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)

A total of 85 patients (68 with coronary heart disease in the presence of effort angina of various functional classes (a major group) and 17 with neurocirculatory++ dystonia and cardialgic syndrome (a control group)) were examined. Heart failure severity and blood flow distribution in the functioning myocardial areas were evaluated in transient ischemia induced by atrial pacing. Three levels of coronary venous blood flow were defined in patients with coronary heart disease. A relationship between the coronary blood flow, disease history duration, and coronary blood flow changes was examined in cardioselective exercise.
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PMID:[Status of coronary venous blood flow in patients with ischemic heart disease in myocardial ischemia induced by the atrial stimulation test]. 189 38

A 59-year-old man developed dystonia and reflex sympathetic dystrophy after receiving high doses of ergotamine for migraine treatment. Ischemia is suggested as the precipitating factor.
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PMID:Dystonia and reflex sympathetic dystrophy induced by ergotamine. 158 44

Three cases of movement disorders secondary to hypoxic-ischemic encephalopathy are reported. Despite similarities among the clinical events, the neurological syndromes produced were dissimilar. Cerebral hypoxia-ischemia typically produces lesions of the globus pallidus that may result in an akinetic rigid syndrome. Due to its unique blood supply, vascular insufficiency is found to be a major factor. Lesions in the putamen also occur, and these tend to be associated with dystonia. Recent evidence supports a specific neuronal sensitivity in the striatum, possibly due to afferent excitatory amino acid connections. These two components and changes in the levels of neurotransmitters during hypoxia-ischemia may interact to produce varied clinical outcomes. These factors must also be considered when planning therapeutic interventions.
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PMID:Hypoxic-ischemic damage of the basal ganglia. Case reports and a review of the literature. 238 37

On the basis of histological and histochemical examinations of 100 postmortem observations of bacterial shock, 4 stages of disorders in the microcirculatory bed and in cell elements of organs in this complication are distinguished. The hemodynamic stage consists in redistribution of the blood flow, alternation of spasm and paresis, and vascular dystonia. In the stage of hemorheological disorders congestion is substituted by stasis, sludging of erythrocytes due to pachyemia. As a result of increased permeability of vessel walls, interstitial edema and early changes of parenchymatous cells of organs occur at the enzymatic level. The addition of DIBC syndrome leads to deeper ischemia of organs and formation of necroses, hemorrhages, acute ulcers. As a consequence, organ insufficiency (adrenal, renal, respiratory) develops.
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PMID:[Organ pathology of bacterial shock]. 667 Sep 42

Patients with coronary heart disease (CHD), neurocirculatory dystonia and acute myocardial infarction showed statistically significant, positive linear correlations between the levels of inosine and hypoxanthine as well as the total concentration in the arterial blood and the blood from the coronary sinus. The correlation analysis ascertained that CHD patients in the initial state exhibited a considerable extraction of inosine by the myocardium as compared to patients with neurocirculatory dystonia and that in electrically stimulated ischemia it was sharply reduced. Electrostimulation in the group of patients with neurocirculatory dystonia had no effect on the rate of inosine extraction. Acute myocardial infarction was related to a higher rate of inosine extraction and to inosine production in the myocardium, the latter being explained by the degradation of adenyl nucleotides in conditions of acute ischemia. It is outlined that the total level of inosine and hypoxanthine in the arterial blood of patients with acute myocardial infarction may indicate the severity of infarction while its variations over time may be prognostically valuable.
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PMID:[Effect of myocardial ischemia on adenine nucleotide metabolism]. 674 86

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.
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PMID:Delayed-onset progressive movement disorders after static brain lesions. 890 76

A 76-year-old man had shown sustained excruciating facial pain in the maxillary region for more than 30 years. Since he was suffering from blepharospasm, facial electromyography was performed and revealed a perioral dystonia. This possible cause of facial pain might have been overlooked had dystonia not been considered and electromyographical studies performed. Repeated intramuscular perioral injections of botulinum toxin brought about complete pain relief. This case shows that involuntary activity of facial muscles can cause a severe chronic pain syndrome. Possible mechanisms include irritation of ascending trigeminal fibers, muscle ischemia due to compression of blood -vessels, or release of pain-producing substances.
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PMID:Facial pain in a case of cranial dystonia: a case report. 995 Jun 30

A series of six patients with movement disorders associated with cerebral arteriovenous malformations (AVM) is reported. The AVMs were classified according to the Spetzler-Martin classification as grade V (one patient), grade IV (four patients), and as grade III (one patient). One patient had action-induced hemidystonia caused by a contralateral frontoparietal AVM which compressed the putamen and was supplied partially by enlarged lenticulostriate arteries. Two patients presented with unilateral cortical tremor associated with contralateral high-frontal cortical/subcortical AVMs sparing the basal ganglia. Another patient developed hemidystonia and hemichorea-hemiballism after bleeding of a contralateral temporooccipital AVM and subsequent ischemia. Two patients had focal dystonia after thalamic and basal ganglia hemorrhage from AVMs. Five patients were operated on. The movement disorder was abolished in one patient postoperatively. Different mechanisms were identified that are relevant for the development of AVM-related movement disorders: mass effect, diaschisis, local parenchymal altered cerebral blood flow, and hemorrhagic or ischemic structural lesions.
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PMID:Cerebral arteriovenous malformations and movement disorders. 1046 3

Liquidators of consequences of the Chernobyl atomic power station accident were found to have cardiovascular regulatory disorders in the late period. A late pressure reaction of systolic blood pressure to exercise was caused by cardiac rhythm rigidity due to the sick sinus syndrome. High exercise tolerance and delayed ischemia were indicative of diminished total peripheral resistance due to the impaired responsiveness of alpha-adrenoblockers in the arterial vessels and of the development of neurocirculatory dystonia. Cardiovascular functional changes in the liquidators are not attended by the higher morbidity rates of hypertensive disease.
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PMID:[The cardiovascular system in liquidators of consequences of the Chernobyl atomic power station accident]. 1534 87


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