Complex Regional Pain Syndrome (CRPS)

Original Editors - Katelyn Koeninger and Kristen Storrie from Bellarmine University's Pathophysiology of Complex Patient Problems project and Yves Hubar 

Top Contributors - Matthias Steenwerckx, Laure-Anne Callewaert, Gwen Wyns, Ine Wittevrongel


Definition/Description

Complex regional pain syndrome (CRPS) is a term for a variety of clinical conditions characterised by chronic persistent pain, and are subdivided into Type I and Type II CRPS. It is a condition that can develop after a limb trauma,[1] and appears mostly in one or more limbs. CRPS can be considered a regional post-traumatic neuropathic pain problem,[2] and like other neuropathic pain disorders, symptoms are a disproportionate consequence of painful trauma or nerve lesion.[3]

Many names have been used to describe this syndrome such as; Reflex Sympathetic Dystrophy, causalgia, algodystrophy, Sudeck’s atrophy, neurodystrophy, and post-traumatic dystrophy. To standardise the nomenclature, the name complex regional pain syndrome was adopted in 1995 by the International Association for the Study of Pain (IASP).[4]

Prevalence

CRPS affects approximately 26 out of every 100,000 people. It is more common in females than males, with a ratio of 3.5:1.[5] CRPS can affect people of all ages, including children as young as three years old and adults as old as 75 years, but typically is most prevalent in the mid-thirties. CRPS Type I occurs in 5% of all traumatic injuries,[6] with 91% of all CRPS cases occurring after surgery.[7]

Clinically Relevant Anatomy

Teasdall et al-2.jpg

CRPS can happen in any body part, but occurs most often in the extremities. The wrist is most frequently affected after distal radial fractures.[8]

The central and peripheral nervous systems are connected through neural and chemical pathways, and can have direct control over the autonomic nervous system. It is for this reason that there can be changes in vasomotor and sudomotor responses without any impairment in the peripheral nervous system. Pain, heat, and swelling are usually not located at the site of injury and there may be no clear damage. Central sensitisation is seen as a main cause for developing CRPS.[9][10]


Figure 1. Nociceptive (painful) information is relayed through the dorsal horn of the spinal cord for processing and modulation before cortical evaluation.[11]

Epidemiology /Etiology

Complex regional pain syndrome can develop after different types of injuries, such as:

  • sprains and strains
  • surgeries
  • fractures
  • contusions
  • crush injuries
  • nerve lesions
  • stroke

Sometimes the provoking injury can occur spontaneously or can not be determined.[12][13][14][15][16][17] One study found that 56% of patients felt their CRPS was due to an ‘on the job’ injury, with the most common type of work related injury occurring in service employments, such as in restaurants, bakeries, and police offices.[18]

The location of CRPS varies from person to person, often affecting the extremities, occurring slightly more in the lower extremities (+/- 60%) than in the upper extremities (+/- 40%). It can also appear unilaterally or bilatearally,[19][20][21] and as mentioned above, occurs regularly in young adults and is more frequent in females than males.[22][23]

The onset is mostly associated with a trauma, immobilisation, injections, or surgery, but there is no relation between the grade of severity of the initial injury and the following syndrome. A stressful life and other psychological factors may be potential risk factors that impact the severity of symptoms in CRPS.[24]

Characteristics/Clinical Presentation

The differences between Type I and Type II are based on a consensus between clinicians and scientists. The definition of Type II (see below) is open to interprtation. For example, post-traumatic neuralgia has different syndromes with different underlying mechanisms, but it can be included in type II. Hence the definition of both types needs to be improved. In both cases, it can be assumed that long-term central changes have occurred. Changes in the somatosensory, sympathetic, peripheral, somatomotor, and neuroendocrine systems can cause changes in the central nervous system. All symptoms of CRPS II show many similarities to those of CRPS I.[25][26][27][28]

CRPS is clinically characterised by sensory, autonomic, and motor disturbances. The table below shows an overview of the different characteristics of CRPS I and II.[29][30][31][32][33][34]

Type
Type I
Type II
Definition
  • Formerly "Reflex Sympathetic Dystrophy (RSD) "
  • Occurs after a trauma remote from the affected extremity, with or without minor nerve damage
  • Formerly "Causalgia"
  • Occurs after injury to a major peripheral nerve



Etiology
  • Minor, soft tissue trauma (sprains, bruises and skin lesions)
  • Bone fracture or surgery
  • Frostbite or burns
  • Stroke
  • Myocardial infarction or lesion of the central nervous system
  • Immobilisation
Sensory disturbances
  • Allodynia and hyperalgesia
  • Hypoesthesia and hypoalgesia
  • Strange, disfigured, or dislocated feelings in limbs[5]
  • Allodynia and hyperalgesia
  • Hypersensitivity of the skin to light mechanical stimulation - some patients report intolerance to air moving over skin[5]
Autonomic disorders + inflammatory symptoms
  • Swelling and edema [6][5][35]
  • Changes of sweating (especially hyperhidrosis)
  • Abnormal skin blood flow
  • Colour changes (redness or pale)[6]
  • Temperature changes[6][5]
  • Limb is cold and sweaty
  • Distal extremity swelling
  • Changes of sweating
  • Abnormal skin blood flow
  • Temperature changes


Trophic changes
  • Thick, brittle, or rigid nails[6]
  • Increased or decreased hair growth
  • Fibrosis
  • Thin, glossy, clammy skin[5]
  • Osteoporosis (chronic stage)
  • Smoothness and mottling of the skin
  • Acute arthritis



Motor dysfunction
  • Weakness of all muscles[6][5][35]
  • Inability to move the extremity
  • Stiffness
  • Tremor[6]
  • Reduced range of motion
  • Severe impairment of complex movements
  • Atrophy[6]
  • Inability to initiate movement of the extremity[6]
  • Stiffness[5]
  • Tremor
  • Dystonia
  • Reduced range of motion



Pain (sympathetic nervous system)
  • Burning and spontaneous
  • Disproportionate in the intensity to the inciting event
  • Increase when the extremity is in a dependent position
  • Elicited by movement and pressure at the joints
  • Not in all cases (pain may not be present in 7% of CRPS sufferers)[6][5][35]
  • Deep, unpleasant, sensitive, surface, dull
  • Ongoing
  • Neuropathic
  • Spontaneous
  • Triggered by movement, loud noises, or strong emotions
  • Deep, unpleasant, sensitive, surface, dull





