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A M E R I C A N A C A D E M Y O F P A I N M A N A G E M E N T 

The Pain Practitioner 

Volume 16, Number 1 • Spring 2006 

CRPS: Grappling with the Mysteries 

SPECIAL EDITION 

Articles, 

Interviews, 

Commentary 

James Giordano, PhD 

James W. Broatch, MSW 

Bradley S. Galer, MD 

Edward C. Covington, MD 

David D. Sherry, MD 

Donald C. Manning, MD, PhD 

Lynn R. Webster, MD 

Keri L. Fakata, PharmD 

Joshua P. Prager, MD, MS 

Philip Getson, DO 

Peter A. Moskovitz, MD 

ALLODYNIA 

Artist: Stephen Spagnoli






Articles, 

Interviews, 

Commentary 












ALLODYNIA 







Articles, 

Interviews, 

Commentary 












ALLODYNIA 


T A B L E O F C O N T E N T S 

SPECIAL ISSUE CRPS: GR APPLING WITH THE MYSTERIES 

EDITOR-IN-CHIEF: Lennie Duensing 

CO-EDITOR OF THIS SPECIAL EDITION: Debra Nelson-Hogan 

MEDICINE AND HUMANITIES EDITOR: James Giordano, PhD 

6 

9 

FEATURES 

16 

22 

32 

40 

50 

59 

63 

68 

72 

74 

82 

Editor’s Corner 

By Lennie Duensing and Debra Nelson-Hogan 

Dolor, Morbus, Patiens: Maldynia, Pain as Illness and Suffering 

By James Giordano, PhD 

RSDSA: Expanding Research, 

Education, and Awareness of CRPS 

By James W. Broatch, MSW, RSDSA Executive Director 

PEOPLE WITH CRPS: THEIR STORIES AND 

ACCOMPLISHMENTS 23 Stephen Spagnoli • 24 Wilson Hulley 

25 Barbara Schaffer • 26 Lisa Delia• 27 Sharon Weiner 

Complex Regional Pain Syndrome: 

New Hope After a Decade of Dispelling Myths 

By Bradley S. Galer, MD 

Exploring Psychosocial Issues in CRPS 

An Interview Edward C. Covington, MD 

When Children Hurt Too Much: Diagnosis and 

Treatment of Amplified Musculoskeletal Pain 

By David D. Sherry, MD 

EMERGING TREATMENT AND DIAGNOSIS 

Neuroimmunologic Approaches to Emerging 

and Potential Therapies for CRPS 

By Donald C. Manning, MD, PhD 

Ziconotide: Promising New Treatment for 

Complex Regional Pain Syndrome (CRPS) 

By Lynn R. Webster, MD, and Keri L. Fakata, PharmD 

New Rechargeable Spinal Cord Stimulator Systems 

Offer Advantages in CRPS Treatment 

By Joshua P. Prager, MD, MS 

The Use of Thermography in the 

Diagnosis of CRPS: A Physicians’ Opinion 

By Philip Getson, DO 

IN CONCLUSION 

A Theory of Suffering 


DEPARTMENTS 

82 Academy News • 84 Classified Advertisements • 85 Directory 

On the Cover: Allodynia by Stephen Spagnoli. This painting in iodine and acrylics is 

an actual imprint of the artist’s body. 

Academy Board of Directors 

President 

Paula L. Gilchrist, LPT, DPM 

Secretary 

Barbara Lum, BS 

Treasurer 

Carl H. McNeely, APRN, PNP 

Co-Chairs, Board of Advisors 

Rick Marinelli, ND, MAcOM, LAc 

Gerald Q. Greenfield Jr., MD 

Director-at-Large 

Christopher Brown, DDS, MPS 

Academy Staff 

Executive Director 

Kathryn A. Padgett, PhD 

Deputy Executive Director 

Marsha Stanton, MS, RN 

Director of Education 

Terry Finigian 

Education Administrator 

Lois Baker 

Director of Pain Program 

Accreditation and Outcomes 

Measurement 

Alexandra Campbell, PhD 

Director of Communications 

and Advocacy 

Lennie Duensing, MEd 

Administrative Assistant 

Mari Fairhurst 

Director of Publications 

Carol Harper, MA 

Director of Sales 

Jillian Manley 

Sales Representative 

Rosemary LeMay 

General Membership Coordinator 

Marcella Mateo 

Credentialing, Office Manager 

Joy McCurry 

Chief Financial Officer 

Connie Mulalley 

Academy Consultants 

Research Consultant 

Edward E. Duensing, MLS 

Copy Editor 

Nan Newell 

The Pain Practitioner is published by the American 

Academy of Pain Management, 13947 Mono 

Way, Ste. A, Sonora, CA 95370, Phone 

209-533-9 7 4 4 , F a x 2 0 9 - 5 3 3 - 9 7 5 0 , and 

Email: aapm@aapainmanage.org, website: 

www. aapainmanage.org. Copyright 2006 

American Academy of Pain Management. All 

rights reserved. Send correspondance to Lennie 

Duensing, MEd, at lduensing@yahoo. com. 

Contact Jillian Manley at 209-533-9744 

regarding advertising opportunities, media kits, 

and prices. 

The Pain Practitioner is published by the 

American Academy of Pain Management solely 

for the purpose of education. All rights are 

reserved by the Academy to accept, reject, or 

modify any submission for publication. The 

opinions stated in the enclosed printed 

materials are those of the authors and do not 

necessarily represent the opinions of the 

Academy or individual members. The Academy 

does not give guarantees or any other 

representation that the printed material 

contained herein is valid, reliable, or accurate. 

The American Academy of Pain Management 

does not assume any responsibility for injury 

arising from any use or misuse of the printed 

material contained herein. The printed material 

contained herein is assumed to be from reliable 

sources, and there is no implication that they 

represent the only, or best, methodologies or 

procedures for the pain condition discussed. It 

is incumbent upon the reader to verify the 

accuracy of any diagnosis and drug dosage 

information contained herein, and to make 

modifications as new information arises. 

All rights are reserved by the Academy to 

accept, reject, or modify any advertisement 

submitted for publication. It is the policy of the 

Academy to not endorse products. Any 

advertising herein may not be construed as an 

endorsement, either expresed or implied, of a 

product or service. 

4 | T H E PA I N P R A C T I T I O N E R | S P R I N G 2 0 0 6

EDITORS’ CORNER | COMPLEX REGIONAL PAIN SYNDROME 

LENNIE DUENSING 

Editor-in-Chief 

CRPS Special Edition 

BY LENNIE DUENSING, EDITOR-IN-CHIEF 

AND DEBRA NELSON-HOGAN, CO-EDITOR, SPECIAL CRPS EDITION 

DEBRA NELSON-HOGAN 

Co-Editor 

“Complex Regional Pain Syndrome (CRPS) is a perplexing 

condition that has been relatively ignored and misunderstood 

by the medical community because it is so unusual.” 

— BRADLEY S. GALER, MD 

THE AMERICAN ACADEMY OF PAIN MANAGEMENT AND 

THE REFLEX SYMPATHETIC DYSTROPHY SYNDROME 

ASSOCIATION have joined together to produce this 

special spring edition of The Pain Practitioner. Entitled, 

“CRPS: Grappling with the Mysteries,” the issue explores 

the most current thinking about Complex Regional Pain 

Syndrome (CRPS) from a variety of perspectives. 

Why an Issue on CRPS? 

WE TOOK ON THIS JOINT PROJECT because CRPS is a condition 

that creates a host of treatment nightmares for clinicians. 

Unfortunately, most healthcare professionals lack education 

about the condition and often delay diagnosis and treatment. 

Worse yet, some healthcare professionals and insurance 

providers still don’t believe the syndrome exists. The McGill 

Pain Scale, however, ranks CRPS pain higher than cancer pain, 

and for many of those living with CRPS, the constant and 

burning pain creates nothing short of a living hell. This is well 

illustrated in the paintings of CRPS sufferer Stephen Spagnoli, 

which appear throughout this issue. (See story on page 22 ) 

In this Issue 

James Giordano, PhD, the publication’s new Medicine and 

Humanities Editor, opens the issue with a commentary entitled, 

“Dolor, Morbus, Patiens: Maldynia, Pain as Illness and 

Suffering.” Giordano addresses the need to comprehend the 

complexity of pain and suffering, and says that, “… scientific 

and humanistic inquiry is fundamental to the provision of 

technically right and morally good care.” 

James W. Broatch, MSW, RSDSA Executive Director, in 

“RSDSA: Expanding Research, Education, and Awareness of 

CRPS,” describes that organization’s work discusses the 

particular challenges that people who have CRPS face, and how 

the 22-year-old organization meets them. There is also a brief 

overview of the new third edition CRPS Clinical Practice 

Guidelines. 

In his article, “Complex Regional Pain Syndrome: New Hope 

After a Decade of Dispelling Myths,” Bradley S. Galer, MD, 

addresses many facets of this generally misunderstood and 

confusing syndrome. Galer looks at the causes of CRPS and 

highlights some of the advances made in recent years that have 

led to a better understanding of this syndrome, dispels myths 

and misconceptions, and describes treatments. 

Edward C. Covington, MD, Director of the Chronic Pain 

Rehabilitation Program at the Cleveland Clinic Foundation, 

discusses the psycho-social issues in CRPS. Covington addresses 

CRPS in relation to personality and cognition, the value of 


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EDITORS’ CORNER | COMPLEX REGIONAL PAIN SYNDROME 

exercise and activity, and various psychological treatments. 

Covington says, “There are people with CRPS who have 

managed to transcend it and have a life. For others, it’s less the 

case that they have CRPS than that ‘CRPS has them.’” 

Pediatric CRPS can be an entirely different syndrome. In his 

article, “When Children Hurt too Much: Diagnosis and 

Treatment of Amplified Musculoskeletal Pain.” David D. 

Sherry, MD, discusses amplified musculoskeletal pain and 

describes the epidemiology, etiology, clinical manifestations, 

diagnosis, and treatment, and outcomes of these conditions 

based on his experience. He says that with the treatment he 

recommends, “Most children do well.” 

The magazine also includes a special section with articles 

focusing on emerging treatments for CRPS (both 

pharmacological and non-pharmacological approaches). An 

article by Joshua P. Prager, MD, explores the use of spinal cord 

stimulation for people with CRPS. Lynn R. Webster, MD, and 

Keri L. Fakata, PharmD, discuss ziconotide, a new, nonnarcotic 

treatment delivered via an intrathecal pump that is a 

treatment option for CRPS patients. Donald C. Manning, 

MD, PhD, describes other emerging treatments, and Philip 

Getson, MD, gives a brief summary of thermography in the 

diagnosis of CRPS. 

The section, People with CRPS: Their Stories and 

Accomplishments, presents stories about five people with CRPS, 

who in spite of their pain, are working in a variety of ways to 

support others with the condition. 

The issue concludes with a compelling and thoughtful 

commentary by Peter A. Moskovitz, MD, called “A Theory of 

Suffering.” Moskowitz puts forth a six-part theory that explores 

the nature of suffering. He concludes by saying, “The capacity 

for suffering is the precursor to natural morality. I stand at the end 

of a long line of scientists and ethicists, some cited here, to repeat 

that empathy and the understanding of suffering, however elusive 

they may be, are the moral obligation of the pain practitioner.… 

The treatment of diseases and injuries includes the treatment of 

pain. The treatment of pain is all about suffering.” 

Debra Nelson Hogan is a communications consultant for RSDSA. 

Adding a New Dimension 

to The Pain Practitioner 

THE ACADEMY WELCOMES JAMES GIORDANO, PHD, 

AS MEDICINE AND HUMANITIES EDITOR 

THROUGH THE PAIN PRACTITIONER, the American Academy 

of Pain Management has provided clinicians with practical 

information about pain management and the latest trends in 

the field. Now, we are taking the publication a step further. 

Starting with this issue, we will be looking at pain, not only 

from scientific and medical perspectives, but from the perspective 

of the humanities as well—a perspective that hopefully 

will give us a greater understanding of the experience of pain, 

and how it expressed by those who suffer with it. 

To this end, the Academy is pleased to welcome James 

Giordano, PhD, as Medicine and Humanities Editor. In this 

role, Dr. Giordano will write provide editorial input and write 

commentary related the theme of the issue. 

“My hope is that we emerge from this Decade of Pain 

Control and Research with knowledge and understanding that 

advances our epistemology of pain, and in so doing, reconcile 

science, medicine and the humanities.” Dr. Giordano says. 

“My goal as Medicine and Humanities Editor of The Pain 

Practitioner is to create a forum for the provision and 

exchange of these ideas—a 

forum in which those who 

treat people with pain are 

empowered by the knowledge 

that can only be provided 

through a lens that 

brings together the 

pragmatic sharpness of biomedicine 

and the sentient 

focus of the humanities.” JAMES GIORDANO, PhD 

Dr. Giordano’s ongoing research focuses on the neuroscience 

and neurophilosphy of pain, agent-based virtue ethics 

in pain research and practice, and neuroethics. He is currently 

a Scholar in Residence at the Center for Clinical Bioethics, 

Georgetown University Medical Center; a Visiting Scholar at 

the Center for Ethics, Dartmouth Medical School; a Fellow 

of the John P. McGovern MD Center for Health, Humanities 

and the Human Spirit, University of Texas Health Sciences 

Center; and, an invited lecturer of the Roundtable in Arts and 

Sciences, Oxford University, UK. He is the author of over 55 

peer-reviewed papers and three books addressing the neuroscience 

of pain, medical philosophy, and bioethics. He is 

the bioethics section editor of the American Journal of Pain 

Management, editor of the Journal of Practical Pain Management, 

and neuroscience editor of the Pain Physician Journal. 


COMMENTARY | GIORDANO 

COMMENTARY: 

Dolor, Morbus, Patiens: 

Maldynia, Pain as 

Illness and Suffering 

BY JAMES GIORDANO, PhD, MEDICINE AND HUMANITIES EDITOR 

AS THE MEDICINE AND HUMANITIES EDITOR for 

The Pain Practitioner, I am grateful for the 

opportunity to write a commentary on the 

papers appearing in this issue on complex 

regional pain syndrome (CRPS). 

TOGETHER, THESE ARTICLES address this frequently misunderstood 

syndrome, convey how an expanding epistemology has 

generated enhanced understanding of the mechanistic basis and 

existential impact of pain as a complexity-based systems event, 

and present the need to develop diagnostic and therapeutic 

approaches that reflect this progressive knowledge. 

The basic and clinical sciences, humanities, and the 

experiential narratives of patients all contribute essential lenses 

through which we can examine and de-mystify the enigma 

of persistent pain. 

I believe that how we come to know about pain 

is equally important as, and provides a pediment for, what 

we know about pain. It is only through the combination of 

distinct domains of knowledge that we can both comprehend 

pain as a dysfunction of the dynamical, nonlinear adaptability 

of the nervous system, and at the same time apprehend the 

manifestations of these changes within the networked-hierarchy 

of interacting systems that is the patient as person. 1 Thus, 

the study of pain conjoins neuroscience to the burgeoning 

discourse of neurophilosophy and, in so doing, may reconcile 

issues in the dialectic surrounding the concepts of disease— 

illness, brain-mind, and ethical dimensions of care. 

Pain as a Spectral Disorder 

I POSIT THAT PAIN CAN BE CONSIDERED TO BE A SPECTRAL 

DISORDER—one that ranges from a symptom of organic insult 

or trauma, to durable, more global pathologic changes occurring 

at multiple levels of the nervous system, ultimately affecting 

the substrates that are involved in and/or elicit behavior, 

emotion, and cognition of the (internal and external) environment 

and, thus, some form of the definable “self.” 2 

I maintain that with progression across this spectrum, the 

disease process of pain increasingly becomes the phenomenal 

illness of pain. Classification and diagnoses must acknowledge 

pain as disease and manifest illness, recognizing, too, that the 

disease process may be durable and immutable (1). 

The arbitrary temporal classifications that rested upon the 

acuteness or chronicity of pain did little to define the etiologic 

and pathophysiologic processes that may cause or perpetuate 

the disorder. Hence, these criteria have been replaced by nosologic 

distinctions (e.g., nociceptive vs. neuropathic; Type I, II, 

III) that have sought to characterize pain according to the 

inherent neurological mechanisms. Woolf, Borsook, and 

Koltzenburg (2) have recently expanded this schema into an 

elegant algorithmic model that thoroughly accounts for stimulus 

dependency and neural basis, enabling both mechanistic 

identification of types of pain and proof of concept evidenced 

in clinical syndrome(s). Certainly, this algorithm can be considered 

to be situated along, and/or be representative of, the pain 

spectrum, as I have proposed. Yet, the “meaning” and manifestations 

of these types of pain still remain implicit in, if not altogether 

absent from, the algorithm of Woolf et al. Almost a 

decade ago, Lippe (3) proposed the use of the term eudynia to 

represent physiologically “normal” or nociceptive pain, and 

maldynia to be “abnormal” pain arising from neuropathic 

processes. These terms have become increasingly popular, but I 

feel that when used alone, they do little to define what “normality” 

and “abnormality” actually mean. Similarly, the sole use 

of the categorization scheme of Woolf and colleagues is some- 

1 These are concepts that are inherent to, and derived from, complexity theory. 

I feel that the use of a complexity-based model of pain is important to fully 

reconcile the notions of disease and illness, and to fit these within a more 

encompassing framework. For a review of complexity theory and its applicability 

to neuroscience and medicine, see: Kelso, JS. Dynamic Patterns: The 

Self-Organization of the Brain and Behavior, Cambridge, MIT Press, 1995; 

Waldrop MM. Complexity: The Emerging Science at the Edge of Order and 

Chaos, NY, Touchstone Books, 1992; Dayan P, Abbott LF. Theoretical Neuroscience: 

Computational and Mathematical Modeling of Neural Systems. Cambridge, 

MIT Press, 2001; and for a straightforward overview, see: Sarder Z, 

Abrams I. Introducing Chaos, Cambridge (UK), Icon Books, 2003. 

T H E PA I N P R A C T I T I O N E R | V O L U M E 16 , N U M B E R 1 | 9

COMMENTARY | GIORDANO 

Comprehending the complexity of … 

suffering involves both scientific and 

humanistic inquiry and is fundamental 

to the provision of technically right 

and morally good care. 

what sterile and does not depict the potentiality of effects 

elicited by a particular type of pain. However, if framed as 

domains within the spectrum of pain, these classifications 

impart insight to mechanism(s), manifestation(s), and broader 

existential meaning. 

Maldynia: The Illness of Pain as Suffering 

I PROPOSE THAT MALDYNIA be reconsidered to be the multidimensional 

constellation of symptoms and signs that represent the syndrome 

of persistent pain as phenomenal illness. Thus, by its nature, 

maldynia (irrespective of initiating cause and/or constituent 

mechanisms) produces, and results from, functional and perhaps 

structurally maladaptive changes in the nervous system that 

evoke, and are reciprocally affected by, alterations in cognition, 

emotion, and behavior. In this way, maldynia is both the conscious 

state of pain and a consciousness of pain as a condition of 

the internal domain of the lived body and existential disattunement 

of the life world. 3 This definition compels a more thorough 

consideration of the philosophical and pragmatic basis of pain 

medicine, for if maldynia is the illness of pain experienced as suffering, 

then the ethical obligations of the pain practitioner are 

soundly-based upon an objective knowledge and subjective affirmation 

that a patient’s pain and suffering are genuine. 4 

Moskovitz describes CRPS as the quintessential maldynic 

syndrome. This is well illustrated by Galer and Covington, who 

note how multiple biological and psychosocial factors contribute 

to, and are affected by, CRPS. The authors take steps to 

reveal CRPS not as an unsolvable mystery or specious myth, 

but as a complicated clinical problem that is explicable and 

treatable. But complicated problems are rarely resolved through 

simple means, and the diagnosis and treatment of CRPS 

require an insightful, innovative approach that is wholly focal to 

the varying pathologic bases and unique, needs of each patient. 

The cornerstone of this approach is accurate diagnosis, (4, 5) 

and Sherry addresses the differential diagnosis of persistent 

musculoskeletal pain in adolescents as an example of how precise, 

timely assessment is essential to establishing and implementing 

what should be done to most effectively treat a particular 

patient with a specific pain disorder. Diagnosis is built 

from generalized and specifically contextual knowledge, and 

Getson examines thermography as a novel technology and technique, 

that, when utilized within an expanded objective and 

subjective diagnostic framework, may afford improved evaluative 

acumen, thereby determining the appropriate type and ultimate 

trajectory of subsequent care. Manning, Webster, and 

Fakata, as well as Prager each discuss this care, and their work 

emphasizes the importance and viability of rational pharmacology 

and new technologies, in an approach that reflects understanding 

of the contributory neuropathic mechanism(s), as well 

as the relational importance of how these mechanisms are 

expressed in the patient. 

I maintain that this latter point is particularly critical to 

treatment. While there is considerable similarity in the underlying 

neural mechanisms of CRPS, their manifestations can be 

widely different, based upon the compound predispositions of 

each person. The clinician must take this into account when 

considering the prudential question of what should be done to 

best meet the medical needs of a given patient at a particular 

point in the disease-illness continuum (4, 6, 7). Such “customization” 

of care allows for evaluation and therapeutics based 

upon multiple levels and domains of evidence and is instrumental 

in providing the right treatment(s) for the right reason(s) (8, 

9). Instead of being inappropriately wedded to a singularly disease-based, 

curative model, this approach embraces a larger, 

more integrative paradigm, (10) that I feel acknowledges and 

communicates to the patient that while cure may not be possible, 

effective, ethical care is both achievable and obligatory. 

Toward a Neurophilosophy of Pain 

GIVEN THE NOTION THAT: 

[1] maldynia induces functional and structural changes in 

the neurological axis from periphery to brain; 

[2] distinct regions in the brain are responsible for the conditions 

and awareness of discriminable consciousness (e.g., 

the cingulate gyrus, parietal, prefrontal, and operculoinsular 

cortex); and 

[3] maldynia-induced changes in these brain regions are capable 

of evoking alteration of the sensed internal state that is consciousness, 

it becomes clear that maldynia (i.e., pain as suf- 

2 There is considerable discussion in the neural sciences (i.e., neurobiology, 

cognitive psychology, [neuro]philosophy) regarding the nature or existence 

of the “self.” To gain insight into recent perspectives of some of the leading 

scholars in this discourse, see: Blackmore S. Conversations on Consciousness: 

What the Best Minds Think About the Brain, Free Will, and What It 

Means to Be Human. Cambridge (UK), Oxford University Press, 2005. 

3 I base this upon the model of levels of conscious processing, first detailed 

in psychological terms by Ray Jackendoff (Consciousness and the Computational 

Mind, Cambridge, MIT Press, 1990); and expanded by Jesse Prinz 

(Furnishing the Mind: Concepts and Their Perceptual Basis, Cambridge, MIT 

Press, 2004) to include neural substrates. I feel that this model fits well 

within a complexity-based paradigm, and bridges neural mechanisms with 

phenomenal experience(s). For further discussion of the phenomenological 

approach to illness and pain, see: Gadamer HG. The Enigma of Health. Stanford, 

Stanford University Press, 1996; Husserl E. Ideas: General Introduction 

to a Pure Phenomenology. NY, Collier, 1962; Svenaeus F. The Hermeneutics of 

Medicine and the Phenomenology of Health. Dordrecht, Kluwer, 2000; and 

Zaner R. The Problem of Embodiment: Some Contributions to a Phenomenology 

of the Body. The Hague, Nijhoff, 1964. 

4 Suffering is an extensive topic of study. One of the leading scholars in this 

field is Eric Cassell. For an overview of his work specific to a discussion of 

suffering and the ethical obligations in caring for those who suffer, see: Cassell 

E. The Healer’s Art, NY, Lippincott, 1976, and, Cassell E. The Nature of 

Suffering, Oxford, Oxford University Press, 1991. 


fering) may be a disorder of the brain that directly or indirectly 

effects a condition of the expressed “mind.” 

In this context, Moskovitz’s work becomes particularly 

noteworthy. Based upon his clinical experience and the current 

body of experimental and philosophical literature, Moskovitz 

has developed a theory that localizes suffering to the cingulate 

gyrus and adjacent limbic forebrain. Certainly, there is evidence 

from recent neuroimaging studies to support the neuroanatomical 

basis of his theory, at least in part (11, 12, 13). An interesting 

dimension of Moskovitz’s thesis is its solidification of 

suffering as a brain event that is evoked by hierarchical mechanisms 

of pain, yet allows (indeed, encourages) a philosophical 

interpretation of whether suffering represents a biological effect 

of the brain state (i.e., a “physical kind”), or is a distinct property 

(i.e., a “mental kind”) that exists as some nonmaterial construct 

of consciousness. 5 Regardless it is knowable in its entirety 

only to the sufferer: even if there were some way to completely 

transpose the pattern of cerebral activation from one person 

directly to another (e.g., from patient to clinician), the subjective 

experience of that identical brain activation would still differ, 

since the connectivities shaped by genotype and the myriad 

of life experiences are so widely variant (14). 

Thus, while Moskovitz’s theory is attractive because it establishes 

a physiological basis and anatomy of pain as suffering, I 

think that it also raises the question of whether suffering can or 

will be knowable through solely objective means. The authentication 

of suffering cannot exclusively rely on technology (4, 6, 

15, 16), and it is here that this thesis to instigate somewhat 

broader considerations. By validating suffering as a neurobiological 

event, Moskovitz makes it resonant with the domain of 

applied biology that constitutes much of the epistemological 

basis for contemporary medicine. Yet, given that these neurobiological 

substrates are in some way foundational to consciousness, 

he astutely states that only contextual, intersubjective knowledge 

can truly afford the clinician an understanding of the unique 

nature of a person’s suffering. I agree, for the focus of the clinical 

encounter is upon the patient, literally as “the one who suffers.” 

Comprehending the complexity of such suffering involves 

both scientific and humanistic inquiry and is fundamental to 

the provision of technically right and morally good care. I maintain 

that this is incontrovertible, and hope that this issue of The 

Pain Practitioner provides a forum to stimulate thought and discussion 

about the future possibilities that such care may offer. 6 

REFERENCES 

1. Giordano J. Bioethics and intractable pain. Practical Pain Management, 

2005 

2. Woolf CJ, Borsook D, Koltzenburg M. Mechanism-based classifications of 

pain and analgesic drug discovery. In: C. Boutra, R. Munglani, WK 

Schmidt (eds.) Pain: Current Understanding, Emerging Therapies, and 

Novel Approaches to Drug Discovery. NY, Marcel Dekker, 2003, pp. 1-8. 

3. Lippe P. An apologia in defense of pain medicine. Clin. J. Pain. 1998, 14 

(3): 189-190. 

4. Giordano J. Toward a core philosophy and virtue-based ethics of pain 

medicine. The Pain Practitioner, 2005, 15(2): 59-66. 

5. Sadler JZ. Diagnosis/anti-diagnosis. In: J. Radden (ed.) The Philosophy of 

Psychiatry: A Companion. NY, Oxford University Press, 2004, pp. 163-179. 

