Pain Syndromes in Neurology

289 Pages·1990·8.198 MB·English

by  Howard L. Fields (Eds.)

Butterworths International Medical Reviews
Neurology
Published titles
1 Clinical Neurophysiology
Erik Stalberg and Robert R. Young
2 Movement Disorders
C. David Marsden and Stanley Fahn
3 Cerebral Vascular Disease
Michael J. G. Harrison and Mark L. Dyken
4 Peripheral Nerve Disorders
Arthur K. Asbury and R. W. Gilliatt
5 The Epilepsies
Roger J. Porter and Paolo L. Morselli
6 Multiple Sclerosis
W. I. McDonald and Donald H. Silberberg
7 Movement Disorders 2
C. David Marsden and Stanley Fahn
8 Infections of the Nervous System
Peter G. E. Kennedy and Richard T. Johnson
9 The Molecular Biology of Neurological Disease
Roger N. Rosenberg and A. E. Harding
Pain Syndromes in
Neurology
Edited by
Howard L. Fields, MD, PhD
Professor of Neurology and Physiology, University of California, San Francisco,
Cahfornia, USA
Butterworths
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First published 1990
© Butterworth & Co. (Publishers) Ltd, 1990
British Library Cataloguing in Publication Data
Pain syndromes in neurology.
1. Man. Nervous system. Pain
L Fields, Howard L.
616.8Ľ472
ISBN 0-407-01124-2
Library of Congress Cataloging-in-Publication Data
Pain syndromes in neurology/edited by Howard L. Fields,
p. cm. - (Butterworths international medical reviews.
Neurology : 8)
Includes bibliographical references.
ISBN 0-407-01124-2
1. Pain-Pathophysiology. 2. Nervous system-Pathophysiology.
I. Fields, Howard L. II. Series.
[DNLM: 1. Nervous System-physiopathology. 2. Pain -
physiopathology. Wl BU98U/WL 704 P1473]
RB 127.P35 1990
616'.0472-dc20
DNLM/DLC 89-22369
for Library of Congress CIP
Photoset by TecSet Ltd.
Printed and bound in Great Britain by Courier International Ltd,
Tiptree, Essex.
Foreword
For almost a quarter of a century (1951-1975), subjects of topical interest were
written about in the periodic volumes of our predecessor. Modern Trends in
Neurology. Although both that series and its highly regarded editor, Dr Denis
Wilhams, are now retired, the legacy continues in the present Butterworths series
in Neurology. As was the case with Modern Trends, the current volumes are
intended for use by physicians who grapple with the problems of neurological
disorder on a daily basis, be they neurologists, neurologists in training, or those in
related fields such as neurosurgery, internal medicine, psychiatry, and rehabilita­
tion medicine.
Our purpose is to produce annually a monograph on a topic in chnical neurology
in which progress through research has brought about new concepts of patient
management. The subject of each monograph is selected by the Series Editors using
two criteria: first, that there has been significant advance in knowledge in that area
and, second, that such advances have been incorporated into new ways of
managing patients with the disorders in question.
The present volume on Neuropathic Pain fits the criteria admirably. Dr Howard
Fields has chosen his contributors well, and they have set forth clearly the current
understanding of the pathophysiology of neuropathic pain and how best to manage
it.
These two criteria have been the guiding spirit behind each volume, and we expect
it to continue. In effect we emphasize research, both in the clinic and in the
experimental laboratory, but principally to the extent that it changes our collective
attitudes and practices in caring for those who are neurologically afflicted.
C. D. Marsden
A. K. Asbury
Series Editors
Preface
The diagnosis and treatment of painful conditions associated with dysfunction of
the peripheral or central nervous system is an important part of neurologic practice.
Although much progress has been made, these conditions are still incompletely
understood and often unresponsive to treatment. This book is intended to address
both of these problems by informing the reader about advances in three areas: first,
the normal anatomy and physiology of pain, second, the pathophysiology of
damaged sensory neurons and third, the diagnosis and treatment of patients with
neuropathic pain.
This is an appropriate time for this book because there has been a great
expansion of knowledge about the neurobiology of pain sensation. We now have a
much more accurate and detailed idea of the normal sensory processing of the pain
message. We have particularly detailed descriptions, in both humans and
subhuman primates, of cutaneous primary afferents. Furthermore, extensive
animal research has elucidated the neural circuitry of the spinal cord dorsal horn,
the first central nervous system relay of input from primary afferent nociceptors.