Symptoms can spread beyond the area of the lesioned nerve in Type II. Ongoing neurogenic inflammation, vasomotor dysfunction, central sensitisation and maladaptive neuroplasticity contribute to the clinical phenotype of CRPS. Genetic and psychological factors can influence the vulnerability to CRPS and also affect the mechanisms that maintain CRPS. Peripheral and central changes can be irreversible. The sympathetic nervous system plays a key role in maintaining pain and autonomic dysfunction in the affected extremity.[36][37]

Patients typically progress through three stages as CRPS develops. CRPS in children does not always follow the same stage patterns and may only slowly improve or, at times, even stagnate.[35]

Stage Time Period Classic Signs and Symptoms[6]
Stage I: acute inflammation: denervation and sympathetic hypoactivity Begins 10 days post injury;
Lasts 3-6 months
Pain: more severe than expected; burning or aching; increased with position, physical condition, or emotional disturbances
Hyperalgesia, allodynia, hyperpathia: lower pain threshold, increased sensitivity, all stimuli are perceived as painful, increased pain threshold then increased sensation intensity (faster and greater pain)
Edema: soft and localised
Vasomotor/Thermal Changes: warmer
Skin: hyperthermia, dryness
Other: increased hair and nail growth
Stage II: dystrophic: paradoxic sympathetic hyperactivity Begins 3-6 months after onset of pain;
Lasts about 6 months
Pain: worsens, constant, burning, aching
Hyperalgesia, allodynia, hyperpathia: present
Edema: hard, causes joint stiffness
Vasomotor/Thermal Changes: none
Skin: thin, glossy, cool due to vasoconstriction, sweaty
Other: thin and rigid nails, osteoporosis and subchondral bone erosion noted on x-rays
Stage III: atrophic Begins 6-12 months after onset of pain;
Lasts for years, or may resolve and reappear
Pain: spreads proximally and occasionally to entire body, may plateau
Edema: hardening
Vasomotor/Thermal Changes: decreased SNS regulation, cooler
Skin: thin, shiny, cyanotic, dry
Other: fingertips and toes are atrophic, thick fascia, possible contractures, demineralisation and ankylosis seen on x-rays

Associated Co-morbidities

CRPS may also be associated with:

  • Arterial Insufficiency[38]
  • Asthma[5]
  • Bone Fractures[35]
  • Cellulitis[38]
  • Central Pain Syndromes[38]
  • Conversion Disorder[38]
  • Depression/Anxiety
  • Factitious Disorder [38]
  • Lymphedema[38]
  • Malignancy[38]
  • Migraines[5]
  • Nerve Entrapment Syndromes[38]
  • Osteomyelitis[38]
  • Osteoporosis[5][35]
  • Pain Disorder[38]
  • Peripheral Neuropathies[38]
  • Rheumatoid Arthritis[38]
  • Scleroderma[38]
  • Septic arthritis[38]
  • Systemic Lupus Erythematosus[38]
  • Tenosynovitis[38]
  • Thrombophlebitis[38]

Differential Diagnosis[39][40]

The differential diagnosis includes the direct effects of the following conditions:

  • Bony or soft tissue injury
  • Peripheral neuropathy, nerve lesions
  • Arthritis
  • Infection
  • Compartment syndrome
  • Arterial insufficiency
  • Raynaud’s Disease
  • Lymphatic or venous obstruction
  • Thoracic Outlet Syndrome (TOS)
  • Gardner-Diamond Syndrome
  • Erythromelalgia
  • Self-harm or malingering
  • Cellulitis
  • Undiagnostic fracture

Diagnostic Procedures

The Budapest criteria (also known as the IASP) has been developed for the diagnosis of CRPS, but improvements still need to be made.[41][42][43] Clinical diagnostic criteria for complex regional pain syndrome are; [44][45][46][47][48][49]:


● Constant pain, higher than the normally perceived pain
● Minimum one symptom in three of the following four symptoms. Categories must be reported:
○ Vasomotor: temperature asymmetry and/or skin colour changes/asymmetry
○ Sensory: hyperalgesia and/or allodynia
○ Sudomotor/edema: changes in sweating
○ Motor/trophic: smaller range of motion,motor dysfunction and/or changes in hair, nails and skin
● Additionally the patient must also show signs of developing symptoms in at least two symptom categories
● No other illness could explain the set of symptoms the patient is presenting with.

CRPS diagnosis is mainly based on patient history, clinical examination, and supportive investigations. A triple phase bone scan is the best method to rule out type I CPRS [50]. The triple-phase bone scan has the best sensitivity, NPV, and PPV compared to MRI and plain film radiographs.


Other tests include;

Infrared thermography
Infrared thermography (IRT) is an effective mechanism to find significant asymmetry in temperature between both limbs by determining if the affected side of the body shows vasomotor differences in comparison to the other side. It is reported having a sensitivity of 93% and a specificity of 89%.[51] This test is hard to obtain so it is not often used for diagnosing of CRPS.[52][53][54]

Sweat Testing
Determining if the patient sweats abnormally. Q-sweat is an adequate instrument to measure sweat production. The sweat samples should be taken from both sides of the body at the same time.[55][56][57]

Radiographic Testing
Irregularities in the bone structure of the affected side of the body can become visible with the use of X-rays. If the X-ray shows no sign of osteoporosis, CRPS can be excluded if the patient is an adult.[58][59][60]

3 phase bone scan
With the use of technetium Tc 99m-labeled bisophosphonates an increase in bone metabolism can be shown. Higher uptake of the substance means increased bone metabolism and the body part could be affected.[61][62]

Bone densitometry
An affected limb often shows less bone mineral density and a change in the content of the bone mineral. During treatment of the CPRS the state of the bone mineral will improve. So this test can also be used to determine if the patient’s treatment is effective.[63]

Magnetic resonance imaging (MRI)
MRIs are useful to detect periarticular marrow edema, soft tissue swelling and joint effusions. And in a later stage atrophy and fibrosis of periarticular structures can be detected. But these symptoms are not exclusively signs of CRPS.[64][65][66]

Sympathetic Blocks
If the patient shows vasomotor or sudomotor dysfunction and severe pain, blocking the sympathetic nerves proves to be an effective technique to evaluate if the sympathetic nervous system is causing the pain to remain. This technique requires local anesthetic or ablation and is successful if at least 50% of the pain is reduced.[67]

Outcome Measures


There are several methods to evaluate CRPS. Each symptom has another test to evaluate its severity. Below is a list of the different types of instruments with their evaluated symptoms.