6. Giordano J. Moral agency in pain medicine: Philosophy, practice and 

virtue. Pain Physician, 2006, 9: 71-76. 

7. Pellegrino ED. For the Patient’s Good: The Restoration of Beneficence in 

Health Care. Oxford, Oxford University Press, 1987. 

8. Turk DC. Customizing treatment for chronic pain patients: who, what, and 

why? Clin. J. Pain, 1990, 6: 255-270. 

9. Giordano J. Pain research: Can paradigmatic revision bridge the needs of 

medicine, science and ethics? Pain Physician, 2004, 7: 459-463. 

10. Bonakdar R. Integrative pain management: A look at a new paradigm. 

The Pain Practitioner, 2005, 15 (1): 15-18. 

11. Bromm B. Brain images of pain. News Physiol. Sci. 2001, 16: 244-249. 

12. Apkarian AV, Thomas PS, Krauss BR, Szeverenyi NM. Prefrontal cortical 

hyperactivity in patients with sympathetically mediated chronic pain. 

Neurosci. Lett., 2001, 311: 193-197. 

13. Bingel U, Quante M, Knab R, Bromm B, Weiller C, Buchel C. Subcortical 

structures involved in pain processing: Evidence from single-trial fMRI. 

Pain, 2002, 99: 313-321. 

14. Coghill RC, McHaffe JG, Yen Y-F. Neural correlates of inter-individual differences 

in the subjective experience of pain. Proc. Nat. Acad. Sci., 2003, 

100 (14): 8538-8542. 

15. Reiser SJ. Medicine and the Reign of Technology. Cambridge, Cambridge 

University Press, 1978. 

16. Sullivan M. Exaggerated pain behavior: By what standard? Clin. J. Pain, 

2004, 20 (6): 433-439. 

5 The definitions of “kind” are used here in the philosophical sense to mean 

a group of things or occurrences that have inherent qualities in common. 

Thus, a “physical kind” refers to those things that are directly arising from, 

and belonging to, a set of purely physiological events. In contrast, a “mental 

kind” refers to those things that may have arisen from something physical, 

but have an inherent and unique set of characteristics that separate 

them from those things that are physiological. The latter characterization 

formalizes that mental processes are different from physiological ones. This 

distinction allows for the fact that consciousness may be emergent from the 

physiological processes of neurons, but also gives substance to the idea that 

conscious processes are in some way “more” than the result of the physiology 

that may have produced them. 

This speaks to the major “schools,” or orientations in contemporary science 

and philosophy of mind, that range from the viewpoint that any mental 

event is wholly reducible to a brain event (e.g., materialism and related 

orientations of theoretically reductive physicalism), to some middle-ground 

positions that allow that brain events produce mind events, but that mind 

events have more expansive characteristics or are greater than the sum of 

the events which produced them (e.g., nonreductive physicalism, property 

dualism, emergence, complementarity) and at the other extreme, the idea 

that there is a discernible mental field that occurs within the brain, but is 

irreducible, and perhaps unknowable (e.g., strict dualism). There are several 

issues in neuroethics that are related to the implications of these distinctions 

(e.g., the nature of the “self,” self-determinism, free will, etc.). 

The philosopher Colin McGinn claims that our study of the mind is at a 

point of “cognitive closure,” given the inherent limitations of the contemporary 

human brain. Instead, I prefer to think, optimistically, that we are on a 

path of extended contemplation that allows us to gain ongoing insight from 

an ever-increasing knowledge base achieved through widening collaboration 

within, and between, multiple disciplines. Again, it is beyond the scope of 

this paper to address the nature of consciousness, but one can see how this 

discussion would nonetheless be important to the study of pain, suffering, 

and the ethics of science and medicine. 

6 Obviously, the extent of the topic of CRPS cannot be completely or fully 

addressed in a volume such as this. For a thorough summary of mechanistic, 

diagnostic, and therapeutic approaches to CRPS, see: Wilson PR, Stanton- 

Hicks M, Harden RN (eds.) CRPS: Current Diagnosis and Therapy. Seattle, 

IASP Press, 2005. 


FEATURE | BROATCH 

RSDSA: Expanding Research, 

Education, and Awareness of CRPS 

BY JAMES W. BROATCH, MSW, RSDSA EXECUTIVE DIRECTOR 

SCIENTISTS AND CLINICIANS ARE STILL BAFFLED by this 

little-known, poorly understood collection of signs and 

symptoms of CRPS—what causes it, why it develops 

in one person and not in another with the same injury, 

why it occurs in more females than males, and why 

children and teens with this syndrome generally get 

better while most adults (80 percent in one prospective 

study) cannot resume prior activities (1). 

The Reflex Sympathetic Dystrophy Syndrome Association 

(RSDSA) deals with issues like these every day. Founded in 

1984 to raise money for research, over the years, our mission 

has broadened to include awareness, education, patient support, 

legislative issues, and the creation of a CRPS patient 

database. Based in Milford, Connecticut, RSDSA has two fulltime 

employees and is guided by a talented 10-member board 

of directors (four of whom have CRPS). Our Scientific Advisory 

Committee is led by R. Norman Harden, MD, and 

Srinivasa N. Raja, MD, and is comprised of some of the key 

thought leaders on CRPS who serve as consults on medical, 

treatment, and research issues. RSDSA has grown into a 

national, nonprofit organization with an annual revenue is 

over $600,000, 90 percent of which is spent on research and 

educational programming. 

Research 

RSDSA is committed to encouraging research to discover the 

cause(s) and cure(s) of CRPS. Why? Because medical professionals 

and the public are still largely unaware of this intensely 

painful and potentially debilitating syndrome. For example, a 

1999 epidemiology study published in PAIN reported that the 

mean number of different physicians who evaluated a CRPS 

patient prior to being seen at a pain center was 4.8 (2). Then in 

2005, an Internet-based survey of 1,362 people with CRPS 

(conducted by Johns Hopkins School of Medicine and funded 

by RSDSA) found that 56 percent of the respondents saw more 

than four physicians prior to being diagnosed with CRPS-not 

much of an improvement! 

Also, the reality is: you can’t cure what you don’t understand! 

Peter Moskowitz, MD, a member of the RSDSA board of 

directors, explains, “Science helps us learn new things, and there is 

much we want to know about CRPS. The best science not only 

helps us know about difficult subjects—and CRPS is a very difficult 

subject—it also tells us how we know what we know and 

informs our understanding of the disease process and its treatment.” 

It is for these reasons that we fund at least two research 

grants (up to $50,000 each) every year. Since 1992, RSDSA has 

funded $732,665 in fellowships and research grants. Recent 

RSDSA-funded grants include: 

❥ Treatment of Complex Regional Pain Syndrome Type I by 

Nitroglycerine, A Web-Based Epidemiological Survey of CRPS-I; 

❥ Identification of CRPS Subtypes and Effective Treatments; 

❥ Changes in CSF Cytokine levels in Reflex Sympathetic 

Dystrophy; Validation of Revised Diagnostic Criteria 

for CRPS/RSD; and, 

❥ Noninvasive Investigation of Human Brain Mechanisms 

Associated with the Development and Treatment of RSD. 

An Outcome of RSDSA Research Funding 

In 2004, we funded a study called Development of a rat model 

of CRPS-I based on partial injury to nociceptive axons. The 

results of this study prompted further research, which evolved 

into a paper written by Anne Louise Oaklander, MD, PhD, 

called Evidence of focal small-fiber axonal degeneration in complex 

regional pain syndrome-I (reflex sympathetic dystrophy). This 

study will be published in Pain and proves that: “CRPS-I now 

has an identified cause takes it out of the realm of so-called 

‘psychosomatic illness.’ (3)” 

Detailed application guidelines for funding can be 

found on our website at: www.rsds.org 

Education and Awareness 

In order to encourage accurate diagnosis and appropriate treatment, 

RSDSA has developed informative educational brochures 

with the assistance of our Scientific Advisory Committee. One 

of the most widely distributed is a screening tool for medical 

professionals—a laminated, two-sided, wallet-sized card that lists 

the signs and symptoms of CRPS Type I on one side and provides 

a pain rating scale on the other. We mailed the card along 

with an informative cover letter to members of the American 


Academy of Family Physicians, the American Academy of Physician 

Assistants, and the American Society of Pain Management 

Nursing. The letter began with the prescient sentence “A minute 

of your time can prevent a lifetime of suffering.” The response 

was enthusiastic. Many of the physicians and nurses were on 

medical- and nursing-school faculties and requested multiple 

copies for their students and fellows. RSDSA members also 

asked for individual copies for themselves and other family 

members and additional copies to distribute to medical professionals 

in their communities. 

In addition, RSDSA is publishing its third edition of 

evidenced-based Clinical Practice Guidelines (in press) and 

the RSDSA Review Digest, a compendium of articles that have 

appeared in the RSDSA Review on the diagnosis, treatment, 

and management of CRPS. Although the articles are archived 

on our website, 42 percent of Americans do not have access to 

the Internet and most medical professionals are too busy 

to thoroughly search our website. The Digest will be a perfect 

companion to the Clinical Practice Guidelines. We expect that 

medical professionals will also distribute the compendium to 

their patients with CRPS. If you would like to receive any of 

our free materials, please call 877-662-7737. 

Each year, staff and volunteers exhibit at major medical, 

insurance, and school nurse conventions and conferences. 

RSDSA believes it is vitally important for its members to attend 

new conferences in order to inform the attendees about our 

programs and educational materials, our top-notch website, 

research funding opportunities, ongoing CRPS clinical trials, 

and to discuss with medical professionals how we can work 

with them to help their patients and improve their practices. 

Shefali Agarwal, MPH, Srinivasa Raja, MD, both from Johns Hopkins School of 

Medicine and Bradley Galer, MD, RSDSA board member, discuss the results of an 

Internet-based epidemiological study funded by RSDSA. 

Patient Support 

At RSDSA, we are acutely aware of the devastation caused by 

the pain of CRPS. People become disabled and marriages fail. 

Families break part and lives are financially ruined. People 

become socially isolated and housebound. In our 2005 Internet 

Survey, 47 percent of the respondents reported that they had 

considered suicide and 15 percent of this group had tried. 

Although there is no hard data on the number of CRPS-related 

suicides, the donations section of our newsletter includes several 

gifts made in memory of individuals who, more often than not, 

have taken their own lives. It is chilling. 

For this reason, although we do not offer formal patient 

services, I do talk to those people who call 

or send email, as does my assistant, Gayle 

Bonavita, and several of our board members 

who have CRPS. 

CRPS Education Bills 

Through grass-roots initiatives, we have 

helped people with CRPS in their efforts 

to get CRPS Awareness legislation 

passed in Delaware, New York, and Pennsylvania; 

similar legislation has been or 

will be introduced in New Jersey, Illinois, 

Oregon, Michigan, and California. The 

legislation mandates that a state’s 

Department of Health conduct medical 

professional and public education programs 

to encourage earlier detection and 

appropriate treatment of CRPS. 

Jim Broatch talks to attendees at the Academy’s annual meeting in San Diego. 



We are acutely aware of the devastation caused by the pain of CRPS. 

People become disabled and marriages fail. Families break part and lives 

are financially ruined. People become socially isolated and housebound. 

CRPS, Social Security, Workers’ 

Compensation, and the Insurance Industry 

Although it is a challenge for most people who apply for Social 

Security Disability benefits, individuals with CRPS are hampered 

by the lack of knowledge and understanding of the syndrome 

itself. In 1999, RSDSA was instrumental in convincing 

the Social Security Administration to issue a special ruling on 

how to adjudicate CRPS claims. We continue to receive letters 

RSDSA Publications 

and email from members 

who have used 

our information to get 

their claims approved. 

Injured employees 

with CRPS do not fare 

well in the Workers’ 

Compensation (WC) 

program. Of the 1,362 

people who completed 

the web-based survey, 

41% reported being 

injured at work; however, 

only a few of 

them obtained workers’ 

compensation benefits. 

Too often, the 

relationship between 

an injured worker and 

the WC insurance carrier 

erupts into a war. 

Treatment is frequently 

delayed and denied. 

In 2005, RSDSA 

exhibited at the conferences 

of two major workers’ compensation groups, the 

Risk and Insurance Management Society and Case Management 

Society of America. We view these conferences as opportunities 

to reach out to case managers and risk managers, 

some of whom still view CRPS as a nebulous, expensive, 

and frequently fraudulent claim. We launched a special newsletter, 

Working Together, Ensuring a Brighter Future, at these conferences. 

Our goal is to develop a mutually beneficial 

relationship. We will distribute our new Clinical Practice Guidelines 

to the insurers to encourage early intervention and appropriate 

treatment, enabling individuals with CRPS to recover 

and return to work. 

RSDSA publishes several free brochures to help people with CRPS/RSD, their families, and their healthcare 

providers. Please call RSDSA at 877-662-7737 to order copies. 

In Pain, Out of Work, and Can’t Pay the Bills, a resource directory, contains information on government programs, patient 

assistance programs, insurance, community and faith-based sources of help, resources for veterans, and much more. 

Recognizing, Understanding, and Treating CRPS/RSD is a quick overview of the syndrome, its telltale signs and symptoms, 

and treatment ideas. It is particularly valuable for those people who are newly diagnosed and their families. 

Helping Children with RSD Succeed in School is a practical guide for parents, teachers, school nurses, and administrators 

on accommodating the school environment for children and adolescents who have CRPS/RSD. 

Treating Complex Regional Pain Syndrome/Reflex Sympathetic Dystrophy Syndrome, A Guide for Therapy contains 

information on evaluation of CRPS/RSD for functional rehabilitation, treatment protocols, and treatment progression. 

CRPS/RSD and Sports Injuries: Prevention is the Name of the Game addresses the risk that athletes have of developing 

the syndrome. New research also links the development of CRPS to some of the surgeries that have traditionally helped 

sports injuries. This brochure is a must-read for athletes, parents, coaches and athletic trainers, as well as those who 

practice sports medicine. 

Telltale Signs & Symptoms Handicard is a quick reference for practitioners. The laminated, credit-card size card features 

the telltale signs of CRPS on one side and a pain scale on the other. This tidy handout has been a great hit among 

healthcare professionals, students, and people who have CRPS/RSD. 

Patient Education 

Linda Lang, an RSDSA board member and coauthor of Living 

with RSDS, described the tremendous losses experienced by an 

individual with CRPS. 

What to Call It —CRPS or RSD? 

IN RECENT YEARS, the medical community has almost universally accepted the term Complex Regional Pain 

Syndrome Type I (CRPS) to describe what had been called Reflex Sympathetic Dystrophy Syndrome (RSD). CRPS is 

a more comprehensive term that denotes the syndrome’s regional nature and that it is not always mediated by the 

sympathetic nervous system. For this magazine, we used whatever term the author chose (CRPS, RSD/CRPS, or RSD). 


Lisa Delia, Maria Brown, and Jim Broatch at the 2005 Achilles Walk for Hope and Possibility fundraiser. 

RSDSA sponsored a team. 

“… [I]n publicizing RSD, we generally focus on the pain, 

not the disabilities that come with it-the legs and hands that no 

longer work, the bones that become osteoporitic, the joints that 

become locked, the muscles that become spastic. … There is an 

awful lot we leave out—how a productive member of society 

can become too disabled to work or take care of her children. 

We don’t discuss the tremendous personal losses—families, 

friends, jobs—that RSD wreaks … (4)” 

We address many of these issues in our publications, such 

as the RSDSA Review (a quarterly newsletter), the Support 

Group Newsletter (a bi-monthly electronic publication), and 

In Pain, Out of Work, Can’t Pay the Bills, a resource directory 

that identifies the governmental and private programs that 

can help low-income families obtain treatment and needed 

medication, pay their bills, and avoid losing their home. 

Originally published in 2001, the directory is now in its third 

edition. We publish several brochures as well, such as 

CRPS/RSD: Prevention is the Name of the Game, which links 

CRPS to sports injuries and the surgeries that traditionally 

follow them. This brochure is written for coaches and trainers, 

and particularly for athletes, a group we believe is at high 

risk for developing the syndrome. 

Website 

Most people with CRPS or persistent pain learn about RSDSA 

by visiting our website, www.rsds.org. In 2005, we had an average 

of 37,000 visits per month. Our highest traffic, 57,000 in 

April, was driven by a People magazine cover story revealing that 

Paula Abdul had been diagnosed with RSD. 

Our website houses all of our educational 

brochures (in PDF format); videos 

or PowerPoint ® presentations from past 

international conferences; scientific articles 

on the diagnosis, treatment, and management 

of CRPS that have appeared in our 

quarterly newsletter or in peer-reviewed 

journals; links to other professional and 

consumer sites; and much more. We 

encourage individuals to sign up to receive 

free electronic alerts about new discoveries, 

clinical trials, articles in the media, legislative 

initiatives, and upcoming events. 

Srinivasa N. Raja, MD, Director 

of Pain Research at Johns Hopkins University 

has created a PowerPoint ® presentation, 

Diagnosis and Treatment Options 

of RSD/CRPS, which can be downloaded 

for use during in-service training or for 

personal edification. 

Join RSDSA 

RSDSA is a vibrant organization that is 

sensitive to the needs and concerns of 

its 6,000 members and the greater 

CRPS community. In the Fall 2005 RSDSA Review, Norman 

Harden, MD, said, “Without RSDSA, progress in fighting the 

syndrome would likely come to a halt. Even basic and essential 

Revised Clinical Practice Guidelines 

THE THIRD EDITION of RSDSA’s Clinical Practice Guidelines 

will be available in hard copy and on the website by the end 

of March. In 2004, RSDSA approved a grant to revise the 

evidence-based Clinical Practice Guidelines, which had not been updated 

since 2002. RSDSA received a grant from the National Organization 

for Rare Diseases, Inc. (NORD) to print and distribute the guidelines. 

R. Norman Harden, MD, Director, Center for Pain Studies, Addison Chair, 

Rehabilitation Institute of Chicago, Chicago, Illinois, edited the guidelines. 

Contributing authors were Stephen Bruehl, PhD, Department of 

Anesthesiology, Vanderbilt University Medical Center, and Allen Burton, 

MD, Department of Anesthesiology and Pain Medicine. The guidelines 

include the following five chapters and a treatment algorithm: 

❥ Introduction and Diagnostic Considerations 

❥ Interdisciplinary Management 

❥ Pharmacotherapy of Complex Regional Pain Syndrome (CRPS) 

❥ Psychological Interventions 

❥ Interventional Therapies 

CRPS can be a difficult syndrome to treat, especially if treatment 

is offered piecemeal rather than in an interdisciplinary fashion as 

recommended. Jim Broatch, Executive Director, says, “Our goal in 

writing these guidelines was to make sure that those individuals 

suffering with CRPS receive the proper diagnosis and appropriate 

treatment. Through education, we hope to minimize patient 

losses as much as we possibly can.” 



information, such as how best to make the diagnosis and what 

causes the disease, is lacking, and these are traditional topics 

funded for research by RSDSA (5).” 

Members include people with CRPS, their families, and 

practitioners. We encourage all of you to join RSDSA. Help us 

to promote greater awareness of CRPS among your medical 

colleagues and to improve the lives of individuals with CRPS 

and their families. 

Together we can make a huge difference. 

REFERENCES 

1. Veldman HJM, Reyen HM, Arntz R, Goris JA. Signs and symptoms of 

reflex sympathetic dystrophy: Prospective study of 829 patients. The 

Lancet 1993; 342; 1012-1015. 

2. Oaklander et al., Evidence of focal small-fiber axonal degeneration in 

complex regional pain syndrome-I (reflex sympathetic dystrophy). Pain. 

2006;120: 235-243. 

3. Allen G, Galer BS, Schwartz L. Epidemiology of complex regional pain 

syndrome; a retrospective chart review of 134 patients. Pain. 

1999;80:539-544. 

4. Lang, L. An Army of Six Million, RSDSA Review. Fall 2004.17:9. 

5. Broatch JW, Every Dollar for Research Counts. RSDSA Review. 

Fall 2005:18:3. 

CORPORATE 

M E M B E R S 

American Academy of Pain 

Management appreciates the 

leadership and support 

of its Corporate Members 

Electromedical Products Intl. Inc 

Endo Pharmaceuticals 

Janssen Pharmaceuticals, Inc 

Ligand Pharmaceuticals 

Eli Lilly and Company 

PainCare Holdings, Inc 

Purdue Pharma, L.P. 


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FEATURE | PATIENT PROFILE 

PEOPLE 

WITH CRPS 

THEIR STORIES AND 

ACCOMPLISHMENTS 

The following are profiles of five remarkable individuals, identified by RSDSA, 

who live with CRPS—and on-going pain. Although their stories are different, 

all have in common the desire and will to make life better for others with the 

condition—and the determination to live full and meaningful lives. 

Stephen Spagnoli 

STEPHEN SPAGNOLI, 46, A FORMER LANGUAGE ARTS TEACHER, MUSICIAN, 

AND COMPOSER FROM QUEENS, NEW YORK, ALWAYS KNEW HE HAD TALENT 

AS A VISUAL ARTIST, BUT HIS LIFE AS A PAINTER DIDN’T BEGIN UNTIL HE 

STARTED RECOVERING FROM A TERRIBLE THREE-YEAR BOUT WITH RSD. This 

experience, he says, was his “wake-up call.” 

In1997, Stephen developed a repetitive stress injury in his right arm 

caused by doing work around his house. Within three weeks, his left arm 

mirrored the same symptoms. Visits to numerous doctors produced no 

results. “I explained to the doctors that having pain in the other arm meant 

the pain had to be neuropathic, but none agreed.” In 1998, a doctor who 

was convinced that Stephen had tennis elbow operated on his right arm. Stephen Spagnoli 

“That’s when the disease exploded and I was diagnosed with RSD,” 

Stephen says. “The pain spread from my arms to my trunk, then to my legs, my face—everywhere. I had a full-body allodynia. I was 

bedridden from 1998 until 2001. I spent 15 hours out of each day in the bathtub. The quality of my life was zero. I was treated 

with heavy doses of morphine, but the drugs did nothing to reduce my pain.” 


The turning point came when Stephen found a doctor in 

Florida who specializes in RSD. “His protocols were different 

from any others I’d heard about. He gave me multiple injections 

along the edge of my spinal cord (not epidurals, but trigger-point-like 

injections). He got me off the morphine and put 

me on Buprenex. That’s when things turned around. I started 

moving and having energy again, and getting the pain under 

control (as opposed to the pain having control of me). I was 

still frail and walking with a cane, and I still had flare-ups, but 

I was no longer praying not to wake up in the morning.” 

When Stephen recovered enough to resume activities, he 

had the rare opportunity to explore “a path not taken” in his 

life before RSD. “I’ve always been an artist but never thought 

of it as a career. I had sold my illustrations to magazines and 

newspapers in the past, but I didn’t start expressing myself 

through painting until I had recovered enough from the RSD. 

When he began painting, Stephen’s work focused solely on 

various aspects of RSD. “Some were visualizations of pain and 

some were tactile (what the allodynia felt like). Some were 

images of despair and loss—the loss of who I was, my ability to 

enjoy being touched, and my sexuality.” 

Today, Stephen works in his studio each day. His abstract 

paintings no longer deal with pain, and he is working on the 

illustrations for a short story that is a metaphor for what he 

went through during his illness and recovery, and a book for 

adolescents. 

“I realized that I had always wanted to be an artist. The 

RSD was my ‘wake-up call’—just like it was a wake-up call in 

every other facet of my life. The RSD was a gift because it 

gave me the space to become what I always should have been. 

It also gave me an appreciation of life and my family.” 

Stephen says, “In a way, I used my paintings as a ‘revenge 

on the disease’ by making it something that could be shown. I 

wanted to put it up to the light.” For people who were beginning 

to have RSD symptoms, he wanted to encourage them 

to seek help immediately. He also wanted to use visual 

imagery to show the doctors who denied that he had RSD, 

that they were wrong. 

Stephen does not know if his condition will continue to 

improve, but he is hopeful. “I’m mobile and I can use my 

hands. I still can’t play ball with my kids, I’m not well enough 

to work out and keep in shape, and I still can’t play my guitar, 

although I try sometimes (Stephen had signed a contract with 

BMI, a music publishing company, prior to his illness). I just 

have to be patient and keep doing what I’m doing.” 

LOVERS 

Soapstone and mixed media on canvas 10x10 

SPASM canvas on canvas 20X18 

“The RSD was a gift because it gave me the 

space to become what I always should have been” 


PEOPLE WITH CRPS | THEIR STORIES AND ACCOMPLISHMENTS 

Wilson H. Hulley 

floor, “pawing” light switches on or off, and 

retrieving items from counters or even the 

WHEN WILSON HULLEY WAS 

refrigerator. Most important for someone 

DIAGNOSED WITH RSD, he 

like Wilson, Star allowed him to be independent-she 

acted as a cane when his bal- 

figured he had two choices: 

cave in and let the syndrome 

ance was compromised and, because his 

and the ensuing disability 

legs are painfully tender to the touch, she 

destroy him or continue to fight for the 

acted as a buffer between him and other 

rights of people with disabilities. Two years 

people in a crowd. 

before the onset of RSD, Wilson had 

Beyond the practical aspects, assistance 

joined the President’s Committee on the 

dogs also provide emotional support. “Pain 

Employment of People with Disabilities. 

places both physical and emotional restrictions 

on our lives, and although medication 

On the Committee, he was Special Assistant 

to the Executive Director, Advisor to 

and other treatment modalities help, those 

the Chairman and to The President, and 

of us disabled by CRPS often can use the 

Wilson Hulley and his assistance dog, Star 

a member of their Executive Staff; Wilson 

‘leg up’ provided by a canine companion. 

helped develop the language for the Americans 

with Disabilities Act, which President George H. Bush can break down the social and physical barriers often imposed 

Also, an affectionate, highly trained canine 

signed into law. 

by a disability,” he says. 

A car accident in 1986 left Wilson with a traumatic brain Wilson continues to be dogged in his fight for the rights of 

injury and the many months of rehabilitation gave him a special 

insight into the challenges that face people with disabilities. CRPS. As a member of the Board of Directors of RSDSA, he 

people with disabilities, and specifically for those who have 

Having held a number of senior management positions in the communicates with others who have the syndrome and has 

private and public sector, Wilson’s resume reads like a “Who’s served as an advocate when necessary. He is particularly interested 

in the plight of returning war veterans who suffer chronic 

Who” and his experience and contacts gave him a definite edge. 

For example, he was working with the Committee when the pain. Beyond the RSD community, Wilson serves on the 

memorial for President Franklin Roosevelt was being designed. Northwest Airlines Customer Advisory Board on Disabilities, 

There was a lot of discussion about whether to portray him for whom he reviews disability policies for both employees and 

in a wheelchair or not. Wilson recalls writing a note to then passengers. Also, having been mugged twice since becoming 

President Bill Clinton that said, “Mr. President. Just do it!” The disabled, Wilson recently retired from the board of directors of 

wheelchair won. 

the National Organization for Victims Assistance. And, he 

Wilson’s “Just do it!” attitude has served him well. For serves as the advisor to the International Association of Assistance 

Dog Partners; where he and Star were honored in 2004 

example, when he realized in 1994 that he needed help getting 

around, he applied for an assistance dog from the National with the Unsung Hero Award; just one of many awards and 

Education for Assistance Dog Services (NEADS) in Princeton, honors he has received in his lifetime of serving others. 

