Fwd: [RSD-WorldNews] Complex Regional Pain Syndrome I in the Upper Extremity

December 16, 2004

Report

Complex Regional Pain Syndrome I in the Upper Extremity

J Mazzola MD, Sourav K Poddar MD and C Hill DO

Current Sports Medicine Reports 2004, 3:261-266

Outline Abstract

Abstract

Introduction

Classification of Regional Pain Syndromes

Causes

Diagnosis

Laboratory and Radiographic Evaluation

Autonomic Testing

Differential Diagnosis

Treatment

Conclusions

References

Complex regional pain syndrome (CRPS) I, formerly known as reflex

sympathetic dystrophy (RSD), is a painful neuropathic condition that

most commonly affects a traumatized extremity. It is characterized by

pain that is out of proportion to the original injury, has a distal

predominance, and is not attributable to a specific peripheral nerve

injury. The name RSD has been changed to CRPS I reflecting the fact

that although sympathetic dysfunction can maintain the painful state,

it is not the essential pathophysiologic lesion. Successful treatment

hinges on early recognition of suspected cases, prompt referral to

pain specialists, and ultimately pain control and return of limb

function. Treatments range from noninvasive medications and therapies

to sympathetic ganglion blockade and sympathectomy. The sports

medicine physician is in an ideal position to recognize CRPS I in its

earliest stages postinjury, and is advised to make prompt referral to

a pain specialist when suspected.

Historically, complex regional pain syndrome (CRPS) I has been

described by a number of physicians since the Civil War as a painful

condition with unusual vasomotor (vascular-related) and sudomotor

(sweat-related) features. CRPS I has had many names through the years,

validating its complex nature and highlighting our incomplete

understanding of its etiology. Disuse of the affected limb is

responsible for a large component of the vasomotor and sudomotor

problems that arise in later stages of the disease if left untreated.

Although the body of epidemiologic studies on CRPS I is incomplete, we

can look to Olmsted County, MN for some help. Sandroni et al. [1]

found 74 cases in their population of 106,470 in 1990, resulting in an

incidence rate of 5.46 per 100,000 person-years at risk and a period

prevalence of 20.57 per 100,000.

Another report performed in an American tertiary pain clinic revealed

the following: CRPS I patients had seen an average of 4.8 physicians

prior to pain clinic referral, and received five types of treatments

prior to and during pain clinic treatment [2]. A total of 17% of

patients had a lawsuit underway and 54% had a workman's compensation

claim ongoing; 47 had the affected limb immobilized by their

physician, and 56% had myofascial dysfunction at the time of

evaluation. Although 51% of patients had received a bone scan, only

53% of those were interpreted as consistent with CRPS I/ reflex

sympathetic dystrophy (RSD) [2]. Lastly, symptoms had persisted a mean

of 30 months prior to pain clinic evaluation. Considering these

alarming statistics and recognizing that early treatment fosters

better outcomes, we propose that sports medicine physicians can

improve patient outcomes with heightened awareness, recognition, and

early referral of suspected cases.

Although the specific cause for CRPS I remains elusive, many

observations implicate central nervous system dysfunction and

peripheral inflammation. Almost universally some sort of trauma will

predate the onset of CRPS I, yet clearly most traumas do not lead to

CRPS I. Some researchers have found decreased perfusion, release, and

turnover of norepinephrine in the affected limb, implicating central

and autonomic nervous system involvement [6]. Others have discovered

markers consistent with an exaggerated regional or neurogenic

inflammatory response, perhaps facilitated by genetic predisposition

[7,8]. Lastly, it appears that individuals with chronic CRPS I have

altered central motor and sensorimotor processing [9,10]. Although

observed in patients with chronic symptoms, the idea that central

processing alterations are involved in CRPS I is a novel one. In a

recent expert review, Stanton-Hicks [11] states plainly that CRPS is a

'neurologic disease involving the brain at several integrated levels.'

More recent studies illustrate sympathetic nervous system involvement.

