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As the download Algodystrophy: counts whole-genome sequencing curves, an n of mutants with 1-Jan or engineered investors will threaten Pacific for digital ethnic pp. Several hypotheses have been offered, including a central mechanism involving the substantia nigra [ 24 ]; a peripheral mechanism involving a primary synapse dysfunction; or altered response to neurotransmitters [ 25 ]. Sympathetic overactivity has been traditionally considered to be the underlying mechanism.
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However, plasma concentrations of adrenaline, noradrenaline and metabolites are lower than in controls [ 26 ], and attempts to quantify the sympathetic skin response have been statistically insignificant [ 27 , 28 ]. One study which attempted to identify abnormalities specific to RSD did not find any consistent histological findings in peripheral nerve or muscle [ 29 ]. Abnormalities of local mediator release, for example, of substance P and vasoactive polypeptides, have been postulated.
No clear culprit has been identified to date.
There is evident localized bone loss which cannot be solely attributed to immobility. The pain is often most severe during stages 1 and 2 when the rate of bone loss is most rapid. Similarities exist between RSD and Charcot's neuroarthropathy of diabetes. Pain may occur in each condition, although Charcot's joints are classically painless.
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Histologically, there is bone loss with a normal underlying bone architecture in RSD, with predominantly trabecular bone resorption [ 30 ], whereas a destructive pattern of bone loss is seen in the Charcot's joint. The Charcot's joint is typically hyperaemic whereas the limb involved by RSD, especially in the later stages, is cooler. The pathogenesis of both conditions remains elusive, but a common pathway towards rapid bone loss does not seem unreasonable.
A painful limb is not subjected to normal weight bearing, and immobility must be considered as a mechanism of bone loss. A variety of treatments has been used with anecdotal success, and there is a great need for randomized controlled studies. Sympathetic blockade, either as a single or repeated procedure has been beneficial in reducing pain.
Diagnosis and Therapy of a Frequent Disease of the Locomotor Apparatus
The use of regional intravenous guanethidine, a favoured agent for this technique, is no more effective than placebo [ 32 , 33 ]. Historically, oral prednisolone was prescribed with little success, often in conjunction with calcium channel antagonists, to reduce the presumed inflammatory response and to increase local blood flow [ 34 — 36 ]. Gabapentin has been used to treat the pain of RSD with anecdotal benefit [ 37 ].
Randomized controlled studies are required to evaluate this further. Calcitonin and the bisphosphonates have also been used with some success. Calcitonin is administered subcutaneously, and there may therefore be compliance implications. However, several papers report success with this treatment in the management of RSD [ 5 , 38 ], although only one was a randomized controlled study. The role of bisphosphonates is being explored as a treatment for RSD. Administration can be oral or intravenous although there are no published data on the role of oral therapy. Intravenous pamidronate is well established in the treatment of Paget's disease and hypercalcaemia associated with malignancy, and has an analgesic and perhaps therapeutic role in patients with metastatic bone disease [ 41 ].
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The analgesic effect of bisphosphonates may have an important role in RSD. Both calcitonin and the bisphosphonates are established treatments for osteoporosis, and their use in RSD where there is localized bone loss is reasonable. Whether generalized osteopenia or osteoporosis is an independent risk factor for RSD has yet to be resolved.
One study of 19 patients indicated lumbar bone density was lower than expected, although this was not a significant finding [ 42 ]. Individuals with lower than average bone density may therefore be at risk of developing RSD following what would have otherwise have been a relatively minor traumatic incident. The vasomotor changes are most marked in the periphery, which aids diagnosis, the clinical signs being more marked than in the knee or hip.
A correct diagnosis may be made earlier, enabling prompt treatment with a better prognosis, although most studies make no attempt to stage the disease, and the natural history remains unclear. No studies have compared outcome of RSD affecting different anatomical sites, although our own experience suggests that RSD of the ankle and foot may have a better prognosis than RSD at other sites. A recent study has looked closely at the role of quantitative ultrasound of the calcaneum in patients with unilateral RSD of the foot [ 42 ]. Ultrasound may therefore be more useful than DEXA in this group of patients, although other causes of unilateral bone loss are not excluded [ ].
One of the difficulties in assessing the efficacy of treatments has been the lack of objective evidence and quantification of the response to treatment. Attempts have been made to quantify the sympathetic response [ 27 , 28 ], but this is unlikely to be very useful as RSD is characterized by vasomotor instability. Bone loss appears to start early in the disease and patchy osteoporosis is evident in cases with a short history.
Quantification of this bone resorption may be an indirect measure of disease progression and resolution. In cases where there is unilateral involvement, the unaffected foot acts as a control, as reported variation between two normal feet is minimal and reproducibility is 0.
Of these, 23 recalled a history of trauma, which ranged from fracture to prolonged vibration from a wheel arch on a bus. Almost all patients had stage 1 or 2 disease at presentation. In those who had stage 3 disease and who were wheelchair bound at presentation, a poorer response to treatment and outcome was seen. Only four patients failed to report improvement by 3 months.
Algodystrophy Diagnosis And Therapy Of A Frequent Disease Of The Locomotor Apparatus
Two of these suffered severe trauma and comminuted fractures, one had established stage 3 disease, and the fourth did not improve with pamidronate and calcitonin but did improve with regional blockade. It is apparent that there is much work to be done to understand the pathogenesis of RSD, so that therapy can be targeted more effectively. Very few randomized controlled studies have been undertaken to confirm reported anecdotal successes in treatment. However, treatments aimed at reducing localized bone loss may be important and should be assessed further.
The chief failure of published research is the lack of quantification of outcome measures. Few studies utilize a simple functional assessment or quality of life assessment. Quantitative ultrasound needs further assessment with regard to the natural history of RSD and then in assessing response to therapy. Patients with RSD of the ankle and foot, who present early with characteristic clinical findings, would be the most appropriate group to target.
The relevance of classification of the different stages of RSD both at the time of diagnosis and in assessing outcome could fuel the need for early treatment and raise awareness of this poorly understood condition. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account.
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