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Acquired Language Disorders A CASE-BASED APPROACH Third Edition Evelyn R. Klein, PhD, CCC-SLP, BCS-CL James M. Mancinelli, PhD, CCC-SLP

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Page 1: Acquired Language Disorders - Plural Publishing · x Acquired LAnguAge disorders: A cAse-BAsed ApproAch Intensity of Treatment 241 Computer-Assisted Technology and Treatment of Aphasia

Acquired Language DisordersA CAse-BAsed ApproACh

Third Edition

Evelyn R. Klein, PhD, CCC-SLP, BCS-CLJames M. Mancinelli, PhD, CCC-SLP

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5521 Ruffin RoadSan Diego, CA 92123

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Copyright © 2021 by Plural Publishing, Inc.

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Library of Congress Cataloging-in-Publication Data

Names: Klein, Evelyn R., author. | Mancinelli, James M., author. Title: Acquired language disorders : a case-based approach / Evelyn R. Klein, James M. Mancinelli. Description: Third edition. | San Diego : Plural Publishing, Inc., [2021] | Includes bibliographical references and index. Identifiers: LCCN 2019029826 | ISBN 9781635500974 (paperback) | ISBN 9781635500981 (ebook) Subjects: MESH: Language Disorders--diagnosis | Language Disorders--therapy | Language Therapy--methods | Aphasia--diagnosis | Aphasia--therapy | Case Reports Classification: LCC RC423 | NLM WL 340.2 | DDC 616.85/5--dc23 LC record available at https://lccn.loc.gov/2019029826

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v

Contents

Introduction xiAcknowledgments xvContributor xvii

Chapter 1. An Overview of Neuroanatomy and Neurophysiology ) 1 Related to Acquired Language Disorders (ALD

The Neuron 1Neurotransmitters 2Sensory 3The Brain: A Brief Review of Structure and Function 4

The Coverings of the Brain, Ventricles, and Cerebrospinal Fluid 5Cerebral Cortex 5The Brainstem 10Subcortical Structures 11The Cerebellum 12

Neural Pathways 13Cerebral Blood Flow 15

Cerebrovascular Accidents 16Brain Imaging and Selected Medical Tests for Acquired Language Disorders 19

CAT Scan or CT Scan 19MRI 19fMRI 20PET Scan 20SPECT Scan 20ASL (Arterial Spin Labeling) 20Examination of the Carotids: Doppler Ultrasound or Auscultation of the Carotids 20Endocardiography 21Angiography 21

References 21

Chapter 2. Assessment and Service Delivery in Acquired Language Disorders 23Approaches to Assessment in Acquired Language Disorders 23Purpose of Assessment 23

Assessment of Language Functions 25Characteristics of Aphasia 25

Definitions of the Clinical Characteristics of the Major Aphasias 27Areas to Consider Using the ALD Target Assessment Model 30

The Target Assessment Snapshot in Acquired Language Disorders 31Screening and Diagnostic Assessment 33

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vi Acquired LAnguAge disorders: A cAse-BAsed ApproAch

Screening Tests 34Diagnostic Assessment in Acquired Language Disorders: Making Sound Decisions 35Selected Assessments for Acquired Language Disorders 37Modifications to Standard Assessments 53

Goal Setting Based on Diagnostic Results 55Service Delivery and the World Health Organization 55

The International Classification of Functioning (ICF) and Living with Aphasia: 55 Framework for Outcome Measurement (A-FROM model)

Service Delivery for People with Acquired Language Disorders 57The Acute Care Setting 57The Rehabilitation Setting 57The Home Care Setting 58The Outpatient Setting 60The Long-Term Care (LTC) Setting 61Monitoring Change and Continuation of Services 63

Documentation of Progress 63Summary 65References 65Appendix 2–A: Functional Communication Connections Octagon 70Appendix 2–B: Quick Reference Diagnostic Chart for Acquired Language Disorders 71

Chapter 3. The Major Nonfluent Aphasias 81Introduction 81Broca’s Type Aphasia 84

Characteristics 84A Functional Analysis of Maurice 87Critical Thinking/Learning Activity 87Treatment Considerations 89Therapeutic Goals Using A-FROM 90

Transcortical Motor Aphasia 91Characteristics 91A Functional Analysis of Vincent 92Critical Thinking/Learning Activity 94Treatment Considerations 95Therapeutic Goals with A-FROM 95

Global Aphasia 97Characteristics 97A Functional Case Analysis for Elizabeth 99Critical Thinking/Learning Activity 99Treatment Considerations 101Therapeutic Goals with A-FROM 102

