Complex Regional Pain Syndrome Type 1 (Reflex Sympathetic Dystrophy)

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Complex Regional Pain Syndrome Type 1 (Reflex Sympathetic Dystrophy)

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Type 1 complex regional pain syndrome (CRPS 1), formerly known as reflex sympathetic dystrophy (RSD), is a clinical syndrome of variable course and unknown cause characterized by pain, swelling, and vasomotor dysfunction of an extremity. This condition is often the result of trauma or surgery. Limb immobility may lead to CRPS 1; in a hemiplegic upper limb after stroke, the syndrome is often termed shoulder-hand syndrome. CRPS 1 may also develop in the absence of an identifiable precipitating event.

Current taxonomy categorizes CRPS 1 as occurring in the absence of definable nerve injury. [1] Type 2 CRPS, causalgia, develops after nerve injury; the term causalgia was coined by Mitchell in 1864 and derives from the Greek for burning pain. In patients with either type 1 or type 2 CRPS, sympathetic mediation of the pain (ie, improvement with sympathetic blockade) may or may not be evident.

CRPS 1 is largely a clinical diagnosis (see Presentation and DDx). Two major approaches to the treatment of early CRPS 1 are sympathetic blockade and anti-inflammatory therapy. Surgical sympathectomy may be considered in patients with refractory CRPS 1 that had initially responded to sympathetic blockade. Spinal cord stimulation is another surgical option. (See Treatment and Medication.)

For discussion of all types of CRPS, see Complex Regional Pain Syndromes

The pathogenesis of CRPS 1 is unknown. Three conditions are deemed important in the development of CRPS 1, as follows:

Susceptibility factors are unknown and may include genetic predisposition (HLA typing) [2, 3, 4] and, in some patients, a tendency toward increased sympathetic activity. This includes cold hands, hyperhidrosis, or a history of fainting.

Healthy individuals have a sympathetic response to injury, with vasoconstriction designed to prevent blood loss and swelling. This initial response soon subsides and gives way to vasodilatation and increased capillary permeability, allowing tissue repair.

In patients with CRPS 1, this sympathetic response continues unabated. The reasons for the perpetuation of the response are unknown but may be related to central dysregulation of nociceptive impulses. This dysregulation may be mediated by wide dynamic range neurons in the spinal cord.

Prolonged ischemia caused by the vasoconstriction produces more pain, establishing a reflex arc that promotes further sympathetic discharge and vasospasm. This is compounded by the local response to trauma, with liberation of substantial amounts of proinflammatory mediators, such as histamine, serotonin, and bradykinin.

The result is a swollen, painful, stiff, nonfunctioning extremity. At least partial sympathetic mediation of this phenomenon is likely because of the ability of sympathetic nerve blockade to relieve pain and other features of CRPS 1 in some patients.

Numerous studies have reported altered brain function in CRPS 1. Researchers have also documented structural alterations in the brain. Pleger et al reported that magnetic resonance imaging (MRI) in patients with CRPS 1 showed altered gray matter structure in dorsomedial prefrontal cortex, as well as increases in gray matter density in the motor cortex contralateral to the affected limb, which were inversely related to decreased white matter density of the internal capsule within that brain hemisphere. [5]

A study by Barad that used structural MRI found that compared with controls, patients with complex regional pain syndrome had decreased gray matter volume in several pain-affect regions (including the dorsal insula, left orbitofrontal cortex, and several aspects of the cingulate cortex) and increased gray matter volume in the bilateral dorsal putamen and right hypothalamus. [6]

Lee et al found that the right dorsolateral prefrontal cortex and left ventromedial prefrontal cortex were significantly thinner in patients with CRPS than in healthy controls. In addition, CRPS patients had longer stop-signal task reaction times and made more perseveration errors on the Wisconsin Card Sorting Test. [7]

CRPS 1 is usually posttraumatic or postsurgical; however, it can occur in a previously healthy extremity with no known trigger.

Penetrating wounds that can lead to CRPS 1 include the following:

Lacerations

Abrasions

Venipuncture

Intramuscular injection of medication or illicit drugs

Gunshot wounds

Other traumatic causes of CRPS 1 include the following:

Crush injuries and blunt trauma

Neck or shoulder injuries

Acute traumatic carpal tunnel syndrome

Chest trauma

Sprain, fracture, or dislocation

Postsurgery CRPS 1 has been reported after the following procedures:

Carpal tunnel release

Dental extractions

Cervical rib resection

Fracture repair (Colles fracture)

Arthroscopy

Local disorders associated with CRPS 1 include the following:

Nerve compression syndromes

Arthritis

Tissue ischemia

Stenosing tenosynovitis

Systemic disorders associated with CRPS 1 include the following:

Myocardial infarction

Stroke

Pancoast tumor

Pancreatic cancer

Herpes zoster

In the United States, an estimated 5% of patients who experience trauma to the upper extremity develop CRPS 1, although this figure is not known with certainty because of confusion over the diagnosis. Extremity immobilization can trigger CRPS 1. Without prophylactic measures (active physical therapy), CRPS 1 can develop in 12-20% of people who experience a hemiplegic stroke.