Massachusetts. Star, a British Black Labrador Retriever, helped Like others who suffer from CRPS, the magnitude of Wilson’s 

personal loss is huge but unlike so many others, he contin- 

Wilson negotiate the world for 10 years (she recently passed 

away at the age of 12. He is awaiting his second assistance dog ues to be empowered to make the world a better, safer, and 

from NEADS). Although we don’t automatically associate assistance 

dogs with people in pain, they can do multiple things 

happier place for those who are disabled. 

that make life manageable, such as picking things up from the 

“ … an affectionate, highly trained canine can break 

down the social and physical barriers often 

imposed by a disability.” WILSON HULLEY 


Barbara Schaffer 

IN 1988, BARBARA SCHAFFER, a 38-year-old vocational rehabilitation 

counselor, developed RSD from a minor injury at 

work. Although her RSD was diagnosed and treated almost 

immediately, the disease progressed rapidly. Exercise exacerbated 

her condition, other complications set in, and nothing 

relieved her pain. Yet in spite of her worsening physical condition, 

Barbara continued working at the job she loved for two 

more years (until the program shut down), and began taking 

action to help others who were living with RSD. 

Shortly after being diagnosed in 1988, Barbara launched an 

RSD support group in her area. And in 1992, she published an 

RSD newsletter and launched the first RSD website. 

Barbara’s group also ran four CME conferences for doctors 

and nurses through Geisinger Medical Center, a tertiary-care 

teaching hospital in the area. 

Two years ago, Barbara worked with others (Rick Ulrich 

and Jenny Dye, both of whom have RSD) to get an RSD bill 

passed in Pennsylvania. “The bill calls for 

educating the public and medical community 

about RSD. We were successful because 

State Representative Merle Phillips worked 

with us. He’d known me and Rick, and he’d 

seen what RSD had done to us. Once the 

bill was passed, the State Department of 

Health held a meeting with providers from 

all over the state who treat people with 

RSD. The purpose of this meeting was to 

find out what the providers wanted done, 

and that’s how the outreach program was 

developed. New York State put out an RSD 

bill the year before, but they’ve didn’t have 

Barbara and Paul Schaffer 

the money to implement it. In Pennsylvania 

the money came out of the Department of Health budget. So 

the implementation may not be as good as we would like, but 

we do have pamphlets in all the Department of Health sites 

and there is RSD information on their website.” Pennsylvania 

is one of the three states in the country to have passed RSD 

legislation. 

Today, at 56, Barbara has had to cut back her activities, but 

that hasn’t stopped her from working for others with RSD. 

Doctors refer patients to her, and she gives support to them 

over the phone. She also contributes her time to RSDSA. Last 

year she assisted RSDSA staff in organizing a conference in her 

area; she writes articles for their newsletter that focus on RSD 

and the arts; and she has worked on the organization’s annual 

fundraising dinner. 

At home, Barbara spends time with her husband (he takes 

care of their three grandchildren while their daughter and 

son-in-law are at work). “I’ve been lucky to be involved with 

my grandchildren. I’m a big part of their lives, which is very 

important to me.” 

Barbara is philosophical about the challenges 

of living with RSD. “I have lost the 

ability to do many of the things that I 

loved, and I have mourned their loss. But I 

continue to find new things to do and new 

ways to do old things. In filling my days 

with activities and friends and my grandchildren, 

I have learned that there are 

many ways I can enjoy life. This is a constant 

challenge because RSD is always 

changing. But isn’t change one of the constants 

of life? I try to remember that life 

has made me no promises, that each day is 

a gift, and that I get to choose whether I 

suffer or enjoy it.” 

“ I try to remember that life has made me no promises, 

that each day is a gift, and that I get to choose 

whether I suffer or enjoy it.” BARBARA SCHAFFER 


PEOPLE WITH CRPS | THEIR STORIES AND ACCOMPLISHMENTS 

Lisa Delia 

KEEP ON MOVING By Ed Delia 

My wife, Lisa, was diagnosed with RSD in May 2003, 

approximately five months after she triggered the 

syndrome by jumping up to squash a bug on the 

ceiling. After being misdiagnosed by two orthopedists, 

Lisa was in physical therapy and not making 

much progress. On the Internet, Lisa found a condition that 

resembled the symptoms she was experiencing. It was RSD. 

Dr. Robert Knobler, a neurologist in Fort Washington, Pennsylvania 

who has treated a lot of people with RSD, started Lisa on 

a regimen of walking and water therapy. Consistent physical 

activity combined with (warm) water therapy seems to help her 

condition. We have found that moving is a must. Move when 

you don’t want to, put the work in every day. Evidence of 

progress comes in months and years. 

Last spring, “movement” escalated when we were introduced 

to the Achilles track club, a worldwide not-for-profit 

organization that encourages people with all types of disabilities 

Valerie Lacey, Emma Delia, Ed Delia, Albee Delia and Lisa Delia at the 

Achilles Walk finish line. 

PHOTO: LORRY MULHERN/CHRIS HERDER, LOTUSPHOTOGR APHERS.COM 

to participate in mainstream athletics. It promotes personal 

achievement and enhanced self-esteem. The founder, Dick 

Traum, was the first amputee to run and finish the New York 

marathon. Achilles was founded in 1983 and now has 110 

chapters worldwide and 40 in the U.S. 

Once a year Achilles sponsors “Hope and Possibility: 5 

miler Run, Walk or Roll.” The participants all have some level 

of disability—blind runners pair with sighted ones, quadriplegics 

compete in wheelchairs, wounded Veterans walk or run. In 

April of 2005, Lisa and I met with Mary Bryant from Achilles. 

She instantly adopted our cause to promote awareness of RSD 

and invited people with RSD to participate. We had less than 

two months to pull this off. 

Lisa called Jim Broatch, the Executive Director of RSDSA 

to see if the organization could help spread the word. RSDSA, 

with Celgene’s financial support, supplied T-shirts and paid the 

entry fee for participants. Lisa sent email to support groups 

across the country, inviting them to come. Her niece, Maria 

Brown, a graphic arts student, created a logo for the poster that 

graced the RSD tent. On June 26, in 82-degree-heat, 25 people 

with RSD, their friends and family, joined thousands of others 

who gathered in Central Park for the event. Our family, 

including my 87-year-old mother and our three children, 

Albee, Daniel, and Emma, joined Lisa and me on 

the track. Some with RSD did the race in wheelchairs, 

and others, like Lisa, used crutches. 

It was not easy; at the four-mile point Lisa was tired 

and hurting, but the people on the sidelines, including 

New York firefighters, were cheering. “You can’t imagine 

the camaraderie you feel you get from support of people, 

like the firefighters and others egging you on,” Lisa said. 

The walk took its toll. For about three weeks afterwards, 

Lisa’s pain flared. Nevertheless, we will be back 

in Central Park this August for the 2006 Achilles Walk. 

In spite of the short notice, Lisa and the group of supporters 

helped raise more than $26,000 for awareness 

last June. We have to keep moving forward. We are 

committed to raising awareness of RSD and the horrible 

pain involved. 

“ You can’t imagine the camaraderie you feel you get 

from support of people, like the firefighters and 

others egging you on.” LISA DELIA 


Sharon Weiner 

SHARON WEINER WAS THE ULTIMATE 

“SUPER MOM.” A full-time career 

woman, a wife, and mother of a son and 

daughter, she always made time to be 

involved with Scouts, PTA, and school 

plays. But when Sharon was diagnosed with 

RSD/CRPS in 1996 at the age of 38, she knew 

her life would have to change. Slowed down, 

but unstoppable, Sharon not only learned to do 

Sharon Weiner 

things in new ways, but she launched a support 

group to help others with the syndrome. 

“When I was first diagnosed with RSD, I was happy to 

know that there was a reason for all this pain, but when I 

started realizing the impact it was going to have on my life, I 

knew I needed to learn more. I found a support group about an 

hour from home and it was the most uninformative, depressing 

thing I had ever gone to. It was a complete ‘woe is me’ meeting. 

The people just wanted to complain and tell their stories. 

When I walked out, I thought, ‘I might as well give up now.’” 

Determined to get a local group started, Sharon went to a 

Reflex Sympathetic Dystrophy Syndrome Association (RSDSA) 

meeting in Atlantic City and found people from her area who 

were interested in joining. As soon as she returned home, she 

arranged for a regular meeting room at a medical center, printed 

flyers, and sent them to all pain centers in the region. The first 

meeting of the group convened in November 1997 and continues 

to meet monthy. 

“We call the group ‘Living with RSD.’ We know there’s no 

cure, so we offer information on how to deal with it. The first 

half-hour of each two-hour meeting is devoted to open discussion. 

The second part of the meeting focuses on a particular 

topic. We’ve offered presentations on self-defense, cooking, legal 

issues, social security, and clothing. Often we address psychosocial 

issues. I don’t always agree the speakers, but I’m committed 

to making information available to people.” 

“Living with RSD” meetings are not limited to people with 

the syndrome; they are also open to family members and 

friends. Most members, however, are women ranging in age 

from their late twenties to early fifties. “At one point we even 

had a fourteen-year-old girl, but many of the issues we address 

are those she didn’t need to deal with yet, such as marital or 

financial problems, how to deal with Workers’ Comp, or how 

to get Social Security.” 

The group also has family sessions in 

which those with RSD/CRPS leave the room 

and family members have the opportunity to 

speak with a psychologist. “This is important 

because CRPS causes rifts in families—the 

dynamics change,” Sharon says. “Family members 

need to understand the limitations of the 

condition, know when to be helpful, and when 

not to be enabling. Getting RSD is particularly 

hard for husbands who were the family breadwinners. 

It’s a huge loss of self-esteem and it’s 

often hard to ask for help. All of us with RSD 

need to understand that we’ve lost part of our 

lives, and we need to go through a grieving process for that.” 

Newcomers to the group receive a packet that contains 

basic RSD information as well as a host of resources and a 

schedule of meetings. Sharon has found that people with 

RSD/CRPS not only find this packet instructive, but they can 

also show it to their families and doctors—because a lot of people 

don’t believe this disease exists. 

In 19????, the support group became a nonprofit organization 

with the help of an accountant with RSD/CRPS. Now, a 

significant part of Sharon’s work is devoted to fundraising. 

“There are no dues, because a lot of people have financial 

problems when they have a long-term syndrome like this. I’m 

not afraid to ask for money or services from other sources, and 

I’m always trying to figure out how we can get jobs done for 

the organization. We’re listed with United Way, and many of 

my friends and family donate through their jobs. We’ve sold 

T-shirts, flower bowls, and lately we’ve been doing flea markets. 

Right now we need money for a mass mailing to healthcare 

professionals and a revamping of our website.” 

“My mother says this work is my ‘calling.’ When I need 

something done, I figure it out. I got that from my father,” 

Sharon says. When he wanted to build something, he got a 

book and built it. Having RSD can be overwhelming, but 

you can’t give up hope. You just have to look for new ways of 

doing things.” 

Although Sharon no longer goes to a regular job, her life is 

full and active—and for her kids, she has never stopped being 

a very super mom. 

“ All of us with RSD need to understand that we’ve 

lost part of our lives, and we need to go through 

a grieving process for that.” SHARON WEINER 


FEATURE | GALER 


COMPLEX REGIONAL 

PAIN SYNDROME: 

New Hope After a 

Decade of Dispelling Myths 

BY BRADLEY S. GALER, MD 


C Fibers Backfiring 

Mixed Media on Canvas 30x60 

Complex Regional Pain Syndrome (CRPS) 

is a perplexing condition that has been 

relatively ignored and misunderstood by the 

medical community because it is so unusual. 

Perhaps the confusion that is invoked by this 

condition is precisely due to its atypical clinical 

presentation: the pain in CRPS patients 

does not follow a pattern expected in painful 

neurologic conditions, the affected body part 

changes color and temperature quite dramat - 

ically, and patients often display protective 

behavior that looks odd to a practitioner. 



TABLE 1 | IASP Diagnostic Criteria (2) 


PAIN SYNDROME TYPE I (RSD) 

❥ The presence of an initiating noxious event, 

or a cause of immobilization 

❥ Continuing pain, allodynia, or hyperalgesia with 

which the pain is disproportionate to any inciting event 

❥ Evidence at some time of edema, changes in skin blood 

flow (skin color changes, skin temperature changes more 

than 1.1°C difference from the homologous body part), 

or abnormal sudomotor activity in the region of the pain 

❥ This diagnosis is excluded by the existence of conditions 

that would otherwise account for the degree of pain 

and dysfunction 


PAIN SYNDROME TYPE II (CAUSALGIA) 

❥ The presence of continuing pain, allodynia, or hyperalgesia 

after a nerve injury, not necessarily limited to the 

distribution of the injured nerve 

❥ Evidence at some time of edema, changes in skin blood 

flow (skin color changes, skin temperature changes more 

than 1.1°C difference from the homologous body part), 

or abnormal sudomotor activity in the region of pain 

❥ This diagnosis is excluded by the existence of conditions 

that would otherwise account for the degree of pain 

and dysfunction 

FURTHERMORE, CRPS OFTEN MAY RESULT from a work-related 

injury and thus may carry suspicion of an ulterior financial 

motive-although this is rarely, if ever, the case. And lastly, often 

the CRPS patient has a comorbid psychiatric condition. The 

net result has been a tendency among many in the medical 

community to keep CRPS patients at arm’s length, ultimately 

making it even more difficult for these patients to receive 

appropriate therapy. 

Fortunately, over the past decade an international group of 

research scientists and clinicians, who are dedicated to advancing 

our understanding and treatment of this difficult condition, 

have made great strides. Although there is still no cure or complete 

understanding of the pathophysiology underlying CRPS, 

most patients can be helped by educated pain practitioners who 

are able to alleviate their CRPS patients’ pain and improve function 

and quality of life with the proper care. This short review 

article will attempt to dispel old myths, summarize advances in 

our understanding of CRPS, and describe promising new 

approaches to therapy. 

What Is CRPS? 

OVER THE PAST DECADE, a great deal has been published in 

medical scientific peer-reviewed journals regarding CRPS (“reflex 

sympathetic dystrophy” and “causalgia”), documenting it as a 

true biomedical clinical disorder with underlying neurological 

pathology in both the peripheral and central nervous systems. 

Numerous attempts have been made to identify common causes 

and features to serve as a basis for effective treatment. International 

pain experts have questioned many of the previously 

long-held medical assumptions regarding this condition by performing 

research to test old hypotheses. Their healthy skepticism 

has resulted in exposing most of these old medical “tenets” as 

myths or half-truths. CRPS is at last being viewed from a datadriven 

scientific and clinical perspective (1, 2). 

A crucial part of this effort has been the attempt by the 

International Association for the Study of Pain (IASP) to more 

accurately define this medical condition, now called “Complex 

Regional Pain Syndrome” (CRPS), and especially to differentiate 

it from other conditions involving nerve pain (2). The new 

IASP diagnostic criteria recognize two syndromes: CRPS I 

and CRPS II [Table 1]. Both are conditions in which pain is 

most often severe and the area affected is characterized by skin 

sensitivity, abnormal color changes, temperature changes, and 

sweating. Not all patients have all these symptoms continuously, 

but they must always have more than just pain and skin 

sensitivity (allodynia and/or hyperalgesia), which are common 

among many neuropathic pain conditions. CRPS II (previously 

called causalgia) differs from CRPS I (or RSD) in being the 

result of identifiable nerve injury; otherwise, they are the same 

symptomatically. By accurately defining CRPS, there is a much 

better chance of finding effective treatments and defining the 

underlying etiology. 

Myth 1 

ONE OF THE MAJOR MYTHS regarding treatment of CRPS is 

that nerve blocks are the key to diagnosis and therapy. Even 

today, physicians commonly confuse the term “sympathetically 

A mistaken notion that heightens undue fear and anxiety in CRPS patients 

is the belief that all CRPS patients will progress through a series of increasingly 

debilitating stages and that CRPS will spread to other parts of the body. 


To date, there is no known predisposing risk factor for developing CRPS. No 

psychological profile has been identified that predisposes one to developing 

CRPS, nor have any data been published that have found a genetic link. 

maintained pain” (SMP) with CRPS. SMP, by definition, 

means only that a patient reports pain relief following a sympathetic 

block; thus, patients with a variety of clinical conditions, 

such as diabetic neuropathy, can also have SMP. Furthermore, 

although nerve blocks may be curative for some patients with 

CRPS, this is not true in all, and probably most, patients. 

For many patients, the majority of their pain is thought to 

be caused by mechanisms independent of the sympathetic 

nervous system (so-called “sympathetic independent pain” 

—SIP), and therefore sympathetic nerve blocks are not 

effective. The authorities have come to acknowledge that the 

cornerstone of CRPS treatment is physical and rehabilitation 

therapy, and not nerve blocks (1, 2). It is crucial to remember 

that the diagnosis of CRPS is a clinical one, based on history 

and examination findings [Table 1], without regard to response 

to sympathetic blocks. 

Myth 2 

A MISTAKEN NOTION that heightens undue fear and anxiety in 

CRPS patients is the belief that all CRPS patients will progress 

through a series of increasingly debilitating stages and that 

CRPS will spread to other parts of the body. A recent study has 

shown that there is no one set of stages that every patient goes 

through, and that the intensity and severity of symptoms/signs 

do not correlate with duration of CRPS (3). This study also 

made the important discovery that there appear to be three distinct 

subgroups of CRPS patients who differ in their grouping 

of CRPS signs/symptoms: 

[1] a relatively minor syndrome with vasomotor 

signs predominating, 

[2] a relatively limited syndrome with neuropathic 

pain/sensory abnormalities 

predominating, and 

MYTH 

[3] a florid CRPS. Although CRPS may indeed 

spread, this does not occur in every patient. 

Moreover, “spreading” of symptoms is often misdiagnosed 

as progressing CRPS. Instead, what 

often happens is that disuse or misuse of the 

affected limb leads to secondary myofascial 

problems, which then can become another independent 

source and site of symptoms. 

Myth 3 

RELATED TO MYTH 2 is the erroneous belief that 

therapy will be unsuccessful unless started early in 

the course of CRPS. Although it is definitely 

important to receive treatment as early as possible, 

patients should not be viewed as hopeless if their CRPS has 

remained undiagnosed or poorly treated for 5 or even 10 years. 

Based on authorities’ experience, patients with CRPS can and 

do respond to a variety of therapies even when they have had 

the condition for many years (1). 

Myth 4 

PERHAPS THE MOST PERVASIVE, DISTURBING, AND DAMAGING 

MYTH is that CRPS is a psychological disorder and is “all in the 

patient’s head.” Unfortunately, this tall tale had been perpetuated 

by many prominent neurologists up until the past few 

years, causing undue pain and suffering, as well as assisting the 

medical-legal-workers compensation systems in denying CRPS 

patients’ right to appropriate (paid-for) healthcare and insurance 

benefits. To some extent, this misguided belief probably 

reflects the unusual nature of CRPS as mentioned earlier. Also, 

like many chronic pain patients, CRPS patients do often 

develop secondary psychological conditions, including depression, 

anxiety, or post-traumatic stress disorder (PTSD), as a 

result of the effect severe pain has on their lives, but not as a 

cause of the condition (1, 2, 4). It is confirmed by scientific 

data that CRPS is not a psychiatric condition. 

What Causes CRPS? 

CRPS IS AN UNDERLYING PAIN CONDITION that is caused by 

abnormality in the nervous system, although standard neurological 

tests are frequently normal (except in CRPS II). Recent 

TABLE 2 | Common Myths 

FACT 

Nerve blocks are the key to therapy. Nerve blocks are effective in only a small 

percentage of CRPS patients. The key 

to therapy is multidisciplinary care 

focused on active rehabilitation of the 

involved body part. 

CRPS progresses through a series of CRPS does not progress through welldebilitating 

stages and will spread. defined stages. There are different subgroups 

of patients with various symptoms. 

CRPS does not spread in every patient. 

Therapy will be unsuccessful CRPS patients may respond to appropriate 

unless started early. 

therapies regardless of when they are started. 

It’s all in your head—CRPS is a CRPS is a chronic neurological condition 

psychiatric condition. 

resulting from a dysfunction in the 

peripheral and central nervous system. 



Although there is still no cure or complete understanding of the pathophysiology 

underlying CRPS, most patients can be helped by educated pain practitioners 

who are able to alleviate their CRPS patients’ pain and improve function 

and quality of life with the proper care. 

animal models for nerve pain have shown that animals suffering 

a nerve injury can display characteristics similar to humans with 

CRPS, including sensitivity to touch and changes in temperature 

and color, as well as “mirror” symptoms, all of which have 

been found to have an underlying neuropathological cause. 

Following injury, the body undergoes a series of physiologic 

responses designed to heal the damage, including an inflammatory 

response that results in changes in the area, such as redness, 

warmth, and swelling. This response is accompanied by changes 

in the nervous system, which registers pain sensations in the surrounding 

area, and results in skin sensitivity, allodynia, and 

hyperalgesia. In effect, many of the signs and symptoms that 

patients with CRPS experience are part of the normal healing 

process These responses usually cease after a short period of time 

but in CRPS they may continue indefinitely. Thus, one hypothesis 

is that CRPS represents a disruption of the healing process 

(1), although it is not known how pain and other CRPS symptoms 

are maintained over months and even years. 

Over the past few years, scientific studies performed with 

CRPS patients have strongly suggested that brain pathologic 

changes may be underlying some patients’ symptoms, which 

are likely reversible. A recent study demonstrated that CRPS 

patients had shrinkage of their somatosensory cortex contra - 

lateral to the affected limb, which was reversed with treatment 

that improved their symptoms (5). 

Is There a Predisposition to Getting CRPS? 

TO DATE, THERE IS NO KNOWN PREDISPOSING RISK FACTOR for 

developing CRPS. No psychological profile has been identified 

that predisposes one to developing CRPS, nor have any data 

been published that have found a genetic link (1, 6, 7). However, 

there is evidence suggesting that increased stress at the 

time of the inciting injury may be a risk factor (1, 6, 7). 

Approach to Treatment 

UNFORTUNATELY, THERE IS NO “MAGIC BULLET” for patients 

with CRPS. When a CRPS patient presents for treatment, most 

authorities generally still recommend a sympathetic nerve block 

to assess whether the patient has SMP (or SIP). If the patient is 

found to have SMP, there is a possibility that a series of these 

blocks may bring significant relief and for a minority of 

patients may be curative. However, patients and physicians 

should be warned not to be disappointed if a trial of one or two 

nerve blocks indicates that this therapy does not work for them. 

Each patient is different in terms of response to nerve blocks 

and medications. Although no treatment has been shown to 

help all patients with CRPS, the good news is that there is a 

long list of treatments that have been shown to ameliorate the 

pain and improve the quality of life for many patients. 

It is the responsibility of each pain provider to become 

familiar with the wide range of treatments reported to help 

patients with CRPS, not just perform invasive procedures, 

which will benefit few patients. Also critical in successfully treating 

CRPS is regular contact among all of the patient’s treating 

healthcare providers so that their efforts can be coordinated. 

Physiotherapy 

A CENTRAL, IF NOT THE KEY, GOAL OF THERAPY is to get the 

painful limb moving to restore normative function (1, 2, 7). 

Methods for accomplishing this goal consist of everything from 

restoring range of motion, slowly increasing tolerance for daily 

activities such as walking and sitting, and reducing sensitivity to 

clothing and other objects in the environment. Defined PT and 

OT techniques that have been used successfully include desensitization, 

stress loading, and a slowly progressive program of 

active exercise. 

Unquestionably, there will be times when patients will not 

want to move, and other times when they will want to move 

too much. The key is to have the patient maintain a systematic, 

long-term, structured program where slow and gradual gains are 

made on a weekly basis, both in the gym and at home. 

Psychotherapy 

PSYCHOLOGICAL ASSESSMENT AND COUNSELING is important, 

not because psychological factors cause CRPS, but because, like 

all chronic pain conditions, CRPS often has profound psychological 

effects on patients and their families. CRPS patients may 

suffer from major depression, anxiety, or post-traumatic stress 

disorder, all of which tend to heighten the perception of pain 

and make rehabilitation efforts more difficult (1, 2, 7). Patients 

who are not optimally treated for these psychological conditions 

simultaneously with their pain will not obtain optimal benefit 

from the overall treatment plan. 

Pharmacotherapy 

BECAUSE THERE IS NO KNOWN CURE FOR CRPS, pharmacotherapy 

is aimed at relieving painful symptoms in order to facilitate 

patient participation in rehabilitation therapy and, over time, a 

return to as much normal activity as possible. Medications 

should be tried one at a time, slowly but aggressively, making 

changes (increasing or decreasing doses, or changing medication) 

over the course of a few days or a week, if necessary, until 

the right agent or combination of agents is found that provides 

the optimal degree of pain relief with the most tolerable side 


effects. It is crucial to perform one medication change at a time 

so that the provider can ascribe improvement or side effects to 

the correct drug. As in treating any chronic pain condition, no 

one drug is effective in every patient, and each patient differs in 

terms of response and dosage required. However, with a persistent, 

systematic approach, most CRPS patients can eventually 

find a medication or group of medicines that provides meaningful 

pain relief (1, 2, 7). 

Athough randomized trials are scarce in CRPS (according 

to published reports and expert opinion), it is recommended 

that medication management be based on 3 classes of drugs 

[Table 3]; (these recommendations also generally comply with 

the recent clinical recommendations published for the treatment 

of neuropathic pain conditions (8)): 

[1] TOPICAL DRUGS (targeted peripheral analgesics), by definition, 

do not deliver meaningful amounts of medication to 

the bloodstream, but act locally on the painful nerves, skin, 

and muscles. Therefore, this class of drugs rarely, if ever, 

produces any systemic side effects. Currently, the only 

FDA-approved topical analgesic is the lidocaine patch 5% 

(Lidoderm ® ), which is indicated for another neuropathic 

pain condition, postherpetic neuralgia. Several publications 

have shown it to be potentially efficacious in other painful 

nerve conditions, including CRPS and diabetic neuropathy, 

as well as inflammatory conditions, such as osteoarthritis 

(9). A case series has shown a compounded form of the 

NDMA-antagonist, ketamine, to be of potential effectiveness 

(10), although caution should always be used when 

using non-FDA formulations. 

[2] ANTICONVULSANT SEIZURE MEDICATIONS are now first-line 

therapies to treat a variety of neuropathic pain conditions. 

Although many of these agents tend to have intolerable side 

effects, gabapentin (Neurontin ® ) and pregabalin (Lyrica ® ) 

are among those that may be better tolerated. 

[3] OPIOID THERAPY has also become a mainstay in the treatment 

of a variety of chronic pain conditions, including neuropathic 

pain states. Drugs in this class include oxycodone 

ER, oxymorphone ER, morphine ER, and the transdermal 

fentanyl patch. Although addiction is believed to be rare in 

properly treated chronic pain patients, practitioners should 

be aware of the behaviors that may reflect misuse and the 

tools that may assist in such evaluation (11). 