An interesting prospective study on patients with distal radius

fractures looked for abnormalities in sympathetic dysfunction

post-trauma [12]. Four of 27 patients went on to develop CRPS I,

whereas two others were labeled as 'borderline.' Astoundingly, in CRPS

I and borderline patients, the sympathetic vasoconstrictor response

was diminished or absent from post-traumatic day 1 throughout the

entire study. By contrast, in non-CRPS patients, sympathetic function

was only minimally abnormal on post-traumatic day 1, but completely

normalized thereafter. Interestingly, CRPS I patients showed impaired

sympathetic function in the uninjured contralateral limb as well.

Birklein et al. [13] found impaired sympathetic vasoconstrictor

reflexes and hyperhidrosis in CRPS I patients that was not seen in

non-CRPS postsurgical patients. Haensch et al. [14] demonstrated

abnormal peripheral sympathetic function in two patients with CRPS I

by a regional decrease in I-123-metaiodobenzyl-guanidine (MIBG) uptake

via scintigraphic imaging. MIBG visualizes and quantifies sympathetic

innervation in vivo and quantifies adrenergic neurodensity and

function. They concluded that partial sympathetic denervation might

contribute to the pathogenic process in CRPS I.

In addition to potential causes, various risk factors have been

identified that increase the risk for developing CRPS I. Clearly,

individuals who have had CRPS I in the past are predisposed to

recurrent episodes. Likewise, trauma and surgery are well-described

risk factors for CRPS I. Stressful life events and psychologic

dysfunction are considered risk factors as well. One of the

highest-quality studies done in this area revealed significant

differences between CRPS I and control patients in stressful life

events (79.2% and 21.4%, respectively). In this same study, men with

CRPS I showed increased anxiety, whereas women showed more depression,

feelings of inadequacy, and emotional instability when compared with

matched controls. Taken together, this study lends support to the

multiconditional model for development of CRPS I [15].

Associated Conditions

Although rare, in a disturbing set of case reports, 22 cases of CRPS

I/RSD were related to various cancers; 12 of these individuals had no

prior noxious event or period of immobilization. Of cancer-related

CRPS I, most cases involved the upper extremity (often bilaterally)

and were most closely associated with ovarian malignancies 16].

Similarly, a small number of case reports of CRPS I after myocardial

infarction and stroke dot the literature.

There is also good evidence that CRPS I can spread, albeit

infrequently, in at least three distinct patterns [17]. The most

common pattern is contiguous spread, usually from distal to proximal

in the affected limb. Other forms of spread include independent spread

and mirror-image spread. Contiguous spread usually occurs after days

to months, whereas independent and mirror-image spread typically occur

months to years after diagnosis.

Although the IASP has not reached consensus on a comprehensive list of

CRPS I signs and symptoms (due to variability in clinical

presentations), et al. [18] have compiled a list of those most

commonly seen (1). It is worth repeating that sympathetic nervous

system involvement is not a requirement for the diagnosis of CRPS I,

as had been implied by its old name, RSD. Currently accepted criteria

for the diagnosis of CRPS I and II adapted from the IASP are presented

in 2 [4,19].

Earlier diagnostic criteria presented by Veldman et al. [20] based on

his study of 829 patients with RSD are as follows: 1) four of the five

following symptoms are present: pain, altered skin color, altered skin

temperature, edema, or reduced range of motion; 2) the symptoms are

present in an area much larger than and distal to the primary injury;

and 3) the symptoms are aggravated by activity of the extremity

A more recent study of 135 adults with upper extremity CRPS I by

Oerlemans et al.21] attempted to identify objective criteria upon

which to base the diagnosis. Their conclusions validated the

following: 1) pain as measured by the visual analog scale with

exertion and the McGill Pain Questionaire was a consistent finding; 2)

skin temperature differences between the dorsum of the affected and

unaffected hand using an infrared thermometer were significant (mean

0.78°C); others have considered a difference of 0.5C to 0.6°C to be

significant; 3) hand volume differences between the two hands averaged

30.4 mL, which is more than two times the expected normal difference

of 12 mL; and 4) active range of motion differences were noted

especially in the wrist and finger joints, with the ulnar fingers

being affected more than the radial ones.