References 103

Chapter 4. The Fluent Aphasias 107Introduction 107Wernicke’s Type Aphasia 108

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Characteristics 108A Functional Analysis of Mildred’s Wernicke’s Aphasia 111Critical Thinking/Learning Activity 113Treatment Considerations 114Therapeutic Goals Using A-FROM 114

Transcortical Sensory Aphasia 115Characteristics 115A Functional Analysis of John’s TSA 117Critical Thinking/Learning Activity 117Treatment Considerations 119Therapeutic Goals Using A-FROM 120

Conduction Aphasia 121Characteristics 121A Functional Analysis of Miriam’s Aphasia 123Critical Thinking/Learning Activity 123Treatment Considerations 123Therapeutic Goals Using A-FROM 125

Anomic Aphasia 127Characteristics 127A Functional Analysis of Sophie’s Aphasia 128Critical Thinking/Learning Activity 130Treatment Considerations 131Therapeutic Goals Using A-FROM 131

References 133

Chapter 5. Other Aphasic Syndromes 135Subcortical Aphasia 135

Introduction 135Characteristics of Subcortical Aphasias 136A Functional Analysis of Winnie’s Subcortical Aphasia 141Critical Thinking/Learning Activity 143Treatment Considerations 143Therapeutic Goals Using A-FROM 144

Primary Progressive Aphasia 146Introduction 146Characteristics 146A Functional Analysis of Luis’s Primary Progressive Aphasia 148Critical Thinking/Learning Activity 150Treatment Considerations 151Therapeutic Goals Using A-FROM 151

Acquired Alexia and Agraphia 153Characteristics 153Alexia 153Agraphia 154A Functional Analysis of Sue’s Alexia 158Critical Thinking/Learning Activity 158

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viii Acquired LAnguAge disorders: A cAse-BAsed ApproAch

Treatment Considerations 158Therapeutic Goals Using A-FROM 160

Aphasia in the Bilingual Person 161Recovery Patterns in Bilingual Aphasia 162Cognitive Control in Differential Aphasia 162A Functional Analysis of Hamid’s Bilingual Aphasia 164Critical Thinking/Learning Activity 166Treatment Considerations 166Therapeutic Goals Using A-FROM 167

References 169

Chapter 6. Right Hemisphere Disorder 173Introduction 173Characteristics 173

Communication Deficits 174RHD and Pragmatic Impairment 174Visual-Perceptual Deficits 175Visuomotor Deficits 175Auditory Perceptual Deficits 176Cognitive Deficits 176A Functional Analysis of Debra 177Critical Thinking/Learning Activity 180Treatment Considerations 180Therapeutic Goals Using A-FROM 181

References 182

Chapter 7. Traumatic Brain Injury 185Introduction 185Characteristics 187

Types of Brain Injury 187Symptoms Related to Localization of the TBI 188Prognostic Considerations in Head Injury 188Premorbid Intelligence 188Age at the Time of Injury 189Duration of Coma 189Posttraumatic Amnesia 189Medical Complications 190Posttraumatic Seizures 190Hydrocephalus 191Spasticity 191

Cognitive-Linguistic Impairment Due to TBI 191Establishing Goals for the Therapeutic Course 193

Postconcussive Syndrome 193Mild TBI (mTBI) 194Rating Scales for Functional Outcomes 195

Rancho Los Amigos (RLA) 195

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contents ix

Disability Rating Scale (DRS) 196General Treatment Issues 196

Errorless Learning 200A Note About Generalization in People with TBI 200A Functional Analysis of Samuel’s TBI 201Critical Thinking/Learning Activity 204Treatment Considerations 204Therapeutic Goals Using A-FROM 205

References 206

Chapter 8. Dementia 209Introduction 209Characteristics 209

Diagnostic Factors 210The Stages of Dementia 212Memory Systems and Dementia 213

Types of Dementia 214Vascular Dementia (VaD) 214Parkinson’s Dementia 215Frontotemporal Dementias (FTD) 216Creutzfeldt-Jakob Disease (CJD) 216Huntington’s Disease 217

Overview of Research on Treatment for Dementia 217A Functional Analysis of Max’s Dementia 219Critical Thinking/Learning Activity 222Treatment Considerations 222Therapeutic Goals Using A-FROM 223