Drugs in Development 

ALTHOUGH DEFINITIVE DATA have not been published, several 

possible exciting new therapies may be available over the next 

few years. Thalidomide is currently being studied, based on the 

positive experience of some patients (12). Also, recent reports 

have shown promise for controlled intravenous infusions of 

ketamine (13). 

Conclusion 

RESEARCH PERFORMED OVER THE PAST DECADE has brought 

much enlightenment to our understanding of CRPS and has 

helped to dispel many myths that had resulted in further pain 

and suffering among CRPS patients. As such, the next decade 

promises more progress, thanks to the many dedicated 

researchers and clinicians worldwide. A new, revised CRPS Treatment 

Guidelines is currently being written by CRPS experts, led 

by Dr. Norman Harden, and should be read by all pain practitioners 

when published. In addition, the pharmaceutical industry 

is very much involved in searching for new therapies to treat 

CRPS and other chronic neuropathic pain conditions. 

REFERENCES 

1. Galer BS, Schwartz L, Allen RJ. Complex regional pain syndromes type I: 

reflex sympathetic dystrophy, and type II causalgia. In: Loeser JD, Butler 

SH, Chapman CR, Turk CDC, eds. Bonica’s Management of Pain. 3rd ed. 

Lippincott Williams & Wilkins; Philadelphia, Penn;2000. 

2. Stanton-Hicks M, Baron R, Boas R, et al. Complex regional pain syndromes: 

guidelines for therapy. Clin J Pain. 1998;14:155-166. 

3. Bruehl S, Harden RN, Galer BS, Saltz S, Backonja M, Stanton-Hicks M. 

Complex regional pain syndrome: are these distinct subtypes and sequential 

stages of the syndrome? Pain. 2002;95:119-124. 

4. Bruehl S, Husfeldt B, Lubenow TR, Nath H, Ivankovich AD. Psychological 

differences between reflex sympathetic dystrophy and non-RSD chronic 

pain patients. Pain. 1996 Sep;67:107-14. 

5. Pleger B, Tegenthoff M, Ragert P, Förster AF, Dinse HR, Schwenkreis P, 

Nicolas V, Maier C. Sensorimotor retuning in complex regional pain syndrome 

parallels pain reduction. Ann Neurol. 2005;57:425-9. 

6. Geertzen JH, de Bruijn-Kofman AT, de Bruijn HP, van de Wiel HB, Dijkstra 

PU. Stressful life events and psychological dysfunction in Complex 

Regional Pain Syndrome type I. Clin J Pain. 1998;14:143-7. 

7. Harden RN. A clinical approach to complex regional pain syndrome. Clin 

J Pain. 2000;16(2 Suppl):S26-32. 

8. Dworkin RH, Backonja M, Rowbotham MC, Allen RR, Argoff CR, Bennett 

GJ, Bushnell MC, Farrar JT, Galer BS, Haythornthwaite JA, Hewitt DJ, 

Loeser JD, Max MB, Saltarelli M, Schmader KE, Stein C, Thompson D, Turk 

DC, Wallace MS, Watkins LR, Weinstein SM. Advances in neuropathic 

pain: diagnosis, mechanisms, and treatment recommendations. Arch Neurol. 

2003;60:1524-34. 

9. Argoff C. Topical treatments for pain. Curr Pain Headache Rep. 

2004;8(4):261-7. 

TABLE 3 | Medications (1, 2, 7, 8) 

DRUG CLASS 

EXAMPLES 

Topical Drugs Lidocaine patch 5% 

(Targeted peripheral analgesics) (Lidoderm®) 

Anticonvulsants 

Opioids 

Gabapentin (Neurontin®) 

Pregabalin (Lyrica®) 

Morphine ER 

Oxycodone ER 

Oxymorphone ER 

Transdermal fentanyl patch 



10. Gammaitoni A, Gallagher RM, Welz-Bosna M. Topical ketamine gel: possible 

role in treating neuropathic pain. Pain Med. 2000;1(1):97-100. 

11. Butler SF, Budman SH, Fernandez K, Jamison RN. Validation of a screener 

and opioid assessment measure for patients with chronic pain. Pain. 

2004;112:65-75. 

12. Rajkumar SV; Rafael Fonseca R; Thomas E. Witzig TE. Complete Resolution 

of Reflex Sympathetic Dystrophy With Thalidomide Treatment. Arch 

Intern Med. 2001;161:2502-2503. 

13. Correll GE, Maleki J, Gracely EJ, Muir JJ, Harbut RE. Subanesthetic ketamine 

infusion therapy: a retrospective analysis of a novel therapeutic 

approach to complex regional pain syndrome. Pain Med. 2004;5:263-75. 

Outcomes 

Measurement 

The Pain Outcomes Profile 

BRADLEY S. GALER, MD, 

is CEO and President of 

Topiceutical, Inc., a 

company that develops 

topical treatments for 

pain and headache. 

Are you Credentialed in Pain Management? 

The Academy offers 3 levels of interdiscliplinary 

pain management credentialing: 

• Diplomate 

• Fellow 

• Clinical Associate 

To receive a copy of the Credentialing Booklet, call the Academy at 

209-533-9744, or download it from the website at www.aapainmanage.org 

E X A M S I T E S 

2006 

Exam date 

Saturday 

June 3, 2006 

Saturday 

June 3, 2006 

Sunday 

Sept. 10, 2006 

Saturday 

Dec 2, 2006 

Saturday 

Dec 2, 2006 

Exam Location 

Los Angeles, CA 

Chicago, IL 

Orlando, FL 

(Annual Conference) 

San Diego, CA 

Orlando, FL 

Application 

Deadline 

April 19, 2006 

April 19, 2006 

August 16, 2006 

October 18, 2006 

October 18, 2006 

A useful measurement tool 

that tracks patients' progress 

throughout treatment for: 

-Pain Intensity- 

-Mobility- 

-Activities of Daily Living- 

-Vitality- 

-Negative Affect- 

-Fear- 

Order forms for the POP Starter Kit 

can be downloaded from the Academy's website at 

www.aapainmanage.org. 

If you are interested in participating in research 

regarding the the Pain Outcomes Profile, 

call Alexandra Campbell, PhD, 

at 209-533-9744, or 

send an email to her at 

alex@aapainmanage.org. 

American Academy of Pain Management • 13947 Mono Way #A • Sonora, CA 95370 

Phone: 209-533-9744• Fax: 209-533-9750 • www.aapainmanage.org 


Concerned About Passing the 

Credentialing Exam? 

Then Take the Pre-exam Track at the 

17th Annual Clinical Meeting 

Who and What: For the first time, the American Academy of Pain Management is offering a 

full-day pre-exam track designed to help members prepare for the Credentialing test. The track 

will be staffed by many of the exam item writers and experts from various disciplines. Participants 

will have an opportunity to listen, ask questions, and understand many of the tenets, 

philosophies, and treatment approaches covered on the Credentialing test. 

When: Pre-exam Track: Thursday, September 7, from 7:30 am to 4:30 pm 

Exam: Sunday, September 10 

Where: Walt Disneyworld Swan and Dolphin, Orlando, Florida 

Cost and Registration: $185 for members and $225 for non-members (includes lunch). 

Registration may be completed in advance through the website or in person the day of 

the pre-conference activity. 

Recommended Reading: Weiner’s Pain Management: A Practical Guide for Clinicians, Seventh Edition 

Take the track, take the test, and become 

a credentialed (Diplomate, Fellow, or 

Clinical Associate) member of the 

American Academy of Pain Management!

INTERVIEW | COVINGTON 

LIFEBOAT mixed media on canvas 36x40 



EXPLORING 

PSYCHOSOCIAL 

ISSUES IN CRPS 

An Interview with Edward C. Covington, MD, Director of the 

Chronic Pain Rehabilitation Program at the Cleveland Clinic Foundation 

Q. What is the current thinking about the relationship 

between the psyche and the soma in CRPS? 

DR. COVINGTON A recent search for articles on CRPS, which 

are being published at the rate of about 100 per year, showed 

that there is still tremendous controversy about the nature 

of this disease, and whether it is a psychiatric rather than a 

medical condition. 

Authors have proposed several theories about how the 

psyche might be related to the soma in this syndrome, and 

each has varying support. Some believe that CRPS is a psychiatric 

illness—a conversion disorder—that there is something 

‘in the head’ that makes it come about. Others see CRPS as a 

result of a psychiatric illness or personality disorder that makes 

some more likely to get it than others. Some contend that CRPS 

causes psychological symptoms or psychiatric illness, while others 

think that psychological factors modify the course of CRPS— 

making it better or worse. Others think that adjustment and 

function in CRPS are determined by psychological factors. 

CRPS AND PERSONALITY 

Q. Are people with particular personalities 

prone to certain diseases? 

DR. COVINGTON There was a very old theory that held that different 

personality types were vulnerable to different illnesses. 

For example, that particular personality types had Crohn’s disease, 

others had migraine headaches, and that other types had 

CRPS. These ideas were widely taught, but never substantiated, 

and had been essentially discredited by the time I was in training 

25 years ago. Few people now believe this theory, although 

occasionally you’ll hear someone refer, for example, to 

migraineurs as compulsive, but this is essentially just folklore. 

Q. What about the relationship between personality 

and CRPS? 

DR. COVINGTON People often mistakenly equate correlation 

with causation. Personalities change when people are miserable 

and unable to function. So CRPS patients may be irritable, 

complaining, or demanding, leading others to conclude that 

these traits led to the disease. Another reason people have 

thought that personality disorders predisposed to CRPS is 

because there are often extreme behavioral changes following a 

trivial injury. Thus the inclination is to think, ‘Oh, c’mon, that 

couldn’t hurt that bad.’ Psychogenic theories also flourished 

because, despite the last twenty years of research, the condition 

remains ill-defined. Its pathophysiology is obscure. We don’t 

have a good understanding of exactly what CRPS is and why 

some people get it and others don’t. 

It is common to assume that when no explanation for a 

condition can be found, then it must be psychogenic. If doctors 

can’t figure it out, perhaps ‘it’s all in the head.’ People with 

fibromyalgia and irritable bowel syndrome have been subjected 

to the same sort of ideas, and I’m convinced that both are 

absolutely organic diseases, as is CRPS. 



Q. Have any studies demonstrated the relationship 

between CRPS and personality abnormalities? 

DR. COVINGTON Cross-sectional, correlational studies demonstrate 

that there is an association between personality abnormalities 

and chronic pain. If you go to any chronic pain unit, you 

will see considerable evidence of personality disorder. By the 

same token, an association can also be shown between obesity 

and diet cola. That does not mean that diet cola causes obesity. 

A common error in medical discussions is to assume that when 

two things are associated, one must cause the other. Obviously, 

this is not the case. 

In a 1993 study of tertiary pain patients, researchers compared 

CRPS patients with patients who had back pain or neuropathic 

pain (1). Findings showed that the CRPS patients were 

just like the neuropathy patients, which is not surprising, since 

CRPS is a neuropathic pain syndrome. Their similarities 

included their symptom reporting, illness behavior, and psychological 

distress. The incidence of disability was a little higher in 

CRPS. When CRPS patients were compared to back pain 

patients, actually the back pain patients tended to have more 

diffuse, ill-explained complaining, and more non-specific symptoms 

than the CRPS patients. Sexual abuse, physical abuse, 

emotional abuse—traumas that we think contribute to the formation 

of physical symptoms in the absence of physical disease, 

were no more prevalent in people with CRPS than in those 

with back ache or neuropathic pain. This is pretty strong evidence 

that old ideas about special sorts of psychiatric profiles of 

CRPS patients were specious. 

Q. How does personality affect the way an individual 

copes with CRPS, or any other disease? 

DR. COVINGTON There’s an old story about a little boy who was 

whistling when he had to shovel manure on Christmas morning. 

When his companion asked how he could be so happy, the 

boy replied, ‘With all this manure, I figure there has to be a 

pony someplace.’ So with all the manure that people have written 

about CRPS, we must wonder, ‘Is there a pony someplace?’ 

That is, is there a kernel of truth here? I think the truth lies in 

the fact that the mind plays a role in all suffering and in all 

function. It’s the mind that copes or fails to do so, whether the 

stress is a stock market crash, the death of a spouse, or a painful 

disease. Among intractable cases, failures of coping and adaptation 

will be disproportionately represented. There are people 

with CRPS who have managed to transcend it and have a life. 

For others, it’s less the case that they have CRPS than that 

‘CRPS has them.’ CRPS has taken over their lives. People who 

have problems with coping and those who have personality 

disorders are the ones most likely to have difficulty dealing 

with a disaster or catastrophe of any kind, including CRPS. 

The problem, of course, is to know whether the person failed 

to cope because of poor coping skills, or whether it was 

because of an unusually severe case of CRPS. 

If we define personality as a bias towards certain ways of 

thinking, behaving, and feeling, then it would stand to reason 

that personality has to affect coping strategies, stress tolerance, 

and even what sorts of things a person finds stressful. Perso - 

nality affects autonomic responses, which contribute to 

sympathetically-maintained pain, and influences a person’s 

needs to escape demands, stress, and responsibility. It determines 

whether a person has healthier ways of dealing with 

stress as well as perseverance in recovery efforts. Thus, 

personality will affect how a person deals with disease, 

and perhaps, his motivation for wellness. 

Q. Does CRPS cause emotional problems? 

DR. COVINGTON There are studies of CRPS in which most 

CRPS patients were contemplating suicide and there are 

contrasting studies in which researchers were surprised to find 

that most CRPS patients were indifferent and happy. Such 

extreme differences in reports are hard to interpret. We do 

know that some people with CRPS are depressed, irritable, 

tense, and anxious, some will abuse substances, some will get in 

trouble with analgesics, some will feel suicidal, some will 

become withdrawn—and some won’t. 

Q. Is there an association between CRPS and 

depression? 

DR. COVINGTON Yes. In a 1988 study, Rudy, Kerns, and Turk 

confirmed that chronic pain is associated with depression (2). It 

was also associated with interference with life; i.e., many people 

with chronic pain had ceased such activities as socializing, going 

to films, having sex, playing with their kids—the things in life 

that gave them joy. These losses were associated with depression. 

Also it was common for people with chronic pain to come 

to see themselves as helpless and trapped and to feel unable to 

do anything about their lives. Those feelings are all associated 

(Continued on page 47) 

We do know that some people with CRPS are depressed, 

irritable, tense, and anxious, some will abuse substances, 

some will get in trouble with analgesics, some will feel 

suicidal, some will become withdrawn—and some won’t. 


CENTER SPREAD

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Who we are 

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serves a broad range of clinicians who treat people with pain. Founded in 1988, 

the Academy has approximately 6,000 members and is the largest interdisciplinary 

pain organization in the United States. 

Why should you join? 

As a member you will be entitled to a host of excellent resources and 

educational benefits: 

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with depression. However, they found that when they controlled 

for interference and ‘self-control,’ pain was no longer 

associated with depression. 

This was an epiphany for me because in years of working in 

a chronic pain rehabilitation program, I had often been surprised 

that some of the most grateful patients were ones who 

had little or no pain relief. When I’d seek an explanation for 

why they were satisfied with a treatment that seemed to have 

failed, they’d reply with such statements as, ‘Yes, but now I have 

my life back!’ 

What this tell us is that if we can help people with pain to 

regain the things in life that bring them joy, and can help them 

regain a sense of empowerment and control over their lives, 

then it may be possible for them to have a good quality of 

life—a life with pleasure and freedom from depression, despite 

persistent pain. This is an especially critical issue because of the 

fact that chronic pain, while often helped, is rarely cured. 

Q. If a person with CRPS is extremely upset, can that 

affect the disease? 

DR. COVINGTON It is clear that psychic factors can modulate 

the disease. There are several studies that show that people had 

marked stress at the time they developed CRPS. And we know 

that autonomic arousal stimulates catecholamine release, so if a 

person with CRPS becomes frightened, angry, has an orgasm— 

anything that causes emotional arousal—it can cause a pain 

discharge at the same time. 

Q. What is the relationship between pain and activity 

in people with CRPS? 

DR. COVINGTON In a 1969 study, a researcher found that many 

of the trophic sequelae (i.e., claw hand, ridge fingers, and skin 

changes) were due to prolonged disuse occasioned by pain. 

He claimed that these changes developed in people who were 

poorly motivated to get well—who were unwilling to overcome 

the stiffness that follows immobilization after trauma. So basically, 

he said that people get CRPS because they’re not exercising 

enough—that getting the disease was their own fault. 

While I dispute the idea that getting the disease was their 

fault, we do know that responses to pain range from normal 

function to invalidism. And we do know from a number of 

studies that simple disuse, overprotection, and immobilization 

will create many characteristics that resemble CRPS (including 

bony demineralization, vasomotor changes, and swelling). A 

very old study of 142 patients found that exercise alone caused 

reversal of edema, trophic changes, and vasomotor signs (3). 

This was a study of young people, and young people do get 

well much more often than adults do. 

So the fact that disuse and immobilization produce signs 

similar to CRPS, together with the fact that use and exercise 

can eliminate some of the signs of CRPS, suggests that behaviors 

are likely to play a major role in the extent to which this 

We don’t have a good 

understanding of exactly 

what CRPS is and why 

some people get it 

and others don’t. 

disease progresses or improves. I doubt that it’s the only factor, 

but it strongly suggests that what patients do in response to the 

disease may strongly impact outcome. 

COGNITION 

Q. Wh at affect does cognition (what a person thinks) 

have on the disease? 

DR. COVINGTON What patients think can disable them. Misunderstandings 

and misinformation can lead to inactivity. A person 

may fear spinal range of motion because the associated pain 

could presage paraplegia or incontinence. The cognition thus 

leads to inactivity which leads to deconditioning. A cycle of 

escalating pain and disability ensues. Fitness and education can 

be curative. And with CRPS, you often see people who seem to 

be more disabled than they ought to be. This disability may 

appear psychiatric when actually it’s a lack of information or 

misinformation—a knowledge deficit. When people are 

informed about what they can do safely, they will sometimes 

get well, at times with no help from health care providers. 

Q. What are some beliefs that can make a person sick? 

DR. COVINGTON Several studies have shown that a belief that 

pain is mysterious and unexplained, or that it connotes body 

damage will increase suffering and dysfunction, even when the 

beliefs are false. If a person sees himself as helpless and fragile, of 

if he sees the world as indifferent, hostile, and without opportunity—such 

beliefs can increase the person’s level of disability. 

The concept of ‘locus of control’ is an important focus of 

work with people in pain. An internal locus of control is characteristic 

of those who see themselves as ‘the captains of their 

ships.’ They tend to be ‘take charge’ or executive types. A 

patient with this attitude is much more likely to do well than 

one who attributes events to fate or to powerful other people. 

Those with an external locus of control are likely to take a 

passive (and therefore ineffective) approach to dealing with 

pain, since they think their efforts are futile. In our rehabilitation 

program we even go to the point of encouraging certain 

patients to wear sweatshirts that say ‘CEO’ to remind them that 

they are the CEOs of their lives as they learn to manage pain. 



The sine qua non of good 

pain treatment is reconditioning. 

I can’t say enough 

good things about helping 

people to get fit. 

The concept of learned helplessness builds on the same 

theme. Those taught by bitter experience that they are powerless 

to change their plight are likely to give up and risk becoming 

depressed, resigned, and passive. The bottom line is that 

those who see themselves as capable are likely to do a lot to try 

to cope with pain. 

Q. In terms of getting better, how do people with an 

external locus of control fare compared to those with 

an internal locus of control? 

DR. COVINGTON ‘Fault and blame’ are potentially very toxic to 

patients in pain. Doug DeGood reported a nice study of this 

subject (4). Patients were asked to respond to a number of questions 

about their pain, several of which dealt with the issue of 

who was to blame for the pain. It was found that patients who 

blamed their pain on others were more likely to be depressed, 

more behaviorally aberrant, more likely to have failed treatment, 

and more pessimistic about the benefit of future treatment. 

Those who did not blame others, who said ‘things happen,’ 

seemed to do better. 

This concept suggests a slogan from Alcoholics Anonymous: 

‘Holding onto resentments is like drinking poison and 

waiting for your enemy to get sick.’ Clinically, we see people 

who are absolutely stuck and destroyed by the grudges they’re 

holding. Although doing so is a challenge, at some point, they 

must relinquish the focus on the person who ‘did them dirty,’ 

and start focusing on the question, ‘How can I have a good life?’ 

OPERANT CONDITIONING 

Q. What role does operant conditioning play in people 

with CRPS? 

DR. COVINGTON All animals tend to repeat behaviors that are 

rewarded, and to reduce behaviors that are not. Imagine a world 

in which that was not true. Animals would fail to return to the 

place where they found water and food, and would fail to avoid 

the place where they’d been attacked. Survival is contingent on 

being programmed to repeat behaviors that are rewarded. 

Unfortunately, behavior is often influenced more powerfully 

by what is immediate than by what is important. Thus, we 

are all at risk of behaving self-destructively in response to 

reinforcers. This is why ‘buy now, pay later’ is so seductive. 

Many behaviors that would promote recovery are unpleasant at 

first. Conversely, many things that are very pleasant at first can 

make you sick. For example, almost every back patient would 

feel better if he simply went to bed. But after a few weeks of 

this, some ‘strenuous’ activity such as tying shoelaces will cause 

pain and send the person back to bed. Thus the rest, which 

causes initial relief, leads ultimately to more pain and less function. 

Therefore it is essential for people in chronic pain to 

consider the long term effects of their choices, as opposed to 

focusing only on what helps immediately. 

Q. For people with CRPS and other chronic diseases 

there are sometimes secondary gains. Would you talk 

about these? 

DR. COVINGTON ‘Secondary gains’ are the good things that 

happen when one is sick—security, increased attention, nurture, 

medications that relieve pain. But there are tremendous 

‘secondary losses’ associated with chronic pain as well. You can 

lose the pride of being the bread winner, the camaraderie of 

co-workers, and a sense of identity. Financial compensation is 

often thought of when the term secondary gain is used, and in 

fact, many chronic pain patients do receive money as a result of 

becoming disabled; however, most remain poor. They have a 

steady but meager source of income, and little hope of more in 

the future, because there won’t be any raises. Nevertheless, the 

‘gains’ of illness can certainly reduce patients’ efforts to recover, 

especially if there are few gains to be had for being well. 

PSYCHOLOGICAL TREATMENTS 

Q. What are some proven psychological treatments 

for CRPS? 

DR. COVINGTON There are several. Probably the most important 

“psychological treatment” is physical therapy. I list it as a 

“psychological” treatment because it not only helps patients 

become strong enough to resume activities that used to give 

them pleasure, it also changes the way they see themselves. It 

helps them feel powerful and less fragile, and it reduces depression 

and anxiety. The sine qua non of good pain treatment is 

reconditioning. I can’t say enough good things about helping 

people to get fit. 

Cognitive therapies, helping people reinterpret their situations 

and their pain in ways that facilitate coping, have been 

shown to improve pain and function in a number of painful 

conditions. 

Another treatment is psychophysiologic training. Often 

this involves biofeedback equipment, which measures muscle 

tension, hand temperature, palmar sweating, and so on. It 

teaches people to relax muscles and reduce sympathetic arousal. 

It helps people feel they have some power over their bodies, 

instead of their bodies having power over them, and it helps 

them understand the effects of emotions on pain. 


It is common for patients in pain initially to reject psychological 

therapies with a retort such as, ‘What does my boss have 

to do with my back ache?’ I may not have an answer to that; 

however, when we hook a patient up in the biofeedback lab, 

and he talks about his boss, and the equipment shows various 

indicators of autonomic arousal and muscle tension, he very 

quickly understands that stress is affecting his body functions. 

This often ‘snares’ a person into the work of examining the role 

of life stresses in their pain, emotional distress, and function. It 

also helps patients learn to calm themselves without a pill. 

Hypnosis is another useful treatment. It helps people learn 

to control body functions they normally can’t control. In 

CRPS, hypnosis changes pain and circulation. It reduces autonomic 

arousal, which reduces sympathetically maintained pain. 

Patients must learn—and practice—self hypnosis for continued 

benefit. Functional brain imaging has demonstrated that hypnosis 

can reduce both physical and emotional pain responses in 

the brain cortex, so that the effects of this psychological treatment 

are clearly physical. 

Psychotherapy is indicated when people are psychologically 

troubled, when it is needed to facilitate behavioral changes, 

and to help ‘jump start’ people when there is a psychogenic 

component to their disability. The most common type with 

pain patients is cognitive behavioral therapy—a cognitive 

restructuring. 

In other instances, support groups can be helpful. Pain 

patients can be remarkably helpful to each other, and often help 

each other find ways out of dilemmas that seemed insoluble. 

People can help each other if there is a caring, trusting environment 

established, and sometimes this can happen without a lot 

of professional input. 

At our clinic we insist on family education and therapy. In 

part this is because an entire family can be adversely affected by 

an illness, and in part it is to teach the family how to maintain an 

environment that promotes wellness rather than regression. This 

often means teaching them when not to provide care and sympathy. 

Families often have pent-up anger because of the effects of 

another’s chronic pain on their lives, and this can poison the 

Many behaviors that 

would promote recovery 

are unpleasant at first. 

Conversely, many things 

that are very pleasant at 

first can make you sick. 

relationship and the patient’s attempt at recovery. It is important 

to address this in order for everyone in the family to feel better. 

Behavior Modification (contingency management) improves 

function, helps people be distracted from pain, normalizes 

mood, and improves quality of life. It is important to consistently 

reinforce well behaviors and not illness behaviors. People 

often mistakenly think that behavior modification means ignoring 

a person with pain, which is clearly counterproductive. You 

don’t ignore the person, you ignore the maladaptive behavior. 

You spend more time and pay more attention, but you try to be 

a friend, a companion, a playmate, or a lover—not a nurse. 

Q. You run a multidisciplinary pain management clinic. 

What is the value of a multidisciplinary approach? 

DR. COVINGTON This is a mystery in some ways. Programs of 

this sort typically treat patients who have failed to receive lasting 

benefit from medications, physical therapy, psychological 

therapies, and a plethora of other interventions. Yet, when they 

are treated in a holistic manner that combines behavioral, medical, 

and rehabilitation approaches, they may ‘blossom’ and feel 

that they have truly recovered their lost selves. They begin to 

play, to laugh, to function sexually, and often to earn an 

income. I suspect that it is the simultaneous use of these disciplines 

in an appropriate environment that helps get patients 

started on a path to recovery that was not achieved with many 

of these techniques in isolation. 

REFERENCES 

1. Ciccone DS, et al. Psychological dysfunction in patients with reflex 

sympathetic dystrophy. Pain. 1997 Jul;71(3):33-33. 

2. Rudy TE, Kerns RD, Turk DC. Chronic pain and depression: toward a 

cognitive-behavioral mediation model. Pain. 1988 Nov;35(2):129-40. 

3. Shumacker HB, Abramson DI, Posttraumatic vasomotor disorders, Surg 

Gynecol Obstet 88 (1949):417-434. 

4. DeGood DE, Kiernan B: Perception of fault in patients with chronic pain. 

Pain. 1996;64(1):153-9. 