No racial predilection exists for CRPS 1. Sexual distribution is equal. Although CRPS 1 can occur in children, the age of onset in most patients CRPS 1 is 30-60 years, and the mean age is 49 years. [8]

A Scottish study estimated that the incidence of CRPS in children 5-15 years of age is 1.2 per 100,000. Girls constituted 73% of patients. Most cases involed a single site, with legs often affected than arms and the right side more often affected than the left. Clear trauma had occurred at the onset of the illness in most cases. Diagnosis was made a median of 2 months (range, 1-12) after the onset of symptoms. [9]

Stanton-Hicks M, Janig W, Hassenbusch S, et al. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain. 1995 Oct. 63(1):127-33. [Medline].

Kemler MA, van de Vusse AC, van den Berg-Loonen EM, et al. HLA-DQ1 associated with reflex sympathetic dystrophy. Neurology. 1999 Oct 12. 53(6):1350-1. [Medline].

Sebastin SJ. Complex regional pain syndrome. Indian J Plast Surg. 2011 May. 44(2):298-307. [Medline]. [Full Text].

Coderre TJ, Bennett GJ. A hypothesis for the cause of complex regional pain syndrome-type I (reflex sympathetic dystrophy): pain due to deep-tissue microvascular pathology. Pain Med. 2010 Aug. 11(8):1224-38. [Medline].

Pleger B, Draganski B, Schwenkreis P, Lenz M, Nicolas V, Maier C, et al. Complex regional pain syndrome type I affects brain structure in prefrontal and motor cortex. PLoS One. 2014. 9(1):e85372. [Medline]. [Full Text].

Barad MJ, Ueno T, Younger J, Chatterjee N, Mackey S. Complex regional pain syndrome is associated with structural abnormalities in pain-related regions of the human brain. J Pain. 2014 Feb. 15(2):197-203. [Medline].

Lee DH, Lee KJ, Cho KI, Noh EC, Jang JH, Kim YC, et al. Brain alterations and neurocognitive dysfunction in patients with complex regional pain syndrome. J Pain. 2015 Jun. 16 (6):580-6. [Medline].

Goebel A. Complex regional pain syndrome in adults. Rheumatology (Oxford). 2011 Oct. 50(10):1739-50. [Medline].

Abu-Arafeh H, Abu-Arafeh I. Complex regional pain syndrome in children: incidence and clinical characteristics. Arch Dis Child. 2016 Aug. 101 (8):719-23. [Medline].

Harden RN, Oaklander AL, Burton AW, Perez RS, Richardson K, Swan M, et al. Complex regional pain syndrome: practical diagnostic and treatment guidelines, 4th edition. Pain Med. 2013 Feb. 14 (2):180-229. [Medline]. [Full Text].

[Guideline] Royal College of Physicians. Complex regional pain syndrome in adults (2nd edition). Available at https://www.rcplondon.ac.uk/guidelines-policy/complex-regional-pain-syndrome-adults. 2018; Accessed: August 17, 2018.

Won AS, Tataru CA, Cojocaru CM, Krane EJ, Bailenson JN, Niswonger S, et al. Two Virtual Reality Pilot Studies for the Treatment of Pediatric CRPS. Pain Med. 2015 Aug. 16 (8):1644-7. [Medline].

Solcà M, Ronchi R, Bello-Ruiz J, Schmidlin T, Herbelin B, Luthi F, et al. Heartbeat-enhanced immersive virtual reality to treat complex regional pain syndrome. Neurology. 2018 Jul 31. 91 (5):e479-e489. [Medline].

O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome. Cochrane Database Syst Rev. 2013 Apr 30. 4:CD009416. [Medline].

Stanton TR, Wand BM, Carr DB, Birklein F, Wasner GL, O’Connell NE. Local anaesthetic sympathetic blockade for complex regional pain syndrome. Cochrane Database Syst Rev. 2013 Aug 19. 8:CD004598. [Medline].

van Hilten BJ, van de Beek WJ, Hoff JI, et al. Intrathecal baclofen for the treatment of dystonia in patients with reflex sympathetic dystrophy. N Engl J Med. 2000 Aug 31. 343(9):625-30. [Medline].