References 224

Chapter 9. Encephalopathy 227Introduction 227Characteristics 228

Drug and Alcohol Intoxication: Two Common Etiologies for Encephalopathy 228A Functional Analysis of Tommy 229Critical Thinking/Learning Activity 232Treatment Considerations 232Therapeutic Goals Using A-FROM 233

References 235

Chapter 10. Selected Treatment Programs and Approaches 237Historical Overview of Efficacy and Evidence in the Treatment of Acquired Language 237

Disorders (ALD) in AdultsRandomized Controlled Trials (rCTs) and Aphasia Treatment 238

Trends in Treatment for Acquired Language Disorders 239Biological and Pharmacologic Interventions 239Using Neuroimaging to Predict Recovery in People with Aphasia 240

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Intensity of Treatment 241Computer-Assisted Technology and Treatment of Aphasia 242AAC for Adults with ALD: Aphasia, PPA, TBI, and Dementia 243The Use of Applications (Apps) in the Rehabilitation of the ALD Patient 244

Selected Treatment Programs for Acquired Language Disorders 245A Treatment Sequence for Phonological Alexia/Agraphia 246Anagram, Copy, and Recall Therapy (ACRT) 247Concurrent Treatment for Reading and Spelling in Aphasia: Oral Reading Treatment 249

(ORT) and Copy and Recall Treatment (CART)Constraint-Induced Language Therapy (CILT) 250Conversational Coaching 252Divergent Word Retrieval 253Life Participation Approach to Aphasia (LPAA) 254Lingraphica® 255Mapping Therapy 257Melodic Intonation Therapy (MIT) 258MossTalk Words (MTW) 260Narrative Story Cards 261Nonsymbolic Movements for Activation of Intention (NMAI) 262Normal Sentence Production 263Oral Reading for Language in Aphasia (ORLA) and ORLA with Virtual Therapist (ORLA-VT) 264Promoting Aphasics’ Communicative Effectiveness (PACE) 265Response Elaboration Training (RET) 266Schuell’s Stimulation Approach 267Semantic Feature Analysis (SFA) 269Sentence Production Program for Aphasia (SPPA) 270SentenceShaper® 272Speech Entrainment 272Treatment of Underlying Forms (TUF) 273Verb Network Strengthening Treatment (VNeST) 273Visual Action Therapy (VAT) 275

References 277

Appendix A. case history Form 283

Appendix B. seven domains Assessment summary sheet 287

Appendix C. cognitive-Linguistic evaluation 289

Appendix d. the World health organization and the international classification 299 of Functioning, disability, and health

Appendix e. the octagon Worksheet for Functional communication 303

Appendix F. test Your Knowledge 305

Index 315

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xi

Introduction

New and experienced clinicians may find it challeng-ing when attempting to integrate theoretical knowl-edge and research into clinical practice. We have noted that it isn’t until the clinician actually encoun-ters a person with a specific disorder that academic knowledge and practice coincide. Given our years of experience as both teachers and practitioners, it is our intention to bridge the gap between theory and practice by providing the reader with a case-based approach to understanding acquired language disor-ders (ALD). To further our goal in making ALD come to life for the reader, we have developed a model that depicts the individual’s language and cognition fol-lowing a cerebrovascular accident or other neurologic event. We refer to this as the ALD Target Assessment Snapshot, and each of the 15 cases that we discuss has a corresponding figure within the chapter.

Our classroom experience has clearly demon-strated that students benefit from the graphic fea-tures of the Target Assessment Snapshot because it facilitates a concrete understanding of the linguis-tic and cognitive characteristics of each case. This model, combined with salient features of the various disorders, case analyses, and treatment consider-ations, connects theoretical knowledge with prac-tical application. In our opinion, this case-based approach matches the needs of speech-language pathologists practicing in health care today.

how the Book Is organized

Each chapter includes a fictional person based upon an actual case that was treated in a health care set-ting, private practice, or home health environment to exemplify a specific acquired language disorder. These case scenarios were developed based on actual patients who the authors or their colleagues have evaluated and treated. Using real clinical cases brings to life each communication impairment for

the learner, who can better conceptualize the spe-cific characteristics of the disorder in the context of a real person. We believe it is essential to under-stand not only the basic pathophysiology of a dis-ease process associated with an acquired language disorder, but also the functional effects it may have on a person’s life. For purposes of anonymity and confidentiality, the patients’ names and identifying information have been changed.

special Features

The 15 cases in this book offer a comprehensive overview of the assessment process, major aphasic syndromes, including bilingual aphasia, right hemi-sphere disorder, traumatic brain injury, dementia, encephalopathy, and other etiologies affecting the ability to communicate. The final chapter provides information about selected treatment programs and therapeutic approaches for individuals with ALD currently in use and new trends in therapeutic inter-vention with the ALD population.

