Spatial and temporal aspects of deep tissue pain assessed by cuff algometry

Complex regional pain syndrome type I (CRPS I) is a chronic painful disease of one extremity that may develop as a disproportionate consequence of a trauma affecting the limbs without overt nerve injury. It is clinically characterized by sensory, motor and autonomic symptoms including vascular abnormalities. Previously, we have reported that pathophysiological alterations of the ongoing sympathetic activity play a crucial role in vasomotor disturbances (Brain 124 (2001) 587). As a companion article, the aim of this study was to evaluate the diagnostic value of skin temperature side differences in consideration of the spontaneous sympathetic vasoconstrictor activity. Twenty-five patients with CRPS I were studied. Fifteen patients with painful limbs of other origin and 20 healthy individuals served as controls. Controlled thermoregulation was performed to change cutaneous sympathetic vasoconstrictor activity by the use of a thermal suit: skin sympathetic vasoconstrictor neurones were activated by whole-body cooling and nerve activity was abolished by whole-body warming. Skin temperature at the affected and unaffected limbs (infra-red thermometry) was measured under resting conditions and continuously monitored during controlled modulation of sympathetic activity. The results showed only minor skin temperature asymmetries between both limbs under resting conditions in most CRPS patients. However, during controlled thermoregulation temperature differences between both sides increased dynamically and were most prominent at a high to medium level of vasoconstrictor activity. In both control groups, there were only minor side differences in temperature both in rest and during thermoregulatory changes of sympathetic activity. When comparing the diagnostic value of skin temperature asymmetries in CRPS I, sensitivity was only 32% under resting conditions, but increased up to 76% during controlled alteration of sympathetic activity. Specificity was 100% at rest and 93% at controlled thermoregulation. We concluded that the degree of unilateral vascular disturbances in CRPS I depends critically on spontaneous sympathetic activity. Taking this into consideration, skin temperature differences in the distal limbs are capable of reliably distinguishing CRPS I from other extremity pain syndromes with high sensitivity and specificity.     

Complex regional pain syndromes

Complex regional pain syndromes (CRPS) (formerly reflex sympathetic dystrophy and causalgia) are neuropathic pain conditions that are initiated by an extremity trauma or peripheral nerve lesion. Clinical definition and scientific understanding of CRPS are still evolving; however, both the clinical picture and therapeutic options are significantly influenced by a dysfunction of the sympathetic nervous system. Recent investigations suggest functional central abnormalities and a peripheral inflammatory component in the pathophysiology of CRPS. Interdisciplinary treatment includes physical, pharmacologic, and invasive interventional therapy, as well as stimulation techniques.     

Pathophysiological Mechanisms Involved in Vasomotor Disturbances in Complex Regional Pain Syndrome and Implications for Therapy: A Review

Complex regional pain syndrome (CRPS) is characterized by continuous pain, disproportional to the initial trauma. It usually spreads to the distal parts of the affected limb. Besides continuing pain, a mix of sensory, sudo‐ and vasomotor disturbances, motor dysfunction, and trophic changes is responsible for physical complaints. Vasomotor disturbance is characterized by changes in skin temperature and color. In CRPS patients with a cold extremity, a decrease in blood flow can cause decreased tissue saturation and tissue acidosis, resulting in ischemic pain. The pathophysiology of vasomotor disturbances is not completely understood. Temperature asymmetry is generally assumed as a result of disturbance in the sympathetic nervous system. Vasodilating drugs and sympathetic blockade have been cornerstones of therapy in cold CRPS for years. However, only a limited part of these patients improve on this kind of therapies. Research has shown a pivotal role for inflammation in the pathophysiology of CRPS. Inflammation can result in endothelial dysfunction. Endothelial function plays an important role in the local regulation of vascular tone. Endothelial dysfunction could be another mechanism responsible for the vasomotor disturbances in cold CRPS. An important goal in the treatment of cold‐type CRPS is the restoration of a normal blood flow. Consequently it is important to distinguish the underlying pathophysiological mechanisms of vasomotor disturbances. A disturbance of the sympathetic nervous system may require another type of treatment than inflammation‐induced endothelial dysfunction. Diagnostic tools to distinguish these underlying pathophysiological mechanisms of vasomotor disturbances would enable a mechanism‐based treatment and improve clinical outcome.     

