Electromyography in CNS Disorders. Central EMG

184 Pages·1984·3.319 MB·English

by  Bhagwan T. Shahani (Eds.)

E L E C T R O M Y O G R A P HY
IN C NS D I S O R D E R S:
C E N T R AL E MG
Edited by
Bhagwan T. Shahani, M.D., D. Phil. (Oxon)
Associate Professor of Neurology, Harvard Medical
School; Director, EMG and Motor Control Unit, Clinical
Neurophysiology Laboratory, Massachusetts General
Hospital, Boston, Massachusetts
With 12 contributing authors
BUTTERWORTH PUBLISHERS
Boston · London
Sydney · Wellington · Durban · Toronto
Copyright © 1984 by Butterworth Publishers
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, without the
prior written permission of the publisher.
Library of Congress Cataloging in Publication Data
Main entry under title:
Electromyography in CNS disorders.
Bibliography: p.
Includes index.
1. Central nervous system—Diseases—Diagnosis.
2. Electromyography. I. Shahani, Bhagwan T.
RC361.E38 1983 616.8 '047547 83-14431
ISBN 0-409-95144-7
Butterworth Publishers
80 Montvale Avenue
Stoneham, MA 02180
10 9 8 7 6 5 4 3 21
Printed in the United States of America.
CONTRIBUTING AUTHORS
B.L. Day, Ph.D. Harald Hefter, Ph.D.
Department of Neurology, Institute Neurology Clinic,
of Psychiatry and King's College University of Düsseldorf,
Hospital, De Crespigny Park, Düsseldorf, West Germany
Denmark Hill,
London, England Völker Homberg, M.D.
Neurology Clinic,
University of Düsseldorf,
Paul J. Delwaide, M.D.
Düsseldorf, West Germany
Professeur Agrégé, Section of
Neurology and Clinical
James W. Lance, M.D.
Neurophysiology, Department of
Professor of Neurology, University
Internal Medicine, University of
of New South Wales; Chairman,
Liège, Liège, Belgium
Department of Neurology, The
Prince Henry Hospital, Sydney,
Milan R. Dimitrijevic, M.D., D.Sc. Australia
Visiting Professor of Clinical
Neurophysiology, The Institute for C. David Marsden, F.R.C.P.,
Rehabilitation and Research; M.R.C. Psych.
Visiting Professor, Department of Professor and Head, University
Rehabilitation, Baylor College of Department of Neurology, Institute
Medicine, Houston, Texas of Psychiatry and King's College
Hospital Medical School,
London, England
Hans-Joachim Freund, M.D.
Professor and Chairman, Neurology
J.C. Rothwell, Ph.D.
Clinic, University of Düsseldorf,
Department of Neurology, Institute
Düsseldorf, West Germany
of Psychiatry and King's College
Hospital, De Crespigny Park,
Karl-Erik Hagbarth, M.D. Denmark Hill,
Professor and Chairman, London, England
Department of Clinical
Neurophysiology, Bhagwan T. Shahani, M.D.,
University Hospital, D. Phil. (Oxon)
Uppsala, Sweden Associate Professor of Neurology,
ν
vi
Harvard Medical School; Director, University of Munich,
EMG and Motor Control Unit, Munich, West Germany
Clinical Neurophysiology Laboratory,
Massachusetts General Hospital,
Boston, Massachusetts Robert R. Young, S.B., M.D.
Professor of Neurology, Harvard
Albrecht Struppler, M.D. Medical School; Director, Clinical
Professor and Head, Department of Neurophysiology Laboratory,
Neurology and Clinical Massachusetts General Hospital,
Neurophysiology, Technical Boston, Massachusetts
PREFACE
Electromyography and electroneurography, in which electrical activity produced
by skeletal muscles and peripheral nerves is studied, have proved to be useful in
investigation and understanding of a variety of neurological disorders. In most
laboratories, however, these electrodiagnostic techniques have been used to help
in the diagnosis of diseases that affect the peripheral nerves, neuromuscular
junctions, or skeletal muscle fibers. Although major advances in electronic and
computer technology have made it possible to study, quantitate, and document
reflex activity in intact human subjects, most neurologists still rely on gross
clinical observations and most electromyographers continue to use conventional
techniques of EMG and nerve conduction studies to differentiate myopathy from
neuropathy. In the past three decades, it has been shown that by using
electrophysiological techniques one can record most of the reflexes (both
proprioceptive and exteroceptive) commonly studied in a clinical setting. These
studies, in addition to providing better insight into the underlying physiological
mechanisms, provide an objective quantitative measure of function of the central
and peripheral nervous systems in man.