Test
Evaluated items
References
Impairment sum score


Pain (VAS and McGill)
Skin temperature
Volume
ROM

[68][69][70][71] [72][73][74]
Grip Strength
Dynamometry
Full fist grip, pinch grip

[75][76]
Foot function (Radboud skills test)
Movements of the foot
[77][78]
Walking stairs
Time, effort, need for assistance
[79][80][81]
Rising and sitting
Getting in and out of car, bed, toilet
[82][83]
Trend (trauma related neuronal dysfunction) symptom inventory
164 items in 10 subscales (sensory, trophic, autonomic, motor, visceral symptoms)
[84][85][86]
Neuropathic pain questionnaire
12 items (see figure below)
[87][88]
Brush allodynia
Brush evoked allodynia
[89]

There is also the CPRS Severity Score (CSS). It includes signs and symptoms that reflect the sensory, vasomotor, sudomotor/edema and motor/trophic disorders of CPRS.
This scoring list evaluates CRPS symptoms separately in order to develop a self-monitoring tool for patients. It is anticipated that this tool will help to facilitate disease management and improve dialogue between patients and their medical team.
Eight symptoms are evaluated at the baseline visit with self-reported ratings of worst pain in the affected area, disability, depression, and quality of life (SF-36).[90][91][92][93]

Examination

The diagnosis is based on the clinical presentation described above. Procedures start with taking a detailed medical history, taking into account any initiating trauma and any history of sensory, autonomic, and motor disturbances, as well as how the symptoms developed, the time frame, distribution and characteristics of pain.. Assessment for any swelling, sweating, trophic and/or temperature increases, and motor abnormality in the disturbed area is important. Skin temperature differences may be helpful for diagnosis of CRPS. The original International Association for the Study of Pain criteria required only a history and subjective symptoms for a diagnosis of CRPS, but recent consensus guidelines have argued for the inclusion of objective findings. [94]

The examination of the affected limb is from the neck downwards and should be carried out at rest, during activity, and during ambulation. [95] Sensory, motor and autonomic dysfunctions are investigated. [96][97][98]

Autonomic dysfunction
The majority of patients with CRPS have bilateral differences in limb temperature and the skin temperature depends of the chronicity of the disease. In the acute stages, temperature increases are often concomitant with a white or reddish colouration of the skin and swelling. where the syndrome is chronic, the temperature will decrease and is associated with a bluish tint to the skin and atrophy. [99]

Motor dysfunction
Studies have shown that approximately 70% of the patients with CRPS show muscle weakness in the affected limb, exaggerated tendon reflexes or tremor, irregular myoclonic jerks, and dystonic muscle contractions. Muscle dysfunction often coincides with a loss of range of motion in the distal joints. [100]

Sensory dysfunction
The distal ends of the extremities require attention when examining a patient with CRPS. However, common findings of regional neuropathic and motor dysfunction have shown us that it is important to broaden the examination both proximally and contralaterally.[101]

Light touch, pinprick, temperature and vibration sensation should be assessed for a complete picture of the CRPS.[102] Most assessments are interlinked, for example, when vibration sensation is highly positive, light touch should also be positive.[103]

To help distinguish the findings of a sensory dysfunction, bilateral comparisons are made. The results should be clear and reliable.[104][105]

Medical Management

Treatment of complex regional pain syndrome should be immediate, and most importantly directed toward restoration of full function of the extremity. There are several options to treat CRPS. [106]

Medical treatment options include;

  • Oral pain relieving medications including corticosteroids and NSAIDs, as well as acupuncture, provide effective pain relief in approximately 20% of those with CRPS, but this is supported by weak evidence.[6]
  • Treatments may be geared to helping patients manage symptoms. Amitriptyline relieves depression and acts as a sleeping aid. Calcium channel blockers can help to improve circulation through SNS effect. Intrathecal baclofen, among other measures, improves motor dystonia.[6]
  • Pain intensity and perception of pain is sometimes relieved through use of an implanted transcutaneous electrical nerve stimulation (TENS) unit.[6] Electrical stimulation of the spinal cord can reduce pain intensity and improve health related quality of life.[107][108] Spinal cord stimulation was more effective than conventional medical management in reducing pain in patients with CRPS type I. [109] and was also shown to be effective in completely eliminating pain in adolescent females 2-6 weeks after stimulation. [110]
  • An excessive inflammatory reaction can lead to the overproduction of free radicals, resulting in the destruction of healthy tissue and possibly leading to CRPS. Free radical scavengers have, therefore, been proposed to curtail the disease process. To date, three free radical scavengers, like dimethyl sulfoxide (DMSO), have been investigated for the treatment of CRPS. [111]
    A scorelist (based on pain, daily activities, edema, color, and ROM) showed greater improvement by dimethyl sulfoxide treatment. DMSO seems to provide a mild improvement in range of motion and vasomotor instability in patients with CRPS.[112]
  • Due to the inflammatory response seen in CRPS, steroids have been used and resulted in significant improvements in pain, oedema and a better post treatment score.[113][114][115]
  • Intravenous immunoglobulin can reduce pain in refractory CRPS.[116]
  • Hyperbaric oxygen therapy is an effective and well tolerated method for decreasing pain, allodynia, oedema, increasing the range of motion in CRPS and also returning the skin colour to a normal colour. [117][118]
  • There is no significant difference between the effectiveness of Dimethylsulfoxide 50% (DMSO) and N-acetylcysteine (NAC) in treating CRPS type I, but DMSO-treatment was more favourable for warm CRPS whereas NAC is more favourable for cold CRPS [119]
  • Low doses of ketamine infusion has been shown to decrease pain in patients with CRPS type I who had been unsuccessful with other conservative methods of management. Ketamine blocks central sensitization by effecting the N-methyl-D-aspartate receptor which has been shown to be effected in CRPS.[120]
[121]
  • Antidepressants may be utilised to treat associated depression.[35]
  • Use of surgical and chemical sympathectomy show moderate improvement in pain scores in patients with CRPS. There were no significant differences found between the surgical and chemical groups when comparing pain scores from day one to four months. More high quality research needs to be done before recommending this as a first line of defence.[122]
  • High frequency repetitive transcranial magnetic stimulation on the motor cortex in addition to pharmacological management was effective in reducing pain. This was demonstrated by the scores on the McGill Pain Questionnaire and Short Form-36 which include different aspects of pain such as sensory-discriminative and emotional-affective.[123]
  • Surgery, casts, and ice should be avoided when treating CRPS because they further aggravate the nervous system. Surgery leads to further stress, inflammation, and immune system disturbances.[35]
  • A stellate ganglion block, or sympathectomy, blocks the nerve pathways causing pain. This may be most beneficial in the early stages of CRPS.[6][5]