Unfortunately, there is no specific blood test that is helpful in the

diagnosis of CRPS I. Plain radiographs are not sensitive or specific

for CRPS I, but are certainly indicated in evaluating a painful,

traumatized limb. Importantly, as a result of longstanding CRPS I and

chronic disuse, osteoporosis of the affected limb can be seen on plain

films. The most frequently used radiographic study in CRPS I has been

three-phase bone scintigraphy (TPBS). Although some retrospective

studies have shown utility of TPBS in confirming the diagnosis of RSD,

criticisms include sampling error, lack of controls, and variability

of TPBS interpretation between radiologists. Sensitivity and

specificity have varied widely; however, it appears that TPBS is most

useful when performed within the first 20 to 26 weeks of onset 22].

Nonetheless, TPBS is not required to diagnose CRPS I.

Autonomic Testing

A number of autonomic tests have been described, yet none have been

adopted as necessary to making the diagnosis of CRPS I. The

sympathetic nervous system has been examined by measuring skin

temperature via infrared thermography [13,23,24]. Sudomotor (sweat)

function has been assessed by resting sweat output and the

quantitative sudomotor axon reflex test (QSART) [11,24]. Sympathetic

vasoconstrictor reflexes have been evaluated by laser-Doppler

flowmetry of the fingertips, measuring peripheral vascular

responsiveness to sympathetic stimuli [12,13]. Lastly, scintigraphy

with MIBG uptake has revealed reductions in perfusion and MIBG uptake

in the affected limb [14]. Although these tests can help provide

objective data when considering CRPS I diagnosis, the equipment is

very specialized and only found in a few specialty clinics. CRPS I

diagnosis remains a clinical one in the hands of an experienced clinician.

Differential Diagnosis

As CRPS I is in part a neuropathic process, the differential diagnosis

must include other causes of neuropathic pain. The disease most

closely related to CRPS I is CRPS II, as discussed above. Albeit

extraordinarily rare, ovarian malignancy should be considered in the

female CRPS I patient without trauma, especially if symptoms are

bilateral. Finally, other potential causes of extremity pain must be

ruled out; specifically vascular, neurologic, orthopedic, immunologic,

rheumatologic, and metabolic diseases.

Treatment options for CRPS I

Given the range of pathophysiologic variables involved, CRPS I remains

a difficult disease to cure. This much is certain: to restore function

to the affected limb, it is imperative to first procure pain relief.

Treatment should begin as soon as possible as the rate of successful

treatment increases dramatically if initiated within 3 months of

symptom onset. Many therapies can be used and a multidisciplinary

approach is most likely to be successful (3).

Noninvasive

Noninvasive treatment options for CRPS I include medications, physical

therapy (PT), occupational therapy (OT), and other modalities.

Individualization of pharmacologic treatment is essential, weighing

the risks and benefits for each patient.

Perhaps the most common pain-relieving medications in use today are

nonsteroidal anti-inflammatory drugs. Despite their breadth of use, in

the setting of CRPS I they have a limited effect. They should be

considered mainly in an adjunctive role with other treatments.

Tricyclic antidepressants have been shown to be effective in treating

neuropathic pain. The best-studied of these is amitriptyline which has

a therapeutic window at doses ranging from 10 to 150 mgd. It should be

noted that these doses are typically subtherapeutic for an

antidepressant effect and it can take patients 1 to 2 weeks to note a

reduction in pain.

Most pain specialists include opioids as part of a comprehensive

treatment plan for CRPS I despite a paucity of evidence. Because

effective pain relief is essential to successful treatment, the early

use of oral opioids is indicated for most patients, particularly if

other agents have failed to adequately control pain.

Unlike opioids, controlled studies for the role of glucocorticoids do

exist and show beneficial analgesic effects in the management of CRPS

I [25]. No other immunosuppressive agents, however, have shown similar

benefits.

The benefits of bisphosphonates and calcitonin have varied.

