Pain Medicine: The Requisites in Anesthesiology (Requisites in Anesthesia)

245 Pages·2006·4.46 MB·English

by  Stephen Abram

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PAIN MEDICINE: THE REQUISITES IN ANESTHESIOLOGY ISBN-10: 0-323-02831-4
ISBN-13: 978-0-323-02831-8
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Notice
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or
appropriate. Readers are advised to check the most current information provided (i) on procedures
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dose or formula, the method and duration of administration, and contraindications. It is the responsi-
bility of the practitioner, relying on his or her own experience and knowledge of the patient, to make
diagnoses, to determine dosages and the best treatment for each individual patient, and to take all
appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editor
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Library of Congress Cataloging-in-Publication Data
Pain medicine : the requisites in anesthesiology / Stephen E. Abram, editor. – 1st ed.
p. ; cm. – (Requisites in anesthesiology series)
ISBN-0-323-02831-4
1. Pain medicine. I. Abram, Stephen E. II. Series.
[DNLM: 1. Pain–drug therapy. 2. Anesthesia. WL 704 P14678 2006]
RB127.P332496 2006
616’.0472–dc22 2005053421
Acquisitions Editor:Joanne Husovski
Developmental Editor:Anne Snyder
Project Manager:David Saltzberg
Design Direction:Steven Stave
Marketing Manager: Emily McGrath-Christie
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1
To the Anesthesiology Residents and Pain Medicine Fellows who have worked
with me in the Pain Clinic over the past 30 years.You have worked tirelessly and
(mostly) without complaint to improve the lives of countless patients suffering
from intractable pain.Your efforts have provided relief,comfort,and hope to our
most vulnerable and underserved patients.
To Pam,for her support and encouragement throughout this project.
Stephen E. Abram,MD
Contributors
Stephen E. Abram, MD Phillip Phan, MD
Professor Senior Anesthesia Resident
Department of Anesthesiology Baylor College of Medicine
Medical College of Wisconsin Houston,Texas
Milwaukee,Wisconsin
Arun Rajagopal, MD
Caridad Bravo-Fernandez, MD Interventional Spine and Pain Clinic
Department of Anesthesiology St.Mark’s Hospital
Medical College of Wisconsin Salt Lake City,Utah
Milwaukee,Wisconsin
Constantine Sarantopoulos, MD, PhD
Mikhail Fukshansky, MD Director
Pain Management Fellow Pain Management Center
Assistant Professor CJ Zablocki Veterans Administration Medical Center
Department of Anesthesiology Milwaukee,Wisconsin
University of Texas MD Anderson Cancer Center Associate Professor
Houston,Texas Department of Anesthesiology
Medical College of Wisconsin
Robert E. Kettler, MD Milwaukee,Wisconsin
Department of Anesthesiology
Medical College of Wisconsin Hariharan Shankar, MD
Milwaukee,Wisconsin Fellow in Anesthesiology
Department of Anesthesiology
Randa Noseir, MD Medical College of Wisconsin
Assistant Professor Milwaukee,Wisconsin
Department of Anesthesiology
Medical College of Wisconsin Mary Lou Taylor, PhD
Milwaukee,Wisconsin Department of Anesthesiology
Medical College of Wisconsin
Therese O’Connor, FFARCSI Milwaukee,Wisconsin
Dip Pain Medicine
Consultant in Anesthesia and Pain Management
Sligo General Hospital
Sligo,Ireland
vii
viii CONTRIBUTORS
Jaya L. Varadarajan, MD Steven J. Weisman, MD
Attending Physician Jane B.Pettit Chair in Pain Management
Jane B.Pettit Pain and Palliative Care Center Children’s Hospital of Wisconsin
Children’s Hospital of Wisconsin Milwaukee,Wisconsin
Milwaukee,Wisconsin Professor
Assistant Professor Departments of Anesthesiology and Pediatrics
Department of Anesthesiology Medical College of Wisconsin
Medical College of Wisconsin Milwaukee,Wisconsin
Milwaukee,Wisconsin
Thomas J. Whalen, MD
Mark S. Wallace, MD Private Practice
Department of Anesthesiology Albuquerque,New Mexico
University of California San Diego
La Jolla,California
Preface
This volume of the Requisites in Anesthesiology series resulted in efficacious therapies. Hopefully this will
was created to provide Anesthesiology residents with change.
