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PubMed1994

A review of reflex sympathetic dystrophy and related syndromes.

Reflex sympathetic dystrophy and related syndromes such as sympathetically maintained pain and causalgia are often confused and over-diagnosed. In an effort to set ground rules and recommendations on these conditions, an attempt is made here to explain the clinical findings and recommendations for treatment. The goal of this article is to aid in reduction of inappropriate diagnosis and subsequent inappropriate management.

Autonomic Nerve Block↗
PubMedDate not supplied

Reflex sympathetic dystrophy syndrome: a review.

Reflex sympathetic dystrophy syndrome is a serious and potentially disabling condition. Early diagnosis and treatment are essential to control the disorder and restore the patient's quality of life. The cardinal clinical features, radiological changes, etiopathologic advances, and current approaches to proper diagnosis and treatment will be discussed.

Humans↗
PubMedDate not supplied

Reflex sympathetic dystrophy involving the foot.

Reflex sympathetic dystrophy often presents with the subjective chief symptom of pain. This paper demonstrates that careful study of the subtle and often cyclical objective signs can be used to assess the state of the disease. It may also evaluate progress of treatment.

Autonomic Nerve Block↗
PubMed1992

The treatment of reflex sympathetic dystrophy syndrome: current concepts.

Reflex sympathetic dystrophy syndrome is the currently accepted term for a disorder that has previously appeared in the literature under a confusing array of designations: causalgia, Sudeck's atrophy, algoneurodystrophy, shoulder-hand syndrome, etc. The disorder, which was first described in 1864, is characterized by pain, swelling, limited range of motion with associated signs of vasomotor instability, trophic skin changes and patchy bone demineralization. It appears as an exaggerated response of an extremity to injury: trauma, infection, phlebitis or numerous other lesions. In 35 per cent of the RSDS patients, no precipitating event can be identified. The rational treatment of these patients should be based on a thorough understanding of its pathogenesis. While the optimal management is still controversial, there is a consensus that the best results will be achieved if treatment is started early and adapted to the clinical stage of the disease. The role of physical therapy is still debatable. Sympathetic interruption, corticosteroids, calcitonin, beta-blocking agents and more recently bi-phosphonates have been advocated. Proper management may result in the prevention of crippling sequelae.

Analgesics↗
PubMed1997

Medical treatment of reflex sympathetic dystrophy.

The treatment of reflex sympathetic dystrophy is not delineated clearly, and there are few controlled studies regarding rehabilitation as medicine. Analgesics, nonsteroidal anti-inflammatory drugs, and intra-articular steroids are used widely, but especially in Europe, calcitonin is the primary treatment at early stages of the disease. Local intravenous injections are used currently in case of failure of the previous treatments. Physical therapy and rehabilitation are needed also to decrease pain and to improve stiffness.

Adrenergic Antagonists↗
PubMed1997

Imaging in reflex sympathetic dystrophy.

The diagnosis of reflex sympathetic dystrophy (RSD) relies on clinical evaluation, scintigraphy or MR imaging, and routine radiographs. Because RSD has variable manifestations with a strong psychogenic overlap, it is desirable to have a noninvasive test to determine the presence of RSD to allow for appropriate treatment. MR imaging allows a differential diagnosis between RSD and other bone lesions. It proves to be a reliable technique in showing and characterizing RSD better than radiographic examination and radionuclide study.

Diagnosis, Differential↗
PubMed1987

Reflex sympathetic dystrophy of the knee.

Reflex sympathetic dystrophy of the knee has been studied in a series of 19 patients. Those diagnosed and treated early (at less than six months) did much better than those diagnosed and treated late. Nevertheless, when these patients were followed up at an average of 3.4 years from onset, not one was completely normal to objective tests with the Cybex II dynameter, an indication of the adverse prognosis with current methods of treatment.

Adolescent↗
PubMed1987

Reflex sympathetic dystrophy following nail biopsy.

Reflex sympathetic dystrophy following a nail unit biopsy in a patient with long-standing, mycologically negative onychomycosis is reported. The significance of this complication is discussed, and the literature on the condition itself is reviewed. It is suggested that although adverse effects occur as a result of nail biopsy, they are infrequent and therefore should not dissuade the clinician from performing the procedure. Biopsy is necessary in order to establish a more accurate diagnosis of nail disease and thus administer more appropriate and effective therapy.

