Guide to Pain Management in Low-Resource Settings
`
`Edited by Andreas Kopf and Nilesh B. Patel
`
`INTERNATIONAL ASSOCIATION FOR THE STUDY OF PAIN®
`
`Grun. Exh. 1020
`PGR for U.S. Patent No. 9,707,245
`
`

`

`

`

`Guide to Pain Management in Low-Resource Settings
`Educational material written for general distribution
`to health care providers by a multidisciplinary
`and multinational team of authors
`
`Editors
`
`Andreas Kopf, MD
`Department of Anesthesiology
`Charité Medical University
`Berlin, Germany
`Nilesh B. Patel, PhD
`Department of Medical Physiology
`University of Nairobi
`Nairobi, Kenya
`
`IASP® • SEATTLE
`
`

`

`© 2010 IASP®
`International Association for the Study of Pain®
`
`All rights reserved. Th is material may be used for educational and training purposes with proper citation of the source.
`Not for sale or commercial use.
`Timely topics in pain research and treatment have been selected for publication, but the information provided and opinions
`expressed have not involved any verifi cation of the fi ndings, conclusions, and opinions by IASP®. Th us, opinions expressed in
`Guide to Pain Management in Low-Resource Settings do not necessarily refl ect those of IASP or of the Offi cers and Councilors.
`No responsibility is assumed by IASP for any injury and/or damage to persons or property as a matter of product liability, neg-
`ligence, or from any use of any methods, products, instruction, or ideas contained in the material herein. Because of the rapid
`advances in the medical sciences, the publisher recommends that there should be independent verifi cation of diagnoses and
`drug dosages. Th e mention of specifi c pharmaceutical products and any medical procedure does not imply endorsement or
`recommendation by the editors, authors, or IASP in favor of other medical products or procedures that are not covered in the
`text. Errors and omissions are expected.
`
`Supported by an educational grant from the International Association for the Study of Pain
`A preliminary version of this text was printed in 2009
`
`