Each chapter is based on a case study and includes eight sections:

n Characteristics of the disorder including neurologic correlates

n Case Scenario providing a brief overview of the case history

n Diagnostic Profile including language expression, speech production, auditory comprehension, reading, written expression, cognition, and behavioral symptoms of the case

n The Target Assessment Snapshot presents a visual representation that captures the type and degree of language impairment as well as any areas of cognition that may be affected.

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xii Acquired LAnguAge disorders: A cAse-BAsed ApproAch

n Functional Analysis consists of a narrative that succinctly summarizes the case and helps the clinician under-stand the impact of the disability on daily life.

n Critical Thinking/Learning Activity poses questions designed to help the student or clinician develop problem-solving and practical skills necessary to maximize the patient’s progress.

n Treatment Considerations provide areas to consider for rehabilitation based on the patient’s strengths and weaknesses, individualized to his/her psychosocial context. General therapeutic objectives are also provided.

n Therapeutic Goals with the A-FROM Model (Aphasia: Framework for Outcome Measurement) is based on the International Classification of Functioning (ICF), disability and health (World Health Organization, 2001). For each of the 15 cases, quality of life goals are provided. The A-FROM model provides a visual representation of the patient’s language and related impairments, communication environment, participation in life situations, and personal factors including identity, attitudes, and feelings (Kagan, 2011). The framework was adapted to provide a profile of treatment considerations for patients with a variety of neurogenic communication disorders, not only aphasia.

The Acquired Language disorders Target Model

We developed the Acquired Language Disorders Target Assessment Snapshot from an embedded lan-guage framework. This model is shown in Figure I–1 and reflects the influence that cognition plays in normal communication and, by extension, in the rehabilitation of people with acquired language disorders. The physical appearance of the model depicts a schematic relationship between language

and cognition as well as the relationship among functional language modalities.

There are five primary domains of the ALD Tar-get Model: Language, Attention, Memory, Executive Functions, and Visual Spatial skills. The Language domain includes four areas: expression, comprehen-sion, reading, and writing. Expression (E) and com-prehension (C) involve the verbal modality; whereas reading (R) and writing (W) involve the visual modality. Although as speech-language pathologists we are clinically oriented to the Language domain, we must not neglect the other four cognitive areas of functioning because they are integral to functional communication.

For an individual who has normal communi-cative functions, the lettered squares (E, C, R, and W) remain attached to the rectangle containing the word Language. For an individual with an acquired language disorder, the lettered squares separate from the Language rectangle, reflecting the level of impairment for that domain. The numbers 1 to 4 are assigned to further reflect the level of severity with 1 being normal (typical) and 4 being severely impaired. For each type of acquired language disor-der, the pattern is different. For example, in a per-son with an expressive nonfluent aphasia (Broca’s), the E square and the W square are placed on or

A�en�on Memory

E

NormalCommunica�onEmbeddedwithinNormalCogni�veFunc�ons

Expression

Execu�veFunc�ons VisualSpa�al

WR

C

Language

Reading Wri�ng

Comprehension

Figure I–1. the Acquired Language disorders target Model.

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introduction xiii

outside the circular border with the subscript 3 or 4 to indicate more impaired functioning. Depend-ing on the acquired language disorder, any or all of these language modalities may be impaired at varying degrees. This ranges from normal, to mild-moderate, to moderate-severe, to severe-profound. Impairment level is depicted in Figure I–2.

The ALD Target Assessment Snapshot includes the cognitive domains of attention, memory, visuo-spatial skills, and executive functions in aphasia that should be considered in a standard evalua-tion for treatment planning (Helm-Estabrooks & Albert, 2004). A line through any of the four cog-nitive domains in each specific case marks that domain as impaired. For example, in an individual with severely impaired executive functions, the box labeled Executive Functions will have a line bisect-ing the word.

how to Use This Book

For the student and the practitioner

n A graphic image of the ALD Target Assess-ment Snapshot representing each disorder enhances the student’s or practitioner’s understanding of cognitive-linguistic changes pertinent to that specific case.

n The value of the case-based approach to ALD is that it facilitates comparisons among types of patients. This optimizes more accurate decision-making for planning treatment. As a learning tool, the case-based approach helps the student or practitioner to attach clinical information to a case that is also represented with a photo image.

n The ALD Target Assessment Snapshot, combined with the Functional Analysis, can be very useful for clinical practice in a health care setting. This permits the student or practitioner to integrate the neurologic, cognitive, linguistic, and functional aspects of each patient to formulate a complete picture for treatment.

n PowerPoint slides are provided to supplement the text and support lectures.

n Many current treatment approaches are provided to assist the practitioner in planning a program for each patient.

n Each case has a one-page diagnostic profile that describes each patient’s language expression, speech, auditory comprehension, reading, written expres-sion, cognition, and behavioral symptoms. In addition, an Assessment Summary Sheet is available to help the clinician develop his or her own patient profile.