Bone demineralisation is not unusual in CRPS patients, so treatment with calcitonin and biphosphonates is suitable. Calcitonin has received considerable interest in the management of CRPS because of its analgesic properties through release of ß-endorphin as well as its inhibition of bone resorption.[124] Biphosphonates are potent inhibitors of bone resorption;

  • Alendronate: less pain and swelling, more range of motion.[125][126][127]
  • Clodronate: less pain, improved global assessment and higher perceived efficacy (patient self evaluated).[128][129][130]
  • Palmidronate: less pain, higher overall improvement (patient self reported), and higher functional assessment scores.[131][132]

Generally biphosphonates have been shown to decrease pain and swelling as well as to increase range of motion for patients with CRPS [133]

Physical Therapy Management

It is difficult to manage CRPS as there is lack of understanding of the pathophysiologic abnormalities, a lack of specific diagnostic criteria and very low quality evidence to treat CRPS. [134] The main goals of treatment are a reduction in pain, preservation of limb function and a return to work. Comorbidities such as depression, sleep disturbance and anxiety also need to be addressed and treated concurrently in a patient centred, multidisciplinary approach.


A combination of physical and occupational therapy are effective in reducing pain and increasing function in patients who have had CRPS for less than 1 year [5]. Physical therapy focuses on patient education about the condition and functional activities. 

Physical therapy intervention could include any of the following:

  • TENS [6][135]
  • Aquatic therapy allows activities to be performed with decreased weight bearing on the lower extremities.[6]
  • Mirror therapy
  • Desensitisation [5]
  • Gradual weight bearing [5]
  • Stretching [5]
  • Fine motor control [5]

It is important to recognise that CRPS typically follows blood vessel pathways, and therefore symptoms may not always follow neural patterns. As a result of the spread pattern, CRPS treatment should also be provided bilaterally, due to the contralateral connections present between the extremities.[35] Treatment should be based on basic principles of pain management (pain and symptom relief, supportive care, rehabilitation) and due to the lack of evidence in treatment of CRPS treatments are based around that of other neuropathic pain syndromes.[136][137]

Acute phase
Immobilisation and contralateral therapy. Intensive active therapy in the acute phase can lead to deterioration.[138]

Chronic phase
Passive physical therapy including manipulation, manual therapy [139], massage [140][141] and mobilisations. Lymphatic drainage can be used to facilitate regression of oedema.[142] Tender areas are recommended to be treated in the following order: more severe before less severe, more proximal and medial before more distally and laterally located points and the area of greatest accumulation of tender areas is treated first. When tender areas are located in a row, the middle is treated first.[143]


Therapeutic exercise including isometric strengthening therapy followed by active isotonic training in combination with sensory desensitisation programs.[144][145] Strength training includes exercises for all four extremities and the trunk.[146] Desensitisation programs contain giving stimuli of different fabrics, different pressure (light or deep), vibration, tapping, heat or cold. The exercises can be stress-loading (f.e. scrubbing, walking, carrying weights), endurance training, written instructions and functional training.[147] When CRPS occurs in the lower extremities, gait re-training is recommended.[148]

Mirror therapy or mirror visual feedback [149]
Mirror therapy contains is where both hands are placed into a box with a mirror separating the two compartments and whilst moving both hands the patient watches the reflection of the unaffected hand in the mirror [150]
There is some evidence to suggest that mirror therapy has the effect of:

  • reducing pain intensity and improve function in post-stroke CRPS [151][152][153]
  • a significant improvement in pain [154]
  • improving function (low quality evidence however) [155]


Graded motor imagery/learning. [156][157][158][159]However, further trials are required [160] [161][162]
GMI plus medical management more effective than medical management plus physiotherapy [163]
GMI may reduce pain and improve function [164]

Relaxation [165][166]
Cognitive-behavioral therapy [167] includes relaxation training, deep breathing exercises and biofeedback.

Neuromodulation or invasive stimulation techniques
Neuromodulation contains peripheral nerve stimulation with implanted electrodes, epidural spinal cord stimulation, deep brain stimulation and electrotherapy.[168] Electrotherapy includes transcutaneous electric nerve stimulation TENS [169][170], spinal cord stimulation (SCS) [171][172][173] and non-invasive brain stimulation (repetitive transcranial magnetic stimulation).[174] These techniques help to reduce pain [175] although further trials are required [176]

Other treatments:
Whirlpool bath/ contrast baths[177]
Vocational and recreational rehabilitation[178]
Psychological therapies: cognitive-behavioral therapy (CBT), operant conditioning (OC), counselling, pain education and relaxation techniques[179][180][181]
-Acupuncture, electroacupuncture[182]
Tactile sensory discrimination training[183][184]
Weight bearing[185]
-Ultrasound therapy
Kinesio taping[186]

Clinical Guidelines

Complex regional pain syndrome in adults UK guidelines for diagnosis, referral and management in primary and secondary care. Royal College of Physicians, May 2012.

Complex regional pain syndrome: practical diagnostic and treatment guidelines, 4th edition. Pain Medicine. 2013, 14: 180-229

Case Reports/ Case Studies

[187]

Resources

Clinical Bottom Line

CRPS is a term for a variety of clinical conditions characterised by chronic persistent pain. There are two types of CRPS and the difference between type I and type II is based on a consensus between clinicians and scientists. All symptoms of CRPS II show many similarities to those of CRPS I.[188][189][190][191] It is difficult to manage CRPS as there is lack of understanding of the pathophysiologic abnormalities and lack of specific diagnostic criteria along with very low quality evidence to treat CRPS.[192] Clinical studies demonstrate a significant improvement following physical therapy, but there needs to be more trials to develop an optimal management programme.