Progress has also been made in our knowledge of the central nervous system
pathways that relay the pain message from the spinal cord to the thalamus and
cortex.
It is clear that knowledge of the normal physiology of pain is critical to our
understanding of clinical pain syndromes. Scientists and clinicians interested in pain
have long been interested in the fascinating and troublesome paradox that damage
to the segmental apparatus or central pathways for nociception can produce
chronic, severe and intractable pain. The first attempt to provide a detailed
explanation of this paradox based on our expanded knowledge of primary afferents
and dorsal horn circuitry was Melzack and Wall's Gate Control Hypothesis,
published in 1965. In the quarter century since that publication appeared our
knowledge of dorsal horn circuitry has grown immensely and with it, the
sophistication of our models of neuropathic pain. We are now aware that there are
multiple factors other than intense stimuli that can generate a pain signal. These
factors include sympathetic nervous system activity, crosstalk between damaged
peripheral axons, hyperactivity in regenerating primary afferents or in deafferented
central pain-transmission neurons.
vn
VIH
It is obvious that better understanding and treatment of painful nervous system
dysfunction will require accurate clinical description as well as animal research that
is both innovative and clinically relevant. In this age of subspecialization, this
means that scientists and clinicians must collaborate and communicate.
Accordingly, this book has two major goals: first, to describe certain painful
conditions that appear to result from dysfunction of the nervous system, and
second, to review those recent advances in the neurobiology of pain that are
directly relevant to understanding how such pain comes about. I am fortunate to
have been able to recruit an outstanding group of neuroscientist and clinician
contributors. I hope that their efforts will prove as informative and stimulating to
the reader as they have been for me.
Howard L. Fields
Contributors
Arthur Κ. Asbury, MD
Van Meter Professor of Neurology, University of Pennsylvania, School of
Medicine, Philadelphia, Pennsylvania, USA
Kim J. Burchiel, MD, FACS
Professor and Head, Division of Neurosurgery, The Oregon Health Sciences
University, Oregon, USA.
James N. Campbell, MD
Associate Professor of Neurosurgery, Johns Hopkins University School of
Medicine, Baltimore, Maryland, USA
Marshall Devor, PhD
Associate Professor and Chairman, Department of Zoology, Life Sciences
Institute, Hebrew University of Jerusalem, Jerusalem, Israel.
Howard L. Fields, MD, PhD
Professor of Neurology and Physiology, Department of Neurology, School of
Medicine, University of California, San Francisco, California, USA
Ronald C. Kramis, PhD
Senior Research Associate, Robert S. Dow Neurological Sciences Institute, Good
Samaritan Hospital and Medical Center, Portland, Oregon, USA
Richard A. Meyer
Principal Professional Staff, Applied Physics Laboratory; Associate Professor of
Surgery and Biomedical Engineering, Johns Hopkins University School of
Medicine, Baltimore, Maryland, USA
Richard Payne, MD
Associate Professor of Neurology, University of Cincinnati Medical Center; Chief,
Neurology Service, VA Medical Center, Cincinnati, Ohio, USA
IX
χ Contributors
Russell Κ. Portenoy, MD
Director of Analgesic Studies, Pain Service, Assistant Attending Neurologist,
Department of Neurology, Memorial Sloan-Kettering Cancer Center; Assistant
Professor of Neurology, Cornell University Medical College, New York, New
York, USA
Srinivasa N. Raja, MD
Assistant Professor, Department of Anesthesiology and Critical Care Medicine,
Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Z. Harry Rappaport, MD
Senior Lecturer in Neurosurgery, Hadassah University Hospital, Jerusalem, Israel
William J. Roberts, PhD
Senior Scientist and Chairman, Robert S. Dow Neurological Sciences Institute,
Good Samaritan Hospital and Medical Center, Portland, Oregon, USA
Ronald R. Tasker, MD
Head, Division of Neurosurgery, Toronto General Hospital; Professor of Surgery,
University of Toronto, Toronto, Ontario, Canada
C. Peter N. Watson, MD, FRCP(C)
Assistant Professor, Department of Medicine, University of Toronto, Toronto,
Ontario, Canada
1
Introduction
Η. L. Fields
INTRODUCTION
The major objective of this book is to present an overview of the chnical features,
pathophysiology and treatment of certain painful conditions that neurologists are
often called upon to see. The focus will be upon those syndromes for which there
have been advances in treatment, clinical description, or relevant areas of basic
research. Of particular importance are advances in understanding of the pain
associated with dysfunction of the nervous system. These conditions (e.g. nerve
entrapments and neuromas, postherpetic neuralgia, causalgia, thalamic syndrome)
take a terrible toll on the patients afflicted by them because they are often severe,
unremitting and refractory to treatment. Fortunately, over the past two decades
significant progress has been made in unravelling the processes set in motion by
neural injury. The search for effective treatments has also started. This chapter
reviews neural mechanisms relevant to pain perception and ends with a brief review
of neuropathic pain.