`

`Contents
`Foreword
`Introduction
`Basics
`1. History, Defi nitions, and Contemporary Viewpoints
`Wilfried Witte and Christoph Stein
`2. Obstacles to Pain Management in Low-Resource Settings
`Olaitan A Soyannwo
`3. Physiology of Pain
`Nilesh B. Patel
`4. Psychological Factors in Chronic Pain
` Harald C. Traue, Lucia Jerg-Bretzke, Michael Pfi ngsten, and Vladimir Hrabal
`5. Ethnocultural and Sex Infl uences in Pain
`Angela Mailis-Gagnon
`6. Pharmacology of Analgesics (Excluding Opioids)
`Kay Brune
`7. Opioids in Pain Medicine
`Michael Schäfer
`8. Principles of Palliative Care
`Lukas Radbruch and Julia Downing
`9. Complementary Th erapies for Pain Management
`Barrie Cassileth and Jyothirmai Gubili
`Physical and Psychological Patient Evaluation
`10. Pain History and Pain Assessment
`Richard A. Powell, Julia Downing, Henry Ddungu, and Faith N. Mwangi-Powell
`11. Physical Examination: Neurology
`Paul Kioy and Andreas Kopf
`12. Physical Examination: Orthopedics
`Richard Fisher
`13. Psychological Evaluation of the Patient with Chronic Pain
`Claudia Schulz-Gibbins
`Management of Acute Pain
`14. Pain Management after Major Surgery
`Frank Boni
`15. Acute Trauma and Preoperative Pain
`O. Aisuodionoe-Shadrach
`16. Pain Management in Ambulatory/Day Surgery
`Andrew Amata
`17. Pharmacological Management of Pain in Obstetrics
`Katarina Jankovic
`
`iii
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`vii
`ix
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`3
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`9
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`13
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`19
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`27
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`33
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`39
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`47
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`59
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`67
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`79
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`93
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`103
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`115
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`119
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`123
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`iv
`Management of Cancer Pain
`18. Abdominal Cancer, Constipation, and Anorexia
`Andreas Kopf
`19. Osseous Metastasis with Incident Pain
`M. Omar Tawfi k
`20. Lung Cancer with Plexopathy
`Rainer Sabatowski and Hans J. Gerbershagen
`21. Lung Cancer with Breathing Problems
`Th omas Jehser
`22. Hematologic Cancer with Nausea and Vomiting
`Justin Baker, Paul Ribeiro, and Javier Kane
`Management of Neuropathic Pain
`23. Painful Diabetic Neuropathy
`Gaman Mohammed
`24. Management of Postherpetic Neuralgia
`Maged El-Ansary
`25. Central Neuropathic Pain
`Maija Haanpää and Aki Hietaharju
`26. Th e Management of Pain in Adults and Children Living with HIV/AIDS
` Glenda E. Gray, Fatima Laher, and Erica Lazarus
`Management of Chronic Noncancer Pain
`27. Chronic Nonspecifi c Back Pain
` Mathew O.B. Olaogun and Andreas Kopf
`28. Headache
` Arnaud Fumal and Jean Schoenen
`29. Rheumatic Pain
`Ferydoun Davatchi
`Diffi cult Th erapeutic Situations and Techniques
`30. Dysmenorrhea, Pelvic Pain, and Endometriosis
`
`Susan Evans
`31. Pain Management Considerations in Pregnancy and Breastfeeding
`Michael Paech
`32. Pain in Sickle Cell Disease
`Paula Tanabe and Knox H. Todd
`33. Complex Regional Pain Syndrome
` Andreas Schwarzer and Christoph Maier
`34. Pain Management in Children
`Dilip Pawar and Lars Garten
`35. Pain in Old Age and Dementia
`Andreas Kopf
`36. Breakthrough Pain, the Pain Emergency, and Incident Pain
`Gona Ali and Andreas Kopf
`37. Pain Management in the Intensive Care Unit
`Josephine M. Th orp and Sabu James
`38. Diagnostic and Prognostic Nerve Blocks
`Steven D. Waldman
`
`Contents
`
`137
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`147
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`155
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`163
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`169
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`179
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`183
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`189
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`195
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`207
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`213
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`221
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`229
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`235
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`245
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`249
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`255
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`269
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`277
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`283
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`293
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`Contents
`39. Post-Dural Puncture Headache