Adult↗
PubMed1998

Reflex sympathetic dystrophy: facts and hypotheses.

Reflex sympathetic dystrophy (RSD) syndrome has been recognized clinically for many years. It is most often initiated by trauma to a nerve, neural plexus, or soft tissue. Diagnostic criteria are the presence of regional pain and other sensory changes following a noxious event. The pain is associated with changes in skin colour, skin temperature, abnormal sweating, oedema, and sometimes motor abnormalities. The clinical course is commonly divided into three stages: first (acute or hyperaemic), second (dystrophic or ischaemic), and third (atrophic) stage. The diagnosis is primarily clinical, but roentgenography, scintigraphy, thermography, electromyography and assessment of nerve conduction velocity can help to confirm the diagnosis. Although a wide variety of treatments have been recommended, the only therapies found to be effective in large studies aim at interfering with the activity of the sympathetic nervous system. To this end, efferent sympathetic nerve activity can be interrupted surgically or chemically. Alternatively, adrenoceptor blockers may be used to relieve pain. Numerous theories have been proposed to explain the pathophysiology. Sympathetic dysfunction, which often has been purported to play a pivotal role in RSD, has been suggested to consist of an increased rate of efferent sympathetic nerve impulses towards the involved extremity induced by increased afferent activity. However, the results of several experimental studies suggest that sympathetic dysfunction consists of supersensitivity to catecholamines induced by (partial) autonomic denervation. Besides, it has been suggested that excitation of sensory nerve fibres at axonal level causes release of neuropeptides at the peripheral endings of these fibres. These neuropeptides may induce vasodilation, increase vascular permeability, and excite surrounding sensory nerve fibres -- a phenomenon referred to as neurogenic inflammation. At the level of the central nervous system, it has been suggested that the increased input from peripheral nociceptors alters the central processing mechanisms.

Animals↗
PubMed1991

Burning pain in an extremity. Breaking the destructive cycle of reflex sympathetic dystrophy.

The pathogenesis of reflex sympathetic dystrophy is controversial, but the condition can result from a major or seemingly minor injury to a limb, or even an insult to an organ, such as stroke or myocardial infarction. Onset can be sudden or insidious. The syndrome is characterized primarily by localized, deep, burning pain in a limb--pain that may not follow any logical distribution. Nonpitting edema, skin hyperesthesia, and guarding of the limb usually accompany the pain. If treatment is not instituted, deformity, contracture, and wasting of the limb can eventually occur. With appropriate therapy, the process can be stopped and often reversed. The keys are a high index of suspicion, early diagnosis, and aggressive treatment.

Clinical Protocols↗
PubMed2005

The predictive value of additional late blood pool imaging to the three-phase bone scan in the diagnosis of reflex sympathetic dystrophy in hemiplegic patients.

Reflex sympathetic dystrophy (RSD) is a relative common sequel after hemiplegia. The diagnosis of RSD in hemiplegic patients presents difficult clinical problems, as the symptoms and signs of RSD are not specific and RSD may be due to reasons other than hemiplegia. Bone scintigraphy has been routinely used for the diagnosis of RSD; however, the optimal acquisition protocols, diagnostic patterns and the utility of quantitation are controversial. This prospective study was conducted to demonstrate the higher predictive value of an additional late blood pool image to the three-phase bone scan compared to the regular three-phase bone scans in RSD patients associated with hemiplegia. Thirty-four RSD patients were enrolled into the study. Bone scans according to the new protocol were obtained for all patients. Those patients with either negative or positive bone scans with no evidence of RSD were followed for 6 months. The patients had positive bone scan findings and were symptomatic at the time of the study. Of these, seven patients (58.3%) subsequently became symptomatic and five patients (41.7%) remained asymptomatic at 6 months. None of the patients with negative bone scans had symptoms of RSD on presentation except one case. We conclude that the addition of a late blood pool image increases the predictive value and has an impact on initiating early treatment in asymptomatic patients.

Aged↗
PubMed1997

Bisphosphonate therapy of reflex sympathetic dystrophy syndrome.