1– Normal2– Mild-ModerateImpairment3– Moderate-SevereImpairment4– Severe-ProfoundImpairment

ImpairedCogni�veFunc�on

A�en�on Memory

E3

W4R2

C1

Language

Execu�veFunc�ons VisualSpa�al

Figure I–2. the key to understanding the Acquired Language disorders target Model.

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xiv Acquired LAnguAge disorders: A cAse-BAsed ApproAch

n Each case includes a set of personal goals pertinent to the patient. In addition, a diagram of the Aphasia: Framework for Outcome Measurement (A-FROM) depicts areas of treatment considerations for the patient’s Participation in Life Situations; Personal Identity, Attitudes, and Feelings; Communication and Language Environment; and Language and Related Impairments (Kagan et al., 2008).

For the Instructor

n An overview of basic neuroanatomy for acquired language disorders is provided.

n This book offers a detailed summary of many formal and informal assessments and treatment programs for those with ALD.

n There are 15 case-based acquired language disorders, each with assessment and treatment considerations, to facilitate class discussion and clinical problem solving.

n PowerPoint slides augment the text and offer important lecture material, diagrams, illustrations, and online links for teaching.

n Charts, tables, and figures including the ALD Target Assessment Snapshot help categorize and concretize the various acquired language disorders.

n Functional treatment can be easily planned using the Functional Communication Connections worksheet.

n A Test Your Knowledge examination is also provided using seven case-based examples.

n The Aphasia Framework for Outcome Measurement (A-FROM) model helps instructors teach students to formulate personal goals pertinent to the patient for Participation in Life Situations; Personal Identity, Attitudes, and Feelings; Communication and Language Environment; and Language and Related Impairments (Kagan et al., 2008).

references

Helm-Estabrooks, N., & Albert, M. L. (2004). Manual of aphasia and aphasia therapy (2nd ed.). Austin, TX: Pro-Ed.

Kagan, A. (2011). A-FROM in action at the Aphasia Institute. Seminars in Speech and Language, 32, 216–228.

Kagan, A., Simmons-Mackie, N., Rowland, A., Hui-jbregts, M., Shumway, E., McEwen, . . . Sharp, S. (2008). Counting what counts: A framework for capturing real-life outcomes of aphasia interven-tion. Aphasiology, 22(3), 258–280. https://doi.org/ 10.1080/02687030701282595

World Health Organization (WHO). (2001). Interna-tional Classification for Functioning, Disability and Health (ICF). Geneva, Switzerland: Author.

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xv

Acknowledgments

We would like to thank Plural Publishing for the opportunity to prepare a third edition of Acquired Language Disorders: A Case-Based Approach for the benefit of students, clinicians, and the patients they serve. We appreciate the support of Barbara Amster, PhD, CCC-SLP, Chair and Program Direc-tor of the Department of Communication Sciences and Disorders, and Kathleen Czekanski, PhD, RN, CNE, Dean of the School of Nursing and Health Sciences. We are also grateful for the guidance and input provided by Plural Publishing from Valerie Johns, Executive Editor; Kalie Koscielak, Associate Acquisitions Editor; Elisa Andersen, Editorial & Mar-keting Assistant; Lori Asbury, Production Manager; Jessica Bristow, Production Assistant, and Carol Elliott, Copyeditor. Our editorial and production

team supported us throughout the process and did so professionally, diligently, and graciously. We are honored that clinicians working with patients with acquired language disorders, as well as professors teaching students about acquired language disor-ders, saw the continued value in this text. We are especially excited and honored that our colleague, Ryan Husak, PhD, CCC-SLP, accepted our invitation to contribute to this edition. The editorial comments and academic information that he provided have been invaluable and enhanced the quality of this third edition. We would also like to thank our gradu-ate assistants, Olivia Scarnulis and Melissa Wojcik, for their diligence in helping us to procure neces-sary information for this text.