EDWARD COVINGTON, MD 

is Director of the Chronic Pain 

Rehabilitation Program at the 

Cleveland Clinic Foundation 


FEATURE | SHERRY 

WHENCHILDREN 

HURTTOOMUCH 

Diagnosis and Treatment of Amplified Musculoskeletal Pain 

BY DAVID D. SHERRY, MD 


There are multiple forms of amplified musculoskeletal 

pain (chronic musculoskeletal pain out of proportion 

to the known stimulus) in children, ranging from 

Complex Regional Pain Syndrome (CRPS) in one limb 

to total body pain. The cause is unknown but may be 

related to trauma, illness, or psychological stress, and 

the incidence seems to be increasing. 

THERE IS A TYPICAL PRESENTATION, mostly among adolescent 

girls with allodynia, marked pain and dysfunction 

disproportionate to the known stimulus, and an 

incongruent affect. Conversion symptoms are not 

uncommon. The treatment is intense exercise therapy 

focused on function, desensitization, and attention to 

concurrent conditions (psychological, mechanical, 

inflammatory). The outcomes are very good, with virtually 

all patients regaining full function and between 80 - 90% 

resolving all pain. These conditions present some of the greatest 

challenges in pediatrics but are also the most rewarding to treat 

because the child goes from being highly disabled to normal. 

Case Presentation 

BETTY WAS AN ATTRACTIVE, bright, athletic 14-year-old girl 

who stepped on a rock at the bottom of a swimming pool and 

hurt her right foot. The skin was not broken, but over the next 

two days her foot became progressively more painful, swollen, 

blue, and cool to the touch. In the emergency department a 

radiograph was normal and a splint was applied. Betty required 

crutches and developed marked tenderness to touch. She was 

put in a cast, but the cast caused so much pain that it had to be 

removed the next day. The pain spread to include her entire 

right leg and also the left foot (although she could bear weight 

on that side), and to both hands (presumably from using 

crutches). She was unable to move her right foot, or her toes, 

which occasionally went numb (although they still hurt). Today, 

she hurts too much to wash or shave her right leg. She cannot 

attend school, because she is fearful that the leg might get 

bumped, and she is unable to concentrate because of the intensity 

of her pain. She cannot sleep well and when she does sleep, 

she wakes frequently with pain. The pain in her right foot is 

greater than 10 out of 10, and her hands and left foot hurt 10 

out of 10. The pain has taken over her life and the life of her 

family. She has seen multiple healthcare practitioners, has had 

numerous tests (all of which are normal), and has either failed 

to respond or has developed unacceptable side effects from a 

host of medications, treatments, and blocks. 

Betty’s symptoms are not unusual for a child with amplified 

musculoskeletal pain. There are multiple forms, usually defined 



TABLE 1 | The Yunus & Masi Criteria 

for Fibromyalgia in Children (4) 

Major: 

___________________________________ 

❥ Generalized musculoskeletal 

aching at 3 or more sites 

for 3 or more months 

❥ Absence of underlying 

condition or cause 

❥ Normal laboratory tests 

❥ Five or more typical 

tender points 

Minor: 

____________________________________________________________________ 

❥ Chronic anxiety 

❥ Numbness 

or tension 

❥ Fatigue 

❥ Poor sleep 

❥ Chronic headaches 

❥ Irritable bowel syndrome 

❥ Subjective soft tissue 

swelling 

Fibromyalgia defined as present if the subject has: 

_______________________________________________________________________________________________________________ 

❥ All 4 major criteria and 3 minor criteria OR 

❥ First 3 major criteria, 4 tender points, and 5 minor criteria. 

by the location or presence of autonomic dysfunction. Children 

with amplified musculoskeletal pain fall into two broad categories: 

those with localized pain and those with diffuse pain (1). 

The most easily recognized type of localized pain is CRPS. 

Children with CRPS have overt autonomic dysfunction that is 

manifested by coolness or cyanosis of the limb and, occasionally, 

increased perspiration or edema. Additionally, many, if not 

most, of these children have localized pain amplification without 

autonomic signs (e.g., cold, blue). In studies of children 

with diffuse pain, fibromyalgia receives the most attention 

(although this term is not often used in conjunction with children 

since it may differ from adult fibromyalgia). Two sets of 

criteria for childhood fibromyalgia have been established. The 

American College of Rheumatology criteria require 11 of 18 

trigger points on the body to be painful along with three 

months of widespread pain (3). The criteria of Yunus and Masi 

require either four or five painful trigger points and multiple 

related symptoms (see Table 1) (4). Determining whether trigger 

points are painful or not is highly subjective. Most children 

will identify these points as tender or sore, and not painful as 

required by the definition. Not all children with diffuse pain 

have painful trigger points, so some do not satisfy the criteria 

for fibromyalgia. Additionally, there are children with intermittent 

localized or diffuse pains, or overlapping features of the 

above, e.g., a cool, blue foot and total body pain. 

Children with amplified musculoskeletal pain are more disabled 

than those with arthritis or with mechanical joint problems, 

and they and their families suffer intensely. In addition to 

their pain, these children often experience isolation from peers 

and are commonly told by medical professionals that they are 

“faking it” or that “it shouldn’t hurt all that much.” This does 

a great disservice to these children and their families. 

Epidemiology 

THERE ARE NO SPECIFIC STUDIES of the 

incidence of childhood amplified musculoskeletal 

pain. Studies of normal schoolchildren 

have found that 1.2% to 6% 

fulfill criteria for fibromyalgia and up to 

7.5% report widespread musculoskeletal 

pain. Children with amplified musculoskeletal 

pain comprise approximately 

10% of children in pediatric rheumatic 

disease clinics, and it is the impression of 

many clinicians that the incidence is 

increasing (5 - 7). 

The average age of onset of amplified 

musculoskeletal pain is preteen to early 

teen. Amplified musculoskeletal pain is 

rare below the age of six years, so diagnosing 

it in young children needs to be done 

with much circumspection; however, children 

as young as two years old have developed it. The majority 

of these children are female (80% in most series), perhaps 

because females have lower pain thresholds and report pain 

more frequently than males. 

Most children with amplified musculo skeletal pain are 

Caucasian. There is a suspicion that the majority are from 

upper socioeconomic levels; however, no race or economic 

level is spared. 

❥ Pain modulation by 

physical activities 

❥ Pain modulation 

by weather factors 

❥ Pain modulation 

by anxiety/stress 

Etiology 

THE ETIOLOGY OF AMPLIFIED MUSCULOSKELETAL PAIN is 

unknown, but it usually can be related to trauma, illness, or 

psychological distress. Most pediatric rheumatologists think the 

latter plays a significant role in most, but not all, children. 

Whether cause or effect, the pain and dysfunction experienced 

by most of these children is such that it inflicts psychological 

havoc on both child and family. Genetic factors have been 

implicated in fibromyalgia and CRPS, and a very weak association 

has been made between fibromyalgia and increased flexibility. 

It is likely that there is a combination of both intrinsic 

factors (such as individual pain threshold, gender, and coping 

strategies) and extrinsic factors (such as previous pain experiences, 

social stresses, modeling of chronic pain behaviors, and 

central and peripheral pain mechanisms) that work together to 

give rise to amplified musculoskeletal pain (8). 

Clinical Manifestations and Diagnosis 

ALTHOUGH EACH CHILD IS UNIQUE, there are enough significant 

similarities in the history and physical examination to 

establish the pattern for most. The typical patient is a mature 

and accomplished adolescent girl who suffers a minor injury or 

illness and then has increasing pain and dysfunction over several 

days to months. The pain may be localized, with or without 

signs of autonomic dysfunction, or it may be diffuse. 


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Not uncommonly it begins as a localized pain and spreads. 

Allodynia (tenderness to a normally nonpainful stimulus) is 

common. Clothing, bumps while riding in the car, and even 

the wind against bare skin will cause pain. Some children, usually 

those with diffuse pain, will have multiple bodily complaints, 

which help define fibromyalgia by the Yunus and Masi 

criteria (see Table 1). These children typically report very high 

levels of pain (10 out of 10) with an incongruently cheerful 

affect, and severe dysfunction. They present themselves as 

mature and accomplished teens who are perfectionistic, and 

who meet the emotional needs of their peers and others rather 

than their own. They are severely incapacitated, much more 

than children with arthritis or mechanical limb pain, and multiple 

physician visits and therapeutic failures are common. 

Autonomic signs seen in CRPS usually consist of coolness 

and cyanosis. These signs may not be apparent at rest but may 

develop after exercising the limb. Occasionally there is increased 

perspiration or dystrophic skin. 

Allodynia is tested by either light touch or gentle pinching 

of a fold of skin. The area of allodynia may vary in location on 

repeated testing. 

Painful trigger points can be found in those with fibromyalgia. 

These points are reported as painful, not tender or sore, 

with 3-4 kilograms of digital pressure. These points are: base of 

occiput, lateral transverse process of C6, mid superior border of 

the trapezius muscle, medial border of the scapula, just superior 

to the spine of the scapula, superior anterior border of the 

medial 2nd rib, 1 cm distal to the lateral epicondyle, mid gluteal 

fold, 1 cm posterior to the greater trochanter, and 1 cm proximal 

to the medical knee mortise (3). Control points should also 

be tested, such as the forehead, thumbnail, shaft of the tibia, and 

outer third of the clavicle (9). Those with painful control points 

are, perhaps, better described as having total body pain. 

Conversion symptoms are fairly common and include 

numbness, bizarre gait, paralysis, or abnormal shaking or 

tremors. Dizziness is a common complaint, but vestibular function 

tests are normal (10). 

Laboratory Tests 

ALL LABORATORY BLOOD AND URINE TESTS ARE NORMAL. 

Radiographs may show osteoporosis, and a bone scan is usually 

normal although it can show decreased uptake, especially in 

CRPS (or spotty increased uptake characteristic of adult CRPS) 

(11). Magnetic resonance images can show edema, but the 

anatomy is otherwise normal. 

Diagnostic Pitfalls 

CHILDREN THOUGHT TO HAVE AMPLIFIED MUSCULOSKELETAL 

PAIN should have a careful evaluation for other causes. The 

most common diagnosis I make in these children is spondyloarthropathy, 

since enthesitis (inflammation at the insertion 

of tendon and ligament into bone) is not a feature most 

These conditions present 

some of the greatest 

challenges in pediatrics 

but are also the most 

rewarding to treat 

because the child goes 

from being highly 

disabled to normal. 

practitioners check for. Malignancies, usually spinal cord 

tumors, are the most serious condition one can miss, so a 

detailed neurological examination is mandatory. Arthritis has 

been mistaken rarely for amplified musculoskeletal pain, but 

it is usually obvious on examination. Rarely will undetected 

thyroid disease in children be manifest as diffuse pain. 

Disease Activity 

INITIALLY AND DURING FOLLOW-UP there needs to be ongoing 

assessment of pain and dysfunction. Self-report, such as a mark 

on a visual analog scale or a rating of 0 - 10 on a verbal scale, is 

adequate to measure pain. Functional measures can be elaborate 

(such as standardized age-appropriate questionnaires) but, in 

practice, asking about school attendance, walking endurance, 

chores, and participation in recreational activities is sufficient. 

Treatment 

INITIALLY, IT IS PARAMOUNT to establish a trusting relationship 

with the child and family. You have to believe that the child is 

in pain since that child has been given both verbal and nonverbal 

messages that the pain is all in his or her head or that he or 

she is malingering. I have found it extremely useful to explain 

the pain in terms of sympathetically mediated pain amplification; 

this approach reinforces the reality of the pain, gives an 

understandable reason for the pain, and is a mechanism with 

which to introduce the treatment strategy (12). 

“Further medical investigation is unnecessary, even if the 

family is convinced that an insidious diagnosis has been overlooked 

or that a test (even if done previously and was normal) 

will establish a diagnosis. 

All medications for pain need to be discontinued. Children 

who are on medications for depression or anxiety disorders may 

need to continue their use, but those treated with antidepressants 

for pain reduction alone should stop taking the drugs. 

Several of the medications used for pain will need to be tapered, 


especially opioids. Opioids should be tapered about 10% per 

day and, depending on the dose, gabapentin should be tapered 

over two to three weeks. Tramadol binds to opioid receptors; 

therefore, those children on a high dose of this medication 

should have it tapered. 

There are no controlled studies of the vast number of treatments 

reported in the literature for the various forms of amplified 

musculoskeletal pain. Treatments are legion and include 

pain medications, antidepressants, gabapentin, transcutaneous 

nerve stimulation, nerve blocks and sympathectomy (for 

CRPS), epidural catheters for continuous drug infusion, pain 

pumps, lidocaine and opioid patches, acupuncture, massage, 

cognitive-behavior therapy, psychotherapy, and exercise therapy. 

Most authors agree that exercise therapy is helpful in 

achieving the best long-term outcomes in all forms of amplified 

musculoskeletal pain. I have found it to be the most helpful 

with the longest-lasting results (13, 14). The nature of the exercise 

therapy, however, is different from what physical and occupational 

therapists are accustomed to (15). The primary goal of 

the program we use is to restore function, so the exercise program 

is very intense and directed at doing normal and aerobic 

activities (such as jumping, climbing stairs, building walking 

speed and endurance, performing sports drills, and carrying 

loads). Pain is not directly treated and is ignored as much as 

possible during the exercise sessions. The vast majority will 

gradually resolve all pain once full function has been restored. 

Allodynia is treated by desensitization with rubbing, vibration, 

and applying textures to the skin. 

Some children can and do carry on this exercise program on 

their own at home once they realize that even though exercising 

hurts, it is not damaging and is, in fact, going to make them 

better. For most children, however, the pain is too great for 

them to exercise at home, so they need to come into the office 

to participate in our program. We give them five hours of exercise 

therapy daily for an average of three weeks. Most children 

will also have improvement in their mood, sleep, and energy 

level, and relief from other somatic complaints once they start 

this intensive exercise program. 

In addition to exercise therapy, the psychodynamics of 

the child and family should be evaluated, since most families 

and children will have significant psychological difficulties. 

These may require individual, family, or marital therapy (or a 

combination of these therapies) (16, 17). 

Good sleep hygiene is helpful and should be mentioned 

even though fixing the sleep problems does not resolve the 

somatic symptoms. Frequently children with amplified musculoskeletal 

pain have a sleep complaint (not a true sleep disorder) 

and having a good night sleep is helpful. This includes going to 

bed only when one is sleepy, not reading or watching television 

while in bed, eliminating caffeine, practicing relaxation techniques, 

eliminating napping, and having a routine for sleeping 

and waking on weekdays and weekends. 

Complementary treatments are frequently sought, but there 

are no data regarding benefit. These treatments include herbal 

therapy, massage, magnet therapy, homeopathy, reflexology, 

aromatherapy, to name a few, but only rarely is any sustained 

benefit reported. We cannot recommend any of these treatments 

and, as with allopathic medications, we discontinue 

them once the diagnosis is made. 

Outcomes 

MOST CHILDREN DO WELL with the described treatment 

approach. The outcome may vary, depending on the form of 

amplified musculoskeletal pain; however, long-term studies in 

children are rare. Most children with CRPS (92% of 103 children 

studied) who were treated with an intense exercise program 

resolved all signs and symptoms and 88% were well after 

five years (14). Less than half of 70 children with CRPS who 

were treated with drugs, blocks, and moderate exercise resolved 

all symptoms; no long-term outcomes were reported (18). 

TABLE 2 | Key Points in the Recognition 

and Treatment of Amplified 

Musculoskeletal Pain in Children 

1 

There is a high index of suspicion 

for the presence of amplified 

musculoskeletal pain in patients 

with these characteristics or 

manifestations: 

❥ Adolescent female 

❥ Mature beyond years 

❥ Accomplished 

❥ Perfectionistic 

❥ Anxious to please 

❥ Prolonged school absence due to 

pain 

❥ Marked dysfunction 

❥ Worsening of pain over time 

❥ Normal examination except pain 

❥ No enthesitis or arthritis 

❥ Normal neurological exam 

❥ Localized pain on examination 

❥ Allodynia 

❥ Autonomic signs 

❥ Incongruent affect 

❥ La belle indifference 

❥ Widespread pain on examination 

❥ Multiple painful points 

❥ Normal laboratory studies 

❥ Failure of all prior therapies 

2 

Once an amplified musculoskeletal 

pain is recognized: 

❥ Acknowledge the pain 

❥ Explain that it is amplified, 

and not indicative of 

underlying damage or disease 

❥ Stop further medical investigations 

❥ Stop medications as appropriate 

❥ Restore function 

❥ Prescribe aerobic exercise, up to 

5 hours daily of intense therapy 

focused on functional activities 

and continuing for 2-4 weeks 

❥ If allodynia is present, desensitize 

with tactile stimulation 

❥ Advise child to resume full-time 

school attendance 

❥ Advise child to resume social 

and recreational activities 

❥ Evaluate the psychological 

dynamics and treat if appropriate 

❥ Anticipate total resolution 

of symptoms 



Children with diffuse pain or fibromyalgia may have more 

long-term pain, depending on the treatment and study (17, 

19). However, 11 of 15 school children identified on screening 

to have fibromyalgia resolved their fibromyalgia after 30 

months (20). It is important to realize that these children were 

not seeking medical help when diagnosed. Cognitive-behavior 

therapy alone was employed in five girls with fibromyalgia, and 

four reported no pain 10 months later (21). 

Children with amplified musculoskeletal pain may develop 

other bodily pains such as headache and abdominal pain (8). In 

the children we have followed, unresolved psychological issues 

contributed to nonpainful poor outcomes such as conversion 

reactions, eating disorders, school avoidance, suicide attempts, 

and acting out behaviors. 

Summary 

AMPLIFIED MUSCULOSKELETAL PAIN IN CHILDREN may vary 

from localized CRPS to widespread, total body pain. Children 

with amplified musculoskeletal pain all suffer significant pain 

and disability and need compassionate care that should include 

a timely and accurate diagnosis, explanation of the possible 

causes of pain, and an effective therapeutic approach (see Table 

2). The diagnosis involves excluding conditions that can cause 

pain and by the typical pattern manifest in most with amplified 

musculoskeletal pain. The psychological aspects involved should 

be formally assessed in all children. Intense exercise therapy 

along with desensitization is the treatment of choice and of 

great benefit to most. Normal function, at a minimum, should 

be restored, and reflected in school attendance and social and 

sports activities. In those in whom the pain continues, cognitive-behavior 

therapy or more formal psychotherapy should be 

pursued. Pharmacological agents should be limited to specific 

indications, not pain. Children with amplified musculoskeletal 

pain and their families challenge one’s diagnostic and therapeutic 

skills, but the outcome is rewarding. Rarely can we so significantly 

alter the course of a condition that renders children 

completely debilitated as we can in those who suffer with 

amplified musculoskeletal pain. 

6. Malleson, P.N., M.Y. Fung, and A.M. Rosenberg, The incidence of pediatric 

rheumatic diseases: results from the Canadian Pediatric Rheumatology Association 

Disease Registry. Journal of Rheumatology, 1996. 23(11): p. 1981-7. 

7. Manners, P.J., Epidemiology of the rheumatic diseases of childhood. Current 

Rheumatology Reports, 2003. 5(6): p. 453-7. 

8. Sherry, D.D., Pain Syndromes, in Adolescent Rheumatology, D.A. Isenberg 

and J.J.I. Miller, Editors. 1998, Martin Dunitz Ltd: London. p. 197-227. 

9. Okifuji, A., et al., A standardized manual tender point survey. I. Development 

and determination of a threshold point for the identification of positive 

tender points in fibromyalgia syndrome. Journal of Rheumatology, 

1997. 24(2): p. 377-83. 

10. Rusy, L.M., S.A. Harvey, and D.J. Beste, Pediatric fibromyalgia and dizziness: 

evaluation of vestibular function. Journal of Developmental & 

Behavioral Pediatrics, 1999. 20(4): p. 211-5. 

11. Laxer, R.M., et al., Technetium 99m-methylene diphosphonate bone scans 

in children with reflex neurovascular dystrophy. Journal of Pediatrics, 

1985. 106(3): p. 437-40. 

12. Sherry, D.D., An overview of amplified musculoskeletal pain syndromes. 

Journal of Rheumatology Supplement, 2000. 58: p. 44-8. 

13. Sherry, D.D., et al., Psychosomatic musculoskeletal pain in childhood: clinical 

and psychological analyses of 100 children. Pediatrics, 1991. 88(6): 

p. 1093-9. 

14. Sherry, D.D., et al., Short- and long-term outcomes of children with complex 

regional pain syndrome type I treated with exercise therapy. Clinical 

Journal of Pain, 1999. 15(3): p. 218-23. 

15. Sherry DD, executive producer. Amplified Musculoskeletal Pain in Childhood. 

Diagnosis and Treatment. A Guide for Physical and Occupational 

Therapists. (Videotape, DVD) MMII, www.childhoodrnd.org 

16. Sherry, D.D. and R. Weisman, Psychologic aspects of childhood reflex neurovascular 

dystrophy. Pediatrics, 1988. 81(4): p. 572-8. 

17. Sherry, D.D. and P.N. Malleson, The idiopathic musculoskeletal pain syndromes 

in childhood. Rheumatic Diseases Clinics of North America, 2002. 

28(3): p. 669-85. 

18. Wilder, R.T., et al., Reflex sympathetic dystrophy in children. Clinical characteristics 

and follow-up of seventy patients. Journal of Bone & Joint Surgery 

American, 1992. 74(6): p. 910-9. 

19. Siegel, D.M., D. Janeway, and J. Baum, Fibromyalgia syndrome in children 

and adolescents: clinical features at presentation and status at follow-up. 

Pediatrics, 1998. 101(3 Pt 1): p. 377-82. 

20. Buskila, D., et al., Fibromyalgia syndrome in children—an outcome study. 

Journal of Rheumatology, 1995. 22(3): p. 525-8. 

21. Walco, G.A. and N.T. Ilowite, Cognitive-behavioral intervention for juvenile 

primary fibromyalgia syndrome. Journal of Rheumatology, 1992. 

19(10): p. 1617-9. 

REFERENCES 

1. Malleson, P.N., M. al-Matar, and R.E. Petty, Idiopathic musculoskeletal 

pain syndromes in children. Journal of Rheumatology, 1992. 19(11): p. 

1786-9. 

2. Merskey, D.M. and N. Bogduk, Classification of Chronic Pain. Descriptions 

of Chronic Pain Syndromes and Definitions of Pain Terms. 1994, Seattle: 

IASP Press. 

3. Wolfe, F., et al., The American College of Rheumatology 1990 Criteria for 

the Classification of Fibromyalgia. Report of the Multicenter Criteria 

Committee. Arthritis & Rheumatism, 1990. 33(2): p. 160-72. 

4. Yunus, M.B. and A.T. Masi, Juvenile primary fibromyalgia syndrome. A 

clinical study of thirty-three patients and matched normal controls. 

Arthritis & Rheumatism, 1985. 28(2): p. 138-45. 

5. Bowyer, S. and P. Roettcher, Pediatric rheumatology clinic populations in 

the United States: results of a 3-year survey. Pediatric Rheumatology Database 

Research Group. Journal of Rheumatology, 1996. 23(11): p. 1968-74. 

DAVID D. SHERRY, MD 

Director, Clinical Rheumatology, 

Attending, Pain Management, 

Professor of 

Pediatrics at The Children's 

Hospital of Philadelphia 

University of Pennsylvania 


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EMERGING TREATMENT AND DIAGNOSIS 

EMERGING 

TREATMENT 

AND DIAGNOSIS 


FEATURE | COMPLEX REGIONAL PAIN SYNDROME 

Neuroimmunologic Approaches to 

Emerging and Potential Therapies 

for Complex Regional Pain 

Syndrome (CRPS) 

BY DONALD C. MANNING, MD, PhD 

Despite a great deal of progress in defining 

Complex Regional Pain Syndrome (CRPS), 

there is still controversy regarding the 

mechanisms involved. 

THEORIES HAVE INCLUDED INFLAMMATION, neuropathic mechanisms, 

ischemic injury and abnormal sympathetic nervous system 

function. To date there is no approved treatment for 

CRPS, and therapies for neuropathic or inflammatory pain 

have given disappointing results, affording many patients only 

partial relief at best (1). Therefore, it is time for a reevaluation 

of CRPS mechanisms to enable new therapeutic opportunities. 

The high female predominance (75%) and the combination of 

inflammatory and neuropathic pain components could be consistent 

with an autoimmune mechanism. Targeting therapies 

toward immune activation involving cytokines, glia, or the 

infiltration of immune cells is a new approach for pain therapy, 

although it has already been employed with some success in 

oncology and rheumatology. 

Neuroimmune activation involves a bidirectional stimulation 

of neurons and immune cells in response to trauma or 

inflammation (2). Immune cells release inflammatory [e.g., 

cytokines tumor necrosis factor (TNF), interleukin (IL)-1 

and IL-6] and anti-inflammatory (e.g., cytokine IL-10) 

molecules and they, in turn, are modulated by neurotransmitters, 

especially the sympathetic nervous system transmitter norepinephrine 

(3,4). Cytokines are polypeptides that can act 

locally, within tissues, or at a distance similar to hormones. 

They regulate replication, development and activation of cells 

in the immune, nervous and hematopoetic systems. The biology 

of the cytokines is complicated in that different cells can 

produce the same cytokine that can in turn have different 

effects or different cytokines can have similar effects or antagonize 

each other depending upon the local environment. 

Cytokines as Chronic Pain Mediators 

TNF, IL-1 AND IL-6 are the cytokines with the best-documented 

pathological roles in neuropathic pain. In healthy animals, 

the administration of IL-1 or TNF alone can produce 

symptoms of neuropathic pain. Spinal neuron activation by 

these cytokines can produce long-term alterations in neuronal 

excitability. Activation of non-neuronal glial cells with extensive 

interconnections within the spinal cord could account for central 

cytokine release (5) as well as the spread of excitation 

beyond traditional neuroanatomical boundaries and reactivation 

of the pain system after new injuries (6). Infusion of IL-1 or 

TNF for adjuvant cancer chemotherapy has been associated 

with an incidence of nearly 50% of pain syndromes or complaints 

of pain and tenderness at the injection site (7-9). 

Whereas TNF and IL-1 play important roles in the 


EMERGING TREATMENT AND DIAGNOSIS | MANNING 

initiation of persistent neuropathic pain, delayed IL-6 production 

is a factor in the maintenance of such pain (10). Another 

set of cytokines such as IL-10 serves to inhibit inflammation 

and immune activation (11). Malfunction of this inflammatory/anti-inflammatory 

cytokine balance could lead to chronic 

pain and inflammatory syndromes. The widespread presence of 

receptors for the cytokines in the sensory nervous system suggests 

that these nerves serve as immunosensors (12) and form a 

link between immune activation and neurobehavioral aspects of 

chronic illness (13). Immune activation and cytokine release 

have also been associated with decreased mood (14) and inhibition 

of certain types of learning and memory (15). Evidence 

from animal studies suggests that the action of tricyclic antidepressants 

on pain and mood may derive from cytokine interactions 

in the brain (16, 17). 