OBJECTIVE: The reflex sympathetic dystrophy syndrome (RSDS) is a painful limb disorder, for which a consistently effective treatment has not yet been identified. The disease is associated with increased bone resorption and patchy osteoporosis, which might benefit from treatment with bisphosphonates, powerful inhibitors of bone resorption. METHODS: Twenty patients with RSDS of foot and hand, were randomly assigned to blind administration of either alendronate intravenously (Istituto Gentili, Pisa, Italy) 7.5 mg dissolved in 250 ml saline solution or placebo saline infusions daily for three days. Two weeks later all patients had an identical treatment course with open labelled alendronate (7.5 mg/day for three days), independent from the results of the first blind treatment. RESULTS: In the patients treated with blind alendronate the diminution in spontaneous pain, tenderness, and swelling (circumference of the affected limb) and the improvement in motion were significantly different from baseline (p < 0.001), from those observed within the first two weeks in the control group (p < 0.01), and from week 2 to week 4 (p < 0.01). In the patients given blind placebo infusions no relevant symptomatic changes were observed after the first two weeks of follow up, but they responded to the open alendronate therapy given afterwards. In 12 patients with RSDS of the hand the ultradistal bone mineral content (BMC) of the affected arm was considerably lower than that of the controlateral arm (mean (SD)) (426(82) mg/cm versus 688(49)). Six weeks after the beginning of the trial BMC rose by 77(12) mg/cm (p < 0.001) in the affected arm, but it did not change in the controlateral. CONCLUSIONS: These results indicate that bisphosphonates should be considered for the treatment of RSDS, producing consistent and rapid remission of the disease.

Adult↗
PubMedDate not supplied

Reflex sympathetic dystrophy following neck dissections.

PURPOSE: Reflex sympathetic dystrophy (RSD), which is a disorder that occurs after injury or surgery on the extremities, has not been reported as a complication of neck dissections until now. A group patients with head and neck cancer have been examined to determine the incidence of RSD in neck dissections. PATIENTS AND METHODS: Forty-six patients with head and neck cancer, who had undergone neck dissections together with the removal of the primary tumor, were evaluated for RSD on their routine controls. RESULT AND CONCLUSION: The presentation of RSD in two patients who were treated with radical neck dissection is probably a result of sympathetic hyperactivity that is secondary to surgical trauma.

Accessory Nerve↗
PubMed1979

Reflex sympathetic dystrophy in two young females.

Reflex sympathetic dystrophy in paediatric patients is a rarely recognized pain syndrome probably of neurovascular origin. The manifectations in two young females consisted of disabling pain and localized hyperesthesia in lower extremities without evident trauma. Sympathetic block followed by active mobilization and, in the patient with atrophic changes, lumbar sympathectomy, resulted in complete recovery. Reflex sympathetic dystrophy should be considered in the differential diagnosis of pain and tenderness in an extremity.

Adolescent↗
PubMedDate not supplied

Reflex sympathetic dystrophy associated with antiepileptic drugs.

Reflex sympathetic dystrophy syndrome (RSDS) complicating antiepileptic drug (AED) therapy is not well acknowledged in the neurologic literature. We report 4 patients with reflex sympathetic dystrophy that occurred while they were receiving AEDs. All patients had shoulder and hand involvement, which in 2 was bilateral, and 1 had ipsilateral foot involvement. Two patients did not respond to a change in AEDs, but all improved with a course of prednisone. One patient with phenobarbital (PB)-associated RSDS relapsed on inadvertent rechallenge with secobarbital. A review of the literature showed that several other fibrosing disorders are associated with AED administration, including Dupuytren's contractures, frozen shoulder, plantar and hand nodules, and Peyronie's disease. RSD associated with AEDs is important to recognize because it may result in permanent disability if treatment is delayed.

Adult↗
PubMed1983

Clinical effects of regional intravenous guanethidine (Ismelin) in reflex sympathetic dystrophy.

Twenty patients with documented reflex sympathetic dystrophy were treated with a series of regional intravenous guanethidine blocks. The mean delay between the first clinical symptoms and the start of guanethidine blocks was 3.6 months. The overall result was good in 11 patients, moderate in two patients and poor in seven patients. Poor results are due mainly to incorrect diagnosis and to application either too late in the third phase or too early in the first phase when only signs of increased blood flow are part of the symptomatology. Side effects, except pain after the injection, were few and of minor importance. The tolerance of the procedure may be improved by preceding the injection of guanethidine by an injection of a local anaesthetic agent. It may be concluded that with correct diagnosis and indication, guanethidine injections may play an important part in the treatment of reflex sympathetic dystrophy and may replace sympathetic blocks with local anaesthetics because of the longer duration of action and lower incidence of serious side-effects.

Adult↗