Logo of bmcneulBioMed Centralsearchsubmit a manuscriptregisterthis articleBMC Neurology
BMC Neurol. 2010; 10: 20.
Published online Mar 31, 2010. doi:  10.1186/1471-2377-10-20
PMCID: PMC2861029

Evidence based guidelines for complex regional pain syndrome type 1

Abstract

Background

Treatment of complex regional pain syndrome type I (CRPS-I) is subject to discussion. The purpose of this study was to develop multidisciplinary guidelines for treatment of CRPS-I.

Method

A multidisciplinary task force graded literature evaluating treatment effects for CRPS-I according to their strength of evidence, published between 1980 to June 2005. Treatment recommendations based on the literature findings were formulated and formally approved by all Dutch professional associations involved in CRPS-I treatment.

Results

For pain treatment, the WHO analgesic ladder is advised with the exception of strong opioids. For neuropathic pain, anticonvulsants and tricyclic antidepressants may be considered. For inflammatory symptoms, free-radical scavengers (dimethylsulphoxide or acetylcysteine) are advised. To promote peripheral blood flow, vasodilatory medication may be considered. Percutaneous sympathetic blockades may be used to increase blood flow in case vasodilatory medication has insufficient effect. To decrease functional limitations, standardised physiotherapy and occupational therapy are advised. To prevent the occurrence of CRPS-I after wrist fractures, vitamin C is recommended. Adequate perioperative analgesia, limitation of operating time, limited use of tourniquet, and use of regional anaesthetic techniques are recommended for secondary prevention of CRPS-I.

Conclusions

Based on the literature identified and the extent of evidence found for therapeutic interventions for CRPS-I, we conclude that further research is needed into each of the therapeutic modalities discussed in the guidelines.

Background

Complex Regional Pain Syndrome type I (CRPS-I) is a condition that causes multiple problems for both patients and practitioners, due to the large variety of available treatment options. The IASP (International Association for the Study of Pain) definition of the syndrome reads as follows: "CRPS Type I is a syndrome that usually develops after an initiating noxious event, is not limited to the distribution of a single peripheral nerve, and is apparently disproportioned to the inciting event. It is associated at some point with evidence of oedema, changes in skin blood flow, abnormal sudomotor activity in the region of the pain, or allodynia or hyperalgesia" [1].

A distinction was made between CRPS type I, formerly known as reflex sympathetic dystrophy (RSD), and type II, where a nerve lesion can be detected (formerly known as causalgia) [1,2].

The condition often starts in an arm or leg, and is characterized by a combination of autonomic, sensory and vasomotor symptoms. Pain, temperature asymmetry impaired movement, change in skin colour, hyperaesthesia, hyperalgesia, hyperpathy, tremor, involuntary movements, muscle spasms, paresis, pseudoparalysis, skin, muscle and bone atrophy, hyperhidrosis and changes in hair and nail growth have been reported in patients with this syndrome [3]. It usually requires long-term, intensive medical therapy whereby many CRPS-I patients are no longer able to perform their usual (social) role in everyday life. As a result, CRPS-I has a major impact on quality of life [4,5].

Various sets of diagnostic criteria are used side by side, and many different therapies have been applied to this patient group. The complexity of this problem, the fact that various disciplines are involved in treatment, and the consequences for the patient's psychosocial functioning mean that a clear, uniform set of guidelines is essential. In the light of the foregoing considerations, a multidisciplinary task force was instigated by the Dutch Society of Rehabilitation Specialists and the Dutch Society of Anaesthesiologists in order to draw up evidence-based guidelines for CRPS-I treatment.

Methods

A multidisciplinary task force was set up in the autumn of 2003. The task force included representatives of all medical and paramedical disciplines engaged in diagnosing and treating patients with CRPS-I, epidemiologists, a representative of the Dutch Association of Posttraumatic Dystrophy Patients and the Dutch Institute for Healthcare Improvement CBO. An even spread between geographical locations, balanced representation of the various societies and bodies involved, and a fair division between members with an academic background and those from a non-academic background was ensured.

Members of the task force were further subdivided into project groups addressing specific areas of CRPS treatment. Relevant articles written in English, German, French, Italian or Dutch were identified by searches in the Cochrane Library, Medline, Embase, Cinahl and Psychinfo, using a search string based on the PICO method (see additional file 1). Reference lists of articles identified were screened for relevant articles that did not come up in the database search, and recent guidelines were consulted. Studies were selected based on their methodological strength (meta-analyses, systematic reviews, randomized controlled trials (RCT's) and controlled trials (CT's)). Systematic reviews and meta-analyses, considered to have the highest evidential strength, were given precedence over individual articles included in the review. In case these studies were not available, comparative cohort studies, comparative patient control trials or non-comparative trials were used in the evaluations. Other important criteria were: adequate size, adequate follow-up, adequate exclusion of selection bias, and whether the results obtained can be generalized to the Dutch health care system. The search covered the period from 1980 to June 2005, although some studies published prior to or after this period were also used for the guidelines.

The members of the project group assessed the quality of these studies on the basis of evidence-based guideline development (EBGD) assessment forms. The studies were then graded according to their strength of evidence as described in table table1.1. Conclusions were formulated based on the available strength of evidence, and described in terms in accordance with the levels shown in table table1.1. These descriptions ranged from clear statements about efficacy ("It is proven that...") for level one down to expressions of expert opinion ("The task force is of the opinion that...") for level four conclusions.

Table 1
Classification of the literature consulted, according to strength of evidence

The project group members produced texts, either individually or in subgroups. These texts comprised background information with respect to the intervention and studies assessed, conclusions regarding the efficacy of the intervention according to strength of evidence and additional considerations concerning treatment related issues (i.e. availability of treatment methods, side effects, cost-effect benefits, consequences for organization of care etc.). All texts including recommendation were discussed at plenary meetings and approved after comments had been taken into account. The plenary project group met ten times to discuss draft texts. The draft guidelines were sent for external review to the participating professional societies (see acknowledgements for details) and were presented and discussed at an open national meeting. Once all comments had been taken into account, the guidelines were adopted by the full project group and sent to the participating professional organisations for final approval. Formal endorsement was obtained in December 2006.

The conclusions for each treatment modality including strength of evidence and underlying literature will be presented in italics in the result section. The final recommendations for the different treatment modalities will be described at the end of this article. A practical algorithm based on these guidelines is presented in additional file 2.

Results

Database and cited reference search revealed 94 relevant studies after selection. These included 25 studies on oral or topical drug interventions, 42 studies on invasive treatments, 15 on paramedical interventions, 4 on primary and 8 on secondary prevention of CRPS. Treatment interventions for children with CRPS, comprising 8 studies were described separately.

Drug treatment

Pain medication

Although analgesics are often used when treating patients with CRPS-I, and their use is described in various treatment protocols and guidelines [6-8], the scientific support for their administration to patients with CRPS-I is very limited.

Paracetamol

The use of paracetamol is described in the context of an adjuvant pain protocol in a study into the efficacy of free radical scavengers in treating CRPS-I (n = 146) [9]. No studies were found evaluating paracetamol as a stand-alone treatment for CRPS-I.

There is no evidence that paracetamol is effective in treating pain in CRPS-I patients (level 4).

NSAIDs

Sixty-one CRPS-I patients were retrospectively evaluated with respect to the effects of 60 mg of keterolac administered by means of a regional intravenous blockade [10]. Twenty-six percent of patients had a complete response, 42% had a partial response and 31% had no response. Patients with allodynia had significantly less response to the treatment. Conflicting data have been published with regard to the use of NSAIDs in patients with neuropathic pain [11].

There is insufficient evidence of the degree of pain control achieved by NSAIDs in CRPS-I patients (level 3:Connelly et al. (C)).

Opioids

One placebo-controlled RCT (n = 43) was found investigating the effects of sustained-release oral morphine on patients who had previously been treated with epidural spinal cord electrical stimulation (ESES) [12]. No significant differences were found between the extent of pain reduction and the average time for ESES to become effective. On average, the morphine group reported 20 side-effects a day, against 2 a day in the placebo group. An uncontrolled study with 9 CRPS I and II patients evaluated the effects of continuous infusion of morphine in the axillary plexus following stellate blockade [13]. Significant pain reduction at rest and at movement and increased grip strength were found. However, the steady-state morphine concentrations were lower than the minimally effective analgesic concentration. There is little information on weak and strong acting opioids in patients with CRPS-I. Systematic reviews on their use for neuropathic pain have found tramadol to be effective [14]. Positive short-term effects have also been reported for strong acting opioids administered for neuropathic and musculoskeletal pain [15].

There is insufficient evidence for the effects of oral opioids in CRPS-I patients on pain (level 3: Harke et al. (B)).

There is insufficient evidence for the effects of infusion of morphine to the axillary plexus on pain in CRPS-I patients (level 3: Azad et al. (C)).

Local anaesthetics

One quasi-experimental study with 7 patients evaluated the effects of lumbar and stellate blockades with lidocaine/bupivacaine compared to placebo (follow up 2-2,5 weeks). No significant differences were found between active and placebo treatment with respect to initial peak pain reduction [16].

An uncontrolled open study investigated the long term effects (mean follow up 32 months, range 7-48 months) of epidural administration of bupivacaine to 14 patients with CRPS-I in the knee [17]. Treatment was continued with continuous administration of a narcotic. No pain control data were described, however, 11 patients were seen to have a complete improvement of CRPS-I symptoms at the end of the follow-up.

There is insufficient evidence to allow any statement about the efficacy of local anaesthetics administered to the sympathetic ganglia in CRPS-I patients (level 3: Price et al. (B), Azad et al (C)).

There is insufficient evidence to allow any statement about the efficacy of epidural administered local anaesthetic to CRPS-I patients. Due to use of different interventions the efficacy of epidural administration of local anaesthetics cannot be determined (level 3: Cooper et al. (C)).

Anaesthetics

The effects of a sub-anaesthetic ketamine infusion (10 mg/hour up to 15-50 mg/hour) was assessed in a retrospective study of 33 patients with CRPS-I or -II [18]. Twelve patients experienced a relapse and had a second course of infusions, three patients had a third course, by which pain disappeared completely in 83% of patients. The average duration of pain reduction (data of 20 patients) was 9.4 months. The side-effects were intoxication, hallucinations, dizziness, nausea, light-headedness and blurred vision.

There are indications that intravenous administration of a sub-anaesthetic dose of ketamine reduces pain in CRPS-I patients (level 3: Correll et al. (C)).

Anticonvulsants

Two placebo-controlled, randomized studies have been found that examined the use of gabapentin in neuropathic pain patients. The first study [19] (n = 307) shows that gabapentin causes a modest but significant reduction in neuropathic pain symptoms eight weeks after the start of treatment. It is unclear what this means for the CRPS-I patients, who made up 28% of the sample population.