Gobelet C, Waldburger M, Meier JL. The effect of adding calcitonin to physical treatment on reflex sympathetic dystrophy. Pain. 1992 Feb. 48(2):171-5. [Medline].

Littlejohn G. Therapy: Bisphosphonates for early complex regional pain syndrome. Nat Rev Rheumatol. 2013 Apr. 9(4):199-200. [Medline].

Varenna M, Adami S, Rossini M, Gatti D, Idolazzi L, Zucchi F, et al. Treatment of complex regional pain syndrome type I with neridronate: a randomized, double-blind, placebo-controlled study. Rheumatology (Oxford). 2013 Mar. 52(3):534-42. [Medline].

[Guideline] Netherlands Society of Anaesthesiologists, Netherlands Society of Rehabilitation Specialists. Updated Guidelines for Complex Regional Pain Syndrome type 1. Available at http://pdver.atcomputing.nl/pdf/Executive_summary_guideline_CRPS_I_2014_docx.pdf. November 2014; Accessed: August 17, 2018.

Taylor RS, Van Buyten JP, Buchser E. Spinal cord stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature and assessment of prognostic factors. Eur J Pain. 2006 Feb. 10(2):91-101. [Medline].

Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med. 2000 Aug 31. 343(9):618-24. [Medline].

[Guideline] National Institute for Health and Care Excellence. Spinal cord stimulation for chronic pain of neuropathic or ischaemic origin. NICE. Available at http://www.nice.org.uk/guidance/ta159. Accessed: September 26, 2014.

[Guideline] Perez RS, Zollinger PE, Dijkstra PU, Thomassen-Hilgersom IL, Zuurmond WW, Rosenbrand KC, et al. Evidence based guidelines for complex regional pain syndrome type 1. BMC Neurol. 2010 Mar 31. 10:20. [Medline]. [Full Text].

Midbari A, Suzan E, Adler T, Melamed E, Norman D, Vulfsons S, et al. Amputation in patients with complex regional pain syndrome: a comparative study between amputees and non-amputees with intractable disease. Bone Joint J. 2016 Apr. 98-B (4):548-54. [Medline].

Cimaz R, Matucci-Cerinic M, Zulian F, Falcini F. Reflex sympathetic dystrophy in children. J Child Neurol. 1999 Jun. 14(6):363-7. [Medline].

Badri T, Ben Jennet S, Fenniche S, Benmously R, Mokhtar I, Hammami H. Reflex sympathetic dystrophy syndrome in a child. Acta Dermatovenerol Alp Panonica Adriat. 2011 Jun. 20(2):77-9. [Medline].

Bean DJ, Johnson MH, Heiss-Dunlop W, Lee AC, Kydd RR. Do psychological factors influence recovery from Complex Regional Pain Syndrome Type-1? A Prospective Study. Pain. 2015 Jul 1. [Medline].

Azari P, Lindsay DR, Briones D, Clarke C, Buchheit T, Pyati S. Efficacy and safety of ketamine in patients with complex regional pain syndrome: a systematic review. CNS Drugs. 2012 Mar 1. 26(3):215-28. [Medline].

T P Sudha Rao, MD Associate Professor of Medicine, Virginia Commonwealth University School of Medicine; Chief, Rheumatology Fellowship Coordinator, Department of Rheumatology, McGuire VA Medical Center

T P Sudha Rao, MD is a member of the following medical societies: American College of Rheumatology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Lawrence H Brent, MD Associate Professor of Medicine, Sidney Kimmel Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, American College of Rheumatology

Disclosure: Stock ownership for: Johnson & Johnson.

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Don R Revis, Jr, MD Consulting Staff, Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Florida College of Medicine

Don R Revis, Jr, MD is a member of the following medical societies: American College of Surgeons, American Society for Aesthetic Plastic Surgery, American Society of Plastic Surgeons, American Medical Association

Disclosure: Nothing to disclose.

Robert E Wolf, MD, PhD Professor Emeritus, Department of Medicine, Louisiana State University School of Medicine in Shreveport; Chief, Rheumatology Section, Medical Service, Overton Brooks Veterans Affairs Medical Center

Robert E Wolf, MD, PhD is a member of the following medical societies: American College of Rheumatology, Arthritis Foundation, Society for Leukocyte Biology

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Lewis Katz School of Medicine at Temple University

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology

Disclosure: Nothing to disclose.

Complex Regional Pain Syndrome Type 1 (Reflex Sympathetic Dystrophy)

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