`Winfried Meissner
`40. Cytoreductive Radiation Th erapy
`Lutz Moser
`41. Th e Role of Acupuncture in Pain Management
`Natalia Samoilova and Andreas Kopf
`Planning and Organizing Pain Management
`42. Setting up a Pain Management Program
`M.R. Rajagopal
`43. Resources for Ensuring Opioid Availability
`David E. Joranson
`44. Setting up Guidelines for Local Requirements
`Uriah Guevara-Lopez and and Alfredo Covarrubias-Gomez
`Pearls of Wisdom
`45. Techniques for Commonly Used Nerve Blocks
`Corrie Avenant
`46. Psychological Pearls in Pain Management
`Claudia Schulz-Gibbins
`47. Clinical Physiology Pearls
`Rolf-Detlef Treede
`48. Herbal and Other Supplements
`Joel Gagnier
`49. Profi les, Doses, and Side Eff ects of Drugs Commonly Used in Pain Management
`Barbara Schlisio
`Appendix
`Glossary
`Andreas Kopf
`
`v
`299
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`303
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`307
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`317
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`321
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`329
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`337
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`341
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`345
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`349
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`351
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`359
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`Guide to Pain Management in Low-Resource Settings
`
`Chapter 33
`Complex Regional Pain Syndrome
`Andreas Schwarzer and Christoph Maier
`
`single nerve, e.g., the whole hand is aff ected following
`In 1865, the neurologist Silas Weir Mitchell reported
`fracture of the radius; (3) usually both joints and nerves
`about soldiers complaining of strong burning pain, pro-
`are aff ected; (4) patients often present with psychological
`nounced hyperesthesia, edema, and reduction of motor
`disturbances. Th ere are no clinical diff erences between
`function of the limb following injuries of the upper or
`CRPS type I and type II; except for the nerve damage.
`lower extremity. Mitchell named these disturbances “cau-
`salgia.” In the following years, these symptoms were de-
`What is the incidence of CRPS, and
`scribed again and again after extremity injuries but were
`are there specifi c triggers?
`labeled diff erently (algodystrophy, refl ex sympathetic dys-
`trophy, Morbus Sudeck). Currently, this disease pattern is
`referred to as complex regional pain syndrome (CRPS).
`CRPS is a rare disease. Approximately 1% of patients de-
`Two types are recognized: CRPS type I without nerve in-
`velop CRPS following a fracture or nerve injury. How-
`jury and CRPS type II associated with major nerve injury.
`ever, exact data on prevalence do not exist. In a current
`study from the Netherlands, the incidence was esti-
`What are the main characteristics
`mated 26/100,000 persons per year, with females being
`of patients with CRPS?
`aff ected at least three times more often than males. In
`another population-based study from the United States,
`As a general rule, the symptoms of CRPS manifest
`the incidence was estimated at 5.5/100,000 persons per
`themselves in the distal extremity (usually in the upper
`year. Th e upper extremity is more often aff ected, and a
`limb, and less often in the lower limb). Almost all pa-
`fracture is the most common trigger (60%).
`tients (90–95%) suff er from pain, which is described as
`What is the explanation for
`burning and drilling and is felt deep in the tissue. Fur-
`development of CRPS?
`thermore, an edema of the aff ected extremity, with an
`emphasis on the dorsal areas (dorsum of the hand or
`In almost all of the patients (90–95%) there is an ini-
`foot) can be observed in almost all patients. Pain and
`tiating noxious event (trauma) in the clinical history.
`edema increase when the limb is hanging down. Further
`Th e reason why only some patients develop CRPS is
`essential disease features are the following: (1) patients
`still unclear. Th ere is also no comprehensive theory
`suff er from sensory, motor, and autonomic impairment;
`that can explain the diversity and the heterogeneity
`(2) the symptoms spread beyond the area of the primary
`of the symptoms (edema, central nervous symptoms,
`damage and cannot be assigned to the supply area of one
`249
`Guide to Pain Management in Low-Resource Settings, edited by Andreas Kopf and Nilesh B. Patel. IASP, Seattle, © 2010. All rights reserved. Th is material may be used for educational
`and training purposes with proper citation of the source. Not for sale or commercial use. No responsibility is assumed by IASP for any injury and/or damage to persons or property
`as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material herein. Because of the rapid advances in the
`medical sciences, the publisher recommends that there should be independent verifi cation of diagnoses and drug dosages. Th e mention of specifi c pharmaceutical products and any
`medical procedure does not imply endorsement or recommendation by the editors, authors, or IASP in favor of other medical products or procedures that are not covered in the text.
`
`