Stellate ganglion blockade (SGB) for refractory index finger pain - a case report

ObjectiveTo identify through case study the presentation and possible pathophysiological cause of complex regional pain syndrome and its preferential response to stellate ganglion blockade.SettingComplex regional pain syndrome can occur in an extremity after minor injury, fracture, surgery, peripheral nerve insult or spontaneously and is characterised by spontaneous pain, changes in skin temperature and colour, oedema, and motor disturbances. Pathophysiology is likely to involve peripheral and central components and neurological and inflammatory elements. There is no consistent approach to treatment with a wide variety of specialists involved. Diagnosis can be difficult, with over-diagnosis resulting from undue emphasis placed upon pain disproportionate to an inciting event despite the absence of other symptoms or under-diagnosed when subtle symptoms are not recognised. The International Association for the Study of Pain supports the use of sympathetic blocks to reduce sympathetic nervous system overactivity and relieve complex regional pain symptoms. Educational reviews promote stellate ganglion blockade as beneficial. Three blocks were given at 8, 10 and 13 months after the initial injury under local anaesthesia and sterile conditions. Physiotherapeutic input was delivered under block conditions to maximise joint and tissue mobility and facilitate restoration of function.ConclusionThis case demonstrates the need for practitioners from all disciplines to be able to identify the clinical characteristics of complex regional pain syndrome to instigate immediate treatment and supports the notion that stellate ganglion blockade is preferable to upper limb intravenous regional anaesthetic block for refractory index finger pain associated with complex regional pain syndrome.     

Early aggressive treatment improves prognosis in complex regional pain syndrome

Complex regional pain syndrome (CRPS) is divided into two types. Type I occurs without obvious nerve injury. In type II, a peripheral nerve injury is present, although pain may not be limited to the distribution of that nerve. Diagnosis rests on the presence of a constellation of symptoms and signs. These include extreme sensitivity, changing skin colour and temperature, trophic changes in the skin, nails and hair, reduced range of motion and loss of function. These features are accompanied by considerable pain for which no other unifying diagnosis can be made. CRPS typically starts with an injury to an extremity which is often seemingly trivial, followed by immobilisation, such as an ankle sprain or Colles' fracture. Instead of the expected resolution of symptoms, persistent pain and dysfunction develop. CRPS usually has an early warm phase that suggests an inflammatory process, with local swelling, erythema and heat. It then progresses to a cold phase, which often goes on for months or years. It is important to keep the affected part moving as much as possible, especially in the early stages. Sensory stimulation, particularly by self-massage, is advised. Aggressive treatment in the early stages improves prognosis. Many cases, especially those with relatively minor symptoms, will resolve spontaneously. Patients who are symptomatically deteriorating, despite regular analgesia, neuropathic agents and physiotherapy, should be referred to a specialist.     

Complex regional pain syndrome: a review of diagnostics, pathophysiologic mechanisms, and treatment implications for certified registered nurse anesthetists

The pathophysiologic mechanisms for complex regional pain syndrome (CRPS) are complex and elusive. The proposed etiologic mechanisms for CRPS include inflammatory responses, peripheral or central sensitization, and sympathetic dysfunction. Anesthesia care of patients with CRPS is challenging. Treatments including physiotherapy, peripheral vasodilators, sympathetic blockade, analgesics, and other systemic medications can help optimize mobility, perfusion, and pain relief for affected patients.     

Despite clinical similarities there are significant differences between acute limb trauma and complex regional pain syndrome I (CRPS I).

In order to analyze the pathophysiology behind the clinical similarity acutely after limb trauma and in acute stages of complex regional pain syndrome (CRPS), 20 patients with external fixation after distal radius fracture (3.5 days after surgery) without signs of CRPS and 24 patients suffering from acute CRPS I (without nerve lesion; duration, 5 weeks) were investigated. Hyperalgesia to heat was tested by a feedback-controlled thermode, and to mechanical stimuli by an impact stimulator. The sympathetic nervous system was examined by measuring skin temperature (infra-red thermography), testing different sympathetic vasoconstrictor reflexes (laser-Doppler flowmetry) and quantitative sudometry after thermal load (thermoregulatory sweat test). We found hyperalgesia to heat after trauma (P<0.001), but not in CRPS, whereas mechanical hyperalgesia was present in both patient groups (trauma: P<0.001; CRPS: P<0.005). Skin temperature was significantly increased on the affected side in both patient groups (acute trauma: P<0.001; CRPS: P<0.005). However, sympathetic failure, as indicated by impairment of sympathetic vasoconstrictor reflexes (P<0.02) and hyperhidrosis (P<0.01), was found exclusively in CRPS patients. Our results indicate that pain and vasomotor disturbances may be generated by different mechanisms acutely after trauma and in acute CRPS. Despite the clinical similarity, additional changes in the peripheral or central nervous system are required for CRPS. In the light of our observations, it seems unlikely that CRPS is a simple exaggeration of post-traumatic inflammation.     