guidelines for the treatment of many common pain prob- As purveyors of medical technology,we are drawn to
lems and to serve as a study guide for the Anesthesiology those therapies that involve technical innovation.Some
board examinations. In addition, we expect that it of these technologies have provided substantial improve-
willserve as a valuable pain management text for anes- ments in the lives of patients who have not benefitted
thesiologists and other specialists involved in the treat- from more conventional treatments.Others have not
ment of acute, chronic, and cancer pain. While a been shown to be of significant benefit.Others are effec-
textbook of this scope cannot provide sufficient depth of tive in a small minority of patients.Unfortunately,these
knowledge for all painful conditions,it should impart a sophisticated and often expensive interventions are inef-
sound basic understanding of many of the pain problems fective for a substantial number,possibly a majority,of
encountered in a community practice. patients with chronic pain.We must therefore rely on the
Pain Medicine has been late in adopting the principles basic tools of pain management that have evolved over
of evidence–based medicine that have been incorpo- the past half century:physical rehabilitation,cognitive-
rated into other medical disciplines.There are many rea- behavioral therapy,pharmacological intervention,and
sons for this.The problems encountered in a pain clinic addiction medicine.These are not therapies that produce
are heterogeneous and include neuropathic,somatic,and dramatic and rapid results,and reimbursement for their
visceral sources of pain,both peripheral and central pain providers is typically poor;but they are essential to the
states,and contributions from psychological issues,sub- successful treatment of most patients with long-standing
stance abuse,psychiatric comorbidities,and antisocial pain.
and self-destructive behaviors.We deal with long-stand- It is the aim of this textbook to provide an introduc-
ing refractory problems for which the accepted thera- tion to the entire range of treatment options available for
pies have low success rates.The ability to successfully patients with intractable pain.There are few treatment
conduct randomized controlled trials under such circum- algorithms or care maps presented,as few have been
stances is limited.Nevertheless,increasing numbers of developed.The trainee in Pain Medicine will be depend-
well-conducted outcome trials and case series are lead- ent on the experience and expertise of faculty mentors
ing us toward therapies with demonstrable efficacy and as he or she learns how to incorporate treatment options
away from those with low chances of success.The emer- into a coherent plan.However,even the least experi-
gence of new outcome data will necessarily lead to enced physician can provide a valuable service to the
changes in therapies.Some of the treatment recommen- most difficult and complex patients by listening carefully,
dations expressed in this book will be abandoned or examining thoroughly,offering to help,and providing
modified;others will be confirmed. explanations. There are two statements that patients
Still other changes will come as the rapid advances in never want to hear: “I don’t know what’s wrong with
the basic science of pain perception are translated into you,”and “There is nothing I can do for you.” We can
clinical therapies.Our understanding of the mechanisms always provide a logical,if not totally proven,explanation
of nociception,neuropathy,and central sensitization has of why a patient has pain,and there is always something
advanced rapidly,but few of these breakthroughs have that can be done to help.