References

  1. O’CONNEL, N.E, Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews. The Cochrane Collaboration, 2013 Apr 30;(4)
  2. RHO, R, Concise Review for Clinicians: Complex Regional Pain Syndrome. Mayo Foundation for Medical Education and Research, 2002, Feb;77(2):174-80
  3. WASNER, G, Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Brain, Volume 124, Issue 3, 1 March 2001, Pages 587–599
  4. TRAN, Q, Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society,  2010 Feb;57(2):149-66
  5. 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 5.13 5.14 5.15 5.16 5.17 Goebel A. Complex regional pain syndrome in adults. Rheumatology 2011;50(10):1739-50.
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 6.16 Cite error: Invalid <ref> tag; no text was provided for refs named Patho_Book
  7. Turner-Stokes L, Goebel A. Complex regional pain syndrome in adults: concise guidance. Clinical Med 2011; 11(6):596-600.
  8. JELLAD, A., Complex Regional Pain Syndrome Type I: Incidence and Risk Factors in Patients With Fracture of the Distal Radius. Archives of Physical Medicine and Rehabilitation, 2014. (level of evidence 2B)
  9. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001.
  10. SHIPTON, E., Complex regional pain syndrome – Mechanisms, diagnosis, and management. Current Anaesthesia and Critical Care, 2009.
  11. TEASDALL, R., Complex Regional Pain Syndrome (reflex sympathetic dystrophy). Clin Sports Med, 2004.
  12. ROSS A.H. et al., The Theoretical Basis for and Treatment of Complex Regional Pain Syndrome with Prolotherapy. Journal of Prolotherapy, 2010. (level of evidence 2C)
  13. BARON, et al., Complex regional pain syndrome: mystery explained? The Lancet Neurology, 2003. (level of evidence 3B)
  14. ALLEN, G., et al., Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Pain,1999. (level of evidence 2B)
  15. SUMITANI M., et al., Complex regional pain syndrome. Rheumatology, 2014. (level of evidence 2C)
  16. JUOTTONEN, K., et al., Altered central sensorimotor processing in patients with complex regional pain syndrome. Pain, 2002. (level of evidence 5)
  17. ATALA, N.S., et al., Prednisolone in Complex Regional Pain Syndrome. Pain Physician, 2014. (level of evidence 2B)
  18. ALLEN, G., et al., Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Pain,1999. (level of evidence 2B)
  19. ROSS A.H. et al., The Theoretical Basis for and Treatment of Complex Regional Pain Syndrome with Prolotherapy. Journal of Prolotherapy, 2010. (level of evidence 2C)
  20. ALLEN, G., et al., Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Pain,1999. (level of evidence 2B)
  21. SUMITANI M., et al., Complex regional pain syndrome. Rheumatology, 2014. (level of evidence 2C)
  22. SRINIVASA N. et al., Complex Regional Pain Syndrome I (Reflex Sympathetic Dystrophy). American Society of Anesthesiologists, 2002. (level of evidence 3B)
  23. SANDRONI, P., et al., Complex regional pain syndrome type I: incidence and prevalence in Olmsted county, a population-based study. Pain, 2003. (level of evidence 2B)
  24. SRINIVASA N. et al., Complex Regional Pain Syndrome I (Reflex Sympathetic Dystrophy). American Society of Anesthesiologists, 2002. (level of evidence 3B)
  25. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  26. WASNER, G., e.a., Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Oxford University Press, 2001. (level of evidence 3A)
  27. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  28. JANIG, W., et al., Complex regional pain syndrome is a disease of the central nervous system. Clinical Autonomic Research, 2002. (level of evidence 5)
  29. WASNER, G., e.a., Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Oxford University Press, 2001. (level of evidence 3A)
  30. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  31. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  32. JUOTTONEN, K., et al., Altered central sensorimotor processing in patients with complex regional pain syndrome. Pain, 2002. (level of evidence 5)
  33. JANIG, W., et al., Complex regional pain syndrome is a disease of the central nervous system. Clinical Autonomic Research, 2002. (level of evidence 5)
  34. GALER, B. et al., Course of Symptoms and Quality of Life Measurement in Complex Regional Pain Syndrome: A Pilot Survey. Journal of Pain and Symptom Management, 2000. (level of evidence 2C)
  35. 35.0 35.1 35.2 35.3 35.4 35.5 35.6 35.7 35.8 Hooshmand H, Phillips E. Spread of complex regional pain syndrome. Vero Beach, Florida. Neurological Associates Pain Management Center.
  36. WASNER, G., e.a., Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Oxford University Press, 2001. (level of evidence 3A)
  37. SUMITANI M., et al., Complex regional pain syndrome. Rheumatology, 2014. (level of evidence 2C)
  38. 38.00 38.01 38.02 38.03 38.04 38.05 38.06 38.07 38.08 38.09 38.10 38.11 38.12 38.13 38.14 38.15 38.16 MD Guidelines, Medical DIsability Advisor. Complex Regional Pain Syndrome: Comorbid Conditions. http://www.mdguidelines.com/complex-regional-pain-syndrome/comorbid-conditions (accessed March 28, 2012).
  39. TURNER-STOKES, L., e.a., Complex regional pain syndrome in adults: concise guidance. Clinical Med, 2011. (level of evidence 5)
  40. MCBRIDE, A., e.a., Complex Regional Pain Syndrome, Current Orthopaedics, 2005. (level of evidence 3A)
  41. HARDEN, R. N., et al., Validation of proposed diagnostic criteria (the ‘‘Budapest Criteria”) for Complex Regional Pain Syndrome. International Association for the Study of Pain, 2010. (level of evidence 1C)
  42. CHOI, E., et al., Interexaminer reliability of infrared thermography for the diagnosis of complex regional pain syndrome. Skin Research and Technology, 2013. (level of evidence 2B)
  43. HARDEN, R. N., Commentary: The Diagnosis of CRPS: Are we there yet?. International Association for the Study of Pain, 2012. (level of evidence 1B)
  44. PEREZ, R., et al., Diagnostic criteria for CRPS I: Differences between patient profiles using three different diagnostic sets. European Journal of Pain, 2007. (level of evidence 2A)
  45. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  46. HARDEN, R. N., et al., Validation of proposed diagnostic criteria (the ‘‘Budapest Criteria”) for Complex Regional Pain Syndrome. International Association for the Study of Pain, 2010. (level of evidence 1C)
  47. HARDEN, R. N., Commentary: The Diagnosis of CRPS: Are we there yet?. International Association for the Study of Pain, 2012. (level of evidence 1B)