Proinflammatory cytokines TNF and IL-6 are specifically 

elevated in tissue fluid in CRPS-affected regions but not in 

nonaffected regions (18). Cerebrospinal fluid levels of IL-6 and 

IL-1 are elevated in patients with CRPS but not in patients 

without pain or with chronic non-CRPS-related pain (19). 

These findings suggest a specific association between cytokines 

and CRPS. 

Immunomodulation as a Strategy for Treating CRPS 

IN IMMUNE-MEDIATED DISEASES, it is important to suppress 

the pathologic elevations of cytokines rather than completely 

blocking them. This approach, known as immunomodulation, 

serves to restore the normal balance in immune function. 

Immunosuppressive agents such as methotrexate (20) and 

leflunomide (21) attenuate tactile hypersensitivity in rodent 

radiculopathy and neuropathy models. Leflunomide is approved 

for clinical use in rheumatoid arthritis and has several antiinflammatory 

actions, including inhibition of IL-1, TNF, 

and the expression of nitric oxide and COX-2 genes. However, 

no clinical studies in chronic neuropathic pain conditions have 

been reported. Caution is advised, because general immunosuppressants 

can increase the risk and reduce the resolution of certain 

types of infection. 

A somewhat unexpected drug class for immunomodulation 

is comprised of the statins or 3-hydroxy-3-methylglutaryl coenzyme 

A (HMGCoA) reductase inhibitors. Reports that statin 

treatment could produce improvement in a model of multiple 

sclerosis (22) have sparked great interest in this class of drugs. 

(23) Treatment with atorvastatin induced the secretion of antiinflammatory 

cytokines (IL-4, IL-5, and IL-10) and inhibited 

the secretion of Th-1 pro-inflammatory cytokines (IL-2, IL-12, 

IFN, and TNF). Another statin, lovastatin, inhibited the 

expression of TNF, IL-1, and IL-6 in rat astrocytes, 

microglia, and macrophages (24). Statins decreased the expression 

of inflammatory mediators in the CNS, including TNF 

(25). The potential clinical benefit of using statins to treat neuropathic 

pain is unexplored, but these agents may be effective 

in preemptive use. How many postoperative or traumatic 

neuropathic pain states have been avoided by concomitant use 

of statins? Future studies may provide some guidance for the 

use of these agents. 

In addition, Shir et al. have reported that dietary fat can 

reduce the neuropathic pain-related behaviors resulting from 

partial sciatic nerve ligation (26). The consumption of unsaturated 

corn or soy oils suppressed tactile allodynia and heat 

hyperalgesia, an effect that was accentuated by dietary protein 

from multiple sources (26). Dietary fats can modulate both 

innate and adaptive immune responses through toll-like receptor-4 

(TLR-4) receptors. TLR-4 functions in the innate 

immune system as a pattern-recognition receptor for pathogens. 

In the rat CNS TLR-4 occurs exclusively on microglia (27). 

TLR-4 can be activated by bacterial wall molecules such as 

endotoxins or lipopolysaccharides and by endogenous ligands 

such as heat shock proteins, proteoglycans, and saturated fatty 

acids released after neural injury and degeneration (28, 29). Saturated 

fatty acids activate TLR-4, but omega-3 polyunsaturated 

fatty acids inhibit agonist-induced TLR-4 activation (30). Partial 

but significant reduction in hyperalgesia and allodynia 

behavior can be accomplished by interfering with the function 

of TLR-4 in microglia (31). This mechanism raises intriguing 

therapeutic possibilities; however, much work remains. 

Inhibitors of Cytokine Production and Function 

GLUCOCORTICOIDS HAVE BEEN USED FOR MANY YEARS 

to treat CRPS and inflammatory diseases. They can modulate 

the immune system and inhibit the production of a wide range 

of inflammatory mediators as well as stimulate the production 

of anti-inflammatory agents. Glucocorticoid utility for chronic 

diseases is severely compromised by a wide range of adverse 

effects, including diabetes, impaired wound healing, and susceptibility 

to infections, metabolic problems, and bone demineralization 

(32). The search for safer and more effective 

inhibitors of inflammatory mediators has yielded several new 

therapeutic agents. Successful use of TNF monoclonal antibodies 

(infliximab) or TNF-receptor fusion protein (etanercept) 

has changed the therapy for rheumatoid arthritis and 

several other chronic inflammatory diseases. Open-label clinical 

reports have claimed rapid resolution of acute sciatica (involving 

spinal root irritation) using TNF inhibitors infliximab 

(33) or entanercept (34). These findings, however, were not 

supported by a larger controlled study of acute radiculopathy 

pain using infliximab (35). There are no reports of these agents 

being used in trials of CRPS therapy. In one small experimental 

report, elevated interstitial cytokine levels from CRPS-affected 

regions are markedly reduced by infliximab treatment coincident 

with a reduction in clinical symptoms (36). Anakinra is a 

recombinant human IL-1-receptor antagonist approved for use 

in rheumatoid arthritis (37), but no studies have looked at its 


FEATURE | COMPLEX REGIONAL PAIN SYNDROME 

By changing our perspective and looking beyond traditional neuroanatomy 

and neurophysiology to understand the body’s response to injury, we may 

uncover new therapeutic strategies. 

ability to alter the development or maintenance of other 

chronic pain states. 

Thalidomide was developed as a sedative and antinausea 

drug, but its teratogenic effects and propensity to cause peripheral 

neuropathy with prolonged use have limited its use. It is 

orally active and functions as an immunomodulator by inhibiting 

the production of a broad range of pro-inflammatory mediators, 

including TNF, IL-1, and IL-6 and by increasing the 

level of IL-10, IL-2, and IFN. It also inhibits the production 

of TNF from human microglial cells (39). Clinically, thalidomide 

has been reported to reduce pain and hyperalgesia in 

Complex Regional Pain Syndrome (CRPS) Type I (40-43). 

Medicinal chemistry efforts have produced several 

generations of immunomodulatory agents derived from thalidomide 

that have decreased toxicity. Lenalidomide, a novel 

immunomodulatory drug with anti-inflammatory properties, 

potently inhibits the secretion of pro-inflammatory cytokines 

(e.g., TNF, IL-1 and IL-6) and stimulates the secretion of 

anti-inflammatory cytokines (e.g., Il-10). Lenalidomide is currently 

approved in the U.S. for the treatment of patients with 

transfusion-dependent anemia due to low- or intermediate-1- 

risk myelodysplastic syndromes with a deletion 5q cytogenetic 

abnormality with or without additional cytogenetic abnormalities. 

Based upon reports of symptomatic improvement of CRPS 

in response to treatment with thalidomide, as well as upon the 

pharmacological properties of lenalidomide, a pilot study was 

undertaken to assess the safety and preliminary efficacy of 

lenalidomide in subjects with unilateral CRPS Type I (44). 

Lenalidomide was used in an open-label study of 40 

patients with unilateral CRPS of at least 1-year duration, optimal 

conventional therapy, and with entry pain levels registering 

at least 4 on a 0-10 pain scale (44). The patients had high levels 

of pain, on average, at baseline (7.1 out of 10) and were taking, 

on average, more than 4 concomitant CRPS pain medications. 

Despite this high degree of prior and current treatment, over 

one third of subjects reported at least 30% improvement and 

one half reported a 20% improvement in pain levels as well as 

broad and significant reductions in CRPS symptoms and sleep 

disturbance. Of the original 40 subjects, 28 continued into an 

extension phase and 14 are still in the study, with continued 

benefit after more than 2 years on the study drug. Data from 

this study demonstrated a good overall safety profile; however, 

as the study was uncontrolled, it is difficult to interpret the precise 

relationship of adverse events to study treatment. Most 

adverse events were mild to moderate in severity and many were 

attributed to the disease rather than to a reaction to the study 

drug. Few subjects required dose reductions or discontinuation 

due to adverse events. The results of this study demonstrate a 

level of safety and efficacy justifying additional study for the 

treatment of CRPS. Controlled studies are currently underway 

in subjects with CRPS. 

Summary 

WE NEED TO FIND NEW APPROACHES to the treatment of 

chronic neuropathic pain and CRPS. By changing our perspective 

and looking beyond traditional neuroanatomy and neurophysiology 

to understand the body’s response to injury, we may 

uncover new therapeutic strategies. This short article cannot 

possibly provide adequate coverage of the extensive literature 

supporting immune- and nervous system interaction, especially 

in pain states. An appreciation of the role played by the 

immune system in injury-induced pain states, as summarized in 

this article, represents a new opportunity. Currently available 

immunomodulators and immunosuppressive agents need to be 

cautiously evaluated for their pain-modulating ability. The 

results of these initial studies will certainly foster more extensive 

therapeutic development efforts. 

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EMERGING TREATMENT AND DIAGNOSIS | MANNING 

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18. Huygen, FJ, et al. Mast cells are involved in inflammatory reactions during 

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19. Alexander, GM., et al. Changes in cerebrospinal fluid levels of pro-inflammatory 

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Abstracts: 11th World Congress on Pain. IASP Press, Seattle. 2005. 

DONALD C. MANNING, 

MD, PhD, Executive Director, 

Neurosciences Clinical 

Research and Development 

Celgene Corporation, 

Summit, New Jersey 

Clinical Associate Professor 

of Anesthesiology and Pain 

Management, University of 

Virginia, Health Sciences 

Center, Charlottesville, Virginia 


ZICONOTIDE: 

Promising New Treatment for Complex 

Regional Pain Syndrome (CRPS) 

BY LYNN R. WEBSTER, MD AND 

KERI L. FAKATA, PHARMD 

Ziconotide is a 

synthetic neuroactive peptide that 

was isolated from a neurotoxin utilized 

by the cone shell snail, Conus Magnus, 

to capture its prey. It is one of 50,000 

peptides isolated from this venom 

that has proven to safely and 

effectively treat chronic severe 

pain in refractory pain patients 

who in most cases failed 

intrathecal (IT) opioid therapy. 

THE FDA APPROVED ZICONOTIDE after a decade of research and 

clinical experience in 1,254 patients. Out of this population, 17 

were reported to have the diagnosis of CRPS. Eleven of these 

patients received ziconotide, and six patients received placebo. 

The reported efficacy for this subset of patients was a mean 

change in the Visual Analog Scale of Pain Intensity (VASPI) of 

25.2 % for patients who received ziconotide, compared to 2.8% 

for patients who received placebo (1). One published case report 

documented complete resolution of nonambulatory bilateral 

lower-extremity CRPS. The patient resumed normal gait after 7 

months of treatment and achieved complete resolution with 

ongoing of therapy (2). As more experience is gained with the 

use of ziconotide, more clinicians are sharing their positive experiences 

in treating CRPS at workshops and clinical meetings. 

Underlying Mechanisms of Pain in CRPS 

IT HAS BEEN PROPOSED that pain in CPRS is neuropathic in 

origin, resulting from both peripheral and central sensitization 

of somatosensory afferent neurons (3,4). Multiple underlying 

mechanisms are responsible for the pain associated with CRPS, 

including regional inflammatory reactions, sympathetic maintained 

pain, stimulus-independent pain, stimulus-evoked pain, 

and peripheral and central sensitization. 

Central sensitization may be the mechanism in which 

ziconotide is effective for relieving pain and symptoms associated 

with CRPS. Transmission of pain from noxious stimuli 

results when the stimulated peripheral afferent neurons that 

contain A and C fibers transmit nociceptive signals by releasing 

chemical signals such as glutamate, aspartate substance P, and 

calcitonin gene-related peptide at the spinal cord. These chemical 

signals are released at the presynaptic end of the peripheral 

neuron in response to an influx of Ca++ into the N-type voltage-sensitive 

calcium channel (N-VSCC). These neurotransmitters 

activate the dorsal horn neurons in lamina II of the spinal 

cord to continue ascending transmission of pain (3,4). 

In central sensitization the peripheral afferents spontaneously 

fire, resulting in the increased sensitivity of the dorsal 

root neuron to input of all forms. In response to inflammation, 


EMERGING TREATMENT AND DIAGNOSIS | WEBSTER & FAKATA 

reorganization of peripheral afferent neurons may occur. Fibers 

that do not normally transmit pain start expressing the pain 

transmitters, so that nonnoxious stimuli that normally activate 

these fibers would transit pain. 

Ziconotide represents a new class of potent analgesics called 

neuronal calcium channel blockers (NCCBs). Its exact mechanism 

of action has not been established in humans; however, 

animal studies confirm its specificity for N-VSCCs found 

throughout the nervous system and concentrated in the spine 

on the presynaptic terminals of peripheral nociceptors. 

Ziconotide blocks the N-VSCC and prevents release of excitatory 

amino acids from the presynaptic terminal, thereby reducing 

the amount of stimulation at the dorsal horn neurons. It is 

proposed that ziconotide may unwind central sensitization over 

time through this mechanism (5). 

Clinical Use of Ziconotide 

ZICONOTIDE IS CURRENTLY FDA-APPROVED for monotherapy in 

patients with chronic severe pain where IT therapy is warranted. 

Currently there are no published clinical data on the 

efficacy of ziconotide in combination with other IT medications. 

The Polyanalgesic Consensus Committee has not made 

any formal recommendations regarding the use of ziconotide as 

monotherapy or in combination with IT therapies at this time 

(6). There is little information on other IT medications in combination, 

yet combination IT therapy has been an accepted 

standard of practice. The rationale for ziconotide in combination 

with other common IT medications is combining different 

mechanisms of action for possible additive or synergistic analgesia. 

Preclinical studies in animals demonstrated additive or synergistic 

effects with opioids, clonidine, and bupivacaine when 

utilized in combination with ziconotide (5). Clinicians who 

wish to use ziconotide in combination with other IT medications 

should first obtain consent. 

Some stability data have been published regarding 

ziconotide in combination with other common IT medications. 

It is important to note that the data represented stability 

with 25 mcg/ml formulation of ziconotide with fixed concentrations 

of other IT meds. Ziconotide was found to have 

relatively good stability with hydromorphone, bupivacaine, 

and baclofen. It was completely stable with clonidine (7-10). 

Formulated IT products such as Infumorph ® (IT morphine) 

and Sublimaze ® (fentanyl) should be avoided because of low 

stability. Ziconotide stability is pH dependent and is most 

stable at pH of 4.5. 

In choosing to use ziconotide in combination with other IT 

meds, a clinician should be aware of some inherent stability 

considerations because ziconotide is a peptide. On the initial 

fill, ziconotide adheres to the titanium in the pump. The initial 

concentration may also be altered by the residual volume in the 

pump. Ziconotide degrades due to exposure to high temperature 

(body temperature), and it is susceptible to oxidation. 

Ziconotide may be most effective 

in reducing pain and preventing 

central sensitization by its 

mechanism of action. 

The authors of this article recommend keeping ziconotide 

at or above a working concentration of 10mcg/ml. This also 

allows for the convenience and practicality of utilizing the100 

mcg/ml (1ml) vial formulation, taking cost of medication into 

consideration. The rinses in the prescribing information can be 

conducted through the following steps: 

[1] dilute 0.5 ml of the 100 mcg/ml formulation to 6 ml (8.33 

mcg/ml); 

[2] rinse the pump three times utilizing 2 ml aliquots of step 1 

above; and, 

[3] utilize the remaining 0.5 ml to dilute to a working concentration 

of 10 mcg/ml in 5 ml, or 5 mcg/ml in 10 ml if 

lower concentration is necessary for first pump fill with 

ziconotide. 

Subsequent refills should occur monthly due to stability 

concerns; however, further rinses are not required. The entire 

vial of 100 mcg/ml 1 ml vial can be used for the refill. The 

same concepts are utilized for monotherapy or compounding 

ziconotide with other IT medications (11). 

Ziconotide is associated with adverse events such as nausea/vomiting, 

dizziness, abnormal gait, abnormal vision, and 

confusion. These adverse events may present themselves within 

the first few days of therapy if treatment is initiated with too 

high of a dose. Experienced clinical investigators realize that 

ziconotide should be started at 1 mcg/day and titrated by 0.5 

mcg/day no more than once a week. This dose is significantly 

lower than the maximum recommended starting dose in the 

prescribing information. Cognitive effects such as memory loss, 

confusion, and psychosis tend to have a later onset of approximately 

three weeks. Therefore, to be safe and to not overshoot 

the therapeutic window, it is advisable to titrate no more often 

than weekly—once a month may be preferable. If adverse 

events do occur, they usually resolve after a dose reduction. 

Early onset adverse events usually resolve in a few days, whereas 

it may take up to three additional weeks to resolve late onset 

adverse events. If patients cannot tolerate adverse events, 

ziconotide may be abruptly removed from the pump without 

any withdrawal sequelae. 

Monitoring Considerations 

PATIENTS SHOULD BE CONTINUALLY ASSESSED for adverse 

events related to ziconotide. They should be instructed to 

immediately notify clinic personnel or to seek emergency 

medical attention if any serious adverse events should occur. 

In clinical studies with ziconotide, a significantly elevated 

serum, Creatinine Kinase isoenzyme MM (CK-MM) found in 

(Continued on page 66) 


UNRIVALED INDEPENDENCE 

COMING SOON… 

©Medtronic, Inc., 2006. All Rights Reserved. Printed in USA.

EMERGING TREATMENT AND DIAGNOSIS | WEBSTER & FAKATA 

skeletal muscle, was common in 40% of patients participating 

mostly in open-label studies. Elevated CK-MM usually 

occurred within the first 2 months of therapy. Other isoenzymes 

were rarely affected. Of all patients studied in clinical 

trials, there was one case of symptomatic myopathy and two 

acute renal failures associated with rhabdomyolysis and 

extreme CK elevation (17, 000-27,000 IU/L) (12). 

A baseline CK should be obtained with another CK at 

2 months, and every 6 months thereafter. CKs should be 

obtained if the patient is exhibiting any new neuromuscular 

symptoms. 

Conclusion 

ZICONOTIDE MAY BE MOST EFFECTIVE in reducing pain and 

preventing central sensitization by its mechanism of action. 

As a result, it may be useful in many patients with CRPS. 

Ziconotide will likely not be first-line therapy for CRPS 

but will have a role when less invasive therapies have been 

exhausted and the pain becomes chronic and severe enough to 

warrant an IT pump. Some clinicians are discussing their success 

treating CRPS through an earlier utilization of ziconotide 

by external catheter. However, prolonged use of external 

catheters increases the risk of meningitis. Immediate pain relief 

should not be expected with the recommended slow titration. 

Treatment with ziconotide will need to be based on the 

individual’s response. Ziconotide has the potential of becoming 

an important analgesic in our armamentarium to treat CRPS. 

REFERENCES 

1. Ziconotide: Use in Reflex Sympathetic Dystrophy, PRI031_ 

Use_in_Reflex_Sympathetic Dystrophy 03 Ref Number:1-6462160, Elan 

Pharmaceutical Inc. 

2. Miljanich GP. Ziconotide: Neuronal Calcium Channel Blocker for Treating 

Severe Chronic Pain. Current Medicinal Chemistry, 2004. 11: 3029-3040. 

3. Ribbers, GM, Geurts AC, Stam HJ, Mulder T. Pharmacologic Treatment of 

Complex Regional Pain Syndrome I: A Conceptual Framework. Archives of 

Physical Medicine and Rehabilitation 2003; 84: 141-146. 

4. Harden RN. Chronic Neuropathic Pain. The Neurologist 2005 11(2): 111- 

122. 

5. Miljanich GP. Ziconotide: Neuronal Calcium Channel Blocker for Treating 

Severe Chronic Pain. Current Medicinal Chemistry, 2004. 11: 3029-3040. 

6. Hassenbusch SJ , Portenoy RK, Cousins M et al. Polyanalgesic Consensus 

Conference 2003: An Update on the Management of Pain by Intraspinal 

Drug Delivery-Report of an Expert Panel. Journal of Pain and Symptom 

Management. 2004, 27(6):540-563. 

7. Shields D, Montenegro R . The Chemical Stability of Admixtures Combining 

Ziconotide and Hydromorphone during Simulated Intrathecal Administration. 

(Abstract) Neuromodulation 2005 Vol 8(in press). 

8. Shields D, Montenegro R, Ragusa M. The Chemical Stability of Admixtures 

Combining Ziconotide and Morphine Sulfate during Simulated 

Intrathecal Administration. (Abstract) Neuromodulation 2005. Vol 8(in 

press). 

9. Shields D, Montenegro R, The Chemical Stability of Admixtures Combining 

Ziconotide and Clonidine during Simulated Intrathecal Administration. 

(Abstract) Neuromodulation 2005. Vol 8(in press). 

10. Shields D, Montenegro R, Ragusa M . The Chemical Stability of Admixtures 

Combining Ziconotide and Bupivacaine during Simulated Intrathecal 

Administration. (Abstract). Neuromodulation 2005 Vol 8(in press). 

11. Webster LR, Fakata KL, Ziconotide for Severe Chronic Pain. Practical Pain 

Management May 2005. 

12. Prialt (ziconotide intrathecal infusion) prescribing information. Elan 

Pharmceutical Inc. 2/2005. 

LYNN R. WEBSTER, MD, 

is Medical Director, CEO, 

Lifetree Pain Clinic, 

Salt Lake City, Utah 

KERI L. FAKATA, PHARMD, 

Lifetree Research and Pain 

Clinic, Clinical/Research 

Pain Management Pharmacist, 

Salt Lake City, UT 


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EMERGING TREATMENT AND DIAGNOSIS | PRAGER 

NEW RECHARGEABLE SPINAL CORD 

STIMULATOR SYSTEMS OFFER 

ADVANTAGES IN CRPS TREATMENT 

BY JOSHUA P. PRAGER, MD, MS 

n April, 2004, the Food and Drug Administration 

(FDA) approved the first rechargeable spinal cord 

stimulator (SCS) system. This system, called Precision, 

TM produced by Advanced Bionics, is the first 

in a new generation of SCS systems that offers a 

significant improvement in stimulation to people 

with CRPS. In early 2005, Advanced Neuromodulation 

Systems received approval for its rechargeable 

system, the Eon Ț M and shortly thereafter Medtronic, 

the largest producer of neurostimulator systems, 

received FDA approval for its Restore TM System. 

This article will briefly review the use of SCS for 

treatment of CRPS and then describe the potential 

of the new systems in improving care and outcomes. 

Reprinted from The RSDSA Review, Fall 2005 


SCS as Part of the CRPS Treatment Algorithm 

IN 1995, the International Association for the Study of Pain 

(IASP) brought together a group of international experts to 

address treatment of CRPS. This was one of four meetings the 

IASP has held in the last two decades regarding various aspects 

of CRPS. Stanton-Hicks published results of the 1995 meeting 

as a treatment algorithm, which indicates that the mainstay of 

CRPS/RSD treatment is physical therapy, and that nerve blocks 

or SCS as adjuvant treatment are important for patients who 

are not adequately progressing with physical therapy alone (1). 

The important point of this article is that SCS can significantly 

enhance CRPS treatment by facilitating physical therapy as part 

of the entire rehabilitation process. 

Stanton-Hicks suggested that the beneficial effect of SCS 

relates not only to pain relief, but it also inhibits or modulates 

the sympathetic outflow to the region where the tingling produced 

by the stimulation is experienced (2). 

SCS and CRPS 

THERE HAVE BEEN NUMEROUS STUDIES of SCS for the treatment 

of CRPS. These studies have been both retrospective and 

prospective randomized. In 1982, Broseta reported the use of 

SCS for CRPS-2 patients with 72 percent having experienced 

excellent results (3). Barolat (4) reported a 73 percent success 

rate of pain in 18 patients with CRPS-1. Kumar (5) discussed 

12 patients treated with SCS for CRPS. Robaina (6) compared 

SCS with TENS in 35 patients with late-stage CRPS-1; 66 percent 

of patients reported good results with SCS, experiencing 

rapid relief of pain and reduction in swelling. Bennett (7) 

examined not only the effect of SCS on CRPS, but also looked 

at the effect of different lead arrays. He found that patient satisfaction 

was markedly improved with dual octapolar leads as 

opposed to traditional quadripolar leads. 

There have been four prospective studies published of 

spinal cord stimulation in CRPS. The first, Calvillo (8) in 

1998, examined 31 patients with CRPS affecting the upper 

extremity with a significant reduction in pain scores compared 

to baseline. Oakley and Weiner (9) observed statistically significant 

reduction in pain and an 80 percent success rate with SCS 

for CRPS. The largest prospective study in CRPS was that of 

Kemler (10), in the New England Journal of Medicine in 2000; 

54 patients with CRPS-1 of one extremity were randomized to 

SCS plus physical therapy or physical therapy alone. A significantly 

greater number of patients with SCS plus physical therapy 

had a much improved global perceived effect than the 

physical therapy group alone. Most recently, Kemler (11) published 

a two-year follow up of the randomized trial. The mean 

pain score in the 24 implanted SCS patients was significantly 

reduced compared to those receiving physical therapy alone; 

63 of the SCS patients reported improvement in their global 

perceived effect. 

Thus, there is significant literature demonstrating the 

success with SCS in treating CRPS. This brief discussion 

above was not meant to thoroughly review or evaluate this 

literature, but merely to call attention to its presence and 

provide a reference list where one can review this information 

in greater detail. 

Rechargeability and its Implication Toward the 

Treatment of CRPS with SCS 

THE ADVENT OF RECHARGEABILITY, being able to recharge the 

SCS battery, creates new opportunities. Previously, when a 

battery failed, the entire pulse generator needed to be replaced, 

which required expensive surgery and was uncomfortable for 

the patient. Rechargeability may significantly reduce the need 

to replace internal pulse generators. 

Many CRPS patients with SCS systems have needed to 

use a lot of power to achieve the pain relief necessary to 

function. In order to reduce the need to replace the internal 

pulse generator, patients have often rationed the amount of 

stimulation by either reducing the power or turning the unit 

off some of the time. Thus, both patient and physician have 

attempted to manage the battery while compromising treatment. 

Rechargeability offers the opportunity to manage the 

patient instead of managing the battery. 

Bennett (12) notes that large arrays produce greater satisfaction 

than traditional quadripolar leads. Rechargeability offers 

the opportunity to use many contacts simultaneously, which 

uses a significantly greater amount of energy. Previously, this 

increased power consumption would have been prohibitive 

in some patients. Rechargeability allows the use of a greater 

number of electrodes at a given time to provide better coverage 

with stimulation. 

There are some reports that increased frequency improves 

stimulation in patients with CRPS. Although this not been well 

documented, it is important to note that higher frequency produces 

higher energy consumption. Higher frequency potentially 

compromises battery life. Thus, rechargeability provides an 

opportunity to fully utilize the potential of any system without 

needing to worry about battery failure. 

Conventional SCS four- and eight-contact leads were 

placed relatively far apart. Oakley and Prager (13) in their 

discussion of SCS, indicate that when SCS leads are placed 

closer together the result is deeper penetration of the spinal 

Rechargeability offers the opportunity to manage the 

patient instead of managing the battery. 


EMERGING TREATMENTS | PRAGER 

cord, which provides a stronger effect. New lead configurations 

have been and will be designed specifically for rechargeable 

systems because the more-effective configurations will use more 

energy. Thus, once again, rechargeability provides a platform to 

allow for a more effective form of stimulation that conventional 

primary cell internal pulse generator source would not support. 