Complex regional pain syndromes: the influence of cutaneous and deep somatic sympathetic innervation on pain

OBJECTIVES: Complex regional pain syndromes (CRPS) can be relieved by sympathetic blockade. Different sympathetic efferent output channels innervate distinct effector organs (ie, cutaneous vasoconstrictor, muscle vasoconstrictor. and sudomotor neurons, as well as neurons innervating deep somatic tissues like bone, joints, and tendons). The aim of the present study was to elucidate in CRPS patients the sympathetically maintained pain (SMP) component that exclusively depends on cutaneous sympathetic activity compared with the SMP depending on the sympathetic innervation of deep somatic tissues. METHODS: The sympathetic outflow to the painful skin was modulated selectively in awake humans. High and low cutaneous vasoconstrictor activity was produced in 12 CRPS type 1 patients by whole-body cooling and warming (thermal suit). Spontaneous pain was quantified during high and low cutaneous vasoconstrictor activity. By comparing the cutaneous SMP component with the change in pain that was achieved by modulation of the entire sympathetic outflow (sympathetic ganglion block), the SMP component originating in deep somatic structures was estimated. RESULTS: The relief of spontaneous pain after sympathetic blockade was more pronounced than changes in spontaneous pain that could be induced by selective sympathetic cutaneous modulation. The entire SMP component (cutaneous and deep) changes considerably over time. It is most prominent in the acute stages of CRPS. CONCLUSIONS: Sympathetic afferent coupling takes place in the skin and in the deep somatic tissues, but especially in the acute stages of CRPS, the pain component that is influenced by the sympathetic innervation of deep somatic structures is more important than the cutaneous activation. The entire sympathetic maintained pain component is not constant in the course of the disease but decreases over time.     

Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome

Complex regional pain syndromes (CRPS, type I and type II) are devastating conditions that can occur following soft tissue (CRPS type I) or nerve (CRPS type II) injury. CRPS type I, also known as reflex sympathetic dystrophy, presents in patients lacking a well-defined nerve lesion, and has been questioned as to whether or not it is a true neuropathic condition with an organic basis. As described here, glabrous and hairy skin samples from the amputated upper and lower extremity from two CRPS type I diagnosed patients were processed for double-label immunofluorescence using a battery of antibodies directed against neural-related proteins and mediators of nociceptive sensory function. In CRPS affected skin, several neuropathologic alterations were detected, including: (1) the presence of numerous abnormal thin caliber NF-positive/MBP-negative axons innervating hair follicles; (2) a decrease in epidermal, sweat gland, and vascular innervation; (3) a loss of CGRP expression on remaining innervation to vasculature and sweat glands; (4) an inappropriate expression of NPY on innervation to superficial arterioles and sweat glands; and (5) a loss of vascular endothelial integrity and extraordinary vascular hypertrophy. The results are evidence of widespread cutaneous neuropathologic changes. Importantly, in these CRPS type I patients, the myriad of clinical symptoms observed had detectable neuropathologic correlates.     

