Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levels of R proteins, immunoglobulins A, M, and G, natural anti-sheep erythrocyte antibodies, active oxygen (superoxide) were measured in the neutrophilic leukocytes in pregnant females at a risk for late gestosis. The examinees were found to have high levels of R proteins, IgA, IgM, natural anti-sheep erythrocyte antibodies, neutrophils capable to restore NST, and low levels of IgG. Teen-agers, old-year primiparas, pregnant females with a history of pyelonephritis, obesity, neuropathy in the prior labour, and hypertensive vegetovascular dystonia constituted a gestosis-risk group. The R-protein test should be considered to be the most informative indicator of a gestosis risk.
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PMID:[Immunity indices in the diagnosis of pretoxicosis in women with an increased risk for the development of late toxicosis]. 165 May 37

The purpose of the work was to evaluate the compensatory and adaptive possibilities of oxygen transport systems in moderate hypoxic hypoxia to define the sensitivity to hypoxia of patients suffering from neurocirculatory dystonia (NCD) with the respiratory syndrome and to elaborate training therapy methods. 40 patients suffering from cardial NCD were examined. Of these, 23 complained of dyspnea. The general hypoxemic test (GHT) was used; parameters of external respiration, hemodynamics, gas composition of blood, and the content of oxidation substrates were examined. Analysis of the clinical picture of respiratory disorders in patients with cardial NCD revealed the differences in their nature. In addition to psychogenic factors of dyspnea, of importance was a decrease in the compensatory and adaptive possibilities of the body as regards hypoxia, which occurs in mental, physical stress, changes in meteorological conditions, in closed premises, and in vegetovascular crises.
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PMID:[A respiratory syndrome in patients with neurocirculatory dystonia]. 181 39

Changes in central hemodynamics, systolic phase structure and capacity for physical work were examined, using respiration ergometry, in patients with neurocirculatory dystonia after a short course of treatment with beta-blockers. It was demonstrated that the treatment resulted in the eukinetic type of circulation, yet changes in physical working capacity showed opposite tendencies: oxygen support of exercise was improved in some patients only. A short-term beta-blocker treatment course can be used as a test of adequacy of the chosen therapy.
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PMID:[Effect of a short course of beta-blocker treatment on the central hemodynamics and work capacity of patients with neurocirculatory dystonia]. 286 4

Synchronous electro- and rheoencephalography were used to study tolerance to moderate hypoxic hypoxia for 30 min at an altitude of 5000 m without additional oxygen supply. As test subject, men with autonomic-vascular dystonia (29-39 years old), 15 men over 40 (41-56 years old), and 16 essentially healthy controls (23-36 years old) were used. The aged volunteers (41-56 years old) did not differ from the controls with respect to their tolerance to hypoxic hypoxia. The men with early symptoms of hypertonic-type dystonia also showed high tolerance to hypoxic hypoxia. The subjects with hypotonic-type dystonia displayed lower tolerance.
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PMID:[Hemo- and neurodynamics of the human brain during exposure to moderate hypoxic hypoxia]. 648 67

The working capacity and the oxygen supply during exercise were studied in 83 patients with neurocirculatory dystonia of various severity and 50 healthy subjects on the basis of the spiroergometric findings. The patients with neurocirculatory dystonia showed a decrease in such parameters of the oxygen supply during "maximum" exercise as the maximum consumption of oxygen at the threshold exercise level, the maximum oxygen pulse, the maximum pulmonary ventilation and the index of the oxygen cost per 1 kgm of work. The correlation of the disorders of the oxygen supply during exercise with the severity of the clinical course of the disease elucidated their relationship: a decrease in the maximum oxygen consumption at the threshold exercise level and an increase in the "oxygen cost" of 1 kgm of work were most pronounced in a group of patients with a severe course of the disease.
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PMID:[The oxygen supply in patients with neurocirculatory asthenia during exercise]. 652 Dec 10

A consistent neurochemical abnormality in Parkinson's disease (PD) is degeneration of dopaminergic neurons in substantia nigra, leading to a reduction of striatal dopamine (DA) levels. As tyrosine hydroxylase (TH) catalyses the formation of L-DOPA, the rate-limiting step in the biosynthesis of DA, the disease can be considered as a TH-deficiency syndrome of the striatum. Similarly, some patients with hereditary L-DOPA-responsive dystonia, a neurological disorder with clinical similarities to PD, have mutations in the TH gene and decreased TH activity and/or stability. Thus, a logical and efficient treatment strategy for PD is based on correcting or bypassing the enzyme deficiency by treatment with L-DOPA, DA agonists, inhibitors of DA metabolism, or brain grafts with cells expressing TH. A direct pathogenetic role of TH has also been suggested, as the enzyme is a source of reactive oxygen species (ROS) in vitro and a target for radical-mediated oxidative injury. Recently, it has been demonstrated that L-DOPA is effectively oxidized by mammalian TH in vitro, possibly contributing to the cytotoxic effects of DOPA. This enzyme may therefore be involved in the pathogenesis of PD at several different levels, in addition to being a promising candidate for developing new treatments of this disease.
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PMID:Tyrosine hydroxylase and Parkinson's disease. 962 67

