severe vasospasm, no signs of subarachnoid hemorrhage or intra-arterial thrombi, no evidence of cervical artery dissection. -
Alexia Without Agraphia
Neuroradiology(1992) 34:210-214 Neuro radiology Springer-Verlag 1992 Alexia without agraphia D. J. Quint I and J. L. Gilmore 2 1Division of Neuroradiology,Department of Radiology,University of MichiganHospitals, Ann Arbor, Michigan,USA 2Department of Neurology,University of Rochester, Rochester, New York, USA Received: September 16, 1991 Summary. Two new cases of alexia without agraphia are mentation and right visual complaints. She had suffered presented. Pertinent clinical findings, anatomy, pathophy- from extensive atherosclerotic peripheralvascular disease siology and differential diagnoses are reviewed. The im- involving both the systemic and cerebral vasculature, portance of carefully examining the inferior portion of the necessitating carotid endarterectomy. The patient denied left side of the splenium of the corpus callosum on CT any "strokes", but did suffer from complications of scle- and/or MR scans in patients who present with this clinical roderma including gastritis, esophagitis and Raynaud's syndrome is stressed. phenomenon and had also had a cervical sympathectomy. The patient did report a vague episode of "loss of con- Key words: Alexia - Agraphia - Disconnection syndrome sciousness" 4-5 months before admission. - Magnetic resonance imaging - Computed tomography General physical examination showed some edema of the legs. Neurologic examination revealed the patient to be oriented to person and place, but not to time. She could Alexia without agraphia or pure word blindness is con- sidered one of the classic disconnection syndromes. Pa- identify letters, but could not read. She could write her name and spell simple words forwards and backwards. Cra- tients retain the ability to write, but are unable to read nial nerve (II-XII) examination demonstrated a right ho- (even words that they have just written) and often have monymous hemianopia. -
Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
A.qxd 9/29/05 04:02 PM Page 1 A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis (i.e., with dorsal column disease). Cross References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circum- stances: normal old age obesity after abdominal surgery after multiple pregnancies in acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neu- rone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis. -
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). -
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. -
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.