Shoulder-hand syndrome after stroke. A complex regional pain syndrome

Complex regional pain syndrome (CRPS) types I and II are neuropathic pain disorders that develop as an exaggerated response to a traumatic lesion or nerve damage, that generally affects the extremities, or as the consequence of a distant process such as a stroke, spinal lesion or myocardial infarction. It rarely appears without an apparent cause. CRPS of upper limbs after stroke is frequently today called shoulder-hand syndrome (SHS). The onset and severity of SHS appears to be related with the aetiology of the stroke, the severity and recovery of motor deficit, spasticity and sensory disturbances. Another important aetiological factor is glenohumeral subluxation. The physiopathology of the disease is still not known. In CRPS, there is an exaggerated inflammatory response and some chemical mediators have been identified and are present in the inflammatory soup around the primary afferent fibres that, through different processes, can induce hyper-excitability of the afferent fibres (peripheral sensitization). It is hypothesized that a localized neurogenic inflammation is at the basis of oedema, vasodilation and hyperhidrosis that are present in the initial phases of CRPS. The repeated discharge of the C fibres causes an increased medullary excitability (central sensitization). Another important factor is the reorganisation of the central nervous system, and in particular this appears to affect the primary somatosensory cortex. The central role of the sympathetic nerve is presently in doubt. However, it is thought that a sub-group of CRPS patients exists in whom a predominant factor is the hyper-activity of the sympathetic nervous system, and that it responds positively to sympathetic block. Diagnosis is clinical and there are no specific tests, nor pathognomic symptoms to identify this disease with certainty. Diagnosis of CRPS after stroke appears more complex than in other pathological situations: the paretic upper arm frequently appears painful, oedematose, with altered heat and tactile sensations and slightly dystrophic skin within a non-use syndrome. Some investigations can aid differential diagnosis with other diseases. Treatment may be non-pharmacological, pharmacological, with psychotherapy, regional anaesthesia, neuromodulation and sympathectomy. In any case there is little evidence that supports the efficacy of the interventions normally used to treat or prevent CRPS-SHS. The key to effective treatment undoubtedly lies in a an expert multidisciplinary team that is co-ordinated and motivated and that treats the disorder with individualised therapy.     

Evolving understandings about complex regional pain syndrome and its treatment

Complex regional pain syndrome (CRPS) is still a puzzling disease. Although pathophysiologic understanding has improved, not every aspect of this challenging neuropathic pain syndrome has been explored. Typical symptoms of CRPS are sensory, motor, and autonomic dysfunctions. In most cases, CRPS occurs after a fracture, limb trauma, or lesion of the peripheral or central nervous system. Sometimes, symptoms develop without any trauma. Recent pathophysiologic concepts basically consider three major mechanisms: enhanced peripheral neurogenic inflammation, dysfunction of the sympathetic nervous system, and structural reorganization in the central nervous system. Moreover, a genetic predisposition may explain increased vulnerability. Treatment usually requires a multidisciplinary approach, including medical and nonmedical therapies. The common therapeutic aim is to maintain or restore normal function of the affected extremity. Beyond highlighting pathophysiologic concepts, this article describes recent therapeutic approaches.     

The symptoms of complex regional pain syndrome type 1 alleviated with lamotrigine: A report of 8 cases

Complex regional pain syndrome type 1 (CRPS) comprises the symptom complex of burning nondermatomal pain, intermittent swelling and discoloration, allodynia, and abnormalities of sudomotor function. Not all patients respond to blockade of the sympathetic nervous system. In this case report we highlight 8 cases with intractable CRPS Type 1 in which the patients derived benefit from the use of lamotrigine in terms of both pain relief and relief of other symptoms.     

Pathophysiology and diagnosis in patients with sympathetically dependent pain

Chronic pain in a distal extremity that is accompanied by autonomic dysfunction in the same region is taken to indicate reflex sympathetic dystrophy. Typically, hyperalgesia to light touch is present in addition to the spontaneous pain. The absence of heat hyperalgesia indicates that the underlying mechanism is central rather than peripheral sensitization. This mechanism is similar to that of secondary hyperalgesia in the intact skin surrounding an injury site. Sympathetically maintained pain (SMP) is diagnosed, when these sensory symptoms are reversible under sympathetic blockade. SMP is not due to hyperactivity of sympathetic efferents but to receptor supersensitivity, probably by overexpression of alpha(1)-adrenergic receptors on nociceptive primary afferents. This way normal levels of norepinephrine can cause pathological spontaneous activity of nociceptors which maintains the central sensitization. Chronic burning pain and cutaneous hyperalgesia may also be independent of the sympathetic innervation of the skin. In this case, central sensitization is maintained by other mechanisms. A role of the sympathetic nervous system in the pathogenesis of pain cannot be deduced simply from the simultaneous presence of sensory and autonomic clinical signs and symptoms. Therefore, sympathetic blockade in a patient initially is a diagnostic procedure, aiming to demonstrate the presence of the symptom SMP. Therapeutic blockade is only indicated after this demonstration. For the substantial number of patients with sympathetically independent pain, other treatment modalities are needed which may for example attack central sensitization.     