In the second study (n = 58) a moderate effect on pain was found, but no significant reductions in other sensory abnormalities were found [20]. Dizziness, sleepiness and fatigue occurred significantly more often in patients taking gabapentin than in patients taking placebo.

There are indications that gabapentin administered at doses of 600 to 1800 mg every 24 hours in the first eight weeks can cause some reduction in pain symptoms suffered by patients with CRPS-I.

There is limited evidence that gabapentin reduces sensory abnormalities such as hyperaesthesia and allodynia. The long-term effect of gabapentin on patients with CRPS-I is not known (level 2: Serpell (B), Van de Vusse et al. (B)).

No studies were found evaluating the effects for other anticonvulsants in relation to CRPS I.

There is no evidence that anticonvulsants such as carbamazepine, pregabalin and phenytoin are effective in reducing pain in CRPS-I patients (level 4).

Antidepressants

No studies testing tricyclic antidepressants on patients with CRPS-I were available.

There is no evidence that antidepressants are effective in reducing pain in patients with CRPS-I (level 4).

Capsaicin

Only one study has been found in which an extremely high dose of capsaicin (5 to 10%) was administered to ten patients with CRPS-I [21]. Doses of this strength can only be spread onto patients' skin if the painful body part is first numbed by epidural anaesthesia.

The investigators claim to have succeeded in 90% of patients in achieving pain reduction. No scientific conclusions can yet be drawn from this open-label study.

There is insufficient evidence that capsaicin is effective in CRPS-I patients (level 4)

Free radical scavengers

A prospective crossover study [22] with 20 patients found a positive effect of dimethylsulphoxide (DMSO) on the function of the affected limb. In 26 CRPS-I patients DMSO was found to be significantly more effective than the conventional regional ismelin block [23] in reducing pain. A randomised double-blind trial conducted with 32 CRPS-I patients [24] showed that 5 times daily use of DMSO in cremor vaselini cetomacrogolis provided significantly better results on CRPS-I symptoms than placebo after two months of treatment. A randomized double-blind study in 146 CRPS-I patients found comparable results for DMSO cream and N-acetylcysteine [9]. In general, DMSO generates lower (direct and indirect) costs than N-acetylcysteine. Subgroup analysis indicates that N-acetylcysteine is more cost effective in patients with a cold form of CRPS-I than DMSO. The opposite holds for warm forms of CRPS-I [25].

DMSO (dimethylsulphoxide) cream (50%) reduces the symptoms of CRPS-I patients (level 2: Perez et al (A2), Geertzen et al. (B); Goris et al. (B), Zuurmond et al. (B)).

It is likely that 600 mg of N-acetylcysteine administered three times a day reduces the symptoms of CRPS-I (level 3: Perez et al. (A2)).

There are indications that 50% DMSO (dimethylsulphoxide) cream is more effective on primary warm CRPS-I while N-acetylcysteine (NAC) is more effective on primary cold CRPS-I (level 3: Perez et al. (C)).

Oral muscle relaxants

Motor symptoms of CRPS-I may include paresis, dystonia, myoclonias and/or tremor. Five descriptive studies have been conducted into movement disorders in CRPS-I patients (n = 5-43) [26-30]. Three of these studies reported that a small number of CRPS-I patients with dystonia/spasms did benefit from treatment with benzodiazepines and high doses of baclofen [28]. No controlled studies have been carried out on the treatment of either dystonia or spasms in patients with CRPS-I. Two descriptive studies report that anticholinergics have never produced (lasting) effects [29,30].

There is insufficient evidence of the efficacy of muscle relaxants in treating movement disorders associated with CRPS-I, such as dystonia and muscle spasms (level 3: Bathia et al. (C), Van Hilten et al. (C), Jankovic et al. (C), Marsden et al. (C), Schwartzman et al. (C)).

Botulin toxin

One study described the use of botulin toxin A to treat 14 patients with very severe tonic dystonia of the hand ('clenched fist') [31]. In four of these patients, the dystonia developed in the context of CRPS-I. An 'overall' improvement in pain and muscle relaxation was achieved in four out of five hands, but the extent of improvement was not described. Other articles report that botulin toxin injections never work, or only work for a short period, and rarely lead to improvement in functionality [27,29].

There is insufficient evidence that botulin toxin A is effective in treating dystonia in CRPS-I patients (level 3: Cordivari et al. (C), Van Hilten et al. (C), Jancovic et al. (C)).

Intrathecal baclofen administration

Intrathecal baclofen therapy (ITB) is an invasive technique that has only been investigated in two patients with CRPS-I alone [32] and seven CRPS-I-dystonia patients [33] whose condition had failed to respond to previous treatment. Only the latter study was preceded by a double-blind placebo-controlled crossover screening procedure aimed to ascertain whether patients would be suitable for having a programmable pump for ITB fitted. Comparison with a placebo revealed that baclofen significantly improved outcomes. Six patients underwent the implant procedure and were monitored for 1.7 years as part of an open trial with varying degrees of success. Zuniga et al. also reported an open trial with ITB on two CRPS-I patients with no motor disorder [32]. Pain, allodynia and autonomic disorders responded well to ITB. The main side-effects of the screening process and continuous administration of ITB are post-puncture headache, diminished consciousness and urine retention [33].

There is insufficient evidence that intrathecal baclofen (ITB) is effective in treating dystonia in CRPS-I patients (level 3: Van Hilten et al. (C), Zuniga et al. (C)).

Corticosteroids

Corticosteroids have been used in open trials (n = 64-69) [34,35] and in one controlled trial (n = 23) [36] to treat CRPS-I, all of limited methodological quality. All the studies found corticosteroids to have a very pronounced beneficial effect.

Corticosteroids may have a positive effect on CRPS-I. Little is known as to the duration and dosage (level 3: Christensen et al. (C), Grundberg et al. (C), Kozin et al. (C)).

Calcitonin

The effects of calcitonin have been evaluated in two meta-analyses and two systematic reviews. The meta-analysis carried out by Kingery et al. [37] reports conflicting findings as to the effects of calcitonin. The systematic review conducted by Van den Berg et al. [38] finds no evidence that calcitonin is effective in cases of CRPS-I. In contrast, the meta-analysis carried out by Perez et al. points to calcitonin having a positive effect on pain on average [39], and the review carried out by Forouzanfar et al. also describes positive results for calcium-regulating drugs (including calcitonin) administered to CRPS-I patients [40].

There is conflicting evidence with respect to the efficacy of calcitonin for treatment of CRPS-I (level 1: Van den Berg et al. (A1), Forouzanfar et al. (A1), Kingery (A1), Perez et al. (A1)).

Bisphosphonates

Three placebo-controlled studies have been carried out to date [40-43]. One study (n = 20) involved administration of alendronate three days in a row [41]. Another study evaluated the efficacy of clodronate (n = 32) [42]. In a third study, treatment comprised alendronate (40 mg: this dose is four times as high as that given for osteoporosis) administered to 40 CRPS-I patients [43]. In the three studies, the parameters in the group of patients treated with bisphosphonates improved significantly more than in the placebo group.

Bisphosphonates have a beneficial effect on the signs of inflammation in patients with CRPS-I. At present little is known as to the optimum dosage, frequency and duration of treatment (level 1: Forouzanfar et al. (A1), Manincourt et al. (A2)).

Calcium-channel blockers

Two studies of moderate quality and size investigated the effect of nifedipine and phenoxybenzamine in treating CRPS-I [44,45]. One retrospective study with 59 patients reports that nifedipine (20 mg per day) or phenoxybenzamine (up to 120 mg/day) are most effective for CRPS-I in the acute phase [44]. Both studies are primarily descriptive and the outcomes are subjective, failing to describe the nature of the improvement in patients' conditions.

There are indications that calcium-channel blockers have some effect in the acute phase of CRPS-I. While they improve blood circulation, they also cause side-effects such as a drop in blood pressure and headache (level 3: Muizelaar et al. (C), Prough et al. (C)).

Invasive treatment

Intravenous sympathetic blockade

Eight studies have been carried out into the effects of intravenous guanethidine on CRPS-I [23,46-52]. The doses administered ranged from 10 to 30 mg. Four of these studies (n = 9-60) were randomized, comparing guanethidine to a placebo (in most cases 0.9% NaCl) [46,48,50,52]. The remaining studies (n = 20-55) examining the effect of guanethidine report a temporary effect in approximately one-third of patients.

Three additional studies were very small (n = 5-7) from which no conclusions can be drawn [53-55]. One study (n = 16) described a temporary effect of intravenous lidocaine on mechanical and thermal allodynia [56]. Intravenous blockades brought about by guanethidine, lidocaine, clonidine, droperidol and reserpine have been investigated in two meta-analyses and one systematic review [37,39,40], which provided no evidence in favour of intravenous sympathetic blockades.

Intravenous sympathetic blockade has no added value (pain reduction) compared to placebo in CRPS-I patients (level 1: Kingery (A1), Forouzanfar et al. (A1), Perez et al. (A1)).

Other intravenous treatment

A number of intravenous drugs have been tested for efficacy. Intravenous regional blockades produced by bretylium and ketanserine were found to achieve a significant reduction in pain in the treatment group [57,58]. Ketanserine (n = 16; 10 mg for upper extremity and 20 mg for lower extremtity administration), and two intravenous applications of bretylium at 1.5 mg/kg with lidocaine (in 12 patients) provided slight pain relief. Intravenous administration of reserpine, droperidol and atropine had no effect [37].

There are indications that 10-20 mg of ketanserine administered by intravenous injection reduces pain in CRPS-I patients. Reserpine, droperidol and atropine do not relieve pain in CRPS-I patients (level 1: Kingery (A1), Hanna et al. (B), Hord et al. (B)).

Percutaneous sympathetic blockade

The literature contains one systematic review of the therapeutic role of local anaesthetic sympathetic blockades in patients with CRPS-I [59]. That review assessed 29 studies performed on 1144 patients with CRPS-I, and concludes that critical examination of the studies raises the question of whether sympathetic blockade is of any benefit at all in CRPS-I. Less than a third of the patients reported temporary relief of pain symptoms following a sympathetic blockade. However, it is unclear whether this is due to a placebo effect.

Routine administration of percutaneous sympathetic blockade in patients with CRPS-I is not useful (level 2: Cepeda et al. (A1)).

Surgical sympathectomy

The efficacy of surgical sympathectomy was addressed in a systematic review [60], based on analysis of retrospective cohort including 7 to 73 individuals [61-65]. All the studies report a clear reduction in pain due to sympathectomy, whereby the extent of pain relief declines over time. Long term follow up studies (> one year) indicate that the chance of success is greatest if treatment is given within three months after the initial trauma [62,63,65].

There are indications that surgical sympathectomy can relieve pain in CRPS-I (level 3: AbuRahma et al. (C), Bandyk et al. (C), Bosco Vieira Duarte (C), Mailis et al. (C), Schwartzman et al. (C), Singh et al. (C)).