`

`250
`joint involvement, etc.). Current attempts explain sin-
`gle symptoms, but not the overall picture. An essential
`hypothesis about the main pathomechanism for de-
`veloping CRPS includes infl ammatory processes. Th is
`point of view is supported by the fact that the classic
`infl ammatory signs (edema, redness, hyperthermia,
`and impaired function) are prominent, especially in the
`early stages of the disease, and that these symptoms are
`positively infl uenced by the use of corticosteroids.
`What is the prognosis of patients
`who have developed CRPS?
`Th e number of favorable cases that heal up spontane-
`ously or following adequate treatment (and avoidance
`of mistreatment), are unknown. Prognosis regarding the
`full recovery of function of the aff ected limb is unfavor-
`able, and only 25–30% of all patients fully recover, ac-
`cording to the degree of severity and their comorbidity.
`Th e extent of the eff ects of osteoporotic changes on the
`prognosis is still unclear. Th e following symptoms point
`to an unfavorable course of the disease: a tendency to
`stiff joints, contracture in the early stages, pronounced
`motor symptoms (dystonia, tremor, and spasticity), ede-
`ma, and psychological comorbidity.
`Which treatment strategies play an
`important role in the management
`of CRPS?
`Treatment should take place in three steps: in the begin-
`ning, treatment of pain at rest and treatment of edema
`have utmost priority. Next to pharmacological treat-
`ment, rest and immobilization are most important. In
`the second stage, the therapy should include treatment
`of the pain during movement as well as during physi-
`cal and occupational therapy. Pain treatment takes a
`back seat in the third stage, when the emphasis is on
`the treatment of functional orthopedic disorders as well
`as on psychosocial reintegration. Th e intensifi cation of
`physical therapy can be limited due to reoccurrence of
`pain or edema. Th e main rule is that the treatment must
`not cause any pain.
`Case report
`Etta, a 58-year-old offi ce worker, had bad luck when
`she left her house on a rainy day and fell on the slip-
`pery steps of her front porch. A fracture of the left distal
`
`Andreas Schwarzer and Christoph Maier
`radius was diagnosed in the hospital. Everything seemed
`fi ne after the fracture was treated by osteosynthesis and
`cast, but within a few days after discharge she felt an in-
`creasing constant burning pain in her forearm, and her
`fi ngers got swollen. When visiting her surgeon, she com-
`plained about the pain, and the cast was removed.
`Are the symptoms a “normal”
`consequence of her fracture?
`After the application of a looser cast and the prescription
`of pain medication, the pain was tolerable, even though
`her fi ngers remained swollen. Six weeks later, the cast was
`removed, and physiotherapy commenced. A few days lat-
`er, Etta reported an increase in swelling after the removal
`of the cast and said she felt a stinging, partly burning pain
`circularly around the wrist, radiating to the fi ngers. Fur-
`thermore, the movement of her fi ngers was reduced; the
`hand was shiny, swollen, and blueish-reddish.
`Once again, is this a “normal”
`consequence of her fracture?
`Dr. Jones, the attending physician, recommended inten-
`sifying the physical treatment and increasing the doses
`of the pain medication. During intensifi cation of physi-
`cal therapy, Etta’s fi ngers were trained forcefully, which
`was very painful. With exercise, the pain and swelling
`increased, and the hand was still bluish-reddish colored
`and shiny. Moreover, Etta noticed an increased growth
`of her fi nger nails and the hair on the dorsum of her left
`hand. Although physical therapy was intensifi ed, the lack
`of mobility of the fi ngers worsened, the hand was con-
`stantly swollen, and the pain was burning and almost
`unbearable, at rest as well as during movement. Etta be-
`came desperate, and Dr. Jones was at the limit of his wis-
`dom on how to help her.
`What should be done?
`Why has Dr. Jones’ therapy failed?
`Six weeks passed, and Dr. Jones referred Etta to a pain
`management center. She was still complaining about
`the pain, which at that point was radiating to the fore-
`arm and elbow as well. Additionally, she reported strong
`functional defi cits in the hand (it was not possible to
`make a fi st, and the fi nger-palm distance was 10 cm).
`In the past few days, she had also noticed a restriction
`in the shoulder movements (especially abduction). Dr.
`Ndungu, the attending doctor from the pain center, rec-
`ognized the problem and recommended an appropriate
`treatment; Etta was lucky.
`
`

