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)

Two patients are presented in whom percutaneous radiofrequency spinal rhizotomy was complicated by contralateral paresis. Both patients were elderly and suffered from cardiac failure, chronic obstructive respiratory disease, and generalized vascular disease. Investigation of the paresis indicated a contralateral ischaemic cord lesion. It is suggested that local haemodynamic changes induced by heat-mediated rhizotomy may compromise oxygen delivery to the adjacent cord, especially in the presence of pre-existent cardiovascular disease.
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PMID:Ischaemic spinal cord lesion following percutaneous radiofrequency spinal rhizotomy. 1193 79

The debilitating loss of function after a stroke has both primary and secondary effects on sensorimotor function. Primary effects include paresis, paralysis, spasticity, and sensory-perceptual dysfunction due to upper motor neuron damage. Secondary effects, contractures and disuse muscle atrophy, are also debilitating. This paper presents theoretical and empirical benefits of aerobic exercise after stroke, issues relevant to measuring peak capacity, exercise training protocols, and the clinical use of aerobic exercise in this patient population. A stroke, and resulting hemiparesis, produces physiological changes in muscle fibres and muscle metabolism during exercise. These changes, along with comorbid cardiovascular disease, must be considered when exercising stroke patients. While few studies have measured peak exercise capacity in hemiparetic populations, it has been consistently observed in these studies that stroke patients have a lower functional capacity than healthy populations. Hemiparetic patients have low peak exercise responses probably due to a reduced number of motor units available for recruitment during dynamic exercise, the reduced oxidative capacity of paretic muscle, and decreased overall endurance. Consequently, traditional methods to predict aerobic capacity are not appropriate for use with stroke patients. Endurance exercise training is increasingly recognised as an important component in rehabilitation. An average improvement in maximal oxygen consumption (VO2max) of 13.3% in stroke patients who participated in a 10-week aerobic exercise training programme has been reported compared with controls. This study underscored the potential benefits of aerobic exercise training in stroke patients. In this paper, advantages and disadvantages of exercise modalities are discussed in relation to stroke patients. Recommendations are presented to maximise physical performance and minimise potential cardiac risks during exercise.
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PMID:Benefits of aerobic exercise after stroke. 872 2

Proinflammatory cytokines exert a number of important effects on vascular reactivity. At one end of the spectrum, certain cytokines may induce vascular paresis leading to profound vasodilatation and hyporesponsiveness to constrictor stimuli. This may be relevant to the pathogenesis of septic shock and other types of inflammatory vasodilatation. At the other end of the spectrum, inflammatory cytokines can impair endothelium-dependent dilatation and the endothelium may lose its ability to respond to circulating hormones or autacoids. This effect may case a predisposition to vessel spasm, thrombosis or atherogenesis. Studies in human vessels suggest that interleukin-1 is particularly important as a mediator of inflammatory dilatation; the underlying mechanisms include induction of the inducible isoform of nitric oxide synthase in vascular smooth muscle, or over-production of nitric oxide from the endothelial isoform of nitric oxide synthase. Induction of the enzyme GTP cyclohydrolase 1 and consequent production of tetrahydrobiopterin contributes to the increase in the activity of endothelial nitric oxide synthase. In contrast, tumour necrosis factor-alpha considerably impairs endothelium-dependent relaxation. The mechanisms of these effects are not yet fully understood, but tumour necrosis factor can induce endothelial dysfunction in human endothelial cells in culture, and human blood vessels in vitro and in vivo. The implications of these observations for cardiovascular disease are discussed.
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PMID:Effects of cytokines on nitric oxide pathways in human vasculature. 991 65

Surgical destruction of a portion of the ventrolateral nucleus of the thalamus is currently the procedure of choice for the treatment of incapacitating tremor and rigidity of parkinsonism. Seventy-three patients were treated by 105 thalamotomies at the University of Alberta Hospital and assessed one to four years later for improvement of function in everyday activities. Fifty-six patients were improved, 12 were unchanged, and five had died. Only two of the deaths were related to the operation. Paresis was permanent in only one patient. Twenty-five patients had bilateral operations and 22 of these showed improvement of function. Contraindications to operation include serious cardiovascular disease, mental deterioration, and those parkinsonian patients whose disability is chiefly due to akinesia, oculogyric crisis, dysphasia or dysarthria.
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PMID:RESULTS OF THALAMOTOMY FOR PARKINSON'S DISEASE. 1407 11

In contrast to Henrik Ibsen's literary work, the author's health during the last years of his life has not attracted much attention. Ibsen suffered from a variety of symptoms due to arteriosclerotic cardiovascular disease. He was first hit by a stroke in March 1900, which resulted in paresis of his left foot. During the summer 1900 he was ill with erysipelas. Thereafter, in 1901 and in 1903, he was hit by two more strokes, which left him with severe right hemiparesis and aphasia. Ibsen's varying health might indicate that he was hit by several additional minor stokes in both hemispheres, most likely tromboembolic cerebral infarcts. During his last years he developed symptoms of cardiac failure, and it was probably an increasing cardiac failure that led to the cardiac arrest that ended his life.
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PMID:[The fatal story--Ibsen's health during the last years of his life]. 1673 52

The search for the causes of medical and psychiatric disorders has gone through 3 historical phases. First, up until the mid-19th century, causes of illness were anecdotally recorded from individual cases, resulting in long and diverse lists for all disorders. Second, in the latter half of the 19th century, with the use of microbiological methods, single causes were found for many infectious diseases that led to specific diagnostic tests, effective preventions, and, in some cases, treatments. Causal thinking in medicine shifted from the earlier multicausal approaches to monocausal theories of etiology. Indeed, proving monocausal etiology became a way to establish the legitimacy of a disorder. Through the writings of Kahlbaum and Hecker, psychiatry was deeply influenced by this monocausal perspective, the importance of which was substantially amplified by a twist of fate: the increasing clinical importance of general paresis of the insane throughout the 19th century and the eventual proof that it too was a monocausal condition. However, in the mid-20th century, the third phase began. With decreasing deaths from infectious diseases, epidemiology and clinical medicine shifted to a chronic disease model in which paradigmatic disorders, such as cancer and cardiovascular disease, were shown to be highly multicausal. Biostatistics evolved from deterministic to probabilistic models of disease risk factors. Paradoxically, at this time, biological psychiatry, then rising to dominance in American psychiatry, vigorously pursued monocausal theories, first of neurochemical origin and then of genetic origin. We were trying to establish the legitimacy of our field by pursuing an outmoded model-that "real" diseases are monocausal. Despite ample evidence to the contrary, monocausal thinking continues to influence our field, for example, in the popular but improbable view that we can, with a few key advances, move easily from descriptive to etiologically based diagnoses.
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PMID:From Many to One to Many-the Search for Causes of Psychiatric Illness. 3121 68