Spinal cord stimulation

Patients with chronic refractory CRPS-I were randomly allocated to spinal cord stimulation (SCS) plus physiotherapy or physiotherapy alone. Trial stimulation proved successful in 24 of the 36 patients; only these patients underwent a procedure to implant a permanent SCS device. Pain intensity reduced by 2.4 cm on a visual analogue scale after six months in the group receiving spinal cord stimulation plus physiotherapy compared to a group receiving only physiotherapy [66]. At two years follow-up, pain decrease in the SCS group was 2.1 cm more than pain decrease observed in the physiotherapy group [67]. Quality of life improved only in the patients with an implanted system; function remained unchanged. Nine of the 24 patients with an implanted system (38%) experienced complications requiring further surgery within two years [66,67].

Two retrospective cohort studies have investigated effects of SCS on pain relief (n = 23-31) [68,69]. All studies relate to carefully selected patients with refractory CRPS-I. There is no scientific evidence for SCS being effective in non-chronic CRPS-I. Complications requiring further surgery do occur in 25-50% of patients [70].

Spinal cord stimulation administered to CRPS-I patients who are carefully selected and undergo successful trial stimulation causes long-term pain reduction and improves quality of life, but does not improve function (level 3: Kemler et al. (A2), Calvillo et al. (C), Kemler et al. (C), Kemler et al. (C)).

Amputation

Amputation is sometimes performed with the aim to improve quality of life of CRPS I patients with severe complications, such as threatening sepsis or severe functional impairment.

Two retrospective studies [60,71] evaluating CRPS I patients undergoing amputation were found. One study evaluating seven patients with upper-limb CRPS-I [71], reported three satisfied, two indecisive and two unsatisfied patients. In another study, 34 amputations were carried out on 28 patients [72] due to pain, recurrent infections and functional impairment. Two patients were pain-free; ten infections were adequately controlled, and functional improvement was achieved in nine cases. CRPS-I relapse occurred in 28 cases, but 24 patients remained satisfied with their amputation.

There is insufficient evidence that amputation positively contributes to the treatment of CRPS-I (level 3: Dielissen et al. (C), Stam et al. (C)).

Paramedical interventions

Physiotherapy

Published articles often recommend 'physiotherapy' as adjuvant treatment, without specifying exactly what this physiotherapy involves. In general, it is emphasized that functional recovery is essential and forms the key to recovery.

A randomized controlled trial (n = 135) showed that physiotherapy given in addition to medical treatment has a clinically relevant effect on the severity of functional impairments [73,74]. Physiotherapy contributes primarily to quicker reduction of pain, abnormal skin temperature, reduced mobility and oedema. In view of the rapid improvement of disorders it is recommended that physiotherapy should be started at an early stage, or soon after the diagnosis is made [73-75], and may be beneficial for chronic CRPS-I [76,77]. Promising results are reported for Mirror therapy (n = 8-13) in reducing pain [78,79]. Standardized pain-contingent physiotherapy aimed at improving patients' ability to cope with the condition has proven to be effective in reducing CRPS symptoms [73,74,80].

Physiotherapy for upper-limb CRPS-I is likely to have a beneficial impact on the disorders and on how patients cope with the condition (level 2: Oerlemans et al. (A2), McGabe et al. (B), Fialka et al (C)).

There are indications that physiotherapy treatment may be beneficial for chronic CRPS-I (level 3: Moseley (B); Van Wilgen et al. (D)).

Physiotherapy should form a part of the standard treatment of CRPS-I (level 4).

Transcutaneous Electrical Nerve Stimulation (TENS)

Articles of limited methodological quality were found describing beneficial effects of TENS in small groups of CRPS-I (n = 10-11) patients [81,82].

There is insufficient evidence that TENS is effective in the treatment of CRPS-I (level 4).

Occupational therapy

We found one RCT evaluating the efficacy of occupational therapy in CRPS-I (n = 135) [74]. Occupational therapy provided in addition to medical treatment had a positive effect on the severity of the functional limitations, and appeared to have a positive impact on activity level [73,74].

Occupational therapy has a positive effect on functional limitations, and is likely to have a positive effect on the activity level of patients with upper-limb CRPS-I (level 3: Oerlemans et al. (A2)).

Rehabilitation medicine

Though no studies have been carried out to date evaluating the efficacy of integrated and coordinated multidisciplinary interventions for CRPS-I, experts argue for a multidisciplinary approach because of the complex nature of the condition, the possibility of a multifactorial cause, and the varying nature of its progress [6,83].

There is no evidence that multidisciplinary treatment is beneficial for CRPS-I patients (level 4: Stanton-Hicks et al. (D), Rho et al. (D)).

Psychological treatment

It has been suggested that CRPS-I might be caused or worsened and maintained by non-organic factors [23,84]. We found one RCT (n = 28) evaluating cognitive behavioural therapy in children with CRPS-I [85]. Retrospective cohort surveys or cross-sectional studies with no control group and limited follow-up are common. No scientific publications of psychological treatments administered to adults were found.

Treatment of children with CRPS I

Drug and invasive treatment in children

Little research has been published on specific drug or invasive treatments for children with CRPS-I. Most of the information is limited to descriptions of multimodal treatments [86,87], with the use of analgesics only mentioned in passing.

In a case study of limited quality, 13 children with CRPS-I (9-16 years old) [88] were evaluated to assess the effect of home administration of continuous peripheral nerve blockade (ropivacaine) combined with intensive physiotherapy. The continuous analgesia was assessed as excellent, with the motor block lasting for a limited time (12 hours). The children were able to walk within 24 hours, and none of them showed signs of CRPS-I two months later.

A case study of limited quality [89] examined continuous intravenous infusions of carbacyclin derivatives administered over three days combined with physiotherapy and psychological consultation. All 7 children with CRPS-I (aged between 6 and 11) were reported to be symptom-free after a follow-up period of 30 months on average (range: 25 to 37 months). Repeated infusion was necessary in two cases.

There is insufficient data to allow any conclusions to be drawn as to the effects of continuous peripheral nerve blockade by means of ropivacaine or continuous intravenous infusion with a carbacyclin derivative in children with CRPS-I (level 3: Dadure et al. (C), Petje et al. (C)).

Physiotherapy for children with CRPS-I

No well-designed trials have been carried out evaluating the effects of physiotherapy modalities in children with CRPS-I. Between 47 and 93% of patients (n = 10-46) are reported to recover after physical therapy [86,90]. Physiotherapy (n = 23) given once a week for six weeks appears to have the same effect as physiotherapy given three times a week for six weeks [85].

The number of children experiencing one or more relapses after treatment ranges from 10 to 48% (n = 10-103) [81,91-93].

There are indications that physiotherapy is helpful for children with CRPS-I. It is not clear which elements of physiotherapy are effective, as different forms of treatment are combined (level 3: Lee et al. (B), Barbier et al. (C), Kesler et al. (C), Maillard et al. (C), Murray et al. (C), Sherry et al. (C), Wesdock et al. (C), Wilder et al. (C)).

There are indications that children with CRPS-I may relapse after receiving physiotherapy (10-48%) (level 3:Lee et al. (B), Barbier et al. (C), Kesler et al. (C), Maillard et al. (C), Murray et al. (C), Sherry et al. (C), Wesdock et al. (C), Wilder et al. (C)).

Occupational therapy of children

An intensive treatment program (n = 23-103), comprising occupational therapy, physiotherapy and hydrotherapy, has been reported to be effective [87,92]. No conclusions can be drawn from the existing literature about children with CRPS-I with regard to the efficacy of occupational therapy.

There are indications that occupational therapy can be beneficial as part of a multidisciplinary approach to treat children with CRPS-I (level 3: Maillard et al. (C), Sherry et al. (C)).

Psychological treatment of CRPS-I in children

Relaxation therapy and biofeedback (described as cognitive behavioural therapy) in combination with physiotherapy has been evaluated for treatment of children with CRPS-I (n = 23) [85]. Relaxation therapy and biofeedback were reported to reduce both pain symptoms and physical function in 57% of cases (n = 72) [91]. It is not possible to ascertain which of the three treatments contributed most to the effects.

No conclusions can be drawn as to the effect of cognitive behavioural therapy on children with CRPS-I (level 2: Lee et al. (B), Wilder et al. (B), Sherry et al. (C)).

Prevention of CRPS-I

Primary prevention

Vitamin C

In a randomized double-blind trial (n = 123), patients with a wrist fracture treated with a plaster cast were referred for treatment with vitamin C (500 mg/day for 50 days) or a placebo. Seven percent of patients in the group taking vitamin C developed CRPS-I, as against 22% of patients in the control group (absolute risk reduction 15%, and number needed to treat 7) [94].

In a cohort study with a historic control group (n = 95), patients with wrist fractures treated by surgery were given vitamin C (1000 mg/day for 45 days). Two percent of patients in the group treated with vitamin C developed CPRS-I, compared to 10% in the control group [95].

It is likely that oral administration of 500 mg of vitamin C per day for 50 days from the date of the injury reduces the incidence of CRPS-I in patients with wrist fractures (level 2: Zollinger et al. (A2), Cazeneuve et al. (B)).

Guanethidine

In a randomized study (n = 71), patients scheduled for surgery for Dupuytren's disease were referred for pre-emptive intravenous guanethidine blockade or a placebo blockade. After eight weeks 13% of the patients taking guanethidine were found to have developed CRPS-I, as against 6% in the control group [96].

There are no indications that perioperative intravenous guanethidine in patients undergoing fasciectomy for Dupuytren's disease has any effect on the incidence of CRPS-I (level 3: Gschwind et al. (A2)).

Calcitonin

In a double blind randomized study, 91 patients undergoing wrist, knee or foot surgery were treated with for 100 IU of thyrocalcitonin administered subcutaneously (from the day of the operation or the trauma once a day for one week and three times a week for three weeks thereafter) or placebo injections. No significant differences were found between placebo and thyrocalcitonin in reducing the occurrence of CRPS-I [97].

There are no indications that subcutaneous administration of calcitonin for four weeks from the onset of the trauma or from the date of surgery can prevent patients developing CRPS-I (primary prevention) (level 3: Riou et al. (B)).

Secondary prevention

Various interventions or combinations of interventions aimed at preventing relapse of CRPS-I have been described, but little adequate research has been carried out. Relapse rates up to 13% (of 47 patients) have been reported despite combined interventions aimed at preventing relapse of CRPS-I (waiting until the symptoms of CRPS-I had abated, minimizing the use of tourniquet, administering vasodilators to encourage circulation, sympathetic blockades and mannitol) [98]. Six percent of patients with a history of CPRS-I (n = 18) treated with calcitonin (100 IU a day s.c. for four weeks) had a relapse of CRPS-I, against 28% of the patients in a historic control group (n = 74) [99]. A retrospective study (n = 50) found that peri-operative stellate ganglion blockade carried out to prevent a relapse of CRPS-I to be unsuccessful in 10% of cases. The relapse rate in an untreated control group was 72% [100].