Profiles of external respiration and circulation, self-assessment of health, mental performance, sensory functions, and peripheral blood were studied in patients with neurocirculatory dystonia in the course of normobaric hypoxic training. The hypoxic training proved to successfully normalize arterial pressure, eliminate cardiac arrhythmias, and benefit general condition. Substantial strengthening of hypoxic resistance was stated along with an oxygen debt reduction during hypoxia, improvement of sensory coordination and mental performance, and activation of erythropoiesis.
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PMID:[Clinical-physiological aspects of normobaric hypoxic training effects on functional status of patients with neurocirculatory dystonia]. 966 81

A toxin produced by legumes of the genus Astragalus and Arthrinium fungi, 3-NPA is a suicide inhibitor of succinate dehydrogenase and causes acute encephalopathy and late onset dystonia. It has been suggested that dopamine (DA) toxicity plays a role in 3-NPA induced brain damage. In order to simulate natural conditions of toxicant intake, adult, male, Sprague-Dawley rats were exposed to 3-NPA weekly for 24-h periods at 10 and 20 mg/40 ml in drinking water. This dosing regimen continued for 3 months with animals from both high and low dose groups sacrificed at the end of each month. Dopamine and its metabolites, 3,4-dihydroxylphenylacetic acid (DOPAC) and homovanillic acid (HVA), were assessed by HPLC-EC in the frontal cortex (FC) and caudate nucleus (CN). Increases of DA concentration were seen in both low and high dose groups in the CN after 1 and 3 months of dosing and in the FC after 2 months of exposure. An increase in DA turnover was observed in the CN of the high dose group following 2 months of dosing. Data suggest an activation of the dopaminergic system after long-term, intermittent exposure to 3-NPA. The production of radical oxygen species associated with DA metabolism may contribute to 3-NPA-induced neurotoxicity.
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PMID:Dopamine toxicity following long term exposure to low doses of 3-nitropropionic acid (3-NPA) in rats. 1090 28

In order to understand the correlation between the clinical and neuroimaging manifestations and the long-term prognosis in delayed encephalopathy after carbon monoxide (CO) intoxication, we retrospectively reviewed 12 patients who had delayed encephalopathy from 89 patients with CO intoxication. There were 8 men and 4 women, with a mean age of 54.4 +/- 17.2 years (range: 11-79 years). All patients had prominent consciousness disturbance in the acute stage and received high flow of O2 or hyperbaric oxygen therapy. All of them regained consciousness within 1-7 days, but subsequently developed delayed encephalopathy. The delayed encephalopathy occurred from 14 to 45 days after recovery from the acute stage. The clinical manifestations included cognitive impairment, akinetic mutism, sphincter incontinence, gait ataxia and extrapyramidal syndromes such as chorea, dystonia, and parkinsonism. Brain MRI revealed multiple lesions in the subcortical white matter and basal ganglia, mostly in the globus pallidus, and to a lesser degree in the putamen, and caudate. In the follow-up period, sphincter incontinence first disappeared. The cognitive impairment improved greatly in the following few months, but the involuntary movements were improved only slightly. Some patients had persistent neurological sequelae, such as dystonia. Similary, the follow-up brain MRI showed a steady improvement. In conclusion, the delayed encephalopathy usually developed 2 weeks to 1.5 months after the acute phase of CO intoxication. Globus pallidus and subcortical white matter were commonly involved. The neurological manifestations improved and correlated roughly with the neuroimaging changes.
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PMID:Delayed encephalopathy after carbon monoxide intoxication--long-term prognosis and correlation of clinical manifestations and neuroimages. 1547 74

Thirty-five men with neurocirculatory dystonia (NCD) aged 24.4 +/- 1.8 and 22 practically healthy men of comparable age were examined. All the patients underwent standard load veloergometric test by step-up technique until submaximum heart rate was achieved. The study found significant increase in myocardial oxygen consumption both at rest and during physical exercise. The author offers quantitative criteria that allow for objective evaluation of disturbances in the regulatory systems that provide response to measured physical load and thus contribute to clinical diagnostics of NCD.
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PMID:[Standardized load test in the diagnostics of neurocirculatory dystonia]. 1766 3


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