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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a personal assessment of true major causalgia and the other reflex dystrophies, related but distinctly separate entities. The clinical picture of causalgia differs only in minor respects from that described by Mitchell over 120 years ago. Its management has, however, been clarified, largely through the extensive experiences of World War II. It is readily recognized and can be treated effectively by sympathetic blocks or sympathectomy together with active exercise. The other reflex dystrophies are far less understood. They appear to have a similar pattern in their early phase and to respond well to a program of exercise and control of edema--a regimen which, because of pain and paresis, cannot be carried out without sympathetic blocks or occasionally sympathectomy. When not recognized early and treated properly, the sympatomatology usually changes dramatically and treatment differs. Often control of edema and active use of the affected part are all that is necessary. Sometimes, in addition to these measures, sympathetic blocks or sympathectomy is required. Guidelines found useful in management are outlined. Puzzling features are discussed.
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PMID:A personal overview of causalgia and other reflex dystrophies. 397 27

Complex-regional pain syndromes (CRPS), formerly known as Sudeck's dystrophy and causalgia, belong to the neuropathic pain syndromes. CRPS may develop following fractures, limb trauma or lesions of the peripheral or central (CNS) nervous system. Occasionally, CRPS may also develop spontaneously. The clinical picture comprises a characteristic clinical triade of symptoms including autonomic (disturbances of skin temperature, colour, presence of sweating abnormalities), sensory (pain and hyperalgesia) and motor (paresis, tremor, dystonia) disturbances. Diagnosis is mainly based on clinical signs. However, additional laboratory, neurophysiological and radiological examinations may help to corroborate correct diagnosis. Several pathophysiological concepts have been proposed to explain the complex symptoms of CRPS: 1, facilitated neurogenic inflammation; 2, pathological sympatho-afferent coupling; 3, neuroplastic changes within the CNS. Furthermore, there is accumulating evidence that genetic factors may predispose for CRPS. Therapy is based on a multidisciplinary approach. Non-pharmacological approaches include physiotherapy and occupational therapy. Pharmacotherapy is based on individual symptoms and includes steroids, free radical scavengers, treatment of neuropathic pain, and finally agents interfering with bone metabolism (calcitonin, biphosphonates). Sympathetic blocks are useful for the treatment of sympathetically maintained pain. Invasive therapeutic concepts include implantation of spinal cord stimulators. This review covers new aspects of pathophysiology and therapy of CRPS.
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PMID:[Complex regional pain syndromes: new aspects on pathophysiology and therapy]. 1744 40

Complex regional pain syndrome (CRPS), formerly known as Sudeck's dystrophy and causalgia, is a disabling and distressing pain syndrome. We here provide a review based on the current literature concerning the epidemiology, etiology, pathophysiology, diagnosis, and therapy of CRPS. CRPS may develop following fractures, limb trauma or lesions of the peripheral or CNS. The clinical picture comprises a characteristic clinical triad of symptoms including autonomic (disturbances of skin temperature, color, presence of sweating abnormalities), sensory (pain and hyperalgesia), and motor (paresis, tremor, dystonia) disturbances. Diagnosis is mainly based on clinical signs. Several pathophysiological concepts have been proposed to explain the complex symptoms of CRPS: (i) facilitated neurogenic inflammation; (ii) pathological sympatho-afferent coupling; and (iii) neuroplastic changes within the CNS. Furthermore, there is accumulating evidence that genetic factors may predispose for CRPS. Therapy is based on a multidisciplinary approach. Non-pharmacological approaches include physiotherapy and occupational therapy. Pharmacotherapy is based on individual symptoms and includes steroids, free radical scavengers, treatment of neuropathic pain, and finally agents interfering with bone metabolism (calcitonin, biphosphonates). Invasive therapeutic concepts include implantation of spinal cord stimulators. This review covers new aspects of pathophysiology and therapy of CRPS.
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PMID:Complex regional pain syndromes: new pathophysiological concepts and therapies. 2018 Aug 38

Although much has been written on the evaluation and management of pelvic ring injuries, only a single case of anterior sacroiliac joint dislocation exists in the literature and was reported in 1976. This article describes 2 additional cases, 1 of a pure anterior sacroiliac dislocation in a 25-year-old man, and 1 of an anterior sacroiliac fracture-dislocation in an 18-year-old man, each treated by a different orthopedic traumatologist at neighboring trauma centers. Both cases were the result of high-energy trauma, and both patients had significant complications resulting from severity of their injuries, including wound dehiscence and causalgia in 1 case and persistent L5-S1 paresthesias and paresis in the other. Closed reduction can be attempted, but in our experience was unsuccessful even with the use of external fixation pins for leverage. We recommend open reduction by an orthopedic traumatologist who will perform definitive fixation. The decision to use an anterior external fixation frame to assist during the patient's resuscitation should be based on the patient's hemodynamic status and concomitant injuries. Despite a high complication rate, operative intervention can return patients to a functional level with minimal residual pain.
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PMID:Anterior sacroiliac dislocation. 2116 94

We present the case of a 33-year-old woman with benign sporadic monomelic amyotrophy of the distal part of the arm, called Hirayama disease. Clinical features included forearm amyotrophy sparing the brachioradialis muscle, cold paresis and causalgia. Neck magnetic resonance imaging was normal in neutral and flexion position. Electromyography showed denervated patterns in the extensor digitorum communis, and conduction studies ruled out multifocal motor neuropathy. Motor evoked potentials were normal. Serum IgG anti-GM1 antibodies were moderately raised but were negative 8 months later. Outcome was favourable within 15 months, with partial motor recovery. Pathogenesis remains controversial: neck flexion induced myelopathy via chronic anterior horn ischaemia due to forward displacement of the posterior wall of the dura mater, or benign variant of lower motor neuron disease? Whatever the pathomechanism is, the clinical features and outcome are the same.
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PMID:A woman with forearm amyotrophy. 2217 Dec 30