Intravenous bisphosphonates have shown improvements in pain, swelling,

and motion of affected extremities [26,27]. Calcitonin given

subcutaneously has shown fleeting effects in pain control in CRPS I [28].

Finally, gabapentin certainly has a role in managing neuropathic pain.

In the setting of CRPS I, data are limited but encouraging [8]. Also,

intrathecal baclofen has been shown to help with the dystonia of late

CRPS I [29].

In addition to pharmacotherapy, the benefits of PT and OT have been

well documented. Oerlemans et al. [30,31] demonstrated that PT and OT

instituted within the first year in patients with CRPS I helped to

reduce pain and improve mobility in the affected limb. Importantly,

active therapy can actually increase pain and disability if instituted

prior to adequate pain management in acute CRPS I. At the same time,

it is generally accepted that many of the late effects of CRPS I can

be avoided if motion is regained in the affected extremity. Although

pain-free motion is ultimately critical to successful treatment, some

have asserted that initial PT/OT should be focused on immobilization

and mirror visual feedback [32]. After better pain relief is achieved,

passive therapy is gradually advanced to isometric and isotonic work

[8], often in concert with a sensory desensitization program.

Free radical scavengers have been effective as part of a treatment

strategy, based on the concept that CRPS I exhibits features of an

exaggerated inflammatory response. More commonly utilized in Europe,

these free radical scavengers include dimethylsulfoxide and

N-acetylcysteine [33].

Invasive

Interventional techniques offer great potential in treating CRPS I. In

concert with the historic belief that the essential lesion was

sympathetic nervous system dysfunction, sympathetic blockade has

traditionally been considered the principal form of treatment. Its

benefit is most predictable in cases where sympathetic signs and

symptoms predominate. When used appropriately and early this modality

may provide complete resolution of symptoms.

Two main techniques are currently used to achieve sympathetic

blockade. The first method involves ipsilateral stellate ganglion

blockade (SGB) with local anesthetic. The length of treatment

typically involves daily blockade for days to weeks. Additional

benefit has been shown with concomitant administration of the oral

tricyclic antidepressant amitriptyline [34]. In addition, patients

with a prior history of CRPS I undergoing surgery of an extremity

showed a lower rate of recurrence when undergoing perioperative SGB [35].

The second method entails intravenous regional sympathetic blockade

(IRSB) of the affected extremity that is blocked with a tourniquet.

Agents investigated include bretylium, guanethidine, and reserpine.

Although isolated studies have shown benefit of IRSB, it cannot be

recommended as the balance of studies and a systematic review suggest

no significant differences between placebo and IRSB [28,36].

Thorascopic sympathectomy has also been shown to have a role in

treatment [37,38]. Classically, this has been performed in patients

who demonstrate at least some response to stellate ganglion blockade.

Singh et al. [37] showed, however, that good or excellent outcomes

could be achieved even in patients who did not respond to SGB. The

main predictor of successful response to surgical sympathectomy was

whether the procedure was performed early (within 3 months). Patients

in a later stage of CRPS I showed a lower rate of good to excellent

results [37].

More recently, an encouraging approach has been validated; namely,

continuous sensory analgesia by regional block of the affected limb.

When used in conjunction with active painless exercise, as a form of

limb desensitization, results of initial studies are promising. One

showed significant improvement in pain and grip strength in 17 of 17

patients 39], whereas the second demonstrated good to excellent

results in 13 of 16 or 81% of patients treated with this modality [40].

New treatments under investigation provide hope for a more definitive

approach to CRPS I. From a pharmacotherapeutic standpoint, medications

that block the N-methyl-D-aspartate receptor, such as ketamine,

dextromethorphane, and memantine, have shown potential in early

studies. Small studies involving irradiation of the stellate ganglion

also show promise [41]. Spinal cord stimulation may have a role for

patients with comorbidities that limit other treatment options [42].

Finally, peripheral nerve and even brain (thalamus and medial

lemniscus) stimulation techniques have been effective in other cases [43].