The application of clinical neurophysiological studies using classical EMG
and nerve conduction techniques to evaluate function of the central nervous
system is termed central EMG.
As the president (1981-1982) of the American Association of Electromyo-
graphy and Electrodiagnosis I organized an international symposium on central
EMG in order to introduce practicing electromyographers to new concepts in
clinical neurophysiology. Distinguished clinical neurophysiologists from
different parts of the world participated in the symposium. Many physicians who
attended the symposium were convinced that electromyographic techniques are
useful in documenting normal and abnormal functions, not only of the peripheral
neuromuscular apparatus, but also of the autonomic and central nervous
systems. The purpose of this book is to introduce neurologists, physiatrists,
neurosurgeons, orthopedic surgeons, clinical electromyographers, and other
interested physicians to the new concept of central EMG. Since many of the
techniques described here are used for studies of motor control in man, this volume
will also be useful for physical therapists and occupational therapists who are
involved in the treatment of patients with disorders of the central nervous system.
It is hoped that this book, which has contributions from scientists whose work has
been responsible for major advances in clinical neurophysiology, will stimulate
interest in wider application of electrophysiological techniques for diagnosis.
ix
χ
monitoring, and treatment of patients seen in departments of neurology,
neurosurgery, rehabilitation medicine, and orthopedic surgery.
I would like to express my gratitude to my clinical neurophysiologist col-
leagues who came from all over the world to participate in the symposium and
for writing reviews highlighting some of their work related to central EMG. My
special thanks also go to my colleague Dr. Robert R. Young for his help and ad-
vice, and to Ms. Susan Wyoral for carefully reviewing the chapter manuscripts,
illustrations, and references. I also wish to thank members of the American
Association of Electromyography and Electrodiagnosis for their support and en-
couragement, and for helping me to organize the first international symposium
for the association. Finally, I wish to thank the publishers for their excellent
cooperation during the preparation of this book.
Bhagwan T. Shahani, M.D., D. Phil. (Oxon)
CHAPTER 1
Pyramidal and
Extrapyramidal Disorders
James W. Lance
PRINCIPLES OF MOTOR CONTROL
Pyramidal and Extrapyramidal Pathways
The motor cortex used to be considered the cerebral center for the control of
movement in which individual muscles or whole patterns of movement were
"represented/' More recently, the motor cortex appears to have been relegated to a
subordinate status and its direct projection to spinal motor neurons, the pyramidal
tract, regarded as little more than an interneuron linking the brain with the spinal
cord. The truth probably lies somewhere in between. Of some 20 million neurons
descending from the motor cortex, only one million proceed to the pyramids of the
medulla, decussating to form the lateral corticospinal tract. The remaining
extrapyramidal, or "parapyramidal, " fibers are distributed to the basal ganglia,
thalamus, red nucleus, pons, and the medullary reticular formation (Phillips and
Porter 1977).
The basal ganglia and cerebellum play a part in the planning or program-
ming of movement as well as feeding back information through the thalamus to
the motor cortex, correcting movements in progress. The final expression of
extrapyramidal activity in the control of muscle tone and of coarse movements
involving axial and proximal muscles (and influencing flexor and extensor
synergies of the limbs) is mediated by the reticulospinal and vestibulospinal
pathways. With this background of extrapyramidal activity, or complementary
to it, is the ability, conferred by the monosynaptic projection from cortex to
spinal motor neuron of pyramidal tract fibers, to use distal muscles discretely for
precise movements of the hands and feet.