  48. WASNER, G., et al., Complex regional pain syndrome - diagnostic, mechanisms, CNS involvement and therapy. International Spinal Cord Society, 2003. (level of evidence 2A)
  49. HODGE, S., et al., Complex Regional Pain Syndrome: The Anatomy Of A Controversy. Anatomy For Litigators: complex regional pain syndrome, p. 163-167. (level of evidence 2A)
  50. Cappello">Cappello Z, Kasdan M, Louis D. Meta-analysis of imaging techniques for the diagnosis of complex regional pain syndrome type I. JHS 2012;37A:288-296.
  51. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  52. PEREZ, R., et al., Diagnostic criteria for CRPS I: Differences between patient profiles using three different diagnostic sets. European Journal of Pain, 2007. (level of evidence 2A)
  53. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  54. CHOI, E., et al., Interexaminer reliability of infrared thermography for the diagnosis of complex regional pain syndrome. Skin Research and Technology, 2013. (level of evidence 2B)
  55. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  56. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  57. CHEMALI, K., et al., α-adrenergic supersensitivity of the sudomotor nerve in complex regional pain syndrome. Annals of Neurology, 2001. (level of evidence 2B)
  58. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  59. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  60. HODGE, S., et al., Complex Regional Pain Syndrome: The Anatomy Of A Controversy. Anatomy For Litigators: complex regional pain syndrome, p. 163-167. (level of evidence 2A)
  61. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  62. HODGE, S., et al., Complex Regional Pain Syndrome: The Anatomy Of A Controversy. Anatomy For Litigators: complex regional pain syndrome, p. 163-167. (level of evidence 2A)
  63. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  64. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  65. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  66. HODGE, S., et al., Complex Regional Pain Syndrome: The Anatomy Of A Controversy. Anatomy For Litigators: complex regional pain syndrome, p. 163-167. (level of evidence 2A)
  67. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  68. SCHASFOORT, F.C., et al., Outcome measures for complex regional pain syndrome type I: an overview in the context of the international classification of impairments disabilities and handicaps. Disability and Rehabilitation, 2000. (level of evidence 2C)
  69. PACKHAM, T., A Systematic Review of Psychometric outcome Assessment in Complex Regional Pain Syndrome. Disability and Rehabilitation, 2012. (level of evidence 2A)
  70. HARDEN, R.N., et al., Development of a Severity Score for CRPS. Pain, 2010. (level of evidence 1C)
  71. OERLEMANS, H.O., et al., Impairment Level Sumscore in Reflex Sympathetic Dystrophy of One Upper Extremity. Archives of Physical Medicine and Rehabilitation, 1998. (level of evidence 2B)
  72. GROENEWEG, J.G., et al., Increased endothelin-1 and diminished nitric oxide levels in blister fluids of patients with intermediate cold type complex regional pain syndrome type 1. BMC Musculoskeletal Disorders, 2006. (level of evidence 1B)
  73. ATALA, N.S., et al., Prednisolone in Complex Regional Pain Syndrome. Pain Physician, 2014. (level of evidence 2B)
  74. FISCHER, S.G., et al., Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Pain Medicine, 2013. (level of evidence 1B)
  75. HOTTA, J., et al., Patients with complex regional pain syndrome overestimate applied force in observed hand action. European Journal of Pain, 2015. (level of evidence 3B)
  76. ATALA, N.S., et al., Prednisolone in Complex Regional Pain Syndrome. Pain Physician, 2014. (level of evidence 2B)
  77. VAN GIJN, J.C., et al., Pain exposure physical therapy may be a safe and effective treatment for longstanding complex regional pain syndrome type 1: a case series. Sage Journals, 2015. (level of evidence 1C)
  78. FISCHER, S.G., et al., Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Pain Medicine, 2013. (level of evidence 1B)
  79. PEREZ R. et al., Measuring perceived activity limitations in lower extremity Complex Regional Pain Syndrome type 1 (CRPS I): test-retest reliability of two questionnaires. Clinical Rehabilitation, 2002. (level of evidence 1B)
  80. PACKHAM, S. Assessment of CRPS. 2015. (level of evidence 5)
  81. FISCHER, S.G., et al., Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Pain Medicine, 2013. (level of evidence 1B)
  82. PEREZ R. et al., Measuring perceived activity limitations in lower extremity Complex Regional Pain Syndrome type 1 (CRPS I): test-retest reliability of two questionnaires. Clinical Rehabilitation, 2002. (level of evidence 1B)
  83. FISCHER, S.G., et al., Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Pain Medicine, 2013. (level of evidence 1B)
  84. SCHASFOORT, F.C., et al., Outcome measures for complex regional pain syndrome type I: an overview in the context of the international classification of impairments disabilities and handicaps. Disability and Rehabilitation, 2000. (level of evidence 2C)
  85. GROENEWEG, J.G., et al., Increased endothelin-1 and diminished nitric oxide levels in blister fluids of patients with intermediate cold type complex regional pain syndrome type 1. BMC Musculoskeletal Disorders, 2006. (level of evidence 1B)
  86. COLLINS, S., et al., Development of a symptoms questionnaire for complex regional pain syndrome and potentially related illnesses: the Trauma Related Neuronal Dysfunction Symptoms Inventory. Archives of Physical Medicine and Rehabilitation, 2008. (level of evidence 3B)
  87. BOUHASSIRAA, D., et al., Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4). Pain, 2004. (level of evidence 1B)
  88. BACKONJA, M., et al., Neuropathic Pain Questionnaire - Short Form. The Clinical Journal of Pain, 2003. (level of evidence 2B)
  89. VAN EIJS, F., et al., Brush-evoked allodynia predicts outcome of spinal cord stimulation in CRPS. European Journal of Pain, 2010. (level of evidence 1B)
  90. KIRSLING, A., et al., The Complex Regional Pain Syndrome Symptom Severity Score (SSS): toward the development of a patient-administered screening tool. Rehabilitation Institute of Chicago. (level of evidence 3B)
  91. HARDEN, R.N., et al., Development of a Severity Score for CRPS. Pain, 2010. (level of evidence 1C)
  92. ATALA, N.S., et al., Prednisolone in Complex Regional Pain Syndrome. Pain Physician, 2014. (level of evidence 2B)