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Contributor

Ryan Husak, PhD, CCC-SLPAssistant ProfessorDepartment of Communication Sciences and DisordersLa Salle UniversityPhiladelphia, Pennsylvania

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Evelyn Klein and James Mancinelli dedicate this book to the people with acquired language disorders and their families whom we have treated.

Their courage and determination are inspirational.

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1

Chapter 1

An overvIew oF neUroAnAToMy And neUrophysIoLogy reLATed

To ACqUIred LAngUAge dIsorders (ALd)

The neuron

The brain has more than 100 billion neurons, or nerve cells. These structures comprise the build-ing blocks of the nervous system and are its func-tional “work horses.” Each neuron is composed of a body, referred to as the soma; filamental extensions called dendrites; and longer fibers called axons. Each neuron has one axonal fiber that can mea-sure from micrometers to meters in length (Figure 1–1). The axon functions as a conductor of elec-trical impulses. Dendrites receive stimuli or input from other neurons, and axons send stimuli to other neurons, glands, or muscles (Webb & Adler, 2008). These neurons communicate with each other elec-trochemically via neurotransmitters (a discussion of neurotransmitters appears in this chapter).

The nervous system has sensory neurons (receptors) and motor neurons (effectors). Sensory neurons are sensitive to light, sound, touch, tem-perature, smell, and chemical input, and transmit sensory information from the environment via the nervous system. Motor neurons receive excitation from other cells and send impulses to the muscles instructing them to contract and to the endocrine

glands to regulate hormonal secretions. Input from sensory neurons can be transmitted to motor neu-rons; for example, a sensory neuron may detect a dangerous stimulus and respond by alerting inter-neurons in the spinal cord to notify the motor neu-rons to remove that body part in danger. At the endpoint or terminal of the nerve cell, neurotrans-mitters are released into the synaptic space between the cells. Neurotransmitters are biochemical com-pounds that help neurons communicate, acting as messengers between them (Figure 1–2).

Axon

Dendrites

Nucleus

AxonHillock

Myelin Sheath

Soma

Figure 1–1. neuron.

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2 Acquired LAnguAge disorders: A cAse-BAsed ApproAch

neurotransmitters

Neurotransmitters are chemicals that assist in the regulation of the brain’s ability to control metabolic

activity, speech and language, motivation, person-ality, mood states, and cognition including atten-tion and memory (Bhatnagar, 2002). Each neuron releases neurotransmitters at the synapse, which is where the bulb of the axon makes contact with the

Dendrites

Nucleus

Axon

Muscle

Soma

AxonHillock

Direction ofNeural Impulse

Myelin Sheath

A

Dendrites

Nucleus

Axon

Muscle

Soma

AxonHillock

Direction ofNeural Impulse

Myelin Sheath

B

Figure 1–2. A. Motor neuron. B. sensory neuron. C. events at synapse.

Terminal

Tip of axonSynaptic

cleft

Receptors

Neurotransmittersreleased

Postsynapticmembrane

C

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1. An overvieW oF neuroAnAtoMY & neurophYsioLogY reLAted to Acquired LAnguAge disorders 3

dendrites. The neurotransmitter passes across the synaptic cleft and bonds with the receptor site on the postsynaptic membrane. This results in a change in the electrical current across the cell membrane and the nerve fibers. The change in the electrical valence of the cell is referred to as the action poten-tial. An excess or depletion of neurotransmitters can have significant effects on functioning. For exam-ple, excess dopamine interacting with other factors has been linked to schizophrenia, and a depletion of dopamine concentration contributes to Parkin- son’s disease.

sensory

There are two main types of neurotransmitters: the small molecules and the large molecules, also known as neuropeptides. The small molecule trans-

mitters include acetylcholine, serotonin, dopamine, norepinephrine, glutamate, histamine, and gamma aminobutyric acid (GABA). In this group, GABA is primarily inhibitory whereas glutamate is excitatory. Yet in many cases, neurotransmitters can be either excitatory or inhibitory depending on the recep-tor site. Dopamine can act in this way. The large molecule neuropeptides include vasopressin, soma-tostatin, neurotensin, enkephalin, and endorphins. These neuroactive substances are hormone-medi-ated and affect the body’s metabolic functioning. A pituitary peptide such as endorphin is opioid-like and functions in pain management. Neuroac-tive peptides may be specific to particular organs and have multiple roles in the body. Both groups of neurotransmitters are crucial to a person’s feelings of pleasure, pain, stress, cravings, the promotion of sleep and rest, and emotional attachment, as well as basic metabolic functioning (Schwartz, 1991; Webb & Adler, 2008) (Table 1–1).

