[Causalgia and other sympathetic reflex dystrophies].
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Few series on reflex sympathetic dystrophy syndrome (RSDS) have included children. The present series reviewed 10 affected children. The group consisted of 9 girls and one boy with an average age at onset of 11 years (5 years to 16 years). The diagnosis was based on the clinical findings of pain, dysesthesia and autonomic system dysfunction. All patients underwent x rays and bone scans. Their results showed great variation. Minor trauma was the most common trigger factor. The lower extremities were more often involved. The treatment consisted of pain relief and progressive mobilization. Less conventional treatments in children, such as calcitonin and bisphosphonate were also used. The severity and duration of the disease varied greatly among these children. Moderate pain and sympathetic dysfunction persisted often up to two years after onset. Reflex sympathetic dystrophy is more common in children than previously thought. There are differences with the adult form in presentation and clinical course: the diagnosis is often delayed, the lower extremities are more often involved, girls are affected more often and idiopathic forms are frequent. Significant emotional dysfunction is found in a majority of patients and they are best treated as inpatients by a multidisciplinary team.
We describe a patient with 4 episodes of reflex sympathetic dystrophy involving 3 limbs occurring over a 4-year period of time. The patient did not respond to steroids but responded well to either sympathetic blocks or sympathectomy.
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We describe a 50-year-old woman who developed severe pain of the left lower limb after an episode of thrombophlebitis. Bone scintigraphy and thermography showed results indicative of reflex sympathetic dystrophy. Laboratory analysis revealed the presence of the lupus anticoagulant. The patient was diagnosed as antiphospholipid syndrome complicated with reflex sympathetic dystrophy of the left lower limb. To our knowledge, this is the first report of a patient with reflex sympathetic dystrophy with underlying antiphospholipid syndrome.
In 26 patients with features of reflex sympathetic dystrophy, venous blood was collected from painful and unaffected limbs. Levels of plasma adrenaline, noradrenaline and its intracellular metabolite, 3,4-dihydroxyphenylethyleneglycol (DHPG), were measured by combined gas chromatography/mass spectrometry. Plasma DHPG was lower on the painful side. Concentration of plasma noradrenaline was also lower on the painful side in patients with widespread allodynia, and in those with hyperhidrosis in the affected hand or foot. These findings do not support the widely held view that autonomic disturbances in reflex sympathetic dystrophy are due to sympathetic overactivity. Rather, they suggest that sweating and changes in peripheral blood flow result from supersensitivity to sympathetic neurotransmitters. After injury, supersensitivity to noradrenaline may also contribute to spontaneous pain and allodynia by disrupting efferent sympathetic modulation of sensation. This would explain why pain and allodynia are relieved by sympathetic blockade, and why noradrenaline rekindles pain in sympathectomized skin.
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Several syndromes derived from the involvement of central and peripheral nervous system and meninges have been reported in the infection by Borrelia burgdorferi. The features of autonomic nervous system involvement have received a marginal attention. Reflex sympathetic dystrophy is an autonomic picture characterized by regional sympathetic hyperactivity which has not been associated with Lyme disease. We report a 16-year-old female with clinical, radiological and scintigraphic features consistent with reflex sympathetic dystrophy. The usual causes of this syndrome were ruled out and antibodies against Borrelia burgdorferi were detected by immunofluorescence, enzyme immunoassay and Western blotting. Specific IgG and IgM levels had a progressive increase during three months. In Lyme borreliosis causes of false positives were excluded. Antigen-antibody bands were detected in increasing number during the evolution, using sonicates of B. burgdorferi and patient's sera with the Western blotting technique. Our data suggest that reflex sympathetic dystrophy is another type of nervous system involvement in the multifaceted Lyme borreliosis.
It has traditionally been accepted that a predisposing psychological field exists with the appearance of the reflex sympathetic dystrophy. Nevertheless, there is no unanimous agreement in this interpretation, since surveys exist unanimous are in favour the reactive character of the psychological effect on reflex sympathetic dystrophy. In this study, we revise literature already published on the subject, present arguments on the psychological evaluation tests carried out to date and propose the possibility of using other test unanimous are easier to manage and to interpret.