  93. FISCHER, S.G., et al., Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Pain Medicine, 2013. (level of evidence 1B)
  94. PENTLAND, B., e.a., Parkinsonism and dystonia. Neurological Rehabilitation, 1997. (level of evidence 2C)
  95. SANDEEP, J., Complex Regional Pain Syndrome. Indian Journal of Plastic Surgery, 2011. (level of evidence 2A )
  96. PENTLAND, B., e.a., Parkinsonism and dystonia. Neurological Rehabilitation, 1997. (level of evidence 2C)
  97. ROMMEL, e.a., Quantitative sensory testing, neurophysiological and psychological examination in patients with complex regional pain syndrome and hemisensory deficits. Ruhr-University, 2000. (level of evidence 1B)
  98. SANDEEP, J., Complex Regional Pain Syndrome. Indian Journal of Plastic Surgery, 2011. (level of evidence 2A )
  99. FRONTERA, W, e.a., Essentials of Physical Medicine and Rehabilitation - Musculoskeletal disorders, pain and rehabilitation. Saunders Elsevier, 2002. (level of evidence 5)
  100. SANDEEP, J., Complex Regional Pain Syndrome. Indian Journal of Plastic Surgery, 2011. (level of evidence 2A )
  101. FRONTERA, W, e.a., Essentials of Physical Medicine and Rehabilitation - Musculoskeletal disorders, pain and rehabilitation. Saunders Elsevier, 2002. (level of evidence 5)
  102. FRONTERA, W, e.a., Essentials of Physical Medicine and Rehabilitation - Musculoskeletal disorders, pain and rehabilitation. Saunders Elsevier, 2002. (level of evidence 5)
  103. FRONTERA, W, e.a., Essentials of Physical Medicine and Rehabilitation - Musculoskeletal disorders, pain and rehabilitation. Saunders Elsevier, 2002. (level of evidence 5)
  104. FRONTERA, W, e.a., Essentials of Physical Medicine and Rehabilitation - Musculoskeletal disorders, pain and rehabilitation. Saunders Elsevier, 2002. (level of evidence 5)
  105. SANDEEP, J., Complex Regional Pain Syndrome. Indian Journal of Plastic Surgery, 2011. (level of evidence 2A )
  106. WASNER, G., et al., Complex regional pain syndrome - diagnostic, mechanisms, CNS involvement and therapy. International Spinal Cord Society, 2003. (level of evidence 2A)
  107. KEMLER M. et al., Spinal Cord Stimulation in Patients with Chronic Reflex Sympathetic Dystrophy. The New England Journal of Medicine, 2000. (level of evidence 2B)
  108. FOROUZANFAR T. et al., Spinal cord stimulation in complex regional pain syndrome: cervical and lumbar devices are comparably effective. British Journal of Anaesthesia, 2004. (level of evidence 2B)
  109. Simpson E, Duenas A, Holmes M, Papaloannou D, Chilcott J. Spinal cord stimulation for chronic pain of neuropathic or ischaemic origin: systematic review and economic evaluation. Health Technology Assessment 2009;13(17):1-179.
  110. Olson GL, Meyerson BA, Linderoth B. Spinal cord stimulation in adolescents with complex regional pain syndrome type I. EUR J PAIN 2008;12(1):53-59.
  111. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  112. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  113. WASNER, G., et al., Complex regional pain syndrome - diagnostic, mechanisms, CNS involvement and therapy. International Spinal Cord Society, 2003. (level of evidence 2A)
  114. CHRISTENSEN, K., et al., The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Scand 1982. (level of evidence 2B)
  115. BRAUS, D.F., et al., The shoulder-hand syndrome after stroke: a prospective clinical trial. Annals of Neurology, 1994. (level of evidence 1B)
  116. GOEBEL, A. et al., Intravenous Immunoglobulin Treatment of the Complex Regional Pain Syndrome: A Randomized Trial, Annals of internal medicine, 2010. (level of evidence 1B)
  117. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  118. KIRALP, M.Z. et al., Effectiveness of Hyperbaric Oxygen Therapy in the Treatment of Complex Regional Pain Syndrome, The Journal of International Medical Research, 2004. (level of evidence 1B)
  119. Perez R, Zuurmond W, Bezemer P, Kuik D, vanLoenen A, deLange J, et al. The treatment of complex regional pain syndrome type I with free radical scavengers: a randomized controlled study. Pain 2003;102(3):297-307.
  120. Goldberg M, Domsky R, Scaringe D, Hirsh R, Dotson J, Sharaf I, et al. Multi-Day Low Dose Ketamine Infusion for the Treatment of Complex Regional Pain Syndrome. Pain Physician 2005;8:175-179.
  121. Arizona Pain. Stellate Ganglion Block. Available from: http://www.youtube.com/watch?v=izOYrLUuNd8 [last accessed 3/29/12]
  122. Straube S, Derry S, Moore RA, McQuay HJ. Cervico-thoracic or lumbar sympathectomy for neuropathic pain and complex regional pain syndrome. Cochrane Database of Systematic Reviews 2010;7:1-14.
  123. Picarelli H, Teixeira M, deAndrade D, Myzkowski M, Luvisotto T, Yeng L, et al. Repetitive Transcranial Magnetic Stimulation Is Efficacious as an Add-On to Pharmacological Therapy in Complex Regional Pain Syndrome Type I. J Pain 2010;11(11):1203-10.
  124. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  125. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  126. WASNER, G., et al., Complex regional pain syndrome - diagnostic, mechanisms, CNS involvement and therapy. International Spinal Cord Society, 2003. (level of evidence 2A)
  127. ADAMI, S., et al., Bisphosphonate therapy of reflex sympathetic dystrophy syndrome. Ann Rheum Dis,1997. (level of evidence 2B)
  128. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  129. WASNER, G., et al., Complex regional pain syndrome - diagnostic, mechanisms, CNS involvement and therapy. International Spinal Cord Society, 2003. (level of evidence 2A)
  130. VARENNA, M., et al., Intravenous clodronate in the treatment of reflex sympathetic dystrophy syndrome. A randomized, double blind, placebo controlled study. Journal of Rheumatology, 2000. (level of evidence 2B)
  131. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  132. ROBINSON, J.N., et al., Efficacy of pamidronate in complex regional pain syndrome type I. Pain Medicine, 2004. (level of evidence 2B)
  133. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  134. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  135. Somers D, Clemente F. Transcutaneous Electrical Nerve Stimulation for the Management of Neuropathic Pain: The Effects of Frequency and Electrode Position on Prevention of Allodynia in a Rat Model of Complex Regional Pain Syndrome Type II. Phys Ther 2006;86:698-709.