ix
1
CHAPTER Pain Pathways
and Mechanisms
CONSTANTINE SARANTOPOULOS
Introduction Mechanisms and Hypotheses Explaining the Different
Pain Pathways Phases of Pain
Peripheral Pathways Phase 1:Brief,Transient Acute Pain
Primary Afferent Fibers Phase 2:Chronic Nociceptive Pain
Cell Bodies Peripheral Mechanisms of Sensitization
Nociceptors Central Sensitization
Distribution of Nociceptors Mechanisms of Central Sensitization
Dorsal Root Ganglia and Dorsal Roots The Role of Excitatory Amino Acids and Tachykinins in the
Entry to Spinal Cord—Lissauer’s Tract Sensitization of Dorsal Horn Neurons
Dorsal Horns of the Spinal Cord Phase 3:Neuropathic Pain
Neurons of the Dorsal Horns Pathophysiologic Mechanisms of Neuropathic Pain
Class 1:Low-Threshold (LT) Cells Neuropathic Pain:Peripheral Mechanisms
Class 2:Multireceptive Cells or Wide Dynamic Range (WDR) Neuropathic Pain:Central Mechanisms
Cells Conclusion
Class 3:Nociceptive Specific (NS) Cells or High-Threshold Reference
(HT) Cells Suggested Reading
Class 4:Deep Cells
Neurochemistry of Primary Afferents
Ascending Pathways
Spinothalamic Tract INTRODUCTION
Spinomesencephalic Tract
Spinoreticular Tract The sensation of pain is the final result of a complex
Spinolimbic Tract and interactive series of mechanisms integrated at all lev-
Postsynaptic Dorsal Column Pathway els of the nervous system from the periphery through the
Supraspinal Systems Contributing to the Processing of Pain spinal cord to the higher cerebral structures. “Pain”
Reticular Activating System describes a conscious,unpleasant sensory and emotional
Thalamus experience that can be induced by a wide variety of events
Limbic System to which humans can be subjected.It can be defined as the
Cerebral Cortex perception of an unpleasant sensation originating from an
Modulation of Nociceptive Information area of the body,produced by actual or potential tissue
Descending Modulatory Systems damage,or described in terms of such damage.However,
The Periaqueductal Gray advances in our knowledge of the physiology of pain over
The Rostral Ventromedial Medulla the last years have lead to other relevant terminology.
Locus Ceruleus,Subceruleus,and Parabrachial Area The emphasis on the stimulus that activates the pain
Intrinsic Interneuron Systems in the Dorsal Horns pathway and its immediate consequences has been rec-
Mechanisms of Pain ognized by the use of the word “nociception,” intro-
Referred Pain and Visceral Pain Phenomena duced by Sherrington in the early 1900s.Nociception is
1
2 PAIN MEDICINE:THE REQUISITES IN ANESTHESIOLOGY
a specialized form of sensory signaling, describing the data of the specificity and pattern theories with the belief
generation, transmission, and processing of information that the “straight-through” connection of the Cartesian
associated with the actual or potential tissue damage.At model was contradicted by the more modern theories;
its simplest level of organization,nociception can be con- they proposed the Gate Control Theory,highlighting the
sidered the electrical,chemical,and synaptic activity in dynamic central nervous system mechanisms as an essen-
the sensory afferent neuron.At higher levels it includes tial component in pain processes.According to the Gate
the motor reflex responses evoked by that stimulus,and Control Theory,large and small diameter nerve fibers proj-
at even higher levels it may describe the response evoked ect to the substantia gelatinosa and the central sensory
by such stimuli that are organized at the brainstem level transmission neurons.Signals of pain (high-threshold sig-
into cardiovascular,hormonal,or other responses to pain. nals) are conveyed by small fibers.Large fibers convey low-
According to Sherrington, pain is a nociceptive reflex threshold,normally nonpainful signals.Input from the large
with a psychical component. “Nociceptors” are the fibers results in activation of central control mechanisms,
peripheral sensory neurons that respond selectively to which subsequently project back and modify the gate con-
noxious stimuli,thus having the capacity to discriminate trol system.This theory forced biomedical sciences to
between painful and nonpainful sensory input. accept the brain as an active system that filters,selects,and
Pain can be produced by activation of the specific noci- modulates inputs.The dorsal horns were also accepted as
ceptors in the periphery,and in this case is characterized active sites at which dynamic activities (i.e.,inhibition,exci-
as “nociceptive” pain. However, it may also result from tation,and modulation) occurred instead of merely passive
injury or alterations to sensory fibers or from disease or transmission stations. The cutting of nerves and pathways
damage to the central nervous system (CNS) itself.This is was gradually replaced by methods to modulate the input,
called “neuropathic”pain.A progressive unraveling of the such as physical therapy,transcutaneous electrical nerve
neuroanatomical substrate and cellular mechanisms stimulation (TENS),or spinal cord stimulation (SCS).
underlying pain has been in process,and an increasing Finally,over the last few years,there has been a sig-
understanding of these mechanisms facilitates the devel- nificant contribution to the understanding of pain from
opment of novel strategies for more effective treatment. the advances in the basic sciences, such as molecular
In the 17th century,René Descartes described man as biology, electrophysiology, and basic pharmacology.