Results of a retrospective study of the treatment of 146 patients with post-traumatic reflex sympathetic dystrophy within upper extremity in various stages were presented. Treatment included the following methods: regional intravenous steroid blocks, mannitol, mannitol combined with dexamethasone, physical therapy, calcitonin and surgery. Uniform, clearly defined criteria of diagnosis of the condition and criteria of assessment of the results were used in the study. Final assessment was carried out 6-15 months after ending of the treatment (mean 11 months). Good result (no pain and full finger flexion) was obtained in 94 patients (64%), moderate (pain only after load or loss of flexion less than 3 cm) in 31 (21%) and poor (pain at rest or reduction of flexion more than 3 cm) in 21 (15%). There was found that method of treatment had not significant effect on the result, except surgical treatment after which the worst results were obtained. Significant effect of duration of the disease on the results of the treatment was noted: the earlier treatment the better results. In spite of satisfactory withdrawal of other signs and symptoms, considerable reduction of grip strength after treatment persisted (mean grip strength ratio 28% of the other side) suggesting functional impairment of the hand. The critical approach to evaluation of the results of the treatment of early reflex sympathetic dystrophy was suggested with regard to spontaneous recovery of the condition in many cases.
BACKGROUND: Intractable pain and sweating dysfunction can occur in patients with reflex sympathetic dystrophy (RSD). We, therefore, investigated autonomic function by measuring sympathetic skin response (SSR) in these patients. This method provides useful information regarding the pathophysiologic changes in and clinical evaluation of RSD. METHODS: Twenty-six RSD patients and 22 age-matched normal subjects were involved in our investigation. Three significant stages of RSD were classified through three-phase bone scanning of the wrist, carpal and metacarpal bones. There were 11 patients in stage I RSD, nine in stage II and six in stage III. SSRs were recorded from the bilateral palms of each subject simultaneously using electrical stimulation of the median nerve in the wrist. Latency and amplitude side ratios were calculated and compared with the control group. RESULTS: The affected/normal (A/N) hand amplitude ratios were significantly lower in stage I RSD, and stage II RSD patients exhibited significantly higher A/N amplitude ratios compared with the control group. A/N amplitude and A/N latency ratios in stage III RSD did not change significantly. The A/N latency ratios in stage I RSD were significantly higher than those of the control group and those of stage II RSD. In one stage I patient and three stage III patients, SSRs were bilaterally unobtainable. CONCLUSIONS: It appears that abnormal SSRs may be associated with autonomic disturbance in RSD patients.
In 16 cases of reflex sympathetic dystrophy of the knee, the authors obtained by drill biopsy 29 bone samples from the epiphyseal and metaphyseal regions of the femur and tibia and 8 cartilagenous samples (including 6 by arthrotomy and 2 after patellectomy). They noted thinning of the cortical bone, lacunae of cortical reabsorption, rarefaction of the trabeculae, of which some were dead, stasis and fibrosis of the bone marrow. The 8 cartilage samples were pathological, with, in particular, fibrosis of the surface cartilage (vascular pannus formation). The association of chondromalacia of the patella with an S.R.D. syndrome of the knee is frequent.
Reflex sympathetic dystrophy (RSD) has been reported in incomplete spinal cord injury patients, most often occurring unilaterally; however to our knowledge, bilateral RSD has not been reported in patients with a central cord syndrome. We report a case of bilateral RSD in a patient with incomplete cervical myelopathy and the clinical picture of central cord syndrome. Diagnosis of RSD was based upon clinical, roentgenographic and scintigraphic findings. Management of RSD included elevation of forearm and hands, gentle active and passive range of movements of all upper extremity joints and systemic corticosteroids. With treatment, pain subsided, the range of motion of the joints improved and the patient achieved good functional recovery.
Five hundred forty-one patients with reflex sympathetic dystrophy (RSD) of the upper extremity were prospectively studied. One hundred fifteen patients complained of pain and/or limited range of motion in the shoulder. Shoulder complaints more often occurred in women (p = .01); age and etiology were not different from patients with RSD without shoulder complaints. Physical examination showed a tendinitis of one or both tendons of the biceps muscle in 109 patients. Seventy one patients were treated with local injection of bupivacaine followed by methylprednisolone. This resulted in permanent relief of complaints in 34 patients, temporary or moderate relief in 31, no difference in 3, increase of complaints in 1 patient, and in 2 patients results were not documented. We conclude that shoulder complaints in RSD occur in a minority of patients and more often in female patients. There are no predisposing factors. The pathophysiologic mechanism for developing shoulder complaints remains unknown. In most cases complaints can be attributed to a bicipital tendinitis for which local injection of bupivacaine followed by prednisolone are both diagnostic and therapeutic.