Assessment of peripheral sympathetic nervous function for diagnosing early post-traumatic complex regional pain syndrome type I

Clinical diagnosis of complex regional pain syndrome type I (CRPS I) in post-traumatic patients is often delayed since the clinical appearance of this disease resembles normal post-traumatic states to a certain extent (pain, edema, loss of function). The purpose of this study was to assess the incidence of specific clinical features in CRPS I patients and normal post-traumatic patients and to evaluate the diagnostic value of a bedside test that measures the sympathetic nervous function. Fifty patients with post-traumatic CRPS I of the upper limb and 50 patients 8 weeks after distal radius fracture with an undisturbed course of disease were subjected to a detailed clinical examination. Pain was assessed using the VAS (visual analog scale), skin temperature measured with an infrared camera and grip-strength with a pneumatic manometer. In CRPS I patients, motor disturbances defined as an impaired active range of motion of the hand, were most frequent (96%, fracture patients: 40%), followed by edema (88%, fracture patients: 80%) and spontaneous pain (VAS 4.0 +/- 2.3, fracture patients: VAS 1.3 +/- 0.6). Systematic temperature differences (>1 degree C) between the affected and unaffected limbs were seen in only 42% of CRPS I patients and in 34% of the fracture patients. Further sensory, sudomotor or trophic changes of the hands were rare. As expected, there were significant differences in the quantity of edema, motor disturbances and sensory disturbances between CRPS I patients and normal fracture patients. However, normal fracture patients still suffered from several of the evaluated symptoms 8 weeks after trauma, which makes an early clinical diagnosis of the complication more difficult. Using a newly developed bedside test, the peripheral sympathetic nervous function was assessed in both groups of patients and in 50 age-matched healthy controls. The decrease in skin blood flow following sympathetic provocation maneuvers, detected by laser Doppler flowmetry, was quantified as sympathetic reactivity. In the affected hands of CRPS I patients, as well as in the contralateral hands, the sympathetic reactivity was obliterated or diminished in contrast to the age-matched controls and normal fracture patients. A multivariate analysis did not reveal any correlation between sympathetic function and the severity of any clinical symptom. Sympathetic reactivity seems to be an independent variable in CRPS I and the test presented may facilitate the difficult clinical diagnosis of this disease.     

Complex regional pain syndrome

Complex regional pain syndrome (CRPS), formerly known as reflex sympathetic dystrophy, is a regional, posttraumatic, neuropathic pain problem that most often affects 1 or more limbs. Like most medical conditions, early diagnosis and treatment increase the likelihood of a successful outcome. Accordingly, patients with clinical signs and symptoms of CRPS after an injury should be referred immediately to a physician with expertise in evaluating and treating this condition. Physical therapy is the cornerstone and first-line treatment for CRPS. Mild cases respond to physical therapy and physical modalities. Mild to moderate cases may require adjuvant analgesics, such as anticonvulsants and/or antidepressants. An opioid should be added to the treatment regimen if these medications do not provide sufficient analgesia to allow the patient to participate in physical therapy. Patients with moderate to severe pain and/or sympathetic dysfunction require regional anesthetic blockade to participate in physical therapy. A small percentage of patients develop refractory, chronic pain and require long-term multidisciplinary treatment, including physical therapy, psychological support, and pain-relieving measures. Pain-relieving measures include medications, sympathetic/somatic blockade, spinal cord stimulation, and spinal analgesia.     

16. Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS), formerly known as reflex sympathetic dystrophy is a pain syndrome with an unclear pathophysiology and unpredictable clinical course. The disease is often therapy resistant, the natural course not always favorable. The diagnosis of CRPS is based on signs and symptoms derived from medical history and physical examination. Pharmacological pain management and physical rehabilitation of limb function are the main pillars of therapy and should be started as early as possible. If, however, there is no improvement of limb function and persistent severe pain, interventional pain management techniques may be considered. Intravenous regional blocks with guanethidine did not prove superior to placebo but frequent side effects occurred.Therefore this technique receives a negative recommendation (2 A–). Sympathetic block is the interventional treatment of first choice and has a 2 B+ rating. Ganglion stellatum (stellate ganglion) block with repeated local anesthetic injections or by radiofrequency denervation after positive diagnostic block is documented in prospective and retrospective trials in patients suffering from upper limb CRPS. Lumbar sympathetic blocks can be performed with repeated local anesthetic injections. For a more prolonged lumbar sympathetic block radiofrequency treatment is preferred over phenol neurolysis because effects are comparable whereas the risk for side effects is lower (2 B+). For patients suffering from CRPS refractory to conventional treatment and sympathetic blocks, plexus brachialis block or continuous epidural infusion analgesia coupled with exercise therapy may be tried (2 C+). Spinal cord stimulation is recommended if other treatments fail to improve pain and dysfunction (2 B+). Alternatively peripheral nerve stimulation can be considered, preferentially in study conditions (2 C+).     