a machine:Man functioned as any other machine,differ- Particular attention is now focused on cellular and sub-
ing only in sensitivity and reasoning capacity.He claimed cellular aspects and signaling mediators as well as the
that the nerves are connected to the sensory endings development of more rationalized treatments for both
and convey the sensations to the brain.Through a nerve, acute and chronic pain.
an effective stimulus makes its way to the brain and pro-
duces the sensation of pain.Luigi Galvani was the first to
suggest,in the late 18th century,the electrical nature of PAIN PATHWAYS
the nerve conduction,and Du Bois-Reymond measured
injury currents in nerves using a galvanometer in 1840. The “pathways of pain”as classically understood,con-
In the following centuries,the foundations of modern sist of a three-neuron chain that transmits pain signals
anatomy and physiology were laid.With the discovery of from the periphery to the cerebral cortex.Starting from
even more detailed knowledge, we have our present the periphery,the first order (or primary afferent) neu-
understanding of the science of pain.However,the views ron has its cell body in the dorsal root ganglion and two
of Descartes have so thoroughly permeated our concepts axons.The peripheral axon projects distally to the tissue
about physiology and anatomy that it has been difficult to it innervates.The proximal axon extends centrally to the
escape them. They have lead to a persistent search of dorsal horn of the spinal cord.In the dorsal horn,this
pain fibers,pathways,and pain centers in the brain.The axon synapses with the second-order neuron,the axon
result was the concept of the pain as a specific projection of which crosses the spinal cord through the anterior
system,which lead to ways to treat severe chronic pain white commissure and ascends in the spinothalamic
with chemical, electrical, or physical “neural blockade,” tracts to the thalamus.At that site,it synapses with the
utilizing a multitude of different ablative or neurosurgical third order neuron,which projects through the internal
lesions.We know now that these procedures frequently capsule and the corona radiata to the postcentral gyrus
fail and the pain tends to return,even in forms worse than of the cerebral cortex,where information is somatotopi-
those we attempt to abolish.This is explained by the cally organized and perceived (Fig.1-1).
dynamic, plastic properties of the neural tissue itself,
something that was not conceived by the early theorists.
Peripheral Pathways
Modern pain theories evolved from a number of diver-
gent views, which have been argued over the last 100 The spinal nerves are formed by the junction of the
years.In the 1960s,Melzack and Wall1integrated the strong anterior (ventral) and posterior (dorsal) spinal roots
Pain Pathways and Mechanisms 3
Figure1-2 Types of nerve fibers involved in sensory
Figure1-1 Basic organization of pathways of pain transmission.(Copyright 2004 Catherine Twomey/Medical Center
transmission from the periphery to the brain.(Copyright 2004 Graphics,Milwaukee,Wisconsin.)
Catherine Twomey/Medical Center Graphics,Milwaukee,
Wisconsin.)
(see Fig.1-1).Motor and autonomic efferent fibers exit The visceral afferents convey sensory information
through the ventral spinal roots,while input of sensory (including pain) from the viscera.They are pure sensory
afferent fibers is through the dorsal roots.After a lim- fibers,but follow the nerves of the autonomic nervous
ited course,the spinal nerves divide into anterior and system and are divided into those that accompany the
posterior primary rami.Thus,sensory and motor fibers sympathetic nerves and those that follow the parasympa-
are distributed to both primary rami.The posterior thetic nerves.Nociceptive information from the abdomi-
rami innervate the posterior (dorsal) spinal and somatic nal and thoracic viscera is transmitted by sensory fibers,
muscular and cutaneous structures (such as the mus- which follow the sympathetic pathways. The visceral
cles and skin of the back),while the anterior rami form afferents that accompany the sympathetic nerves tra-
the various neural plexuses and peripheral nerves of verse the prevertebral ganglia (e.g., the ganglia in the
the body. celiac plexus) without synapsing,reach the paravertebral
The peripheral nerves are composed of axons from sympathetic chain via the splanchnic nerves, and then
somatic and visceral (autonomic) systems,with sensory reach the segmental nerves (T1 to L2) via the white rami
(afferent) and motor (efferent) components in each sys- communicantes (or sometimes the grey),and finally their
tem.Somatic sensory fibers from several spinal nerves cell bodies in the dorsal root ganglia (Figs.1-3 and 1-4).