Cost-Effectiveness of SCS 

TAYLOR ET AL (14) recently reviewed the cost effectiveness of 

SCS for treating chronic pain. They conclude that in the 

medium to long term, SCS is economically favorable compared 

to other therapies for people with CRPS. Taylor indicates that 

pay back ranged from 15 months to five years after the SCS 

was implanted. The pay back period was sensitive to the efficiency 

level of the battery/electrode life and the amount of 

patient usage. However, this review was performed before 

rechargeable batteries. Considering the advantages of rechargeability, 

it is possible that pay back will be shortened and that 

the costs of SCS plus physical therapy will be lower than the 

cost of physical therapy alone. SCS initial costs are offset by a 

reduction in healthcare expenditures after the implant. 

The Future with Rechargeability 

THE RELEASE OF RECHARGEABLE SYSTEMS has prompted the 

development of many new lead configurations that will 

enhance the effectiveness of SCS for the CRPS patient. New 

leads and extensions are currently in development. In particular, 

one product that will be available in the near future will allow 

four limbs to be treated simultaneously from a single-pulse generator. 

For patients with advanced four-limb CRPS, this eliminates 

the need for multiple systems; four limbs can be treated 

with a rechargeable single-pulse generator that, despite high 

energy consumption, will not require frequent replacement. 

Summary 

SPINAL CORD STIMULATION has a demonstrated efficacy in 

treating patients with CRPS when it is used in conjunction 

with a comprehensive rehabilitation program. Rechargeability 

enhances the ability to perform stimulation without requiring 

as frequent internal pulse generator battery replacements. 

SCS is cost effective in CRPS and future developments will 

enhance its effectiveness. 

REFERENCES 

1. Stanton Hicks, M. et.al. An updated interdisciplinary clinical pathway for 

CRPS: Report of an expert panel. Pain Practice 2002; 2(1):1-16. 

2. Stanton-Hicks M., Spinal cord stimulation for the management of complex 

regional pain syndromes. Neuromodulation 1999; 2(3):193-201. 

3. Broseta J, et.al. Chronic epidural dorsal column stimulation in the treatment 

of causalgia pain. Appl Neurophys 1982;45: 190-194. 

4. Barolat G. Schwartzman R., et.al., Epidural spinal cord stimulation management 

of reflex sympathetic dystrophy. Stereotact Funct Neurosurg 

1999; 53:29-39. 

5. Kumar K., et.al., Spinal cord stimulation is effective in the management 

of reflex sympathetic dystrophy. Neurosurgery 1997; 40:503-508. 

6. Robaina F. J., et.al., Transcutaneous electrical nerve stimulation and 

spinal cord stimulation for pain relief in reflex sympathetic dystrophy. 

Stereotact Funct Neurosurg 1989; 52(1): 53-62. 

7. Bennett D. S., et.al., Spinal cord stimulation for complex regional pain 

syndrome (RSD): A retrospective multicenter experience from 1995-1998 

of 100 patients. Neuromodulation 1999;2:202-210. 

8. Calvillo O, et.al., Neuroaugmentation in treatment of complex regional 

pain syndrome of the upper extremity. Acta Orthop Belg 1998; 64: 57- 

62. 

9. Oakley, J. and Weiner, R. L., Spinal cord stimulation for complex regional 

pain syndrome: A prospective study of 19 patients at two centers. Neuromodulation 

1999; 2:47-50. 

10. Kemler, M.A., et.al., Spinal cord stimulation in patients with chronic reflex 

dystrophy. N Engl J Med 2000; 43:618-24. 

11. Kemler, M.A., The effect of spinal cord stimulation in patients with 

chronic reflex sympathetic dystrophy: Two years followup of the randomized 

control trial. Ann Neurol 2004; 55:13-18. 

12. Bennett, D.S., ibid. 

13. Oakley, J., Prager, J., Mechanism of spinal cord stimulation. Spine. 27 

(22):2574-2583. 

14. Taylor, R. S., The cost effectiveness of spinal cord stimulation: 

A systematic review of the literature. J Pain Symptom Manage 2004; 

27 (4): 370-8. 

JOSHUA P. PRAGER, MD, 

MS, is Director, Center for 

the Rehabilitation of Pain 

Syndromes (CRPS), Departments 

of Internal Medicine 

and Anesthesiology, David 

Geffen School of Medicine 

at UCLA, Los Angeles, 

California. 


OPINION | GETSON 

The Use of Thermography in the 

Diagnosis of CRPS: A Physician’s Opinion 

BY PHILIP GETSON, DO 

EXPERTS WHO EVALUATE PATIENTS WITH CRPS make the diagnosis 

based upon history and physical examination. However, 

because of the wide variation in symptom complexes, not every 

individual presents with the “classic” symptoms that are frequently 

associated with CRPS (e.g., temperature change, color 

change, and hair growth change). 

In the past, attempts have been made to diagnosis CRPS 

with triple phase bone scans. Some literature suggests that these 

are about 40% accurate, but I believe that in reality the number 

is closer to 15%. This test is frequently non-specific in its representation, 

and rarely do radiologists offer a diagnosis of CRPS 

when they have not been provided with that historical information. 

Electrodiagnostic testing (EMGs), CAT Scans, MRIs, etc., 

have no appreciable value in assisting in the diagnosis of CRPS. 

Thermography has been utilized in medical application 

since the 1950s. Prior to that it had, and still does have, industrial 

applications. The use of infrared imaging for neuromuscular 

purposes dates back to the 1960’s and has continued despite 

lack of widespread acceptance. Numerous articles have been 

written regarding the value of thermography in the diagnosis 

of sympathetically mediated pain syndromes and work in this 

area continues. The July 2002 United States Department of 

Health and Human Services document on reflex sympathetic 

dystrophy, suggests thermography as the diagnostic tool for the 

evaluation of CRPS. 

In the 24 years since I began using neuromuscular thermography 

in my practice, we have examined thousands of patients 

with neuromuscular disorders. Using electronic thermographic 

apparatus, the cameras (which were initially driven by liquid 

nitrogen) are now hi-tech computer-generated images that 

allow us to view the nervous system by measuring changes in 

skin temperature. These changes are controlled by the sympathetic 

nervous system and alterations in the sympathetics cause 

alterations in thermal (infrared) imaging which do not conform 

to dermatomal patterns. 

While electrodiagnostic testing may show a radiculopathic 

pattern, such testing often errs because EMGs measure motor 

function as opposed to sensory function, which is the fundamental 

basis for CRPS. The mechanism of thermal imaging 

allows for perception of altered skin temperature to one-tenth 

of one degree centigrade. The lack of symmetry which is out of 

conformation to dermatomal distribution patterns goes a long 

way to confirming the clinical diagnosis of CRPS. 

Measurements taken on an individual within approximately 

the first six months of the onset of the pathology will show the 

affected side to be warmer than the contra lateral side by temperature 

gradient in excess of 0.9 degrees centigrade (considered 

by this observer to be the standard for sympathetically mediated 

thermal asymmetry). Frequently this asymmetry exceeds 1.5 or 

2 degrees and is clearly not the result of vascular pathology per 

se. After approximately six months the pattern changes with the 

affected side being the “cold side.” It is therefore imperative 

that a history of the traumatic event which precipitated CRPS 

be afforded the thermographic expert. 

As can be seen from the images (included with this article), 

the temperature differential is often dramatic. While the human 

hand is capable of perceiving significant temperature differential 

between two sides, the thermal imaging camera is hundreds of 

times more sensitive and the temperature scale (unlike the 

human hand) and can be adjusted to incorporate variations 

in room and human body temperature, which varies from 

individual to individual. Additionally, this author is currently 


collecting data that clearly indicates that the migratory pattern 

of CRPS can be documented as much as six to nine months 

prior to the occurrence of symptomatology in a limb that has 

been affected with sympathetically-mediated dysfunction, but 

has not yet become symptomatic at the time the images were 

performed. It is fascinating to see patients who offer verbal 

complaints (in completed schematic diagram) about one limb, 

yet manifest thermal abnormalities in an entirely separate area. 

(See attached images). 

In addition to the benefits in diagnosing sympathetically 

mediated pain syndromes, new thermographic cameras have the 

potential to offer real-time imaging capabilities that could allow 

monitoring of an affected limb during the surgical implantation 

of a spinal cord stimulator. By stimulating the affected nerve 

(thereby causing a “warming” of the damaged limb), the surgeon 

could place the leads accurately and “know” they were in 

the exact place to afford the individual the maximum benefit 

to be derived from such implantation. This would reduce the 

randomization factor currently in place by allowing for an 

electronic “road map” which otherwise does not exist. Similar 

use of thermal imaging for surgical or chemical ablations of 

sympathetic nerve dysfunction is possible. 

In conclusion, thermographic (infrared) imaging appears to 

be the best, if not only diagnostic tool, that should be utilized 

by the clinician for objectification of a 

clinical diagnosis of sympathetically 

mediated pain syndromes. The overused 

adage, “A picture is worth 1000 

words” is particularly applicable here, 

not only to assist the clinician in making 

the diagnosis, but to add verification 

to the patients’ symptoms, 

particularly in instances where they have 

been led to believe they are “crazy” 

because conventional diagnostic testing 

does not offer objective evidence of 

their symptom complex. 

Research on thermographic imaging 

is on-going, but as a diagnostic tool, 

much of its potential remains untapped. 

The number of people who have benefited 

from the conclusive diagnosis of 

CRPS by thermographic means continues 

to grow, thereby allowing clinicians 

an opportunity for earlier intervention 

of treatment to an affected body part. 

PHILIP GETSON, DO, has 

been certified by the American 

Academy of Thermology, 

the American Herschel 

Society, the Academy of 

Neuromuscular Thermology 

and is a Diplomate of the 

American Medical Infrared 

Association. He has lectured 

extensively in the field of 

Thermography especially as 

to its usage in the diagnosis 

of R.S.D. He is currently 

working on three separate 

papers on the subject. 

Available for Purchase 

Thriving Pain Clinic 

Convenient Downtown Chicago Location 

Adjacent to Northwestern Hospital 

State-of-the-art surgical facility, 

best equipment 

Bilingual staff, expert training 

Extensive patient list 

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fax to 773-348-0076 for more information. 


IN CONCLUSION | MOSKOVITZ 

A Theory of 

Suffering 

BY PETER A. MOSKOVITZ, MD 

I present here a personal theory of suffering. It differs from previous efforts to 

understand suffering by proposing that the nature of suffering is evolutionary 

and neurobiological, rather than metaphysical, phenomenological, or linguistic. 

In this theory I argue six interrelated premises: 

1. Persistent grief or fear evokes distinct bodily disturbances (somatic markers) that are experienced as suffering; 

2. When pain evokes fear and grief, it has the same effect on the maps in the brain’s body-sensing regions as do fear and grief alone; 

3. Suffering is not an emotion, but it is an “emotionally competent stimulus,” capable of evoking emotions; 

4. The neural substrate for the experience of suffering requires, in part, the anterior cingulate cortex; 

5. The evolution of suffering is essential to the com munication of emotion and to mammalian nurturing; and 

6. The capacity for suffering is the experiential precursor of empathy and altruism, which are the components of natural morality. 

CRPS as the Quintessential Maldynic Pain Disorder 

James Giordano used the term maldynia to address and describe the trajectory of chronic pain and stated that maldynia “… evokes 

considerable suffering, but the (direct) cause of this is pain qua [as] illness (1).” “Pain” and “suffering” are distinct experiences; suffering 

has causes other than pain. The suffering of grief, for example, is often severe and some 

At Right 30”x40” oil on board. 

Matt Sesow is an independent 

American artist residing in 

Washington, DC. Visit his 

website at www.sesow.com 

74 | T H E PA I N P R A C T I T I O N E R | S P R I N G 2 0 0 6 




even think it can be mortal. Fear, particularly in association 

with an event or object that is only vaguely in awareness (as 

with anxiety), causes terrible suffering. Who has not used the 

expression “I was frightened to death”? Our attitudes toward 

suffering, and therefore toward pain, come, in part, from the 

observation that pain is often associated with grief and fear, 

which are not “objective” physical impairments. 

Complex Regional Pain Syndrome (CRPS) is characterized 

by pain that is out of proportion to the inciting injury or tissue 

damage and thus represents the quintessential maldynic (1, 2) 

pain disorder. CRPS commonly begins with a physical impairment, 

and although the injury sometimes appears to be trivial, 

the subsequent pain and disability of CRPS are severe. 

Although often confused, “disability” and “physical impairment” 

are independent, and this confusion has harmful effects. 

For example, both doctor and patient may wrongly assume that 

when the physical impairment (disease) is treated, the disability 

(illness) will cease. Furthermore, many physicians harbor a 

judgmental disdain (only thinly veiled) for “non-organic” pain 

and illness behavior, and nowhere is this failing more evident 

than in the care of patients with CRPS. In addition, and in 

spite of advancing science, a segment of the medical profession 

still thinks that CRPS does not exist at all, that there is a “dystrophic 

personality,” or that patients with CRPS are emotionally 

disturbed or malingering. The suffering of people with 

CRPS is further compounded when the legal system, compensation 

agencies, and the medical profession treat the experience 

of suffering itself with both passive and active disregard. 

There Is No Suffering Without Fear or Grief 

Our understanding of suffering has traditionally been more 

metaphysical than neurobiological. Eric Cassell described in 

detail how pain and disease threaten the integrity of the “facets 

of personhood,” a composite of qualities that Antonio Damasio 

referred to as “the autobiographical self” (3, 4). In my own 

practice, I have seen patients who descend relentlessly from an 

acute lumbar injury into chronic pain and disability under such 

a threat. The most memorable have been laborers whose identity 

as strong providers for their families, in part a culturally 

defined role, was threatened by physical impairment. “Independent” 

evaluators saw the increased disability as a vaguely inauthentic 

secondary gain. The disc impairment was authentic; 

however, the pain was suspect because the suffering that 

increased the perception of pain—the loss of self-regard and 

self-respect, loss of income, loss of customary role behavior, loss 

of sexual capacity and identity, the stress of the medico-legal 

conflict—was not “legitimate.” 

Cassell defined and illustrated over a dozen “existential 

domains of the person,” as reframed within a phenomenological 

context by Giordano (1). For each of the facets of personhood, 

as discussed by Cassell, the threat to the integrity of the individual 

resulted in fear, loss, and the fear of loss of any of the 

“facets of personhood.” When lost, these facets—cultural background, 

habitual and accustomed behaviors, life experiences, 

expectations, attachments to family and friends, secret relationships, 

thoughts, aspirations, and bodily function—become 

objects of grief. The fear of losing them is painful. Such is the 

suffering of chronic pain and illness (5). Suffering increases the 

noxious perception of disease and recalls associations between 

suffering and diverse antecedents and causes of injury, disease, 

and suffering long past. Suffering is not simply the affective 

experience of pain, for suffering does not exist without the 

emotions of fear and grief. 

PREMISE 1 

Fear and grief evoke bodily disturbances, 

the experience of which is suffering. 

I PROPOSE THAT PERSISTENT GRIEF AND FEAR evoke distinct 

bodily disturbances that are experienced as suffering. The 

somatic and visceral effects of grief and fear on the body proper 

produce a characteristic perception of the maps in the brain’s 

body-sensing regions. I propose that the feelings of fear and 

grief are experienced as suffering. A definition of suffering, like 

this one, that invokes the “somatic marker” hypothesis of neurologist 

and humanist Antonio Damasio, implies a neural substrate 

for the experience of suffering (4, 6, 7). And that is what 

I intend to propose. Damasio’s language and theories of consciousness 

inform much of my thinking. 

A Classification of Emotions 

SUFFERING IS NOT AN EMOTION; it is the awareness or feeling 

of the bodily effects of the emotions of fear and grief. Fear and 

grief are two of the six primary emotions, which also include, 

according to Paul Ekman’s classification, joy, surprise, disgust, 

and anger (8). The fact that Damasio, in his recent work, 

accepts this classification gives it greater cogency (9). Each of 

the primary emotions has unique facial expressions and, to a 

lesser degree, vocal tone and body posture or movement. The 

facial expressions of primary emotions are recognizable across 

cultural boundaries (where display rules differ) (10), and are, to 

some extent, recognizable across species. 1 

I am persuaded to think, with arguable economy, that social 

and other secondary emotions are combinations of primary 

emotions that are superimposed on appetites or drive states, 2 

1 Primatologists and dog lovers need no convincing from me. 

2 I am not aware of a comprehensive, biologically based classification of 

appetites and drives. For the sake of argument, here are ten: thirst, hunger, 

oxygenation, elimination, thermal regulation, rest, lust, curiosity, 

mastery/dominance, and attachment. 


and experienced in three time frames (past, present, and future). 3 

Consider some examples: guilt and shame are varieties of disgust 

in differing social contexts. When disgust is directed outward, it 

may take the form of disdain; when combined with anger, it 

may turn to recrimination and vengeance. The experience of primary 

emotions is modified by the virtually infinite variety of 

states of mind, particularly considering that the associations of 

long-term memory are unique representations of objects and 

events. One potential criticism of this taxonomy is that it is 

reductive or deterministic. I refute such criticism by calculating 4 

the unlimited variety of the precursors of suffering, values, and 

behavior. The present discussion is about suffering; but I cannot 

ignore the fact that creativity cannot be predicted by a reduction 

to finite elements. Our appetites for curiosity and mastery will 

sometimes motivate us to think and do outrageous and wonderful 

things. When considering the variety of experiences that 

result in suffering, most observers recall the opening of Tolstoy’s 

Anna Karenina: “All happy families resemble one another; every 

unhappy family is unhappy in its own fashion.” 

PREMISE 2 

When pain evokes fear and grief, the effect on the 

maps in the brain’s body-sensing regions is the 

same as for fear and grief alone. 

I PROPOSE THAT CHRONIC PAIN, OR SEVERE ACUTE PAIN, 

evokes fear and grief and that the pain-evoked fear and grief 

have the same effect on the maps in the body-sensing regions of 

the brain as do fear and grief alone. When pain evokes fear or 

grief by threatening the existential domains of the individual, as 

in Cassell’s formulation, the suffering that results is qualitatively 

no different from any other form of suffering. The differences 

in the varieties of the experience of suffering, I propose, arise 

from its context—what Cassell referred to as “the meaning” of 

suffering. The current technology of neuroscience does not have 

the resolution to address, no less to validate, this theoretical 

postulate. I have no doubt that it will. 

PREMISE 3 

Suffering is not an emotion, but is an “emotionally 

competent stimulus” capable of evoking emotions. 

FEAR AND GRIEF, THE PROPOSED ANTECEDENTS OF SUFFERING, 

ARE EMOTIONS. I propose that suffering is not. Emotions evoke 

action, somatic and visceral motor activity, and aversive behavior 

in the face of fear and disgust. I propose that if fear and 

grief do not evoke suffering, they do motivate corrective or 

aversive action in the face of danger or loss. 5 

I am persuaded to think that suffering does not evoke aversive 

or corrective behavior by itself. Suffering is involutional, 

resulting in withdrawal, stasis, and inaction. Suffering is interior 

and isolating. Suffering is experienced as distress, misery, agony, 

anguish, torment, wretchedness, despair, hopelessness, excruciation, 

and woe. When we are lonely, we seek companionship. 

When we “suffer” the death of a loved one, we shut ourselves 

off and rely on the cultural rituals of the funeral, wake, or 

receiving of friends and family to provide resilience and connection 

to others. We recognize and admire the resilience of those 

who console others around them, even though everyone has 

experienced the same loss or, in the case of danger, the same 

jeopardy and fear. 

I have portrayed suffering as leading to inaction and stasis. 

I propose that with the evolution of suffering, the emotions of 

disgust and anger took on the role of decreasing the intensity of 

suffering by motivating action. Such actions often appear to be 

maladaptive when they are resentful or hostile. The ancient role 

of disgust was to protect against injury from contamination by 

waste, decay, and contagion. To experience disgust at the perception 

of an abstract stimulus or of a benign object is a recent 

response. Rage once served for aggressive display and dominance 

in reproductive and survival conflicts. Now, exploitation 

and dominance, as expressed in revenge, are more common. 6 

Although Elisabeth Kubler-Ross’s work has been criticized after 

her death, her well-known monograph on loss and grief 

demonstrates how suffering evokes disgust and rage (11). 

3 Time frames include the “past” from long-term memory, both declarative 

and non-declarative; the “present” from short-term memory (the answer to 

Emily Webb’s question [from Thornton Wilder’s Our Town] is: no, we do 

not experience life as we live it, we experience it after it happens); and the 

“future” as representations of anticipated objects and events (5). 

4 The calculation of possible states of mind multiplies six primary emotions, 

10 drive states, three time frames, and an arbitrary ordinal scale of intensity 

for the contribution of each of the other three dimensions. Even if many of 

the cells of such a matrix are empty, the product is a number beyond 

comprehension. 

5 For example, if I am afraid of a bull moose, I wait until he leaves and do 

not cross the valley to fish where he is feeding. But I do not suffer for it, 

unless he is feeding at the edge of the best pool in the river. 

6 We easily intuit the ancient survival value of fear, surprise, disgust, and anger; 

however, we might consider the role of disgust and anger in meliorating suffering 

when we recall the media frenzy that accompanies any human tragedy. 

Accusation, scapegoating, recrimination, and revenge follow hard upon fear 

and grief. A good example is the Sago Mine explosion in January 2006. After 

days of intense rescue efforts, a rumor spread that 1 miner was dead and that 

12 survived. The opposite was true and the truth was not transmitted to the 

community for 3 hours. The disgust and rage that followed were severe, 

arguably out of proportion to the offence. For many, rage and disgust were 

easily turned against the media for exploiting the suffering of the lost miners’ 

families. Perhaps we cleave to the suffering of others to validate our own 

resilience, but our reactions only reveal our vulnerability. 



Comorbidities Decrease Resilience and 

Increase Suffering 

EVERY CLINICIAN KNOWS that patients are more likely to lack 

resilience in the face of pain if they “suffer” from other emotions 

or drive states. Pre-existing depression or any of the 

hyper-arousal syndromes—obsessive compulsive disorder, generalized 

anxiety, panic disorder, focal phobias, post-traumatic 

stress disorder—will exacerbate the experience of pain, and any 

of these impairments can be caused by the suffering of chronic 

pain (12). Distinguishing cause from effect is difficult. When a 

drive state alone causes suffering, it might be sufficient to 

address the physiologic need: for example, rehydrate a person 

suffering from thirst. This is seldom the case in medical practice, 

least of all in pain management. Treating the disease 

without addressing the suffering that it causes will not suffice. 

A complete discussion of ethics and morality as they apply to 

the role of the practitioner is not possible here. It is well presented 

by Giordano in his work, cited earlier. 

Suffering as Disequilibrium of 

Frustrated Appetites and Emotions 

ANOTHER WAY TO VIEW THE VARIETY of the precursors of suffering 

is in terms of equilibrium and disequilibrium. I propose 

that suffering is the result of disequilibrium in any form: dehydration 

from thirst, starvation from hunger, shortness of breath, 

the ennui of confinement, prolonged separation from a friend 

or loved one. Although it is possible that each of these drive 

states, alone, is sufficient to cause suffering, I propose that suffering 

is mediated by fear and grief when the drive state is prolonged 

or severe, not unlike the suffering when chronic pain 

evokes fear or grief. We do not suffer from mild thirst; we simply 

get a glass of water. Thirst that evokes bodily pain, exhaustion, 

and fear of injury or death is another matter and thus a 

cause of suffering. 

PREMISE 4 

The neural substrate for the experience of suffering 

requires, in part, the anterior cingulate cortex. 

A NUMBER OF OBSERVATIONS persuade me to think that the 

anterior cingulate cortex (ACC) and its connectivities to the 

posterior cingulate cortex, the ventromedial prefrontal cortex, 

the amygdala, the hippocampus and the anterior insula, play an 

important, if not central, role in the experience of suffering. 

The central nervous system is not merely computational; yet, I 

choose a useful, if not precise, analogy of the ACC as the 

“CPU” that processes internal and external information that 

results in the experience of suffering. The physiologic process 

by which these structures, circuits, networks, and systems operate 

to produce suffering is unknown. Neuroscientists use such 

concepts as synergy, resonance, reverberation, synchrony, and 

synchronous oscillation when trying to explain the hypothetical 

mechanisms underlying suffering or certainty. 

As a medical student, I was fascinated by a patient whose 

midline brain tumor involving the ACC 7 produced a curious 

insensitivity to pain. The young man felt pain after his surgery, 

and reacted protectively to it, but it didn’t “bother” him. What 

was thought to be a type of “insensitivity to pain” was, I now 

propose, the elimination of the experience of suffering that 

would be caused by pain in the presence of an intact ACC. I 

propose that the patient’s experience was more than an inability 

to “interpret” pain, as in “asymbolia” (13). 

Anterior cingulotomy or prefrontal leucotomy relieves the 

suffering of chronic pain without eliminating the pain itself. 

Such neurosurgical procedures decrease pain behavior and disability 

without eliminating nociception (14). Damasio reports 

the experience of a man with intractable, totally disabling 

trigeminal neuralgia and quotes his response the next day after 

undergoing anterior, prefrontal leucotomy: “...the pains are the 

same, but I feel fine now (4).” 

Neuroimaging has validated the neural basis of semantic 

and sensory parameters of pain that are assessed through the 

McGill Pain Questionnaire (MPQ), almost 30 years after its 

development by Ronald Melzack and Warren S. Torgerson (15, 

16 ). Such findings further suggest the role of the ACC in the 

experience of suffering. Scoring of the MPQ divides the list of 

descriptive words for pain into distinct “sensory” and “affective” 

pain rating indices. Neuroimaging of subjects with chronic 

pain, when challenged with words from the sensory word list, 

revealed activation of areas associated with processing of 

somato-sensory nociception. When subjects heard words from 

the affective word list, there was increased activity in the insula 

and ACC (16, 17, 18). Melzack did not use the word “suffering” 

in his extensive, statistical validation of the MPQ, 

although I think that the word applies to the affective list. One 

observation by Melzack illustrates how the prejudices of clinicians 

affected pain assessment, then as now: “… patients are 

pleased to see (or hear) words which they use to describe their 

pain to family and friends but which they would not tell the 

physician because he may consider them psychologically 

unsound; the administrator thus often senses the patient’s relief 

at seeing such words in a list, implying that they are acceptable 

and sound descriptors” (19). Those “taboo” words were ones 

that describe suffering (splitting, exhausting, cruel, frightful, 

excruciating, etc.), as opposed to the sensory words (burning, 

stabbing, throbbing, pressing, stinging, etc.). 

7 The famous neurologist Houston Merritt made the diagnosis— 

without CT or MRI. 


Functional (f)MRIs of subjects in a state of mind characterized 

by grief reveal activation of the posterior cingulate cortex 

(20). Recent observations suggest that a predisposition to 

depression is related to abnormal (and variably asymmetrical) 

feedback circuits that link the ACC and the amygdala, which is 

responsible for the experience of fear (21). 

