Contents

  1  Neuroanatomical and neuropathological framework of speech and language

Introduction

Gross anatomy of the nervous system

Summary

  2  Aphasia syndromes

Introduction

Models of language – a brief history

Classification of aphasia

Bostonian Aphasia Syndromes

Lurian aphasia syndromes

Methods of lesion localization in aphasia

Magnetic resonance imaging

Summary

  3  Subcortical aphasia syndromes

Introduction

Role of subcortical structures in language: historical perspective

Neuroanatomy of the subcortical region

Aphasia syndromes associated with striatocapsular and thalamic lesions

Language disorders associated with cerebellar lesions

Models of subcortical participation in language

Role of subcortical structures in language: evidence from neurosurgical lesions

Role of subcortical structures in language: evidence from functional neuroimaging

Language disorders in degenerative subcortical syndromes

Summary

  4  Speech-language disorders associated with traumatic brain injury

Introduction

Classification of traumatic brain injury

Epidemiology of traumatic brain injury

Biomechanics of head injury

Neuropathophysiology of traumatic brain injury

Medical management of traumatic brain injury

Language disorders subsequent to traumatic brain injury

Speech disorders subsequent to traumatic brain injury

Summary

  5  Language disorders subsequent to right-hemisphere lesions

Introduction

Lateralization of language function

Linguistic functions of the right hemisphere

Other neuropsychological sequelae of right-hemisphere damage

Development of language lateralization: evidence from focal brain lesions and hemispherectomy

Language functions of the right hemisphere: evidence from commissurotomy

Anatomical differences between the left and right hemispheres

The role of the right hemisphere in recovery from aphasia

Summary

  6  Language disturbances in dementia syndromes

Introduction

Types of dementia

Language disorders in cortical dementias

Relationship between the language of dementia and aphasia

Summary

  7  Language disorders associated with diseases of the cerebral white matter

Introduction

Language disorders in multiple sclerosis

Language disorders in Binswanger’s disease

Language disorder in progressive multifocal leukoencephalopathy

Summary

  8  Neurological disturbances associated with aphasia

Introduction

Apraxia

Apraxia of speech

Alexia and agraphia

Agnosia

Gerstmann syndrome

Summary

  9  Dysarthrias associated with upper and lower motor neurone lesions

Introduction

Flaccid dysarthria (lower motor neurone dysarthria)

Spastic dysarthria (upper motor neurone dysarthria)

Summary

10  Dysarthrias associated with extrapyramidal syndromes

Introduction

Models of hypokinetic and hyperkinetic movement disorders

Hypokinetic dysarthria

Hyperkinetic dysarthria

Summary

11  Dysarthrias associated with lesions in other motor systems

Ataxic dysarthria

Mixed dysarthria

Summary

12  Acquired childhood speech-language disorders

Introduction

Acquired childhood aphasia

Acquired childhood dysarthria

Summary

Index

This edition first published 2010

© 2010 John Wiley & Sons Ltd

First edition published by Chapman and Hall 1990

First edition reprinted by Chapman and Hall 1992, 1994, 1995

First edition reprinted by Stanley Thornes 1997

© Bruce Murdoch

Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientific, Technical and Medical business with Blackwell Publishing.

Registered office

John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United Kingdom

Editorial office

John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United Kingdom

For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at

www.wiley.com/wiley-blackwell.

The right of the author to be identified as the author of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

Library of Congress Cataloging-in-Publication Data

Murdoch, B. E., 1950–

Acquired speech and language disorders : a neuroanatomical and functional neurological approach / Bruce E. Murdoch. – 2nd ed.

p. ; cm.

Includes bibliographical references and index.

ISBN 978-0-470-02567-3 (pbk. : alk. paper) 1. Language disorders. 2. Brain damage. 3. Neuroanatomy. I. Title.

[DNLM: 1. Language Disorders–physiopathology. 2. Speech Disorders–physiopathology.

3. Language Disorders–etiology. 4. Nervous System–anatomy & histology. 5. Nervous System Diseases–complications. 6. Speech Disorders–etiology. WL 340.2 M974a 2010]

RC423.M738 2010

616.85′5–dc22

2009014223

A catalogue record for this book is available from the British Library.

1 2010

1

Neuroanatomical and neuropathological framework of speech and language

Introduction

Human communication in the form of speech-language behaviour is dependent upon processes which occur in the nervous system. Consequently, knowledge of the basic structure and function of the human nervous system is an essential prerequisite to the understanding of the anatomical, physiological and pathological basis of human communication disorders. With this in mind, the materials presented in the present chapter are intended to provide the reader with an introductory knowledge of the anatomy of the human nervous system. Such knowledge is necessary prior to discussion of the signs, symptoms and neurological mechanisms underlying the various acquired neurogenic speech-language disorders in later chapters. Where necessary, more detailed information regarding the anatomy of specific brain structures important for speech-language function is provided in subsequent relevant chapters.