often fuse to form peripheral nerves. However, each From there,both the somatic and the visceral information
spinal nerve still conveys cutaneus sensory input from follow a similar course toward the cerebral cortex.
aconceptually discrete area of skin.These discrete areas Most visceral afferents from the sigmoid colon,rectum,
are called dermatomes and provide a clinically useful neck of the bladder, prostate, and cervix of the uterus
sensory map of the body surface (but there is some over- accompany the parasympathetic efferent fibers entering
lap and nonuniformity in their distribution).The cuta- the cord in the dorsal roots of S2 to S4.The visceral affer-
neous somatic input retains a radicular organization,as ents of the vagus nerve have their cell bodies in the nodose
do the bone (sclerotomes) and the muscles (myotomes) ganglion and transmit information such as bloating,disten-
afferents. tion,and nausea-like sensations,but not pain,except per-
The nerve fibers are characterized by their degree of haps from those innervating the hypopharynx and the
myelination, diameter, and velocity of electrical signal upper respiratory tract.They can, however, modify the
conduction. The A fibers are large, myelinated, and of responsiveness of the nociceptive dorsal horn neurons.
rapid conduction.The Αα subtype convey motor signals
to the muscles.The Aβ fibers convey sensory such as
touch, pressure, and proprioception, and the Aγ inner- PRIMARY AFFERENT FIBERS
vate muscle spindles.The Aδ fibers convey signals of
touch,heat,and pain faster than the C fibers,which also Any tissue noxious alterations that involve extreme
convey similar modalities that are non-myelinated, mechanical distortion,thermal stimulation,or changes in
smaller, and slower.Aδ and C fibers are referred to as the chemical milieu at the peripheral sensory terminals
small fibers,while the Aβare called large fibers(Fig.1-2). will evoke the verbal report of pain in humans and
The B fibers are small myelinated fibers,which convey efforts to escape in animals as well as more complex
preganglionic sympathetic signals.Pain signals are con- responses.The circuitry that serves the transduction and
veyed by a subpopulation of the small fibers. encoding of this information,starts with the activation of
4 PAIN MEDICINE:THE REQUISITES IN ANESTHESIOLOGY
Figure1-3 Transmission of pain signals from visceral organs via the sympathetic chain and
spinal nerves.(Copyright 2004 Catherine Twomey/Medical Center Graphics,Milwaukee,Wisconsin.)
the nociceptors, the subsequent depolarization of the
primary afferent axons,the transmission of the informa-
tion to the bodies of the neurons in the dorsal root gan-
glia,and finally to the synapses with the dorsal horn cells
(see Figs.1-1,1-2,and 1-3).
Cell Bodies
The cell bodies of the primary afferent somatic fibers
are located in the dorsal root ganglia (DRG).The cell bod-
ies of the primary afferent visceral fibers are also located
in the DRG,but some of these visceral afferents may have
cell bodies in the sympathetic ganglia or organs of origin.
Nociceptors
The primary afferent fibers encode and convey differ-
ent modalities of sensation.They are classified as noci-
ceptors (if they respond to high-threshold noxious
stimuli),mechanoreceptors (if they encode and convey
mechanical information), thermoreceptors (responsible
for thermal information),chemoreceptors (for chemical
information),and so forth.
Nociceptors belong either to the Aδ or the C type of
sensory fibers (see Fig.1-2) but not all Aδand C fibers are
nociceptive fibers.Most Aδ and C fibers have free nerve
endings without any specialized structures (such as the
Meissner’s and Pacinian corpuscles or the propriocep-
Figure1-4 Transmission of pain signals from upper abdominal
tive endings).About 75% of the Aδ,and a variable number
viscera.Celiac plexus.(Copyright 2004 Catherine
Twomey/Medical Center Graphics,Milwaukee,Wisconsin.) of C, respond to low-threshold mechanical,chemical,