A retrospective study (n = 1200) found that 1% of the patients undergoing anterior cruciate ligament surgery receiving pre-emptive analgesia (comprising administration of paracetamol and NSAIDs before surgery) combined with multimodal analgesia experienced a relapse of CPRS-I. The CRPS-I relapse rate for a control group, taking painkillers only as required after surgery, was 4% [101].

In a randomized double-blind study in 84 patients with a history of CRPS-I in the hand or arm scheduled for hand or arm surgery, intravenous regional blockade with lidocaine and clonidine (1 μg/kg) showed a relapse rate for clonidine of 10% against 74% in the group receiving only lidocaine [100]. Case studies point to a possible beneficial effect of regional anaesthesia, such as brachial plexus block and epidural anaesthesia [101].

Despite lack of evidence, the task force is of the opinion that operations are preferably postponed until CRPS-I signs are minimal. Preferably, regional anaesthetic techniques such as brachial plexus blockade and epidural anaesthesia should be used (level 4)

There are indications that stellate blocks and intravenous regional anaesthesia using clonidine (not guanethidine) offer protection (level 3: Reuben et al. (A2)).

There are indications that the use of multimodal analgesia offers protection (level 3: Reuben (A2).

There are indications that daily administration of 100 IU of salmon calcitonin s.c. (peri-operatively for four weeks) can prevent a relapse of CRPS-I (level 3: Kissling et al. (B)).

Discussion

Besides scientific evidence, other aspects are important in the formulation of guidelines, such as patient perspectives, availability of special techniques or expertise, organisational aspects, social consequences and costs. For the present guidelines these considerations were for a part based on Dutch perspectives. The conclusions based on scientific publications were set into the context of daily practice, and advantages and disadvantages of the various possible policies considered. The final recommendations are the result of the evidence available in combination with these considerations. This procedure followed in the present guideline development provides the opportunity to incorporate the debate between project group members in the formulation of recommendations, in order to make the guideline transparent and bring the recommendations in line with general practice.

Based on the presented evidence based evaluation of CRPS-I literature, in combination with additional considerations with regard to availability of treatment methods, side-effects, cost-benefits and consequences for organisation of care, recommendations endorsed by the participating professional societies were formulated, described additional file 3. In addition to these guidelines the task force is of the opinion that regular consultation between practitioners is desirable in order to provide uniform and clear information to the patient. In line with these observations, the task force advocates that patients should be actively informed about CRPS-I and possible consequences of this complaint, whereby verbal as well as written information should be provided. Although there is no evidence of for specific psychological profile or predisposition for patients with CRPS-I, there may be reasons to carry out further psychological investigation. Possible psychological factors maintaining and/or aggravating the syndrome need to be determined.

A limitation of the guidelines presented in this article is that only articles published up to 2006 were included, and possible relevant findings published after this date couldn't be incorporated in the present guidelines as a consequence of the formal procedure (see method section), involving the approval of participating professional societies. An additional search based on the search string used for these guidelines, revealed 45 additional articles [108-152], possibly providing information that could lead to amendment of this guideline. These articles comprised one retrospective chart review [121], one prospective cohort [120], six case series [117,125,127,128,132,133], 14 clinical trials [109,111,112,119,122,123,126,131,135,138,140,146,147,150], two controlled clinical trials [130,136], 16 RCT's [108,113,114,116,124,129,134,137,139,141,143,145,146,148,149,152], four systematic reviews/meta analyses [110,115,142,144], and one treatment guideline [118]. Interventions evaluated therein were piroxicam [114], gabapentin [126], intrathecal baclofen [146], sympathetic blockade (lumbar, stellate ganglion and intravenous) (n = 5) [122,123,134,143,149], corticosteroids (n = 3) [114,119,135], calcium regulating medication (bisphosphonates, calcitonin) (n = 4) [110,116,138,142], NMDA antagonists (magnesium sulphate, ketamine, memantine) (n = 9) [111,121,125,131,140,146-148,152], free radical scavengers (mannitol, vitamin C) (n = 3) [129,135.137], nitric oxide regulating medication (n = 3) [133,141,151], spinal cord stimulation (n = 5) [112,115,120,128,132], regional anaesthesia (n = 2) [113,117], physiotherapy and rehabilitation medicine (physiotherapy, mirror therapy, manual lymph drainage, vibratory stimulation, functional restoration, sensorimotor retuning, behavioural therapy, occlusional splints) (n = 11) [108,109,124,126,127,130,136,139,144,145,150]. Fifteen studies evaluated a combination of interventions, and four controlled studies used an active control. Two studies addressed primary prevention of CRPS I [117,129]. These studies will have to be evaluated in the next formal adaptation of these guidelines. In addition, since the publication of these guidelines information provided in two studies included in these guidelines [100,101] has been retracted due to scientific misconduct of the author. Recommendations based on these data (i.e. secondary prevention using pre-, per- and postoperative pain control and regional blockades with clonidine) therefore have to be regarded with caution.

Based on the identified literature and the extent of evidence found therein for therapeutic interventions for CRPS-I, we can conclude that further research is needed into each of the modalities discussed in these guidelines. This includes specifically treatment approaches recommended (or not advised) in these guidelines based on expert opinion, such as the use of botulin toxin and tricyclic antidepressants. Scientific data is also lacking with respect to treatment-related aspects, such as the role of the multidisciplinary approach, problems relating to work and communication with the patient and his or her family and close friends.

The project group considers that particular attention needs to be paid to further development of the diagnostic process. This development must be accompanied by research into possible underlying pathophysiological mechanisms (such as genetic factors) associated with CRPS-I, with particular attention being paid to possible sub-groups of the condition related to these underlying mechanisms.

With regard to drug treatment, further investigation is needed into the efficacy of pain medication and the percutaneous sympathetic blockade. More research is also needed into the use of drugs and invasive treatment with children suffering from CRPS-I.

In terms of paramedical treatment, the emphasis must be placed on the difference between pain contingent and a time contingent approach. Research is needed into the effects of various interventions on more long-standing (chronic) CRPS-I and into a multidisciplinary approach to CRPS-I.

Conclusions

For pain treatment, the WHO analgesic ladder is advised with the exception of strong opioids. For neuropathic pain, anticonvulsants and tricyclic antidepressants may be considered. For inflammatory symptoms, free-radical scavengers (dimethylsulphoxide or acetylcysteine) are advised. To promote peripheral blood flow, vasodilatory medication may be considered. Percutaneous sympathetic blockades may be used to increase blood flow in case vasodilatory medication has insufficient effect. To decrease functional limitations, standardised physiotherapy and occupational therapy are advised. To prevent the occurrence of CRPS-I after wrist fractures, vitamin C is recommended. Adequate perioperative analgesia, limitation of operating time, limited use of tourniquet, and use of regional anaesthetic techniques are recommended for secondary prevention of CRPS-I.

Based on the literature identified and the extent of evidence found for therapeutic interventions for CRPS-I, we conclude that further research is needed into each of the therapeutic modalities discussed in the guidelines.

Conflicts of interests

The authors declare that they have no competing interests.

Authors' contributions

All authors have read and approved the final manuscript.

RSGMP is the main author of this manuscript. He participated in establishing the guidelines presented in this manuscript, and contributed to assessment of literature and drawing up text on which these guidelines were based.

JHBG is co-author of this manuscript, and chairman of the guideline development task force. He participated in establishing the guidelines presented in this manuscript, and contributed to assessment of literature and drawing up text on which these guidelines were based.

PEZ, PUD, ILTH, WWAZ and CJGMR are co-authors of this manuscript, and participated as section chairman of the task force for sections of the guidelines. They participated in establishing the guidelines presented in this manuscript, and contributed to assessment of literature and drawing up text on which these guidelines were based.

Pre-publication history

The pre-publication history for this paper can be accessed here:

http://www.biomedcentral.com/1471-2377/10/20/prepub

Supplementary Material

Additional file 1:

Search strategy used to identify studies on CRPS. This file contains the search strings used for literature retrieval for the present guidelines.

Additional file 2:

Practical algorithm. This file contains a practical treatment algorithm based on the recommendations described in these guidelines.

Additional file 3:

Recommendations and additional considerations. This table contains the final recommendations endorsed by the professional societies participating in the guideline development, and the additional considerations related to these recommendations.

Acknowledgements

The present article provides a summary of the full version of these guidelines. The complete version of the guidelines can be obtained from at the following link: http://www.cbo.nl/thema/Richtlijnen/Overzicht-richtlijnen/Neurologische-aandoeningen/

These EBGD guidelines were developed as a result of an initiative taken by the Dutch Society of Rehabilitation Specialists (VRA) and the Dutch Society of Anaesthesiologists (NVA). The development of these guidelines was made possible by the Order of Medical Specialists (umbrella organization for all medical specialists) with methodological support from the Dutch Institute for Healthcare Improvement CBO. The authors would like to acknowledge their fellow members of the CRPS task force for their contributions to the development of the guideline: T. Beems MD, neurosurgeon, St Radboud University Medical Centre, Nijmegen; H.R. van den Brink MD PhD, rheumatologist, Alkmaar Medical Centre, Alkmaar; F. van Eijs MD, anaesthesiologist, St. Elisabeth Hospital, Tilburg; Prof Em R.J.A. Goris MD PhD, surgeon, Nijmegen; W.A.J.J.M. Haagh MD PhD, Maastricht University Hospital, Maastricht; J.J. van Hilten MD PhD, neurologist, Leiden University Medical Centre, Leiden; F.J.P.M. Huygen MD PhD, anaesthesiologist, Erasmus Medical Centre, Rotterdam; M.A. Kemler MD PhD, resident plastic surgeon, University Medical Center, Amsterdam; Prof M. van Kleef MD PhD, anaesthesiologist, Maastricht University Hospital; L. van der Laan MD PhD, surgeon, Amphia Hospital, Breda; H.M. Oerlemans MSc PhD, physiotherapist, St Radboud University Medical Centre, Nijmegen; J. Patijn MD PhD, neurologist, Maastricht University Hospital; J.M. Ruijgrok MD PhD, rehabilitation specialist, Maastricht University Hospital; F.G. Slebus MD, insurance physician, University Medical Centre, Coronel Institute, Amsterdam; S.D. Strackee MD, plastic surgeon, University Medical Centre, Amsterdam; Prof D. Tibboel MD PhD, child physician, Erasmus Medical Centre - Sophia Children's Hospital, Rotterdam; P. Theuvenet MD, anaesthesiologist, Alkmaar Medical Centre, Alkmaar; P.J.M. Veldman MD PhD, surgeon, De Tjongerschans Hospital, Heerenveen; L.A.W. van de Ven-Stevens MSc, occupational therapist, St Radboud University Medical Centre, Nijmegen; A.C.L.P.J. Verhoeven MD PhD, insurance medicine specialist, University Medical Centre, Coronel Institute, Amsterdam; G.J. Versteegen PhD, psychologist, Groningen University Medical Centre; H. Wemekamp MD, general physician, Amsterdam. External consultant W. Kuis MD PhD, child physician, University Medical Centre - Wilhelmina Children's Hospital, Utrecht.