  136. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  137. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  138. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  139. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  140. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  141. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  142. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  143. COLLIN, C., Physical Therapy Management of Complex Regional Pain Syndrome I in a 14-Year-Old Patient Using Strain Counterstrain: A Case Report. J Man Manip Ther., 2007. level of evidence 4)
  144. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  145. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  146. STANTON-HICKS, M., et al., Complex Regional Pain Syndromes: Guidelines for Therapy. The Clinical Journal of Pain, 1998. (level of evidence 5)
  147. STANTON-HICKS, M., et al., Complex Regional Pain Syndromes: Guidelines for Therapy. The Clinical Journal of Pain, 1998. (level of evidence 5)
  148. COLLIN, C., Physical Therapy Management of Complex Regional Pain Syndrome I in a 14-Year-Old Patient Using Strain Counterstrain: A Case Report. J Man Manip Ther., 2007. level of evidence 4)
  149. SMITH, T., How effective is physiotherapy in the treatment of complex regional pain syndrome type I? A review of the literature. Musculoskeletal care, 2005. (level of evidence 3A)
  150. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  151. MCGABE, C.S., et al., Mirror visual feedback for the treatment of complex regional pain syndrome (Type 1). Current Pain and Headache Reports, 2008. (level of evidence 2A)
  152. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  153. BOWERING, K. J., The effects of graded motor imagery and its components on chronic pain: a systematic review and meta-analysis. The American Pain Society, 2013. (level of evidence 1A)
  154. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  155. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  156. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  157. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  158. MOSELEY, G.L., Graded motor imagery is effective for long standing complex regional pain syndrome: a randomised controlled trial. Pain, 2004. (level of evidence 1B)
  159. SMITH, T., How effective is physiotherapy in the treatment of complex regional pain syndrome type I? A review of the literature. Musculoskeletal care, 2005. (level of evidence 3A)
  160. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  161. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  162. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  163. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  164. MOSELEY, G.L., Graded motor imagery is effective for long standing complex regional pain syndrome: a randomised controlled trial. Pain, 2004. (level of evidence 1B)
  165. BRUEHL, S., Psychological interventions. In: Harden RN editor(s). Complex regional pain syndrome: treatment guidelines. Reflex Sympathetic Dystrophy Syndrome Association, 2006 (level of evidence 1C)
  166. SMITH, T., How effective is physiotherapy in the treatment of complex regional pain syndrome type I? A review of the literature. Musculoskeletal care, 2005. (level of evidence 3A)
  167. LEE, B., et al., Physical therapy and cognitive-behavioral treatment for complex regional pain syndromes. Pain Treatment Service, 2002. (level of evidence 2B)
  168. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  169. OAKLANDER, A., et al., Evidence of focal small-fiber axonal degeneration in complexfckLRregional pain syndrome-I (reflex sympathetic dystrophy). Pain, 2006. (level of evidence 1B)
  170. SMITH, T., How effective is physiotherapy in the treatment of complex regional pain syndrome type I? A review of the literature. Musculoskeletal care, 2005. (level of evidence 3A)
  171. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  172. ALBAZAZ, R. N., et al., Complex Regional Pain Syndrome: A review. Annals of Vascular Surgery Inc., 2008. (level of evidence 2A)
  173. KENLER, M., et al., The effect of Spinal Cord Stimulation in Patients with Chronic Reflex Sympathetic Dystrophy: Two Years’ Follow-up of the Randomized Controlled Trial. Annals of Neurology, 2004. (level of evidence 1B)
  174. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  175. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  176. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  177. DEVRIMSEL, G., et al., The effects of whirlpool bath and neuromuscular electrical stimulation on complex regional pain syndrome. J. Phys. Ther. Sci., 2015. (level of evidence 3B)
  178. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  179. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  180. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  181. BRUEHL, S., Psychological interventions. In: Harden RN editor(s). Complex regional pain syndrome: treatment guidelines. Reflex Sympathetic Dystrophy Syndrome Association, 2006 (level of evidence 1C)
  182. SMITH, T., How effective is physiotherapy in the treatment of complex regional pain syndrome type I? A review of the literature. Musculoskeletal care, 2005. (level of evidence 3A)
  183. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  184. BOWERING, K. J., The effects of graded motor imagery and its components on chronic pain: a systematic review and meta-analysis. The American Pain Society, 2013. (level of evidence 1A)
  185. TRAN, Q., e.a., Treatment of complex regional pain syndrome: a review of the evidence. Canadian Anesthesiologists’ Society, 2010. (level of evidence 1A)
  186. ANANDKUMAR, S.; MANIVASAGAM, M., Multimodal physical therapy management of a 48-year-old female with post-stroke complex regional pain syndrome. Physiother Theory Pract, 2014. (level of evidence 3B)
  187. CNN. CNN Report on Reflex Sympathetic Dystrophy. Available from: http://www.youtube.com/watch?v=jaTlI6bfF64 [last accessed 3/28/12]
  188. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)
  189. WASNER, G., e.a., Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Oxford University Press, 2001. (level of evidence 3A)
  190. BARON, R., Complex regional pain syndromes. Curr Pain Headache Rep., 2001. (level of evidence 2A)
  191. JANIG, W., et al., Complex regional pain syndrome is a disease of the central nervous system. Clinical Autonomic Research, 2002. (level of evidence 5)
  192. O’CONNEL, N.E., e.a., Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews (Review). The Cochrane Collaboration, 2013. (level of evidence 3A)