The Basal Ganglia
The caudate nucleus and pu tarnen (neostriatum) receive afferent fibers from
almost all parts of the neocortex, particularly the sensorimotor area (Denny-
Brown 1962). Fibers from the neostriatum project through the globus pallidus
and substantia nigra to the thalamus, where they make two important connec-
1
2 ELECTROMYOGRAPHY IN CNS DISORDERS: CENTRAL EMG
tions. The first of these is in the ventrolateral thalamic nucleus, from which ef-
ferents pass to the motor cortex, thus completing a loop between cortex and basal
ganglia (Fig. 1.1). Although the ventrolateral thalamic nucleus is also a relay station
between the cerebellum and motor cortex, there is little integration at this site of the
output from basal ganglia and cerebellum in the modulation of cortical activity.
The second connection made by basal ganglia fibers in the thalamus takes
place in the medial nuclei, which have reciprocal connections with the midbrain
reticular formation (Fig. 1.2), thought to be responsible for the control of muscle
tone by the basal ganglia.
The discharge of cells in the caudate nucleus and putamen is regulated by a
nigrostriatal pathway using dopamine as a transmitter (Fig. 1.3), while a pathway
in the reverse direction from neostriatum to substantia nigra releases gamma-
aminobutyric acid. The degeneration of the substantia nigra in Parkinson's
disease releases the basal ganglia from a restraining influence so that its links with
Figure 1.1 Cortico-strio-thalamo-cortical loop. Corticofugal fibers concerned with the
programming and feedback of movement pass to the caudate nucleus (CN) and putamen
(P). The caudate nucleus and putamen project to the ventrolateral nucleus of the thalamus
(Th) via the globus pallidus (GP) and substantia nigra (SN) and thence to the motor cortex
(MC). (ST = subthalamic nucleus; RF = reticular formation.)
PYRAMIDAL AND EXTRAPYRAMIDAL DISORDERS 3
MC
Figure 1.2 Reciprocal connections of the basal ganglia with the reticular formation. Fibers
from the caudate nucleus (CN) and putamen (P) project through the globus pallidus (GP)
to medial thalamic nuclei and thence to the reticular formation of the midbrain. Fibers
from the substantia nigra (SN) feed into the same pathway. The reticular formation pro-
jects back through the medial thalamic nuclei to the caudate nucleus.
the motor cortex and the reticular formation become hyperactive, causing tremor
and increased muscle tone.
Another circuit with a predominantly inhibitory influence joins the globus
pallidus with the subthalamic nucleus (see Fig. 1.3). Damage to the subthalamic
nucleus or its projections causes wild rotary and flinging movements of the con-
tralateral limbs, known as hemiballismus.
The Cerebellum
The cerebellar hemispheres develop in complexity with the cerebral cortex as the
phylogenetic scale is ascended, comprising 88% of the human cerebellum (Eccles
1977). The intermediate zone, which runs parallel to the vermis and lateral to it,
forms a closed loop with the motor cortex (Fig. 1.4). It receives proprioceptive in-
formation from the spinal cord, as well as afférents from the cortex (by a crossed
4 ELECTROMYOGRAPHY IN CNS DISORDERS: CENTRAL EMG
MC
Figure 1.3 Reciprocal connections modulating basal ganglia function, with the sub-
thalamic nucleus (ST) (interruption of this pathway causes hemiballismus), and with the
substantia nigra (SN). Striatonigral neurons inhibit SN cells by the release of gamma-
aminobutyric acid. The nigrostriatal pathway, which uses dopamine as a transmitter and
degenerates in Parkinson's disease, inhibits cells in the putamen and caudate nucleus.
pathway synapsing in the pons), and projects back to the motor cortex through
the globose and emboliform nuclei. This cortico-ponto-cerebello-cortical path-
way monitors pyramidal tract activity in relation to limb position, providing on-
line correction of movement. The circuit takes about 20 msec to complete in the
human brain (Eccles 1977). In addition to this feedback function, the intermediate
zone may initiate movements in response to a proprioceptive stimulus.
The lateral zone of the cerebellar hemispheres receives afférents from area 6
and from sensorimotor association areas, such as 5 and 7 (Fig. 1.5), that play a
part in the planning of movement. Some follow the cortico-ponto-cerebellar
route and end on Purkinje cells as mossy fibers, while others synapse in the in-
ferior olive (which introduces a delay of about 10 msec into the system) before
ending as climbing fibers. The mode of interaction between mossy and climbing
fibers is not fully understood. The lateral zones of the cerebellar hemispheres pro-
ject back to the sensorimotor cortex through the ventrolateral thalamus, and are