Participating professional societies:

Royal Dutch Society for Physical Therapy, Dutch College of General Practitioners, Dutch Professional Association of Psychologists, Dutch Orthopaedic Association, Dutch Multidisciplinary Association for the Study of Pain (Dutch EFIC chapter), Netherlands Society of Neurosurgeons, Dutch Association of Posttraumatic Dystrophy Patients, Netherlands Association for Occupational and Industrial Medicine, Dutch Association of Occupational Therapy, Netherlands Society of Surgery, Netherlands Society of Paediatric Medicine, Netherlands Society of Neurology, Netherlands Society for Plastic Surgery, Netherlands Society of Rheumatology, Netherlands Society for Insurance Medicine.

References

  • Merskey H, Bogduk K. Classification of chronic pain: definitions of chronic pain syndromes and definition of pain terms. Seattle: IASP Press; 1994.
  • Stanton-Hicks M, Janig W, Hassenbusch S, Haddox JD, Boas R, Wilson P. Reflex sympathetic dystrophy: changing concepts andtaxonomy. Pain. 1995;63:127–133. doi: 10.1016/0304-3959(95)00110-E. [PubMed] [Cross Ref]
  • Veldman PH, Reynen HM, Arntz IE, Goris RJ. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet. 1993;342:1012–1016. doi: 10.1016/0140-6736(93)92877-V. [PubMed] [Cross Ref]
  • Geertzen JH, Dijkstra PU, Groothoff JW, ten Duis HJ, Eisma WH. Reflex sympathetic dystrophy of the upper extremity--a 5.5-year follow-up. Part II. Social life events, general health and changes in occupation. Acta Orthop Scand Suppl. 1998;279:19–23. [PubMed]
  • Geertzen JH, Dijkstra PU, Groothoff JW, ten Duis HJ, Eisma WH. Reflex sympathetic dystrophy of the upper extremity--a 5.5-year follow-up. Part I. Impairments and perceived disability. Acta Orthop ScandSuppl. 1998;279:12–18. [PubMed]
  • Stanton-Hicks M, Baron R, Boas R, Gordh T, Harden N, Hendler N. Complex regional pain syndromes: Guidelines for therapy. Clin J Pain. 1998;14:155–166. doi: 10.1097/00002508-199806000-00012. [PubMed] [Cross Ref]
  • Raja SN, Grabow TS. Complex regional pain syndrome I (reflex sympathetic dystrophy) Anesthesiology. 2002;96:1254–1260. doi: 10.1097/00000542-200205000-00031. [PubMed] [Cross Ref]
  • Kirkpatrick AF. Reflex sympathetic dystrophy/complex regional pain syndrome (RSD?CRPS) 2003. http://www.rsdfoundation.org/en/en_clinical_practice_guidelines.html#Treatment
  • Perez RS, Zuurmond WW, Bezemer PD, Kuik DJ, van Loenen AC, de Lange JJ. The treatment of complex regional pain syndrome type I with free radical scavengers: a randomized controlled study. Pain. 2003;102:297–307. doi: 10.1016/S0304-3959(02)00414-1. [PubMed] [Cross Ref]
  • Connelly NR, Reuben S, Brull SJ. Intravenous regional anesthesia with ketorolac-lidocaine for the management of sympathetically-mediated pain. Yale J Biol Med. 1995;68:95–99. [PMC free article] [PubMed]
  • Namaka M, Gramlich CR, Ruhlen D, Melanson M, Sutton I, Major J. A treatment algorithm for neuropathic pain. Clin Ther. 2004;26:951–979. doi: 10.1016/S0149-2918(04)90171-3. [PubMed] [Cross Ref]
  • Harke H, Gretenkort P, Ladleif HU, Rahman S, Harke O. The response of neuropathic pain and pain in complex regional pain syndrome I to carbamazepine and sustained-release morphine in patients pretreated with spinal cord stimulation: a double-blinded randomized study. Anesth Analg. 2001;92:488–495. doi: 10.1097/00000539-200102000-00039. [PubMed] [Cross Ref]
  • Azad SC, Beyer A, Romer AW, Galle-Rod A, Peter K, Schops P. Continuous axillary brachial plexus analgesia with low dose morphine in patients with complex regional pain syndromes. Eur J Anaesthesiol. 2000;17:185–188. [PubMed]
  • Duhmke RM, Cornblath DD, Hollingshead JR. Tramadol forneuropathic pain. Cochrane Database Syst Rev. 2004. p. CD003726. [PubMed]
  • Kalso E, Edwards JE, Moore RA, McQuay HJ. Opioids in chronic non-cancer pain: systematic review of efficacy and safety. Pain. 2004;112:372–380. doi: 10.1016/j.pain.2004.09.019. [PubMed] [Cross Ref]
  • Price DD, Long S, Wilsey B, Rafii A. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglia of complex regional pain syndrome patients. Clin J Pain. 1998;14:216–226. doi: 10.1097/00002508-199809000-00008. [PubMed] [Cross Ref]
  • Cooper DE, DeLee JC, Ramamurthy S. Reflex sympathetic dystrophy of the knee. Treatment using continuous epidural anesthesia. J Bone Joint Surg Am. 1989;71:365–369. [PubMed]
  • Correll GE, Maleki J, Gracely EJ, Muir JJ, Harbut RE. Subanesthetic ketamine infusion therapy: a retrospective analysis of a novel therapeutic approach to complex regional pain syndrome. Pain Med. 2004;5:263–275. doi: 10.1111/j.1526-4637.2004.04043.x. [PubMed] [Cross Ref]
  • Serpell MG. Gabapentin in neuropathic pain syndromes: a randomised, double-blind, placebo-controlled trial. Pain. 2002;99:557–566. doi: 10.1016/S0304-3959(02)00255-5. [PubMed] [Cross Ref]
  • Vusse AC van de, Berg SG Stomp-van den, Kessels AH, Weber WE. Randomised controlled trial of gabapentin in Complex Regional Pain Syndrome type 1 [ISRCTN84121379] BMC Neurol. 2004;4:13. doi: 10.1186/1471-2377-4-13. [PMC free article] [PubMed] [Cross Ref]
  • Dobbins WR, Staats PS, Levine HL, Allen RW, Campbell JN, Pappagallo P. Trestment of intractable pain with topical large dose of capsaicin: preliminary report. Anesth Analg. 1998;86:579–583. doi: 10.1097/00000539-199803000-00027. [PubMed] [Cross Ref]
  • Goris RJ, Dongen LM, Winters HA. Are toxic oxygen radicals involved in the pathogenesis of reflex sympathetic dystrophy? Free Radic Res Commun. 1987;3:13–18. doi: 10.3109/10715768709069764. [PubMed] [Cross Ref]
  • Geertzen JH, de Bruijn H, Bruijn-Kofman AT, Arendzen JH. Reflex sympathetic dystrophy: early treatment and psychological aspects. Arch Phys Med Rehabil. 1994;75:442–446. doi: 10.1016/0003-9993(94)90169-4. [PubMed] [Cross Ref]
  • Zuurmond WW, Langendijk PN, Bezemer PD, Brink HE, de Lange JJ, van Loenen AC. Treatment of acute reflex sympathetic dystrophy with DMSO 50% in a fatty cream. Acta Anaesthesiol Scand. 1996;40:364–367. doi: 10.1111/j.1399-6576.1996.tb04446.x. [PubMed] [Cross Ref]
  • van Dieten HE, Perez RS, van Tulder MW, de Lange JJ, Zuurmond WW, Ader HJ. Cost effectiveness and cost utility of acetylcysteine versus dimethyl sulfoxide for reflex sympathetic dystrophy. Pharmacoeconomics. 2003;21:139–148. doi: 10.2165/00019053-200321020-00006. [PubMed] [Cross Ref]
  • Marsden CD, Obeso JA, Traub MM, Rothwell JC, Kranz H, La CF. Muscle spasms associated with Sudeck's atrophy after injury. Br Med J (Clin Res Ed) 1984;288:173–176. doi: 10.1136/bmj.288.6412.173. [PMC free article] [PubMed] [Cross Ref]
  • Jankovic J, van der Linden C. Dystonia and tremor induced by peripheral trauma: predisposing factors. J Neurol Neurosurg Psychiatry. 1988;51:1512–1519. doi: 10.1136/jnnp.51.12.1512. [PMC free article] [PubMed] [Cross Ref]
  • Schwartzman RJ, Kerrigan J. The movement disorder of reflex sympathetic dystrophy. Neurology. 1990;40:57–61. [PubMed]
  • van Hilten JJ, Beek WJ van de, Vein AA, van Dijk JG, Middelkoop HA. Clinical aspects of multifocal or generalized tonic dystonia in reflex sympathetic dystrophy. Neurology. 2001;56:1762–1765. [PubMed]
  • Bhatia KP, Bhatt MH, Marsden CD. The causalgia-dystoniasyndrome. Brain. 1993;116(Pt 4):843–851. doi: 10.1093/brain/116.4.843. [PubMed] [Cross Ref]
  • Cordivari C, Misra VP, Catania S, Lees AJ. Treatment of dystonic clenched fist with botulinum toxin. Mov Disord. 2001;16:907–913. doi: 10.1002/mds.1186. [PubMed] [Cross Ref]
  • Zuniga RE, Perera S, Abram SE. Intrathecal baclofen: a useful agent in the treatment of well-established complex regional pain syndrome. Reg Anesth Pain Med. 2002;27:90–93. [PubMed]
  • van Hilten BJ, Beek WJ van de, Hoff JI, Voormolen JH, Delhaas EM. Intrathecal baclofen for the treatment of dystonia in patients with reflex sympathetic dystrophy. N Engl J Med. 2000;343:625–630. doi: 10.1056/NEJM200008313430905. [PubMed] [Cross Ref]
  • Kozin F, Ryan LM, Carerra GF, Soin JS, Wortmann RL. The reflex sympathetic dystrophy syndrome (RSDS). III. Scintigraphic studies, further evidence for the therapeutic efficacy of systemic corticosteroids, and proposed diagnostic criteria. Am J Med. 1981;70:23–30. doi: 10.1016/0002-9343(81)90407-1. [PubMed] [Cross Ref]
  • Grundberg AB. Reflex sympathetic dystrophy: treatment with long-acting intramuscular corticosteroids. J Hand Surg [Am] 1996;21:667–670. doi: 10.1016/S0363-5023(96)80023-2. [PubMed] [Cross Ref]
  • Christensen K, Jensen EM, Noer I. The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Scand. 1982;148:653–655. [PubMed]
  • Kingery WS. A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain. 1997;73:123–139. doi: 10.1016/S0304-3959(97)00049-3. [PubMed] [Cross Ref]
  • Berg P van den, Bierma-Zeinstra S, Koes B. Therapy for Reflex Sympathetic Dystrophy [Dutch] Huisarts Wet. 2002;45:166–171.