Sensory

Motor

Gray matter

White matter

Dorsal root ganglion

Sensoryinput

Motor outputVentral root

Figure 1–3. spinal cord cross-section.

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4 Acquired LAnguAge disorders: A cAse-BAsed ApproAch

The Brain: A Brief review of structure and Function

The central nervous system consists of the brain and spinal cord. Each segment of the spinal cord has both sensory and motor nerves that innervate our skin, organs, and muscles (Figure 1–3). During brain development in childhood, neurons create new connections with other neurons. At birth, the brain

weighs about 350 grams (12 ounces) and is about 1,000 grams (2.2 pounds) at 1 year old. For an adult, the brain weighs approximately 1,200 to 1,400 grams (2.6 to 3.1 pounds) and does not have the ability to create new connections with other neurons, as most neurons cannot be replaced. This section dis-cusses the brain’s covering, the ventricles, and the following major structures of the central nervous system: the cerebral cortex, brainstem, subcortical structures, cerebellum, and the neural pathways.

Table 1–1. selected neurotransmitters

neurotransmitter distribution proposed Impact

Acetylcholine it is the primary neurotransmitter of the peripheral nervous system (pns) and important to the central nervous system (cns) as well. it is concentrated in the basal forebrain, striatum, and reticular formation. it is also concentrated within regions of the brainstem involved with cognition and memory.

involved in voluntary movement of skeletal muscles and viscera including spinal and cranial nerves. drugs that affect cholinergic activity within the body impact heart rate, bladder function, digestion, and may cause dry mouth. this neurotransmitter is also important to sleep-wake cycles. decreased cholinergic projections on muscle cells are found in myasthenia gravis. decreased projections in the hippocampus and orbitofrontal cortex are related to Alzheimer’s disease.

dopamine concentrated in neuronal groups in the basal ganglia. dopaminergic projections originate in the substantia nigra and have terminals in the cortex, amygdala, and nucleus accumbens.

decreased dopamine in the brain is linked to parkinson’s disease. An increase of dopamine in the forebrain is linked to schizophrenia. dopamine is involved in cognition and motivation and is related to wanting pleasure associated with love and addiction.

norepinephrine norepinephrine neurons are found in the pons and medulla. Most are in the reticular formation and locus ceruleus.

important to maintaining attention and focus. it increases excitation in the brain and is involved in wakefulness and arousal. it is also associated with the sympathetic nervous system and feelings of panic, fight, or flight.

serotonin synthesized from the amino acid tryptophan and found in blood platelets and the gastrointestinal tract. terminals are localized in nerve pathways from the nuclei at the center of the reticular formation.

controls mood, regulates sleep, involved in perception of pain, body temperature, blood pressure, and hormonal functioning. Low levels are associated with depression. it is also involved in memory and emotion.

gABA A major neurotransmitter with cells found in the cerebral cortex, cerebellum, and hippocampus. gABA projections are inhibitory from the striatum to the globus pallidus and substantia nigra to the thalamus.

Loss of gABA in the striatum is linked to a degenerative disease that causes involuntary abnormal movements (huntington’s chorea). it is associated with the inhibition of motor neurons.

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The Coverings of the Brain, ventricles, and Cerebrospinal Fluid

There are three layers of tissues, the meninges, which protect the brain. They include the dura mater, arachnoid membrane, and pia mater. Between the arachnoid membrane and pia mater is the subarach-noid space. This space contains blood vessels and cerebrospinal fluid (CSF).

The CSF protects the brain. It is a clear and colorless fluid that circulates throughout the brain and the spinal cord cushioning and protecting them from injury. There are four ventricles within the brain: two lateral ventricles, the third ventricle, and the fourth ventricle. Each ventricle contains the cho-roid plexus, which is the structure that produces the CSF. The CSF flows from one ventricle to the next and finally into the subarachnoid space. It is reab-sorbed back into the blood. The lateral ventricles are connected to the third ventricle, and the third ventricle is connected to the fourth. Blockage in any of the spaces can cause CSF to back up, leading to a number of serious medical conditions includ-ing hydrocephalus, which increases pressure on the brain (Figures 1–4 and 1–5).

