Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients had a characteristic motor paresis that was dramatically improved by sympathetic block. The cause of this paresis could not be determined by the usual neurological examinations. It was similar to reflex sympathetic dystrophy in that the patients experienced severe pain, swelling, coldness, and muscle atrophy in the affected limbs or other parts of the body in the course of their illness. However, the motor paresis could precede the pain or develop after the pain had disappeared. Even in the absence of pain, the motor paresis was exacerbated by sympathetic stimulation using epinephrine, norepinephrine (nor-adrenalin), or isoproterenol hydrochloride (Proternol) loading and was improved by regional intravenous infusion of reserpine or by sympathetic ganglion block. Loading with pilocarpine, atropine sulfate (Bosmin), and edrophonium chloride (Antirex) did not influence the paresis. This motor paresis is thought to be due to abnormally increased sympathetic tone and may be considered a motor form of reflex sympathetic dystrophy. However, motor paresis closely related to sympathetic dysfunction is quite a new condition that we call "sympathetic motor paresis." This is important clinically because a long-standing effect can be expected from permanent sympathetic ganglion block with dehydrated ethanol.
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PMID:Motor paresis improved by sympathetic block. A motor form of reflex sympathetic dystrophy? 273 Mar 81

The case of a patient who was involved in a car crash is presented. On the right side her wrist and zygomatic arch were fractured. At both localizations she developed a painful syndrome. The diagnosis of reflex sympathetic dystrophy of her arm was made within 3 weeks after the injury and therapy instituted. The pain in her face and skull were accompanied by vasomotor changes which increased after exercise and by hypesthesia, hyperpathia, paresis, and hyperhidrosis. Disorders of the cranial nerves were excluded by physical examination and electromyography and structural disorders by CT scanning. The diagnosis reflex sympathetic dystrophy of the head was made one year after the injury. The problems in diagnosis are discussed.
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PMID:Reflex sympathetic dystrophy of the head: case report and discussion of diagnostic criteria. 829 37

Post-stroke edema of the paretic hand constitutes an additional, functional, and esthetic nuisance for the patient. Although often encountered in daily practice, it is not even mentioned in the stroke chapters of the various textbooks. The phenomenon is far from being elucidated and various aspects are still obscure. In this study we tried to estimate the extent of post-stroke hand edema (PSHE) in a sample of elderly patients. The study group consisted of 188 elderly post-stroke nursing patients with hemi or only hand paresis. Seventy, age matched, non-paretic patients were examined as controls. The basis of comparison was the difference in circumference between the two arms at three sites: mid-finger, hand, and wrist as measured in the control group. Values above two standard deviations (S.D.) of the mean difference in circumference of the controls, at two or three sites, were considered as edema. Edema of the paretic hand was detected in 37% of post-stroke patients. Most (about three-quarters), could be classified as simple PSHE, while the rest may have had reflex sympathetic dystrophy (RSD).
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PMID:Edema of the paretic hand in elderly post-stroke nursing patients. 1669 Jan 45

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