  • Perez RS, Kwakkel G, Zuurmond WW, de Lange JJ. Treatment of reflex sympathetic dystrophy (CRPS type 1): a research synthesis of 21 randomized clinical trials. J Pain Symptom Manage. 2001;21:511–526. doi: 10.1016/S0885-3924(01)00282-2. [PubMed] [Cross Ref]
  • Forouzanfar T, Koke AJ, van Kleef M, Weber WE. Treatment of complex regional pain syndrome type I. Eur J Pain. 2002;6:105–122. doi: 10.1053/eujp.2001.0304. [PubMed] [Cross Ref]
  • Adami S, Fossaluzza V, Gatti D, Fracassi E, Braga V. Bisphosphonate therapy of reflex sympathetic dystrophy syndrome. Ann Rheum Dis. 1997;56:201–204. doi: 10.1136/ard.56.3.201. [PMC free article] [PubMed] [Cross Ref]
  • Varenna M, Zucchi F, Ghiringhelli D, Binelli L, Bevilacqua M, Bettica P. Intravenous clodronate in the treatment of reflex sympathetic dystrophy syndrome. A randomized, double blind, placebo controlled study. J Rheumatol. 2000;27:1477–1483. [PubMed]
  • Manicourt DH, Brasseur JP, Boutsen Y, Depreseux G, Devogelaer JP. Role of alendronate in therapy for posttraumatic complex regional pain syndrome type I of the lower extremity. Arthritis Rheum. 2004;50:3690–3697. doi: 10.1002/art.20591. [PubMed] [Cross Ref]
  • Muizelaar JP, Kleyer M, Hertogs IA, DeLange DC. Complex regional pain syndrome (reflex sympathetic dystrophy and causalgia): management with the calcium channel blocker nifedipine and/or the alpha-sympathetic blocker phenoxybenzamine in 59 patients. Clin Neurol Neurosurg. 1997;99:26–30. doi: 10.1016/S0303-8467(96)00594-X. [PubMed] [Cross Ref]
  • Prough DS, McLeskey CH, Poehling GG, Koman LA, Weeks DB, Whitworth T. Efficacy of oral nifedipine in the treatment of reflex sympathetic dystrophy. Anesthesiology. 1985;62:796–799. doi: 10.1097/00000542-198506000-00017. [PubMed] [Cross Ref]
  • Jadad AR, Carroll D, Glynn CJ, McQuay HJ. 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. doi: 10.1016/0885-3924(94)00064-R. [PubMed] [Cross Ref]
  • Kaplan R, Claudio M, Kepes E, Gu XF. Intravenous guanethidine in patients with reflex sympathetic dystrophy. ActaAnaesthesiol Scand. 1996;40:1216–1222. [PubMed]
  • Livingstone JA, Atkins RM. Intravenous regional guanethidine blockade in the treatment of post-traumatic complex regional pain syndrome type 1 (algodystrophy) of the hand. J Bone Joint Surg Br. 2002;84:380–386. doi: 10.1302/0301-620X.84B3.11901. [PubMed] [Cross Ref]
  • Hennart D, Leon M, Sylin P, Appelboom T. Sympathetic nerve blocks in refractory sympathetic dystrophy syndrome. Acta Orthop Belg. 1999;65:83–85. [PubMed]
  • Glynn CJ, Basedow RW, Walsh JA. Pain relief following post-ganglionic sympathetic blockade with I.V. guanethidine. Br J Anaesth. 1981;53:1297–1302. [PubMed]
  • Driessen JJ, van der Werken C, Nicolai JP, Crul JF. Clinical effects of regional intravenous guanethidine (Ismelin) in reflex sympathetic dystrophy. Acta Anaesthesiol Scand. 1983;27:505–509. doi: 10.1111/j.1399-6576.1983.tb01996.x. [PubMed] [Cross Ref]
  • Ramamurthy S, Hoffman J. Intravenous regional guanethidine in the treatment of reflex sympathetic dystrophy/causalgia: a randomized, double-blind study. Guanethidine Study Group. Anesth Analg. 1995;81:718–723. doi: 10.1097/00000539-199510000-00011. [PubMed] [Cross Ref]
  • Malik VK, Inchiosa M-AJ, Mustafa K, Sanapati MR, Pimentel M-CJ, Frost EA. Intravenous regional phenoxybenzamine in the treatment of reflex sympathetic dystrophy. Anesthesiology. 1998;88:823–827. doi: 10.1097/00000542-199803000-00036. [PubMed] [Cross Ref]
  • Reuben SS, Sklar J. Intravenous regional anesthesia with clonidine in the management of complex regional pain syndrome of the knee. J Clin Anesth. 2002;14:87–91. doi: 10.1016/S0952-8180(01)00346-4. [PubMed] [Cross Ref]
  • Kettler RE, Abram SE. Intravenous regional droperidol in the management of reflex sympathetic dystrophy: a double-blind, placebo-controlled, crossover study. Anesthesiology. 1988;69:933–936. doi: 10.1097/00000542-198812000-00020. [PubMed] [Cross Ref]
  • Wallace MS, Ridgeway BM, Leung AY, Gerayli A, Yaksh TL. Concentration-effect relationship of intravenous lidocaine on the allodynia of complex regional pain syndrome types I and II. Anesthesiology. 2000;92:75–83. doi: 10.1097/00000542-200001000-00017. [PubMed] [Cross Ref]
  • Hanna MH, Peat SJ. Ketanserin in reflex sympathetic dystrophy. A double-blind placebo controlled cross-over trial. Pain. 1989;38:145–150. doi: 10.1016/0304-3959(89)90232-7. [PubMed] [Cross Ref]
  • Hord AH, Rooks MD, Stephens BO, Rogers HG, Fleming LL. Intravenous regional bretylium and lidocaine for treatment of reflex sympathetic dystrophy: a randomized, double-blind study. Anesth Analg. 1992;74:818–821. doi: 10.1213/00000539-199206000-00007. [PubMed] [Cross Ref]
  • Cepeda MS, Lau J, Carr DB. Defining the therapeutic role of local anesthetic sympathetic blockade in complex regional pain syndrome: a narrative and systematic review. Clin J Pain. 2002;18:216–233. doi: 10.1097/00002508-200207000-00002. [PubMed] [Cross Ref]
  • Mailis A, Furlan A. Sympathectomy for neuropathic pain. Cochrane Database Syst Rev. 2003. p. CD002918. [PubMed]
  • Bosco Vieira DJ, Kux P, Magalhaes Duarte DF. Endoscopic thoracic sympathicotomy for the treatment of complex regional pain syndrome. Clin Auton Res. 2003;13(Suppl 1):I58–I62. [PubMed]
  • Schwartzman RJ, Liu JE, Smullens SN, Hyslop T, Tahmoush AJ. Long-term outcome following sympathectomy for complex regional pain syndrome type 1 (RSD) J Neurol Sci. 1997;150:149–152. doi: 10.1016/S0022-510X(97)00078-6. [PubMed] [Cross Ref]
  • Singh B, Moodley J, Shaik AS, Robbs JV. Sympathectomy for complex regional pain syndrome. J Vasc Surg. 2003;37:508–511. doi: 10.1067/mva.2003.78. [PubMed] [Cross Ref]
  • Bandyk DF, Johnson BL, Kirkpatrick AF, Novotney ML, Back MR, Schmacht DC. Surgical sympathectomy for reflex sympathetic dystrophy syndromes. J Vasc Surg. 2002;35:269–277. doi: 10.1067/mva.2002.121065. [PubMed] [Cross Ref]
  • AbuRahma AF, Robinson PA, Powell M, Bastug D, Boland JP. Sympathectomy for reflex sympathetic dystrophy: factors affecting outcome. Ann Vasc Surg. 1994;8:372–379. doi: 10.1007/BF02133000. [PubMed] [Cross Ref]
  • Kemler MA, Barendse GA, van Kleef M, de Vet HC, Rijks CP, Furnee CA. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med. 2000;343:618–624. doi: 10.1056/NEJM200008313430904. [PubMed] [Cross Ref]
  • Kemler MA, de Vet HC, Barendse GA, Wildenberg FA van den, van Kleef M. The effect of spinal cord stimulation in patients with chronic reflex sympathetic dystrophy: two years' follow-up of the randomized controlled trial. Ann Neurol. 2004;55:13–18. doi: 10.1002/ana.10996. [PubMed] [Cross Ref]
  • Calvillo O, Racz G, Didie J, Smith K. Neuroaugmentation in the treatment of complex regional pain syndrome of the upper extremity. Acta Orthop Belg. 1998;64:57–63. [PubMed]
  • Kemler MA, Barendse GA, van Kleef M, van den Wildenberg FA, Weber WE. Electrical spinal cord stimulation in reflex sympathetic dystrophy: retrospective analysis of 23 patients. J Neurosurg. 1999;90:79–83. [PubMed]
  • Turner JA, Loeser JD, Bell KG. Spinal cord stimulation for chronic low back pain: a systematic literature synthesis. Neurosurgery. 1995;37:1088–1095. doi: 10.1097/00006123-199512000-00008. [PubMed] [Cross Ref]
  • Stam HJ, Rijst HV. The results of amputation in reflex sympathetic dystrophy of the upper extremity - an analysis of 7 cases. Physical Med Rehabil. 1994;4:134–136.
  • Dielissen PW, Claassen AT, Veldman PH, Goris RJ. Amputation for reflex sympathetic dystrophy. J Bone Joint Surg Br. 1995;77:270–273. [PubMed]
  • Oerlemans HM, Oostendorp RA, de Boo T, Goris RJ. 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. doi: 10.1016/S0304-3959(99)00080-9. [PubMed] [Cross Ref]
  • Oerlemans HM, Oostendorp RA, de Boo T, van der Laan L, Severens JL, Goris JA. Adjuvant physical therapy versus occupational therapy in patients with reflex sympathetic dystrophy/complex regional pain syndrome type I. Arch Phys Med Rehabil. 2000;81:49–56. doi: 10.1053/apmr.2000.0810049. [PubMed] [Cross Ref]
  • Severens JL, Oerlemans HM, Weegels AJ, 't Hof MA, Oostendorp RA, Goris RJ. Cost-effectiveness analysis of adjuvant physical or occupational therapy for patients with reflex sympathetic dystrophy. Arch PhysMed Rehabil. 1999;80:1038–1043. doi: 10.1016/S0003-9993(99)90057-6. [PubMed] [Cross Ref]
  • van Wilgen CP, Geertzen JH, Dijkstra PU. Complex regional pain syndrome type I, treated as a chronic pain syndrome. Ned TijschriftFysiother. 2002;112:69–76.
  • Fialka V, Wickenhauser J, Engel A, Schneider B. Sympathetic reflex dystrophy. Effectiveness of physical therapy treatment of Sudeck's syndrome. Fortschr Med. 1992;110:146–148. [PubMed]