PAIN PATHWAYS
Three major processes underly sensory experiences that are produced by stimuh:
transduction, transmission and perception. In this context transduction refers to the
process by which a stimulus is converted to receptor membrane depolarization and
then nerve impulses. In the somatosensory system this process normally occurs in
the peripheral terminals of dorsal root ganglion cells (primary afferents). Primary
afferents fall into distinct classes determined by the specific types of stimuli they
respond to and the conduction velocity of their axons. Those that respond with
increased discharge to stimuli that are tissue damaging or potentially tissue
damaging are termed primary afferent nociceptors (PANs). Once impulses are
generated in the PANs the process of transmission begins. Transmission includes
the conduction of nerve impulses in PAN axons to the spinal cord (or trigeminal
nucleus in the brain stem), synaptic activation by the PANs of second-order
pain-transmission neurons (e.g. spinothalamic tract cells) and the conduction of
1
2 Introduction
impulses in these central pain-transmission neurons to the brain structures that
underly subjective perception.
Primary afferent nociceptors
A peripheral nerve contains axons that differ widely in their cross-sectional
diameter, degree of myelination and conduction velocity (CV). The axons of the
primary afferents fall into three distinct groups: A-ß (diameter 6-22 μm, heavily
myelinated, CV 33-75 m/s), Α-δ (diameter 2-5 μm, thinly myelinated, CV
5-30 m/s) and C fibers (diameter 0.3-3 μm, unmyelinated, CV 0.5-2 m/s) [1,2]. To
which of these axonal groups classes do the primary afferent nociceptors belong?
At one level, there is a straightforward experimental approach to this question.
One needs only to determine the response properties of an afferent and measure its
conduction velocity. In fact, cutaneous nociceptors are defined by their character­
istic discharge pattern. Using mechanical or thermal stimuli, PANs discharge when
the stimulus intensity is at or above the level reported as painful when delivered to
the normal skin of a human subject. Characteristically, PANs discharge with
increasing frequency to stimuH of increasing intensity within the range reported as
painful (Figure 1.1). Using these criteria most PANs fall into one of two groups of
afferents: the unmyelinated C fibers and small-diameter myelinated or Α-δ group
{see Chapter 2 for details). Few, if any, belong to the A-ß group.
The large myelinated primary afferents in the A-ß group respond to low-intensity
mechanical stimuli and show no increase in discharge frequency to more intense
stimuli. Thus the A-ß fibers cannot selectively signal the presence of potentially
tissue-damaging stimuli. Consistent with this is the observation that in awake
human subjects, electrical stimulation of A-ß afferents elicits sensations that are
not painful. In fact, there is evidence that selective activation of A-ß afferents may
actually inhibit nociceptive transmission at the spinal level [3,4].
Despite the evidence against a positive contribution of A-ß afferents to pain
perception, recent studies suggest that, under certain conditions, especially when
there is nerve damage, activity in A-ß afferents can elicit pain (e.g. see the
discussions by Roberts and Kramis in Chapter 4 and by Raja, Meyer and Campbell
in Chapter 2 in this book). Thus, although activity of PANs is sufficient to elicit the
sensation of pain, it is likely that activity of PANs is not always required for a
stimulus to evoke pain. This illustrates the crucial point that the term nociceptor
refers to the type of stimuli to which a particular primary afferent responds, as
opposed to the type of sensation it produces when it is active. Under normal
conditions, nociceptors respond to intense stimuli and, when they are active,
consistently elicit the sensation of pain. Under pathological conditions, activity in
afferents that are not nociceptors can elicit pain.
The peripheral terminals of primary afferent nociceptors are sensitive to one or
more of the following types of stimulus: thermal, mechanical or chemical. The most
ubiquitous PAN can be activated by all three types of stimuli and is thus termed the
poly modal nociceptor. Most poly modal nociceptors have axons that are unmyeli­
nated. The other major classes of PAN respond only to relatively intense
mechanical (high-threshold mechanoreceptors) or to both intense mechanical and
thermal stimuU (mechanothermal nociceptors). The latter two classes of nociceptor
usually have axons that are myelinated.