`

`Complex Regional Pain Syndrome
`What are Dr. Ndungu’s options
`for further diagnostic procedures?
`Based on the diagnostic criteria defi ned by IASP (see
`below) and the course of the disease, Dr. Ndungu diag-
`nosed a complex regional pain syndrome. Upon start of
`the treatment at the pain center, he explained to Etta
`the disease pattern and the principles of therapy, which
`require her active cooperation, understanding, and pa-
`tience because progress may be slow, with relapses and
`periods of stagnation. He prescribed Etta a splint and
`recommended that she position the hand and the fore-
`arm higher than the heart, until the edema is reduced.
`Coxibs (celecoxib) and anticonvulsants (gabapentin)
`were prescribed as pain medications. Physical and occu-
`pational therapy was started one week after the decrease
`of the edema and the pain at rest.
`Are there any other therapeutic options?
`What are the main rules for therapy?
`At the beginning of physical therapy, focus was put on
`the shoulder, and 2 weeks later, normal mobility was re-
`gained. Th e progress of improvement in hand function
`was much slower. As soon as Etta exercised too strongly
`with her hand or used it for household tasks, the edema
`developed again and the pain became stronger. After ap-
`proximately 3 months, with physical and occupational
`therapy, Etta was able to achieve an improvement in
`hand function and a reduction in pain. It took 6 more
`months before she was able to return to her offi ce and op-
`erate her computer with her left hand.
`Was this a typical course of CRPS?
`Th is case exemplifi es a typical course of CRPS with re-
`spect to sex, age, injury, and symptoms. However, espe-
`cially in the early stages of the disease, it is often diffi -
`cult to diff erentiate between the symptoms of CRPS and
`the normal or slightly delayed fracture healing. Th e di-
`agnosis of CRPS is possible only after the development
`of typical symptoms, such as an impairment of sensory,
`vasomotor, motor, and sudomotor function. In Etta’s
`case, attention should be focused on two typical clini-
`cal phenomena: fi rst, the negative infl uence of forced
`physical exercises on the further course of the disease,
`and second, the commonly observed involvement of the
`shoulder during the course of the disease. Th e mobility
`of the elbow joint is mostly unaff ected, whereas abduc-
`tion and rotation of the shoulder joint are often dis-
`abled. Patience and individually adjusted physical activ-
`ity are essential requirements for patients.
`
`251
`
`What are the clinical
`symptoms of CRPS?
`Th e clinical pattern of CRPS is characterized by sen-
`sory, motor, and autonomic impairment. Additionally,
`patients with CRPS often feel as if the hand or the foot
`does not belong to them anymore or as if it is not per-
`ceptible or controllable; movements can only be per-
`formed under direct visual control (“neglect-like syn-
`drome”). Furthermore, the following features occur in
`almost all cases:
`• Th e impairment due to CRPS is disproportionate
`to the inciting event.
`• Th ere is a tendency for a distal generalization
`for all symptoms, i.e., not a single fi nger, but the
`whole hand is aff ected, and the hand is more
`strongly aff ected than the forearm.
`• Th e joint and soft tissue structures are also aff ect-
`ed, with according mobility impairment.
`• An edema, depending on position and physi-
`cal activity, usually occurs, especially in the early
`stages of the disease.
`Sensory impairment: Spontaneous pain and hy-
`peralgesia in the hand or foot, which is not restricted to
`the supply area of a single peripheral nerve, are main
`characteristics of the clinical pattern of CRPS. Th e pain
`is described as burning and is felt in the deep tissues;
`additionally, sudden pain attacks, described like electri-
`cal shocks, are often present. A periarticular pressure
`pain of the fi nger joints is almost always present. As a
`rule, strong hypersensitivity to mild painful stimuli (hy-
`peralgesia) or pain following usually nonpainful stimuli
`(allodynia) can be observed.
`Motor impairment: In 90% of all cases, the vol-
`untary motor function of all distal muscles is impaired.
`Complex movements, such as fi st closure or fi nger-
`thumb opposition, are restricted. Th ese movements are
`only possible under visual control. Approximately 50%
`of patients with involvement of the upper limb develop
`a tremor; dystonia or spasticity is seldom found.
`Autonomic impairment: Skin temperature dif-
`ferences of more than 2°C between the aff ected and
`the unaff ected extremity are often present (the aff ected
`side is warmer in about 75% of cases), and they corre-
`spond to an altered skin blood fl ow. About 60% of pa-
`tients have hyperhidrosis, and 20% have hypohidrosis.
`In the early stages, hair and nail growth on the aff ected
`extremity is often increased, in the further course of the
`disease it is often decreased. Dystrophic symptoms (i.e.,
`
`