Conclusions

Complex regional pain syndrome I remains an unusual cause of upper

extremity pain, but is distinguished by its unique constellation of

symptoms and signs in the absence of a specific nerve injury. Pain out

of proportion to the inciting injury, edema, and vasomotor and

sudomotor changes are the principal diagnostic clues. Because clinical

diagnosis and treatment initiation is best handled by a pain

specialist, prompt referral is indicated when suspected. Treatments

are many and include pharmacotherapy as well as regional and stellate

blocks. Timely treatment is critical to achieving ultimately

successful outcomes.

Papers of particular interest have been highlighted as:

• of special interest

•• of outstanding interest

1. Sandroni P, Benrud-Larson LM, McClelland RL: Complex regional

pain syndrome type I: incidence and prevalence in Olmsted County, a

population-based study.

Pain 2003, 103:199-207. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

2. G, Galer BS, Schwartz L: Epidemiology of complex regional

pain syndrome: a retrospective chart review of 134 patients.

Pain 1999, 80:530-544. [Publisher Full Text] OpenURL

Return to citation in text: [1] [2]

3. Soucacos PN, Diznitsas LA, Beris AE: Reflex sympathetic

dystrophy of the upper extremity. Clinical features and response to

multimodal management.

Hand Clin 1997, 13:339-354. [PubMed Abstract] OpenURL

Return to citation in text: [1]

4. Stanton-Hicks M, Janig W, Hassenbusch S: Reflex sympathetic

dystrophy: changing concepts and taxonomy.

Pain 1995, 63:127-133. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1] [2]

5. Verdugo RJ, Campero M, Ochoa JL: Phentolamine sympathetic block

in painful polyneuropathies. Further questioning of the concept of

'sympathetically maintained pain.

' Neurology 1994, 44:1010-1014. OpenURL

Return to citation in text: [1]

6. Drummond PD, Finch PM, Smythe GA: Reflex sympathetic dystrophy:

the significance of differing plasma catecholamine concentrations in

affected and unaffected limbs.

Brain 1991, 114:2025-2036. [PubMed Abstract] OpenURL

Return to citation in text: [1]

7. Vanderlaan L, Goris RJA: Reflex sympathetic dystrophy, an

exaggerated inflammatory response?

Hand Clin 1997, 13(3):373-384. OpenURL

Return to citation in text: [1]

8. Wasner G, Schattschneider J, Binder A: Complex regional pain

syndrome-diagnostic, mechanisms, CNS involvement and therapy.

Spinal Cord 2003, 41:61-75. [PubMed Abstract][Publisher Full Text] OpenURL

• An exhaustive review of the current CRPS literature with 170

references. Includes a particularly good breakdown of pathophysiologic

mechanisms.

Return to citation in text: [1] [2] [3]

9. Ribbers GM, Mulder T, Geurts AC: Reflex sympathetic dystrophy

of the left hand and motor impairments of the unaffected right hand:

impaired central motor processing?

Arch Phys Med Rehabil 2002, 83:81-85. [PubMed Abstract][Publisher Full

Text] OpenURL

Return to citation in text: [1]

10. Juottonen K, Gockel M, Silen T: Altered central sensorimotor

processing in patients with complex regional pain syndrome.

Pain 2002, 98:315-323. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

11. Stanton-Hicks M: Complex regional pain syndrome.

Anesthesiol Clin N Am 2003, 21:733-744. OpenURL

•• The most up to date comprehensive review by one of the true

leaders in the field of CRPS.

Return to citation in text: [1] [2]

12. Schurman M, Gradl G, Zaspel J: Peripheral sympathetic function

as a predictor of complex regional pain syndrome type I (CRPS I) in

patients with radial fracture.

Auton Neurosci 2000, 86:127-134. [PubMed Abstract][Publisher Full

Text] OpenURL

• The only prospective study found demonstrating measurable

sympathetic dysfunction from the earliest stages post trauma. Suggests

a possible genetic predisposition for patients who develop CRPS I.

Return to citation in text: [1] [2]

13. Birklein F, Kunzel W, Sieweke N: Despite clinical similarities

there are significant differences between acute limb trauma and

complex regional pain syndrome I (CRPS I).