  • McCabe CS, Haigh RC, Ring EF, Halligan PW, Wall PD, Blake DR. A controlled pilot study of the utility of mirror visual feedback in the treatment of complex regional pain syndrome (type 1) Rheumatology (Oxford) 2003;42:97–101. doi: 10.1093/rheumatology/keg041. [PubMed] [Cross Ref]
  • Moseley GL. Graded motor imagery is effective for long-standing complex regional pain syndrome: a randomised controlled trial. Pain. 2004;108:192–198. doi: 10.1016/j.pain.2004.01.006. [PubMed] [Cross Ref]
  • Oerlemans HM, Oosterhof J. Phyiotherapy for posttraumatic dystrophy/complex regional pain syndrome type I: analysis of a physiotherapy treatment protocol. Ned Tijdschr Fysiother. 2003;113:2–10.
  • Kesler RW, Saulsbury FT, Miller LT, Rowlingson JC. Reflex sympathetic dystrophy in children: treatment with transcutaneous electric nerve stimulation. Pediatrics. 1988;82:728–732. [PubMed]
  • Robaina FJ, Dominguez M, Diaz M, Rodriguez JL, de Vera JA. Spinal cord stimulation for relief of chronic pain in vasospastic disorders of the upper limbs. Neurosurgery. 1989;24:63–67. doi: 10.1097/00006123-198901000-00010. [PubMed] [Cross Ref]
  • Rho RH, Brewer RP, Lamer TJ, Wilson PR. Complex regional pain syndrome. Mayo Clin Proc. 2002;77:174–180. doi: 10.4065/77.2.174. [PubMed] [Cross Ref]
  • Van Houdenhove B, Vasquez G, Onghena P, Stans L, Vandeput C, Vermaut G. Etiopathogenesis of reflex sympathetic dystrophy: a review and biopsychosocial hypothesis. Clin J Pain. 1992;8:300–306. [PubMed]
  • Lee BH, Scharff L, Sethna NF, McCarthy CF, Scott-Sutherland J, Shea AM. Physical therapy and cognitive-behavioral treatment for complex regional pain syndromes. J Pediatr. 2002;141:135–140. doi: 10.1067/mpd.2002.124380. [PubMed] [Cross Ref]
  • Murray CS, Cohen A, Perkins T, Davidson JE, Sills JA. Morbidity in reflex sympathetic dystrophy. Arch Dis Child. 2000;82:231–233. doi: 10.1136/adc.82.3.231. [PMC free article] [PubMed] [Cross Ref]
  • Maillard SM, Davies K, Khubchandani R, Woo PM, Murray KJ. Reflex sympathetic dystrophy: a multidisciplinary approach. Arthritis Rheum. 2004;51:284–290. doi: 10.1002/art.20249. [PubMed] [Cross Ref]
  • Dadure C, Motais F, Ricard C, Raux O, Troncin R, Capdevila X. Continuous peripheral nerve blocks at home for treatment of recurrent complex regional pain syndrome I in children. Anesthesiology. 2005;102:387–391. doi: 10.1097/00000542-200502000-00022. [PubMed] [Cross Ref]
  • Petje G, Radler C, Aigner N, Walik N, Kriegs AG, Grill F. Treatment of reflex sympathetic dystrophy in children using a prostacyclin analog: preliminary results. Clin Orthop Relat Res. 2005. pp. 178–182. [PubMed] [Cross Ref]
  • Barbier O, Allington N, Rombouts JJ. Reflex sympathetic dystrophy in children: review of a clinical series and description of the particularities in children. Acta Orthop Belg. 1999;65:91–97. [PubMed]
  • Wilder RT, Berde CB, Wolohan M, Vieyra MA, Masek BJ, Micheli LJ. Reflex sympathetic dystrophy in children. Clinical characteristics and follow-up of seventy patients. J Bone Joint Surg Am. 1992;74:910–919. [PubMed]
  • Sherry DD, Wallace CA, Kelley C, Kidder M, Sapp L. Short- and long-term outcomes of children with complex regional pain syndrome type I treated with exercise therapy. Clin J Pain. 1999;15:218–223. doi: 10.1097/00002508-199909000-00009. [PubMed] [Cross Ref]
  • Wesdock KA, Stanton RP, Singsen BH. Reflex sympathetic dystrophy in children. A physical therapy approach. Arthritis Care Res. 1991;4:32–38. doi: 10.1002/art.1790040107. [PubMed] [Cross Ref]
  • Zollinger PE, Tuinebreijer WE, Kreis RW, Breederveld RS. Effect of vitamin C on frequency of reflex sympathetic dystrophy in wrist fractures: a randomised trial. Lancet. 1999;354:2025–2028. doi: 10.1016/S0140-6736(99)03059-7. [PubMed] [Cross Ref]
  • Cazeneuve JF, Leborgne JM, Kermad K, Hassan Y. Vitamin C and prevention of reflex sympathetic dystrophy following surgical management of distal radius fractures. Acta Orthop Belg. 2002;68:481–484. [PubMed]
  • Gschwind C, Fricker R, Lacher G, Jung M. Does peri-operative guanethidine prevent reflex sympathetic dystrophy? J HandSurg [Br] 1995;20:773–775. [PubMed]
  • Riou C, Daoudi Y, Langlais F, Pawlotsky Y, Cheverry C. Can algodystrophy be prevented by thyrocalcitonin? Rev Chir Orthop Reparatrice Appar Mot. 1991;77:208–210. [PubMed]
  • Veldman PH, Goris RJ. Surgery on extremities with reflex sympathetic dystrophy. Unfallchirurg. 1995;98:45–48. [PubMed]
  • Kissling RO, Bloesch AC, Sager M, Dambacher MA, Schreiber A. Prevention of recurrence of Sudeck's disease with calcitonin. Rev Chir Orthop Reparatrice Appar Mot. 1991;77:562–567. [PubMed]
  • Reuben SS, Rosenthal EA, Steinberg RB, Faruqi S, Kilaru PA. Surgery on the affected upper extremity of patients with a history of complex regional pain syndrome: the use of intravenous regional anesthesia with clonidine. J Clin Anesth. 2004;16:517–522. doi: 10.1016/j.jclinane.2004.02.001. [PubMed] [Cross Ref]
  • Reuben SS. Preventing the development of complex regional pain syndrome after surgery. Anesthesiology. 2004;101:1215–1224. doi: 10.1097/00000542-200411000-00023. [PubMed] [Cross Ref]
  • Kemler MA, Furnee CA. Economic evaluation of spinal cord stimulation for chronic reflex sympathetic dystrophy. Neurology. 2002;59:1203–1209. doi: 10.1001/archneur.59.7.1203. [PubMed] [Cross Ref]
  • Vacariu G. Complex regional pain syndrome. Disabil Rehabil. 2002;24:435–442. doi: 10.1080/09638280110108869. [PubMed] [Cross Ref]
  • Cup EH, Ven-Stevens LA van de, Corstens-Mignot MA. Complex regional pain syndrome type I (CRPS-I): Stadard occupational therapy for CRPS-I of the upper extremity. Ned Tijdschr Ergother. 1999;27:122–126.
  • Hardy MA, Hardy SG. Reflex sympathetic dystrophy: the clinician's perspective. J Hand Ther. 1997;10:137–150. [PubMed]
  • Hareau J. What makes treatment for reflex sympathetic dystrophy successful? J Hand Ther. 1996;9:367–370. [PubMed]
  • Marx C, Wiedersheim P, Michel BA, Stucki G. Preventing recurrence of reflex sympathetic dystrophy in patients requiring an operative intervention at the site of dystrophy after surgery. Clin Rheumatol. 2001;20:114–118. doi: 10.1007/s100670170080. [PubMed] [Cross Ref]
  • Moseley GL. Is successful rehabilitation of complex regional pain syndrome due to sustained attention to the affected limb? A randomised clinical trial. Pain. 2005;114:54–61. doi: 10.1016/j.pain.2004.11.024. [PubMed] [Cross Ref]
  • Pleger B, Tegenthoff M, Ragert P, Forster AF, Dinse HR, Schwenkreis P. Sensorimotor retuning [corrected] in complex regional pain syndrome parallels pain reduction. Ann Neurol. 2005;57:425–429. doi: 10.1002/ana.20394. [PubMed] [Cross Ref]
  • Chauvineau V, Codine P, Herisson C, Pellas F, Pelissier J. What is the place of diphosphonates in the treatment of complex regional pain syndrome I? Ann Readapt Med Phys. 2005;48:150–157. [PubMed]
  • Goldberg ME, Domsky R, Scaringe D, Hirsh R, Dotson J, Sharaf I. Multi-day low dose ketamine infusion for the treatment of complex regional pain syndrome. Pain Physician. 2005;8:175–179. [PubMed]
  • Harke H, Gretenkort P, Ladleif HU, Rahman S. Spinal cord stimulation in sympathetically maintained complex regional pain syndrome type I with severe disability. A prospective clinical study. Eur J Pain. 2005;9:363–373. doi: 10.1016/j.ejpain.2004.09.003. [PubMed] [Cross Ref]
  • Frade LC, Lauretti GR, Lima IC, Pereira NL. The antinociceptive effect of local or systemic parecoxib combined with lidocaine/clonidine intravenous regional analgesia for complex regional pain syndrome type I in the arm. Anesth Analg. 2005;101:807–811. doi: 10.1213/01.ane.0000166980.45162.1c. [PubMed] [Cross Ref]
  • Kalita J, Vajpayee A, Misra UK. Comparison of prednisolone with piroxicam in complex regional pain syndrome following stroke: a randomized controlled trial. QJM. 2006;99:89–95. doi: 10.1093/qjmed/hcl004. [PubMed] [Cross Ref]
  • 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;10:91–101. doi: 10.1016/j.ejpain.2005.02.004. [PubMed] [Cross Ref]
  • Sahin F, Yilmaz F, Kotevoglu N, Kuran B. Efficacy of salmon calcitonin in complex regional pain syndrome (type 1) in addition to physical therapy. Clin Rheumatol. 2006;25:143–148. doi: 10.1007/s10067-005-1153-2. [PubMed] [Cross Ref]
  • Jenson MG, Sorensen RF. Early use of regional and local anesthesia in a combat environment may prevent the development of complex regional pain syndrome in wounded combatants. Mil Med. 2006;171:396–398. [PubMed]
  • Harden RN, Swan M, King A, Costa B, Barthel J. Treatment of complex regional pain syndrome: functional restoration. Clin J Pain. 2006;22:420–424. doi: 10.1097/01.ajp.0000194280.74379.48. [PubMed] [Cross Ref]
  • Bianchi C, Rossi S, Turi S, Brambilla A, Felisari G, Mascheri D. Long-term functional outcome measures in corticosteroid-treated complex regional pain syndrome. Eura Medicophys. 2006;42:103–111. [PubMed]