`

`252
`skin and muscle atrophy, connective tissue fi brosis) are
`typical for the later stages of the disease; however, they
`are not always found.
`What are the diagnostic
`criteria for CRPS?
`CRPS is a clinical diagnosis. Th ere are no laboratory
`parameters that confi rm the presence or absence of the
`disease. Patchy demineralization especially in the peri-
`articular regions appears in the radiography some weeks
`or months after the disease begins, but it can be seen in
`less than 50% of patients with CRPS. CT and MRI ex-
`aminations are not specifi c for the diagnosis of CRPS.
`However, triple-phase bone scintigraphy plays an im-
`portant role for the diagnosis of CRPS during the fi rst
`year after trauma. Band-shaped increased radionuclide
`accumulation in the metacarpophalangeal and interpha-
`langeal joints of the aff ected extremity during the min-
`eralization phase is a very specifi c diagnostic criterion.
`Th e current diagnostic criteria are listed below
`according to Harden and Bruehl [3]. Aside from diff er-
`entiation between sensory, vasomotor, sudomotor, and
`motor impairment, the physician should discriminate
`between anamnestic hints (symptoms) and current clin-
`ical signs during the physical examination.
`
`Andreas Schwarzer and Christoph Maier
`What is the diff erential
`diagnosis for CRPS?
`In the clinical routine, it is most essential to diff erenti-
`ate between CRPS and a delayed healing of a trauma
`or complaints after long-term immobilization. In the
`case of CRPS, not only an increase in pain intensity,
`but also a change in the characteristics of pain usually
`occurs. Diff erential diagnosis is nerve or plexus injury,
`especially after an operation to treat nerve entrapment
`syndromes (carpal tunnel syndrome). However, in these
`cases, the symptoms are limited to the area supplied
`by the injured nerve. Autonomic impairment does not
`prove the diagnosis of CRPS. Furthermore, self-injuri-
`ous behavior is another diff erential diagnosis to CRPS.
`What are the treatment
`options for CRPS?
`Th e treatment of CRPS should be based on a multidisci-
`plinary approach. Next to pain treatment, the recovery
`of limb function should play an important role.
`Pharmacological options: Traditional NSAIDs
`(ibuprofen 3 × 600 mg) or COX-2 inhibitors (celecox-
`ib 2 × 200 mg) can be taken temporarily for treatment
`of CRPS pain. Additionally, metamizol (4 × 1000 mg)
`
`1
`2
`2.1
`2.2
`
`3
`
`3.1
`3.2
`
`Sudomotor/edema
`2.3
`2.4 Motor/trophic
`
`Table 1
`Diagnostic criteria for CRPS (according to Harden and Bruehl [3])
`Persistent pain, which is disproportionate to any known inciting event
`Th e patient must report at least one symptom in three of the following categories (anamnestic hints):
`Sensory
`Reports of hyperesthesia and/or allodynia
`Vasomotor
`Reports of temperature asymmetry and/or skin color changes and/or skin
`color asymmetry
`Reports of edema and/or sweating changes and/or sweating asymmetry
`Reports of decreased range of motion and/or motor dysfunction (weakness,
`tremor, dystonia) and/or trophic changes (hair, nails, skin)
`Th e patient must display at least one sign in two or more of the following categories during the current
`physical examination:
`Sensory
`Vasomotor
`
`Evidence of hyperesthesia and/or allodynia
`Evidence of temperature asymmetry and/or skin color changes and/or skin
`color asymmetry
`Evidence of edema and/or sweating changes and/or sweating asymmetry
`Evidence of decreased range of motion and/or motor dysfunction (weakness,
`tremor, dystonia) and/or trophic changes (hair, nails, skin)
`Th ere is no other diagnosis that would otherwise account for the signs and symptoms and the degree of
`pain and dysfunction.
`
`Sudomotor/edema
`3.3
`3.4 Motor/trophic
`
`4
`
`