The nervous system is an extremely complex organization of structures which serves as the main regulative and integrative system of the body. It receives stimuli from the individual’s internal and external environments, interprets and integrates that information and selects and initiates appropriate responses to it. Consider this process in the context of a spoken conversation between two persons. The words spoken by one partner in the conversation, in the form of sound waves, are detected by receptors in the inner ear of the second partner and conveyed to the cerebral cortex of the brain via the auditory pathways where they are perceived and interpreted. Following integration with other sensory information, a response to the verbal input is formulated in the language centres of the brain and then passed to the motor areas of the brain (i.e. areas that control muscular movement) for execution. Nerve impulses from the motor areas then pass to the muscles of the speech mechanism (e.g. tongue, lips, larynx, etc.) leading to the production of a verbal response by the second person.

Speech is produced by the contraction of the muscles of the speech mechanism, which include the muscles of the lips, jaw, tongue, palate, pharynx and larynx as well as the muscles of respiration. These muscle contractions, in turn, are controlled by nerve impulses which descend from the motor areas of the brain to the level of the brainstem and spinal cord and then pass out to the muscles of the speech mechanism via the various nerves which arise from either the base of the brain (cranial nerves) or spinal cord (spinal nerves). Likewise, language is also dependent on processes which occur in the brain, particularly in the cerebral cortex.

Gross anatomy of the nervous system

For the purposes of description, the nervous system can be arbitrarily divided into two large divisions: the central nervous system and the peripheral nervous system. The central nervous system comprises the brain and spinal cord, while the peripheral nervous system consists of the end organs, nerves and ganglia, which connect the central nervous system to other parts of the body. The major components of the peripheral nervous system are the nerves which arise from the base of the brain and spinal cord. These include 12 pairs of cranial nerves and 31 pairs of spinal nerves respectively. The peripheral nervous system is often further subdivided into the somatic and autonomic nervous systems, the somatic nervous system including those nerves involved in the control of skeletal muscles (e.g. the muscles of the speech mechanism) and the autonomic nervous system including those nerves involved in the regulation of involuntary structures such as the heart, the smooth muscles of the gastrointestinal tract and exocrine glands (e.g. sweat glands). Although the autonomic nervous system is described as part of the peripheral nervous system, it is really part of both the central and peripheral nervous systems. It must be remembered, however, that these divisions are arbitrary and artificial and that the nervous system functions as an entity, not in parts. The basic organization of the nervous system is summarized in Figure 1.1.

Histology of the nervous system

Cell types

The nervous system comprises many millions of nerve cells, or neurones, which are held together and supported by specialized non-conducting cells known as neuroglia. The major types of neuroglia include astrocytes, oligodendrocytes and microglia. It is the neurones that are responsible for conduction of nerve impulses from one part of the body to another, such as from the central nervous system to the muscles of the speech mechanism to produce the movement of the lips, tongue and so on for speech production. Although there are a number of different types of neurones, most consist of three basic parts: a cell body (also known as a soma or perikaryon) which houses the nucleus of the cell; a variable number of short processes (generally no more than a few millimetres in length) called dendrites (meaning ‘tree-like’) which receive stimuli and conduct nerve impulses; and a single, usually elongated, process called an axon, which in the majority of neurones is surrounded by a segmented fatty insulating sheath called the myelin sheath. A schematic representation of a neurone is shown in Figure 1.2.

Figure 1.1 Basic organization of the nervous system.

Figure 1.2 Structure of a typical motor neurone.

The cytoplasm of a neurone contains the usual cell organelles (e.g. mitochondria) with the exception of the centrosome. Mature neurones cannot divide or replace themselves because of the lack of a centrosome. In addition to the usual organelles, however, the cytoplasm of nerve cells also contains two organelles unique to neurones: Nissl substance (chromidial substance) and neurofibrils. Seen with the light microscope Nissl substance (bodies) appears as rather large granules widely scattered throughout the cytoplasm of the nerve cell body. Nissl bodies specialize in protein synthesis, thereby providing the protein needs for maintaining and regenerating neurone processes and for renewing chemicals involved in the transmission of nerve impulses from one neurone to another. Seen with the light microscope neurofibrils are tiny tubular structures running through the cell body, axon and dendrites. Although the function of the neurofibrils is uncertain, it has been suggested that they may facilitate the transport of intracellular materials within the neurone. In Alzheimer’s disease, the neurofibrils become abnormally twisted, a feature used in the diagnosis of this condition (see Chapter 6).

In contrast to neurones, neuroglial cells (also often simply referred to as glial cells) contribute to brain function mainly by supporting neuronal functions. Although based on current evidence their role appears to be subordinate to that of the neurones, without glial cells the brain could not function properly. Astrocytes are the most numerous of the glial cells and are widely distributed in the central nervous system. These cells fill spaces between neurones and lie in close proximity to both neurones and capillaries. Evidence suggests that an essential role for astrocytes is the regulation of the chemical content of the extracellular space (e.g. astrocytes envelop synaptic junctions in the brain and thereby restrict the spread of neurotransmitter molecules released by neurones). Further, special proteins found within the membranes of astrocytes may be involved in the removal of many neurotransmitters from the synaptic cleft. In addition to regulating neurotransmitters, astrocytes also regulate the concentration of substances present within the extracellular space that have the potential to interfere with normal functioning of the neurones (e.g. astrocytes regulate the concentration of potassium ions in the extracellular fluid in the brain).

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!

Lesen Sie weiter in der vollständigen Ausgabe!