Pain 2001, 93:165-171. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1] [2] [3]

14. Haensch CA, Jorg J, Hartmut L: I-123-metaiodobenzyl-guanidine

uptake of the forearm shows dysfunction in peripheral sympathetic

mediated neurovascular transmission in complex regional pain syndrome

(CRPS I).

J Neurol 2002, 249:1742-1743. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1] [2]

15. Geertzen JHB, de Bruijn-Kofman AT, de Bruijn HP: Stressful

life events and psychological dysfunction in complex regional pain

syndrome type I.

Clinical Journal of Pain 1998, 14:143-147. [PubMed Abstract][Publisher

Full Text] OpenURL

Return to citation in text: [1]

16. Mekhail N, Kapural L: Complex regional pain syndrome type I in

cancer patients.

Curr Rev Pain 2000, 4:227-233. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1]

17. Maleki J, LeBel AA, GJ: Patterns of spread in CRPS I.

Pain 2000, 88:259-266. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

18. PR, Low PA, Bedder MD: Diagnostic algorithm for complex

regional pain syndromes.

In Reflex Sympathetic Dystrophy: A Reappraisal (Progress in Pain

Research and Managaement vol 6). Edited by: Edited by Janig W

Stanton-Hicks M. IASPPress (Seattle); 1996:93-105. OpenURL

Return to citation in text: [1]

19. Wong GY, PR: Classification of complex regional pain

syndromes-new concepts.

Hand Clin 1997, 13:319-325. [PubMed Abstract] OpenURL

Return to citation in text: [1]

20. Veldman PHJM, Reynen HM, Arntz IE: Signs and symptoms of

reflex sympathetic dystrophy: prospective study of 829 patients.

Lancet 1993, 342:1012-1016. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

21. Oerlemans HM, Oostendorp RAB, de Boo T: Signs and symptoms in

complex regional pain syndrome type I/reflex sympathetic dystrophy:

judgment of the physician versus objective measurement.

Clin J Pain 1999, 15:224-232. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1] [2]

22. Lee GW, Weeks PM: The role of bone scintigraphy in diagnosing

reflex sympathetic dystrophy.

J Hand Surg 1995, 20A:458-463. OpenURL

Return to citation in text: [1]

23. Gulevich SJ, Conwell TD, Lane J: Stress infrared

telethermography is useful in the diagnosis of complex regional pain

syndrome, type I (formerly reflex sympathetic dystrophy).

Clin J Pain 1997, 13:50-59. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

24. Chelimsky TC, Low PA, Naessens JM: Value of autonomic testing

in reflex sympathetic dystrophy.

Mayo Clin Proc 1995, 70:1029-1040. [PubMed Abstract] OpenURL

Return to citation in text: [1] [2]

25. Christensen K, Jensen EM, Noer I: The reflex sympathetic

dystrophy syndrome response to treatment with systemic corticosteroids.

Acta Chir Scand 1982, 148:653-655. [PubMed Abstract] OpenURL

Return to citation in text: [1]

26. Adami S, Fossaluzza V, Gatti D: Bisphosphonate therapy of

reflexsympathetic dystrophy syndrome.

Ann Rheum Dis 1997, 56:201-204. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1]

27. Varenna M, Zucchi F, Ghiringhelli D: Intravenous clodronate in

the treatment of reflex sympathetic dystrophy syndrome. A randomized,

double blind, placebo controlled study.

J Rheumatol 2000, 27:1477-1483. [PubMed Abstract] OpenURL

Return to citation in text: [1]

28. RSGM, Kwakkel G, Wouter WA: Treatment of reflex

sympathetic dystrophy (CRPS I): a research synthesis of 21 randomized

clinical trials.

J Pain Symptom Manage 2001, 21:511-526. [PubMed Abstract][Publisher

Full Text] OpenURL

•• A particularly excellent evidence-based review of CRPS I

treatments as of 2001. Includes an excellent table that reviews all

cited studies in a simple format.