`

`Complex Regional Pain Syndrome
`and opioids (controlled-release) can be prescribed. Th e
`most important adjuvants for the treatment of neuro-
`pathic pain are tricyclic antidepressants (amitriptyline)
`and anticonvulsive drugs (gabapentin). After taking into
`consideration their possible contraindications and their
`anticholinergic eff ects, the physician should increase
`the dose slowly. Furthermore, the dose should be high
`enough before its effi cacy is evaluated. Th e dose of ami-
`triptyline should be initially 25 mg in the evening (alter-
`natively 10 mg). Th e dose can be increased every seven
`days in 25-mg steps up to a maximal dose of 75 mg. Th e
`starting dose of gabapentin is 3 × 100 mg, and the dose
`should be increased in 300-mg steps every three days.
`A dose of at least 1800 mg/d should be achieved. Espe-
`cially in cases of arthrogenic pain (particularly during
`physical examination), oral glucocorticoids are indicat-
`ed (prednisolone in decreasing doses of 90/60/30/10/5
`mg for 14 days).
`Invasive therapies: Th e sympathetic nervous
`system can be blocked either by unilateral anesthetic
`blockades of the lower cervical sympathetic ganglion
`(stellate ganglion) (10–15 mL bupivacaine 0,5%) or by
`blocks of the lumbar or thoracic sympathetic chain (5
`mL bupivacaine 0.5%). Intravenous regional anesthe-
`sia blocks are seldom performed because of poor eff ect
`and painful procedures. Th e indication for a sympa-
`thetic block is pain at rest despite immobilization and/
`or pronounced allodynia. Sympathetic blocks not only
`reduce the pain, but can often also improve the motor
`and autonomic impairment. However, it is important to
`prove that the sympatholysis was technically successful
`by noting a signifi cant skin temperature increase in the
`supplying area.
`Nonpharmacological options: As long as pain
`at rest prevails, therapy should be restricted to consis-
`tent immobilization of the aff ected extremity in a po-
`sition higher than the heart, supported by a splint and
`by lymphatic drainage. After a distinct decrease of the
`pain, physical and occupational therapy come to the
`fore. Initially, the proximal joints of the aff ected and the
`contralateral extremity should be treated. Especially in
`cases of sensory impairment and allodynia, desensitiza-
`tion exercises are indicated. Th e main treatment prin-
`ciple should start with stimulus adaptation, followed by
`exercises aiming at pain-free mobility and improvement
`of fi ne motor skills, and ultimately movements against
`strong resistance.
`Th erapy for CRPS, with regard to the use of medi-
`cal and nonmedical treatment, does not require any
`
`253
`particular setting and meets the standards of a com-
`munity or primary care level. Th e application of nerve
`block techniques should be reserved for specialized pain
`management centers (“referral hospital level”). Th e ad-
`vantage of treatment in specialized pain management
`centers is, besides the reliability of making the diagnosis
`of CRPS and the use of sympathetic blocks, the greater
`experience in dosing the physical and the occupational
`treatment—fi nally, it is perhaps the most essential issue
`for the function recovery of the aff ected extremity.
`What are today’s insights about
`the pathophysiology of CRPS?
`Currently, there is no global pathophysiological concept
`that explains all the symptoms in CRPS. Th ere are sev-
`eral possible explanations. Next to hints for a genetic
`predisposition, infl ammation seems to play an impor-
`tant role. In the context of a neurogenic infl ammation,
`C fi bers and some receptors may release neuropeptides,
`inducing clinical signs such as vasodilatation and ede-
`ma. Additionally, experts are discussing the concept of a
`disease of the central nervous system, in which changes
`of the aff erent neurons, such as pathological connec-
`tions with the sympathetic nervous system, may cause
`spontaneous and evoked pain. Th e pattern of symptom
`spread resembles that of diseases of the central nervous
`system. Th e central nervous dysregulation is assumed
`to result in maladaptation, for example a change in the
`ambient temperature induces an inadequate reaction of
`skin blood fl ow and sudomotor function. Furthermore,
`cortical reorganization processes seem to play an im-
`portant role, wherein the degree of the reorganization
`correlates positively with the spread of the mechanical
`hyperalgesia and the pain, which in turn is reversible us-
`ing the appropriate treatment.
`Pearls of wisdom
`• Th ree important aspects account for the diag-
`nosis of CRPS: pain or functional impairment,
`which is disproportionate to the inciting event;
`hints of sensory, vasomotor, sudomotor, or motor
`impairment in the past; and current fi ndings of
`sensory, vasomotor, sudomotor, or motor impair-
`ment in the clinical examination
`• Th e treatment must not induce pain. If a treat-
`ment procedure leads to escalation of pain, this
`procedure must be given up. Th e following three
`
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`254
`
`therapeutic steps should be followed: fi rst, treat-
`ment of the pain and edema; second, treatment
`of the pain, allowing movement; and third, treat-
`ment of the functional orthopedic impairment.
`• Th e intensity of physiotherapy must be reduced if
`pain increases again or after a new physical trau-
`ma.
`References
`
`[1] Baron R, Schattschneider J, Binder A, Siebrecht D, Wasner G. Relation
`between sympathetic vasoconstrictor activity and pain and hyperalge-
`sia in complex regional pain syndromes: a case-control study. Lancet
`2002;359:1655–60.
`[2] Birklein F, Schmelz M. Neuropeptide, neurogenic infl ammation and
`complex regional pain syndrome (CRPS). Neurosci Lett 2008;437:199–
`202.
`[3] Harden RN, Bruehl S. Diagnostic criteria: the statistical derivation of
`the four criterion factors. In: Wilson PR, Stanton-Hicks M, Harden RN,
`editors. CRPS: current diagnosis and therapy, Progress in pain research
`and management, vol. 32. Seattle: IASP Press; 2005.
`
`Andreas Schwarzer and Christoph Maier
`[4] Maihöfner C, Handwerker HO, Neundörfer B, Birklein F. Patterns of
`cortical reorganisation in complex regional pain syndrome. Neurology
`2003;61:1707–15.
`[5] Moseley GL. Graded motor imagery for pathologic pain: a randomized
`controlled trial. Neurology 2006;67: 2129–34.
`[6] Nelson DV, Brett RS. Interventional therapies in the management of
`complex regional pain syndrome. Clin J Pain 2006;22:438–42.
`[7] Pleger B, Ragert P, Schwenkreis P, Förster AF, Wilimzig C, Dinse H,
`Nicolas V, Maier C, Tegenthoff M. Patterns of cortical reorganization
`parallel impaired tactile discrimination and pain intensity in complex
`regional pain syndrome. Neuroimage 2006;32:503–10.
`[8] Rowbotham MC. Pharmacological management of complex regional
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`
`Websites
`
`http://www.mayoclinic.com/health/complex-regional-pain-syndrome/
`DS00265
`http://www.iasp-pain.org/AM/Template.cfm?Section=WHO2&Template=/
`CM/ContentDisplay.cfm&ContentID=4174
`
`