  • Kemler MA, de Vet HC, Barendse GA, Wildenberg FA van den, van KM. Spinal cord stimulation for chronic reflex sympathetic dystrophy--five-year follow-up. N Engl J Med. 2006;354:2394–2396. doi: 10.1056/NEJMc055504. [PubMed] [Cross Ref]
  • Webster LR, Walker MJ. Safety and efficacy of prolonged outpatient ketamine infusions for neuropathic pain. Am J Ther. 2006;13:300–305. doi: 10.1097/00045391-200607000-00004. [PubMed] [Cross Ref]
  • Paraskevas KI, Michaloglou AA, Briana DD, Samara M. Treatment of complex regional pain syndrome type I of the hand with a series of intravenous regional sympathetic blocks with guanethidine and lidocaine. Clin Rheumatol. 2006;25:687–693. doi: 10.1007/s10067-005-0122-0. [PubMed] [Cross Ref]
  • Ackerman WE, Zhang JM. Efficacy of stellate ganglion blockade for the management of type 1 complex regional pain syndrome. SouthMed J. 2006;99:1084–1088. [PubMed]
  • Moseley GL. Graded motor imagery for pathologic pain: a randomized controlled trial. Neurology. 2006;67:2129–2134. doi: 10.1212/01.wnl.0000249112.56935.32. [PubMed] [Cross Ref]
  • Sinis N, Birbaumer N, Gustin S, Schwarz A, Bredanger S, Becker ST. Memantine treatment of complex regional pain syndrome: a preliminary report of six cases. Clin J Pain. 2007;23:237–243. doi: 10.1097/AJP.0b013e31802f67a7. [PubMed] [Cross Ref]
  • Tan AK, Duman I, Taskaynatan MA, Hazneci B, Kalyon TA. The effect of gabapentin in earlier stage of reflex sympathetic dystrophy. Clin Rheumatol. 2007;26:561–565. doi: 10.1007/s10067-006-0350-y. [PubMed] [Cross Ref]
  • Tichelaar YIGV, Geertzen JHB, Keizer D, van Wilgen CP. Mirror box therapy added to cognitive behavioural therapy in three chronic complex regional pain syndrome type I patients: a pilot study. Int JRehab Res. 2007;30:181–188. doi: 10.1097/MRR.0b013e32813a2e4b. [PubMed] [Cross Ref]
  • Verdolin MH, Stedje-Larsen ET, Hickey AH. Ten consecutive cases of complex regional pain syndrome of less than 12 months duration in active duty United States military personnel treated with spinal cord stimulation. Anesth Analg. 2007;104:1557–1560. doi: 10.1213/01.ane.0000264087.93163.bf. [PubMed] [Cross Ref]
  • Zollinger PE, Tuinebreijer WE, Breederveld RS, Kreis RW. Can vitamin C prevent complex regional pain syndrome in patients with wrist fractures? A randomized, controlled, multicenter dose-response study. J Bone Joint Surg Am. 2007;89:1424–1431. doi: 10.2106/JBJS.F.01147. [PubMed] [Cross Ref]
  • Gay A, Parratte S, Salazard B, Guinard D, Pham T, Legre R. Proprioceptive feedback enhancement induced by vibratory stimulation in complex regional pain syndrome type I: an open comparative pilot study in 11 patients. Joint Bone Spine. 2007;74:461–466. doi: 10.1016/j.jbspin.2006.10.010. [PubMed] [Cross Ref]
  • Kiefer RT, Rohr P, Ploppa A, Nohe B, Dieterich HJ, Grothusen J. A pilot open-label study of the efficacy of subanesthetic isomeric S(+)-ketamine in refractory CRPS patients. Pain Med. 2008;9:44–54. doi: 10.1111/j.1526-4637.2006.00223.x. [PubMed] [Cross Ref]
  • Olsson GL, Meyerson BA, Linderoth B. Spinal cord stimulation in adolescents with complex regional pain syndrome type I (CRPS-I) Eur J Pain. 2008;12:53–59. doi: 10.1016/j.ejpain.2007.02.007. [PubMed] [Cross Ref]
  • Groeneweg G, Niehof S, Wesseldijk F, Huygen FJ, Zijlstra FJ. Vasodilative effect of isosorbide dinitrate ointment in complex regional pain syndrome type 1. Clin J Pain. 2008;24:89–92. doi: 10.1097/AJP.0b013e318156db3b. [PubMed] [Cross Ref]
  • Manjunath PS, Jayalakshmi TS, Dureja GP, Prevost AT. Management of lower limb complex regional pain syndrome type 1: an evaluation of percutaneous radiofrequency thermal lumbar sympathectomy versus phenol lumbar sympathetic neurolysis--a pilot study. Anesth Analg. 2008;106:647–649. doi: 10.1213/01.ane.0000298285.39480.28. [PubMed] [Cross Ref]
  • Zyluk A, Puchalski P. Treatment of early complex regional pain syndrome type 1 by a combination of mannitol and dexamethasone. JHand Surg Eur Vol. 2008;33:130–136. [PubMed]
  • Moseley GL, Zalucki N, Birklein F, Marinus J, van Hilten JJ, Luomajoki H. Thinking about movement hurts: the effect of motor imagery on pain and swelling in people with chronic arm pain. Arthritis Rheum. 2008;59:623–631. doi: 10.1002/art.23580. [PubMed] [Cross Ref]
  • Perez RS, Pragt E, Geurts J, Zuurmond WW, Patijn J, van Kleef M. Treatment of patients with complex regional pain syndrome type I with mannitol: a prospective, randomized, placebo-controlled, double-blinded study. J Pain. 2008;9:678–686. doi: 10.1016/j.jpain.2008.02.005. [PubMed] [Cross Ref]
  • Breuer B, Pappagallo M, Ongseng F, Chen CI, Goldfarb R. An open-label pilot trial of ibandronate for complex regional pain syndrome. Clin J Pain. 2008;24:685–689. doi: 10.1097/AJP.0b013e318175920f. [PubMed] [Cross Ref]
  • Fischer MJ, Reiners A, Kohnen R, Bernateck M, Gutenbrunner C, Fink M. Do Occlusal Splints Have an Effect on Complex Regional Pain Syndrome? A Randomized, Controlled Proof-of-concept Trial. Clinical Journal of Pain. 2008;24:776–783. doi: 10.1097/AJP.0b013e3181790355. [PubMed] [Cross Ref]
  • Kiefer RT, Rohr P, Ploppa A, Dieterich HJ, Grothusen J, Koffler S. Efficacy of ketamine in anesthetic dosage for the treatment of refractory complex regional pain syndrome: an open-label phase II study. Pain Med. 2008;9:1173–1201. doi: 10.1111/j.1526-4637.2007.00402.x. [PubMed] [Cross Ref]
  • Groeneweg G, Huygen FJ, Niehof SP, Wesseldijk F, Bussmann JB, Schasfoort FC. Effect of tadalafil on blood flow, pain, and function in chronic cold complex regional pain syndrome: a randomized controlled trial. BMC Musculoskelet Disord. 2008;9:143. doi: 10.1186/1471-2474-9-143. [PMC free article] [PubMed] [Cross Ref]
  • Brunner F, Schmid A, Kissling R, Held U, Bachmann LM. Biphosphonates for the therapy of complex regional pain syndrome I--systematic review. Eur J Pain. 2009;13:17–21. doi: 10.1016/j.ejpain.2008.03.005. [PubMed] [Cross Ref]
  • Carroll I, Clark JD, Mackey S. Sympathetic block with botulinum toxin to treat complex regional pain syndrome. Ann Neurol. 2009;65:348–351. doi: 10.1002/ana.21601. [PMC free article] [PubMed] [Cross Ref]
  • Daly AE, Bialocerkowski AE. Does evidence support physiotherapy management of adult Complex Regional Pain Syndrome Type One? A systematic review. Eur J Pain. 2009;13:339–353. doi: 10.1016/j.ejpain.2008.05.003. [PubMed] [Cross Ref]
  • Duman I, Ozdemir A, Tan AK, Dincer K. The efficacy of manual lymphatic drainage therapy in the management of limb edema secondary to reflex sympathetic dystrophy. Rheumatol Int. 2009;29:759–763. doi: 10.1007/s00296-008-0767-5. [PubMed] [Cross Ref]
  • van Rijn MA, Munts AG, Marinus J, Voormolen JH, deBoer KS, Teepe-Twiss IM. Intrathecal baclofen for dystonia of complex regional pain syndrome. Pain. 2009;143:41–47. doi: 10.1016/j.pain.2009.01.014. [PubMed] [Cross Ref]
  • Sigtermans M, Noppers I, Sarton E, Bauer M, Mooren R, Olofsen E. An observational study on the effect of S(+)-ketamine on chronic pain versus experimental acute pain in Complex Regional Pain Syndrome type 1 patients. Eur J Pain. 2010;14:302–307. doi: 10.1016/j.ejpain.2009.05.012. [PubMed] [Cross Ref]
  • Collins S, Zuurmond WW, de Lange JJ, van Hilten BJ, Perez RS. Intravenous magnesium for complex regional pain syndrome type 1 (CRPS 1) patients: a pilot study. Pain Med. 2009;10:930–940. doi: 10.1111/j.1526-4637.2009.00639.x. [PubMed] [Cross Ref]
  • Meier PM, Zurakowski D, Berde CB, Sethna NF. Lumbar sympathetic blockade in children with complex regional pain syndromes: a double blind placebo-controlled crossover trial. Anesthesiology. 2009;111:372–380. doi: 10.1097/ALN.0b013e3181aaea90. [PMC free article] [PubMed] [Cross Ref]
  • Moseley GL, Wiech K. The effect of tactile discrimination training is enhanced when patients watch the reflected image of their unaffected limb during training. Pain. 2009;144:314–319. doi: 10.1016/j.pain.2009.04.030. [PubMed] [Cross Ref]
  • Groeneweg JG, Huygen FJ, Niehof SP, Wesseldijk F, Bussmann JB, Schasfoort FC. No recovery of cold complex regional pain syndrome after transdermal isosorbide dinitrate: a small controlled trial. J Pain Symptom Manage. 2009;38:401–408. doi: 10.1016/j.jpainsymman.2008.10.006. [PubMed] [Cross Ref]
  • Sigtermans MJ, van Hilten JJ, Bauer MC, Arbous MS, Marinus J, Sarton EY. Ketamine produces effective and long-term pain relief in patients with Complex Regional Pain Syndrome Type 1. Pain. 2009;145:304–311. doi: 10.1016/j.pain.2009.06.023. [PubMed] [Cross Ref]

Articles from BMC Neurology are provided here courtesy of BioMed Central
PubReader format: click here to try

Formats:

Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...

Links

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...