Return to citation in text: [1] [2]

29. van Hilten BJ, van de Beek WJT, Hoff JI: Intrathecal baclofen

for the treatment of dystonia in patients with reflex sympathetic

dystrophy.

N Engl J Med 2000, 343:625-630. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1]

30. Oerlemans HM, Goris JA, deBoo T: Do physical therapy and

occupational therapy reduce the impairment percentage in reflex

sympathetic dystrophy?

Am J Phys Med Rehabil 1999, 78:533-539. [PubMed Abstract][Publisher

Full Text] OpenURL

Return to citation in text: [1]

31. Oerlemans HM, Oostendorp RAB, de Boo T: Pain and reduced

mobility in complex regional pain syndrome I: outcome of a prospective

randomised controlled clinical trial of adjuvant physical therapy

versus occupational therapy.

Pain 1999, 83:77-83. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

32. McCabe CS, Haigh RC, Ring EFJ: A controlled pilot study of the

utility of mirror visual feedback in the treatment of complex regional

pain syndrome (type I).

Rheumatology 2003, 42:97-101. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1]

33. RSGM, Zuurmond WWA, Bezemer PD: The treatment of complex

regional pain syndrome type I with free radical scavengers: a

randomized controlled study.

Pain 2003, 102:297-307. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

34. Karakurum G, Pirbudak L, Oner U: Sympathetic blockade and

amitriptyline in the treatment of reflex sympathetic dystrophy.

Int J Clin Pract 2003, 57:585-587. [PubMed Abstract] OpenURL

Return to citation in text: [1]

35. Reuben SS, Rosenthal EA, Steinberg RB: Surgery on the affected

upper extremity of patients with a history of complex regional pain

syndrome: a retrospective study of 100 patients.

J Hand Surg 2000, 25A:1147-1151. OpenURL

Return to citation in text: [1]

36. Jadad AJ, Caroll D, Glynn CJ: Intravenous regional sympathetic

blockade for pain relief in reflex sympathetic dystrophy: a systematic

review and a randomized, double-blind crossover study.

J Pain Symptom Manage 1995, 10:13-20. [PubMed Abstract][Publisher Full

Text] OpenURL

Return to citation in text: [1]

37. Singh B, Moodley J, Shaik AS: Sympathectomy for complex

regional pain syndrome.

J Vasc Surg 2003, 37:508-511. [PubMed Abstract][Publisher Full Text]

OpenURL

Return to citation in text: [1] [2] [3]

38. Krasna MJ, Jiao X, Sonett J: Thorascopic sympathectomy.

Surg Lap Endo Perc Tech 2000, 10:314-318. [Publisher Full Text] OpenURL

Return to citation in text: [1]

39. Azad SC, Beyer A, Romer AW: Continuous axillary brachial

plexus analgesia with low dose morphine in patients with complex

regional pain syndromes.

Eur J Anaesth 2000, 17:185-188. [Publisher Full Text] OpenURL

Return to citation in text: [1]

40. Marjic K, Pirc J: The treatment of complex regional pain

syndrome (CRPS) involving upper extremity with continuous sensory

analgesia.

Eur J Pain 2003, 7:43-47. [PubMed Abstract][Publisher Full Text] OpenURL

Return to citation in text: [1]

41. Basford JR, Sandroni P, Low PA: Effects of linearly polarized

0.6-1.6 M irradiation on stellate ganglion function in normal subjects

and people with complex regional pain (CRPS I).

Las Surg Med 2003, 32:417-423. [Publisher Full Text] OpenURL

Return to citation in text: [1]

42. Ahmed SU: Complex regional pain syndrome type I after

myocardial infarction treated with spinal cord stimulation.

Reg Anesth Pain Med 2003, 28:245-247. [PubMed Abstract][Publisher Full

Text] OpenURL

Return to citation in text: [1]

43. Hassenbusch SJ: Long-term results of peripheral nerve

stimulation for reflex sympathetic dystrophy.

J Neurosurg 1996, 84:415-423. [PubMed Abstract] OpenURL

Return to citation in text: [1]

December 16, 2004