Activation of the ACC is observed in experiments in conflict 

resolution (22). In fMRI studies by Joshua Greene and colleagues, 

subjects who elect a rational solution to a moral 

dilemma also show activation of the ACC as a marker of “conflict,” 

along with activation of areas of the brain associated with 

cognitive processing (23, 24). My response to Greene’s summary 

of data and interpretations from the “crying baby” 8 experiments 

supports my theory (25). After reading the “crying baby 

dilemma,” I concluded, with difficulty, that I would select the 

rational solution: I would smother my own crying baby rather 

than expose the hiding place of my fellow villagers to a nearby, 

wartime enemy that would surely kill us all. The emotional resolution 

to the dilemma (do not smother the baby regardless of 

the consequences) is “easier” (Greene observed shorter reaction 

times). After reading Greene’s article (25), I was unable to sleep, 

distressed by thoughts of my own children and six-month-old 

granddaughter and by images of William Styron’s Sophie 9 , mortally 

suffering for the choice she had made. I speculated that 

the rational resolution to the crying baby dilemma requires 

more time and produced my own reaction, in part, because the 

somatic markers for decision-making in the crying baby 

dilemma include those of suffering. My painful obsessions and 

insomnia resulted from fear and grief—the emotional cost of 

my rational choice—even though the stimulus was fictional, 

just like the one in Styron’s novel and the subsequent movie. To 

quote Goethe, “To act is easy, to think is hard, to act according 

to our thought is troublesome.” 10 PREMISE 5 

The evolution of suffering is essential to the 

communication of emotion and to mammalian 

nurturing. 

THE QUALITIES OF SUFFERING that result in withdrawal, isolation, 

and stasis—misery, hopelessness, despair, torment, 

anguish, etc.—are grievous and fearsome indeed. In the evolution 

of species, such qualities and their resulting inaction would 

appear to impart a serious survival and reproductive disadvantage. 

It would follow, then, that a capacity for suffering should 

be extinguished by natural selection. Why, then, does suffering 

exist with such negative effects on the human condition? 11 I 

propose that suffering evolved, paradoxically, to impart survival 

and reproductive advantage. 

The increasing size of the brain relative to body mass (a 

development that paleontologists and physical anthropologists 

call “encephalization” 12 ) imparts survival and reproductive 

advantage (26). Increasing encephalization required that offspring 

are born neurologically immature, which is a serious survival 

disadvantage. 13 I propose that the resolution to the 

apparent paradox is the evolution of nurturing: an altruistic 

behavior that permits an individual to cooperate with another 

and relinquish its independence for the survival of the offspring. 

According to Paul MacLean, the transition from fish, 

amphibians, and reptiles—many, but not all, of which abandon 

their young—to mammals that protect them, play with them, 

have distinctive cries of separation and grieve for their loss, 

requires the paleopallium, the midbrain, the limbic system, 

specifically the circuit of Papez and the ACC (27). I propose 

that the full complement of primary emotions, mediated by the 

paleopallium, is the currency of mammalian nurturing and its 

invariable sequence: attachment, individuation, and separation. 

Suffering and empathy are the means of receipt and distribution 

of that currency. 14 I conclude, therefore, that suffering and 

8 “It is wartime, and you and some of your fellow villagers are hiding from 

enemy soldiers in a basement. Your baby starts to cry, and you cover your 

baby’s mouth to block the sound. If you remove your hand, your baby will 

cry loudly, the soldiers will hear, and they will find you and the others and 

kill everyone they find, including your baby. If you do not remove your 

hand, your baby will smother to death. Is it okay to smother your baby to 

death in order to save yourself and the other villagers?” (25) 

9 Meryl Streep played Sophie in the film adaptation of William Styron’s 

novel Sophie’s Choice. Sophie, upon arriving at a Nazi concentration camp, 

must choose between her two children. One will be taken from her and, 

she assumes, killed. She is allowed to keep the other child with her. Neither 

child survives. Sophie, years later, in the United States, commits suicide. 

10 From Wilhelm Meister’s Apprenticeship, Book VII, chapter 9. 

11 Twentieth-century existentialism simply gave up on rationalizing the role of 

suffering in the human condition and concluded that suffering is the human 

condition. The question of how suffering survives evolution is the same as 

the one that philosophers and scientists ask about altruism in its conflict 

with exploitation: how can it resist extinction? 

12 The rank order of the “encephalization quotient” (EQ) of mammals (humans 

7.4, dolphins 5.3, nonhuman primates 2.1-2.5, elephants 1.9, whales 1.8, 

canines 1.2, felines 1.0, equines 0.9, ungulates 0.8, rodents 0.4-0.5) well 

approximates the prevalence of animal behaviors that imply empathy, 

as we know it. 

13 Another troublesome paradox of the human condition is that we are capable 

of reproduction at the age of about 13 years, but the parts of the brain that 

are responsible for the control of impulsive behavior do not mature until 

the age of 21, if ever. 

14 A corollary to the hypothesis that a capacity for suffering requires the paleopallium 

or limbic system is the proposition that, birds not withstanding, 

most pre-mammalian species do not suffer, since they lack the neurological 

machinery to do so. The obverse proposition is that all mammals, to one 

degree or another, possess the capacity for suffering. It is, therefore, ethically 

safe to be very careful in the manner in which we conduct animal research. 



empathy evolved together, in their primal forms, as essential for 

mammalian nurturing. The capacity for empathy requires the 

capacity for suffering. 

PREMISE 6 

The capacity for suffering is the experiential 

precursor of empathy and altruism, which are 

the components of values and natural morality. 

MOST OBSERVERS AGREE that empathy is the antecedent of 

altruism (29). Explanations of altruism that rely on self-interest, 

enlightened self-interest, kin or group advantage, or strategic 

decision-making are either irrational or fail empirical validation. 

I propose that the survival and reproductive advantages of suffering, 

empathy, and altruism are inextricably related. 

Suffering, Empathy, and Mirror Neurons 

THE THEORY OF EMPATHY—and, arguably, a theory of suffering—took 

an important turn with the discovery by Giacomo 

Rizzolatti and colleagues (29) of “mirror neurons” in primates. 

The current understanding of mirror neurons was recently summarized 

by Rizzolatti and Craighero (30). Mirror neurons are 

specialized nerve cells that form systems in several areas of the 

brain that are involved in motor functions. According to the 

theory, when a person observes the face of another, mirror neurons 

appear to evoke in the observer the sensation that the 

observed facial muscle activity would evoke. They do not stimulate 

the observer to duplicate the activity, only to feel as 

though it had. We know that the feeling of the facial muscle 

activity that is characteristic of an emotion evokes the feeling of 

the emotion. Ekman demonstrated that a person who naively 

“makes the face” of sadness by practicing specific facial muscle 

activity in a pattern that is characteristic of grief, will feel sad 

(31). It follows that when a person observes another in grief, 

mirror neurons evoke the feeling of the observed facial expression. 

According to Damasio’s somatic marker theory, and 

Ekman’s observations, the feeling of sensations from the body 

proper (even if the body is observing at rest) that are concordant 

with a grieving face is an “emotionally competent stimulus”: 

the feelings evoke the experience of grief. 15 The operation 

of mirror neurons in humans has been well demonstrated for 

simple motor activity. The theory linking mirror neurons to 

suffering, empathy, and values is well on the way to validation, 

and, validation not withstanding, it makes wonderful sense. 

Thus far I have proposed that there is a relationship 

between suffering, the capacity for empathy and altruism, and 

that the relationship establishes a neural basis for natural morality. 

When I refer to altruism, I mean that which consists of fairness, 

generosity and regard for others—social emotions and 

values. 16 I use the term natural morality to distinguish it from 

imposed morality, which is commonly associated with belief 

systems and mythology. 17 I believe that altruism is fragile while 

exploitation is robust. Cooperation between evolving individuals 

did not come easily. The longest period of evolution, as 

much as 2.9 billion years, 18 passed while avaricious, self-protective, 

single-celled organisms “learned” how to tolerate each 

other and cooperate in order to form more efficient and adaptable 

multi-celled creatures. 19 

Conclusions 

IN THIS PAPER I proposed that suffering is the feeling of bodily 

disturbance that is evoked by fear or grief primarily, or as a 

response to (a) unresolved drives (thirst, hunger, oxygenation, 

lust, attachment, etc.) or (b) the experience of pain as it threatens 

the integrity of the existential domains of the autobiographical 

self. The disability of illness (as opposed to the impairment 

of disease) is the effect of suffering as an awareness of the bodily 

effects of grief and fear, particularly (but not exclusively) when 

evoked by pain. 

I offer this theory of suffering in an effort to make suffering 

more than just “the story of pain,” the “language of pain,” 

or the “emotional aspects of pain.” I have proposed that the 

neural substrate of suffering is as real as that of nociception or 

fear. Similarly, the burden of suffering is real, even though our 

patients use words to describe the experience that are variable 

to the point of idiosyncrasy. It is a fatuous conceit to say, “I 

feel your pain (or suffering).” No one, neither practitioner 

nor patient, can experience the pain or suffering of the other. 

That is the interior nature of consciousness and the inherent 

15 One aspect of the science of mirror neurons is important for the pain 

practitioner who is trying to comprehend the suffering of a patient who 

sits with a stooped posture, rocking aimlessly, protecting a withdrawn, 

deformed extremity, with the facial expression of fear and grief. Mirror 

neurons do not appear to evoke mimicry, only the feeling of mimicry. 

Mirror neurons, therefore, do not put practitioners at risk of identification, 

a state of mind in which the observer is motivated to behave like the 

patient. This is, no doubt, extending limited knowledge too far, but the 

ethical distinction between empathy and identification in clinical practice 

cannot be overstated. Some practitioners may fear empathy, lest they identify 

with the patient and lose clinical perspective in formulating a cogent 

diagnosis and appropriate plan of care. The advancing science of mirror 

neurons does not eliminate the risk of identification, but it doesn’t 

make it inevitable either. 

16 This is often referred to by the outmoded term psychological altruism, to distinguish 

it from biological altruism, cooperation that promotes survival of the 

species but not the individual. Biological altruism is observed in organisms 

lacking a central nervous system. 

17 In this context I define natural morality as the predisposition to good (as 

opposed to right) behavior that does not require, or is independent of, the 

existence of a supernatural power or intelligence. For a discussion of natural 

law and morality, I refer the reader to Alfonso Gomez-Lobo (32). 

18 For those who are interested, a representative evolutionary time-line includes: 

Earth cools, water and atmosphere form, 4.1 BYA (billion years ago); singlecelled 

organisms appear, 3.9 BYA; sexual reproduction appears, 1.2 BYA; 

multi-celled organisms appear, 1.0 BYA; the Cambrian explosion occurs, 

0.55 BYA. 

19 We share half of our genome with the common yeast whose cooperative skills 

go no further than forming colonies. The rest of evolution seems easy in 

comparison. 


separation between the observer and the observed. Empathy is 

the best we can manage, and if we can muster it to action, that 

is good enough. 

I believe that the capacity for suffering is the precursor of 

natural morality. I stand with numerous scientists and ethicists, 

some cited here, to declare that empathy and the understanding 

of suffering, however elusive they may be, are the moral obligation 

of the pain practitioner. The pain patient has a reciprocal 

obligation. Honesty and trust go both ways. Patients deceive 

their physicians for a host of reasons, some intentional, some 

not. Mistrust at the outset of the relationship thwarts communication. 

Mistrust is prejudicial and ethically corrosive. The 

moral role of the pain practitioner is to trust the patient’s 

reports and expressions of suffering. We cannot measure suffering, 

nor can we even be certain of its presence. But we can 

explore with the patient the habits, goals, desires, expectations, 

roles, attachments—in short, any and every facet of the 

patient’s life, some hidden from awareness, that are threatened 

by the experience of pain. The treatment of diseases and 

injuries includes the treatment of pain. The treatment of pain 

is all about suffering. 

The author acknowledges the help of Linda Sutton in the preparing 

the manuscript and of Russell Stevenson and James Giordano in 

formulating and organizing the ideas in it. 

REFERENCES 

1. Giordano J. Toward a core philosophy and virtue-based ethic of pain 

medicine. Pain Practitioner. 2005 Summer; 15 (2): 59-66. 

2. Giordano J. The neurobiology of nociceptive and anti-nociceptive systems. 

Pain Physician. 2005; 8: 277-291 

3. Cassell EJ. The nature of suffering and the goals of medicine. II. Oxford: 

Oxford University Press, 1991, 2004. 

4. Damasio AR. Descartes’ error: Emotion, reason and the human brain. New 

York: Grosset/Putnam Book, 1994. 

5. Leder D. Toward a phenomenology of pain. Rev Existential Psychology 

and Psychiatry, 1984; 9: 29-43. 

6. Damasio AR. The feeling of what happens: Body and emotion in the making 

of consciousness. New York: Harcourt-Brace, 1999. 

7. Damasio AR. Looking for Spinoza: Joy, sorrow, and the feeling brain. New 

York: Harcourt-Brace, 2003. 

8. Ekman P. Emotions Revealed: Recognizing Faces and Feelings to Improve 

Communication and Emotional Life. New York: Times Books, 2003. 

9. Damasio AR. The neurobiological grounding of human values. Changeux 

J-P, et al (ed) Neurobiology of human values. Berlin: Springer-Verlag, 

2005. 

10. Ekman P. Emotions inside out. 130 Years after Darwin’s “The Expression of 

the Emotions in Man and Animal.” Ann N Y Acad Sci. 2003; Dec;1000:1- 

6. 

11. Kubler-Ross E. On death and dying. New York: Simon-Schuster/Touchstone, 

1969. 

12. Gatchel RJ, Turk DC. Psychosocial factors in pain: Clinical perspectives. 

New York: Guilford Press, 1999. 

13. Grahek, N. Objective and subjective aspects of pain. Philosophical Psychology. 

1991; 4:249-66. 

14. White JC, Sweet WH. Textbook of Stereotactic and Functional Neurosurgery. 

New York: McGraw-Hill; 1998. 

15. Melzack R, Torgerson WS. On the language of pain. Anesthesiology. 1971 

Jan; 34(1):50-9. 

16. Peyron R, Garcia-Larrea L, Gregoire MC, et al. Functional imaging of brain 

responses to pain. A review and meta-analysis. Neurophysiol Clin. 2000; 

30: 263-288. 

17. Ploghaus A, Narain C, Beckmann CF, et al. Exacerbation of pain by anxiety 

is associated with activity in a hippocampal network. J Neuroscience. 

2001; 21(24): 9896-9903. 

18. Koyama T, McHaffie JG, Laurienti PJ, Coghill RC. The subjective experience 

of pain: Where expectations become reality. Proc Natl Acad Sci. 

2005 Sep 6; 102(36):12950-5. 

19. Melzack R. The McGill pain questionnaire: Major properties and scoring 

methods. Pain. 1975; 1: 277-299. 

20. Grundel H, O’Connor MF, Lindsey L, et al. Functional neuroanatomy of 

grief: An fMRI study. Am J Psychiatry. 2003; 160: 1946-1953. 

21. Pezawas L, Meyer-Lindenberg A, Drabant EM, et al. 5-HTTLPR polymorphism 

impacts human cingulate-amygdala interactions: a genetic susceptibility 

mechanism for depression. Nature Neuroscience. 2005; 8: 

828-834. 

22. Bitvinick MM, Braver TT, Barch DM, et al. Conflict monitoring and cognitive 

control. Psychol Rev. 2001; 108: 624-652. 

23. Greene JD, Sommerville R, Nystrom LE, et al. An fMRI investigation of 

emotional engagement in moral judgment. Science. 2001; 293: 

2105-2108. 

24. Greene JD, Nystrom LE, Engell AD, et al. The neural bases of cognitive 

conflict and control in moral judgment. Neuron. 2004; 44: 389-400. 

25. Greene JD. Emotion and cognition in moral judgment: Evidence from 

neuroimaging. Changeux J-P, et al (ed) Neurobiology of human values. 

Berlin: Springer-Verlag, 2005. 

26. Macphail EM. Brain and Intelligence in Vertebrates. Clarendon Press, 

Oxford, 1982. 

27. MacLean PD. Cerebral evolution of emotion. Lewis M, Haviland JM (ed) 

Handbook of emotions. New York: Guilford Press, 1993. 

28. Toi M, Batson CD. More evidence that empathy is a source of altruisticmotivation. 

Journal of Personality and Social Psychology. 1972; 43, 

281-292. 

29. Rizzolatti G, Scandolara C, Matelli M, et al. Afferent properties of 

peri-arcuate neurons in macaque monkeys. I. Somatosensory responses. 

Behav Brain Res. 1981; 2:125-146. 

30. Rizzolatti G, Craighero L. Mirror neuron: A neurological approach to 

empathy. Changeux J-P, et al (ed) Neurobiology of human values. Berlin: 

Springer-Verlag, 2005. 

31. Ekman P. Facial expression. Dalgleish T, 

Power M. (ed) Handbook of cognition and 

emotion. New York: John Wiley & Sons, 1999. 

32. Gomez-Lobo A. Morality and the human 

goods: An introduction to natural law ethics. 

Washington, DC: GTU Press, 2002. 

PETER A. 

MOSKOVITZ, MD 


AC ADEMY NEWS | AMERICAN ACADEMY OF PAIN MANAGEMENT 

ACADEMY NEWS 

The Academy Welcomes 

New Credentialing 

Coordinator, Christine Wright 

CHRISTINE WRIGHT joined the American 

Academy of Pain Management in December 

2005 as the Credentialing Coordinator. 

Christine is responsible for tracking/coordinating 

credentialed member and CHRISTINE WRIGHT, 

Credentialing 

credential eligible applicant processes. She 

Coordinator 

will also 

be involved in the coordination of exhibitor 

booths for the 17th Annual Clinical 

Meeting in Orlando. 

Christine recently moved to California from Boise, Idaho, 

where she worked the State of Idaho for the last 25 years. 

There she provided direct and indirect services for consumers 

and employees and met many interesting challenges including: 

developing and coordinating a volunteer program in an institutional 

setting, identifying appropriate and cost effective medical 

transportation resources for consumers, participating with multiple 

agencies in the restructuring of human resources, and 

developing a new employee orientation program. 

Newly Credentialed 

DIPLOMATE 

Kenneth J. Allan, MD 

Rafael F. Aviles, MD 

Alyn LaMar Benezette, DO 

Anjum Bux, MD 

Robert J. Byrnes, DO 

Jacqueline Chanlatte, MD 

Jeffrey M. Cox, MD 

Sydney H. Crackower, MD 

Jay Finke, MD 

Kenneth W. Gibson, DO 

Allison W. Hanley, MD 

James M. Hawk, MD, PA 

Jonathan M. Hirsch, MD, PC 

Michael S. Lazzopina, MD 

Edmund K.T. Liem, DDS 

Bettina T. Limjoco, MD 

Manoj Maggan, DDS 

Don C. McLarey II, MD 

Enrico A. Melson, MD 

Sunil Shanker Naik, MD 

Sardha M. Perera, MD 

Aida Suarez Phelan, MD 

Kathryn A. Powell-Francis, MD 

Chikka M. Raju, MD, MAGD 

Challa V. Reddy, MD 

Keric J. Shiepis, DC 

Louis Greene Stanfield, CRNA, PhD 

Robert M. Stein, DVM 

Lloyd Stolworthy, MD 

Mark R. Stover, DMD 

Susan M. Thibault, DPM 

Robert N. Ulseth, MD 

Shailesh P. Upadhyay, MD 

Bradley W. Wargo, DO 

Norman H. Wasserman, MD 

Igor Wilderma, MD 

FELLOW 

Jayne D.Andrews, CRNA 

Cindy Cornell, BSN, RN 

Dennis C. McCraney, PA-C 

CLINICAL ASSOCIATE 

Paul C. Pollachek, RN, BS 

Thank You 

The Academy Thanks the Following People for 

Their Generous Donations 

Davis Bregman, MD 

Victoria I. Brightman, DPM 

Jose A. Cumba, DMD 

Albert C. Cura, MD 

Andrew Davy, MD 

Leonard B. Goldstein, DDS, PhD 

Heusent A. James, MD 

IN MEMORY 

Valerie Gerard Dillon, MD 

Kathleen A. Presutto-Nelson, MD 

John E. Freeman 

Juan F. Legarreta-Lopez, MD 

Andres Vega, MD 

C Samuel Verghese, MD, PhD 

Oops! In the last issue of The Pain Practitioner, we forgot 

to acknowledge two of our photographers (pages 80-81): 

Dr. Hal Blatman and Nancy Holland. 

82 |T H E PA I N P R A C T I T I O N E R | S P R I N G 2 0 0 6

N O W A V A I L A B L E ! 

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CL ASSIFIED ADS & DIRECTORY | AMERICAN ACADEMY OF PAIN MANAGEMENT 

CLASSIFIED ADS 

To place a classified advertisement in the directory, 

call Jillian Manley at the Academy at (209)533-9744 

or send an email to jillian@aapainmanage.org. 

R ATES 

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Birmingham, Alabama: Multispecialty 

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DIRECTORY 

To place an advertisement in the directory, call Jillian Manley at 

(209)533-9744 or send an email to jillian@aapainmanage.org. 

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RESOURCES | CRPS 

RESOURCES FOR CRPS 

Organizations 

Reflex Sympathetic Dystrophy Syndrome Association of America (RSDSA) 

RSDSA provides comprehensive information on education, treatment, and research for practitioners and lay people. Information is available as print 

pieces or on their website, www.rsds.org. RSDSA publishes a quarterly newsletter, a bi-monthly electronic newsletter and several brochures and 

booklets. One of its landmark publications, In Pain, Out of Work, Can’t Pay the Bills, is a resource directory for people who are financially devastated by 

CRPS. The organization’s web-housed article archive has more than 80 peer-reviewed articles on various aspects of CRPS. 

Address: 99 Cherry St. • Milford, CT 06460 

Telephone: 877-662-7737 

Email: info@rsds.org 

Website: www.rsds.org 

International Research Foundation for RSD/CRPS 

This is a nonprofit organization dedicated to education and research on Reflex Sympathetic Dystrophy and Complex Regional Pain Syndrome. The primary 

mission of the Foundation is to establish an international research network which will help educate medical professionals and support research worldwide. 

Address: USF Medical Clinics c/o Dr. A. Kirkpatrick 

12901 Bruce Downs Blvd., MDC59 • Tampa, FL 33612 

Telephone: 813-907-2312 

Email: info@rsdfoundation.org 

Website: www.rsdfoundation.org 

National Institute of Neurological Disorders and Stroke (NINDS) 

The mission of NINDS is to reduce the burden of neurological disease. NINDS has a listing of clinical trials for neuropathic pain. The information page 

that has been condensed from its former fact sheet. It also has a list of clinical trials recruiting people with CRPS. 

Address: NIH Neurological Institute 

P.O. Box 5801 • Bethesda, MD 20824 

Telephone: 800-352-9424 or (301) 496-5751 

Website: www.ninds.nih.gov/ 

National Organization for Rare Disorders (NORD) 

NORD is a clearinghouse for information concerning disorders affecting fewer than 200,000 individuals worldwide and features valuable information 

on CRPS. 

Address: National Organization for Rare Disorders 

55 Kenosia Avenue • PO Box 1968 • Danbury, CT 06813-1968 

Telephone: 203-744-0100 

Tollfree: 800-999-6673 (voicemail only) 

Email: orphan@rarediseases.org 

Website: www.rarediseases.org 

For Grace 

For Grace is a nonprofit organization devoted to raising awareness of Reflex Sympathetic Dystrophy in the medical community and general public. 

Address: For Grace 

PO Box 1724 • Studio City, CA 91614 

Telephone: 818-760-7635 

Email: rsdaware@forgrace.org 

Website: www.forgrace.org 

American RSDHope 

This nonprofit group is made up of patients, parents and friends whose mission is to spread information to anyone and everyone who asks or will listen. 

Address: American RSDHope 

PO Box 875 • Harrison, ME 04040 

Email: rsdhope@mail.org 

Website: www.rsdhope.org 

Promoting Awareness of RSD and CRPS in Canada 

Website: www.rsdcanada.org/parc/english/index.html 

Books 

Living With RSDS, A guide to coping with Reflex Sympathetic Dystrophy Syndrome, by Linda Lang and Peter Moskovitz, MD. This book is available 

from the RSDSA home office for $15 or from Amazon.com. 

Positive Options for Reflex Sympathetic Dystrophy (RSD): Self Help and Treatment, by Elena Juris. This book is available from Amazon.com. 

Medifocus Guide—contains over 90 pages of information including a clear description of the condition, treatment options, the latest research and a 

worldwide directory of RSDS professionals. It is available from the RSDSA website, www.rsds.org. 


Or register online at www.aapainmanage.org 

Register now for the Academy’s 2006 Clinical Meeting in Orlando: 

Beyond Boundaries: Forging New Alliances in Pain Management. 

Name 

Profession 

Address 

City State Zip 

Daytime Phone/Email (required) / 

Pre-meeting, Meeting Registration (Thursday) Amount Amount Paid 

Member* $ 185 

Non-Member $ 225 

*Employees of Pain Program Accredited Facilities may register at Member rate 

Clinical Meeting Registration (Fri., Sat., Sun.) Early Bird After 7/1 On-Site Amount Paid 

Member* $ 375 $ 420 $ 475 

Non-Member $ 550 $ 585 $ 640 

Full-Time Student Member ** $ 50 $ 60 $ 70 

Full-Time Student Non-Member ** $ 85 $ 95 $ 125 

One Day $ 250 $ 260 $ 280 

Awards Luncheon (Saturday 12:35 - 2:00 pm) $ 35 $ 35 $ 35 

You must register and pay for luncheon prior to conference, cannot sign up on-site 

*Employees of Pain Program Accredited Facilities may register at Member rate 

Membership 

Individual Membership $ 195 $195 $195 

Amount Paid 

Student Membership** $ 50 $ 50 $ 50 

**Must provide proof of student status 

Total Payment $ 

Method of payment Visa Mastercard Discover Check Enclosed (US Funds Only) 

Credit Card # 

Expiration Date Verification Number Signature 

Please mail or fax completed Registration Form to: 

For AAPM Office Use Only 

American Academy of Pain Management 

13947 Mono Way #A 

Sonora, CA 95370 

Phone 209-533-9744 

Fax 209-533-9750 

Bring 

a guest! 

The Academy is offering complimentary guest badges for the Exhibit Hall on Friday and Saturday. Badges will be 

available at the registration desk. 


A m e r i c a n A c a d e m y o f P a i n M a n a g e m e n t 

Beyond Boundaries 

Orlando 

September 7–10, 2006 

FORGING NEW ALLIANCES IN PAIN MANAGEMENT 

17th 

ANNUAL CLINICAL MEETING 

Walt Disney World 

Swan and Dolphin 

1500 Epcot Resorts Boulevard 

Lake Buena Bista, FL 32830 

407-934-4888 

A m e r i c a n A c a d e m y o f P a i n M a n a g e m e n t 

13947 Mono Way #A • Sonora, California 95370 

NONPROFIT ORG. 

U.S. POSTAGE 

PAID 

CERES, CA 

PERMIT NO. 86

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