Cerebral Cortex

The cerebral cortex is also referred to as the cere-brum and it composes the largest part of the brain. It is involved in complex thought and executive func-tions, learning, personality, movement, touch, vision, and is divided into two hemispheres: right and left. The outer surface of each hemisphere is composed of gray matter that contains nerve cell bodies (more than 6 billion), glial cells, capillaries, axons, and dendrites. The gray matter directs sensory or motor stimuli to the interneurons of the central nervous system for responsiveness via synaptic activation. White matter consists of axons that travel through-out the cortex. These structures are referred to as white matter because of the color of the myelinated sheaths that wrap each axon. The color reflects the fact that they consist primarily of lipids, or fatty material. As noted in the section on neurons, the axon is responsible for carrying information away from the brain to the periphery. These axons form tracts, and the tracts take the information to their intended destination. Two neurologic diseases that manifest white matter changes are multiple sclero-sis, which destroys the myelin shield surrounding the axons, and Alzheimer’s disease. In Alzheimer’s disease, these white matter changes produce amy-loid plaques.

The two hemispheres of the brain primarily receive sensory information from the contralateral side of the body and affect movement on the con-tralateral side of the body. The two hemispheres are separated by a longitudinal fissure, but com-municate by two large bundles of axons, the corpus callosum, composed of cortical association fibers, and subcortical connections. The proper and effi-cient functioning of the corpus callosum is critical to the transmission of information between the left and right hemispheres. The left hemisphere typi-cally is best for processing speech and language and is involved in verbal memory. The right hemisphere has been known to process paralinguistic informa-tion and pragmatics, as well as providing skills with nonlinguistic information that is visual, spatial, emo-tional, and musical.

The cerebral cortex integrates sensory and motor signals in order to execute the primary sen-sory, motor, and association area functions. The

Lateral ventricles

Third ventricle

Fourth ventricle

Figure 1–4. ventricles.

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sensory areas of the cortex receive input from the environment such as touch, taste, smell, vision, and hearing. The motor areas are responsible for mus-cular activity throughout the body. The association areas of the cortex connect the sensory and motor systems and give humans the ability to integrate the sensory (afferent) and the motor (efferent) informa-tion, permitting normal function.

The following website provides an overview of midsagittal brain structures and functions: http://www.psych.ualberta.ca/~ITL/brain/ (Figure 1–6). This figure illustrates structures of the subcortex and cerebellar, and brainstem regions.

Lobes of the Brain

Each hemisphere is composed of four lobes: the frontal, temporal, parietal, and occipital (Figure 1–7). The left side of the brain generally controls the right side of the body, and the right hemisphere con-

trols the left side of the body. Damage to either hemisphere can result in paralysis or lost sensation. Weakness on one side of the body is referred to as hemiparesis, and paralysis on one side of the body is referred to as hemiplegia. Thus, if a person has a left hemispheric stroke with a paralysis on the right side of the body, that person has a right hemiple-gia. If the right side is only weak, it is then a right hemiparesis.

The following website provides an overview of the lobes of the brain and their associated functions: http://www.stanford.edu/group/hopes/basics/brain tut/ab4.html. The lateral views provide further detail of the structural landmarks and functional associa-tion areas of a cerebral hemisphere (Figure 1–8).

The Frontal Lobes. The frontal lobes are at the most anterior part of the brain. The anterior limit of the frontal lobe is dorsal and posterior to the bony case of the eyes. The posterior limit of the frontal

Skin of scalp

Periosteum

Bone of skull

Dura mater

Arachnoid

Subarachnoidspace

Cerebral cortex

Arachnoid granulation

Superior sagittal sinus

Dura mater

Figure 1–5. Meninges.

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lobes is the precentral gyrus. The posterior portion of the frontal lobe is specialized for control of move-ment. In humans, the frontal lobe is critical for lan-guage production. The prefrontal area is important for planning and initiation, judgment and reason-ing, concentration, emotional range, disinhibition of behaviors, and adaptation to change. Functions of the frontal lobes are essential to consciousness

and let us appropriately judge what we are doing in the environment and how we initiate and respond to life’s events. Proper functioning assists with our emotional response and expressive language choices. Essentially, the frontal lobes make us aware of our conscious actions. Our emotional responses, memory for habits, motor activities, and expressive language are all mediated by the frontal lobe.

Fornix, body

Fornix, columnThalamus

Choroid plexus

Posteriorcommissure

Pineal

Superiorcolliculus

Inferiorcolliculus

Cerebellum

Medulla

Pyramid

Basilar ponsMamillary body

Optic chiasm

Hypothalamus

Anteriorcommissure

Corpus callosum, body

Figure 1–6. Midsagittal view of the brain.