Complex regional pain syndrome: A review of evidence-supported treatment options

Complex regional pain syndrome consists of pain and other symptoms that are unexpectedly severe or protracted after an injury. In type II complex regional pain syndrome, major nerve injury, often with motor involvement, is the cause; in complex regional pain syndrome I, the culprit is a more occult lesion, often a lesser injury that predominantly affects unmyelinated axons. In florid form, disturbances of vasoregulation (eg, edema) and abnormalities of other innervated tissues (skin, muscle, bone) can appear. Because of these various symptoms and the difficulty in identifying causative lesions, complex regional pain syndrome is difficult to treat or cure. Complex regional pain syndrome has not been systematically investigated; there are few controlled treatment trials for established complex regional pain syndrome. This article reviews the existing studies (even if preliminary) to direct clinicians toward the best options. Treatments for other neuropathic pain syndromes that may be efficacious for complex regional pain syndrome also are discussed. Some common treatments (eg, local anesthetic blockade of sympathetic ganglia) are not supported by the aggregate of published studies and should be used less frequently. Other treatments with encouraging published results (eg, neural stimulators) are not used often enough. We hope to encourage clinicians to rely more on evidence-supported treatments for complex regional pain syndrome.     

Zur Entstehung und Therapie des Schmerzsyndroms bei der sympathischen Reflexdystrophie

Reflex sympathetic dystrophy (RSD) is a disease of the extremities that can be elicited by different factors, occurring at different sites (e.g., trauma, herpes zoster, myocardial infarction). Independently of its etiology, however, the clinical symptoms of RSD are found most often in distal parts of the extremities affected (hand or foot). In a generalized distribution pattern, the following signs, representing a triad of autonomic, motoric and sensory disturbances, are commonly observed in these regions: 1. dysregulation of blood flow to the skin and of sweating, together with diffuse swelling, 2. impairment of movement and muscular strength; 3. diffuse sensory skin disturbances and spontaneous pain of ariable character (e.g., burning, throbbing, aching, shooting). Pain sensation is generally diffuse; in most cases it is deep and less often, superficial (probably representing bone or skin pain, respectively). This triad occurs at the very onset of RSD. If the distribution pattern is generalized, it can be used as a diagnostic criterion for RSD. Our experimental results support the idea of disturbances of skin blood flow related to abnormal vasoconstrictor outflow. This assumption is primarily based on two observations: 1. 73% of 97 RSD patients (upper extremity affected) showed systematic side differences in fingertip temperatures at room temperature. All points measured on the affected side had higher (n=51) or lower (n= 20) temperature values than corresponding sites on the healthy extremity. Such systematic side differences were found only in 16% out of 79 healthy subjects (p相似文献   

Pathogenesis of complex regional pain syndrome (CRPS)

Neuropathic pain results from injury to neural structures within the peripheral or central nervous systems. Such injury promotes spontaneous and ectopic firing of nerves as well as reorganization of the nervous system. Neuropathic pain persists chronically. Patients who suffer from neuropathic pain exhibit persistent or paroxysmal pain without apparent immediate cause or pain hypersensitivity after tissue damage. This hypersensitivity is manifest as hyperalgesia and allodynia. Complex regional pain syndrome, CRPS is a category of neuropathic pain and is further divided into type I(reflex sympathetic dystrophy: RSD) and type II(causalgia). CRPS is characterized by localized autonomic dysregulation in the affected area with vasomotor and/or sudomotor changes, edema, colour difference, sweating abnormality, and atrophy.     

Complex Regional Pain Syndrome Type I: Neuropathic or Not?

Complex regional pain syndrome (CRPS) is clinically characterized by pain, abnormal regulation of blood flow and sweating, edema of skin and subcutaneous tissues, active and passive movement disorders, and trophic changes. It is classified as type I (reflex sympathetic dystrophy) and type II (causalgia). CRPS cannot be reduced to one system or to one mechanism only. In the past decades, there has been absolutely no doubt that complex regional pain syndromes have to be classified as neuropathic pain disorders. This situation changed when a proposal to redefine neuropathic pain states was recently published, which resulted in an exclusion of CRPS from neuropathic pain disorders. We analyzed the strength of the scientific evidence that supports the neuropathic nature of complex regional pain syndromes.