Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008489 (chorea)
 2,102 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

US and British studies have shown significantly higher incidence of strokes due to thromboembolism, subarachnoid hemorrhage, and cerebral venous thrombosis in users of oral contraceptives, particularly high estrogen formulations. Estrogen increases plasma levels of fibrinogen and the clotting factors VII, VIII, IX, X, and XII; enhances platelet aggregation; and suppresses antithrombin III and the fibrinolytic system. Estrogen may also cause immune-mediated vasculitis. The risk of strokes increases for women over 35 and smokers. Estrogen-induced chorea, including chorea of pregnancy, may be due to direct dopaminergic action of estrogens or to an accumulation of dopamine in the brain caused by competitive binding to the dopamine-degrading enzyme catechol-o-methyltransferase. Epileptics taking anticonvulsants and oral contraceptives have 25 times the risk of pill failure as normally expected, due to metabolism of anticonvulsants, such as phenytoin, phenobarbital, primidone, carbamazepine, and ethosuximide, by the hepatic microsomal enzyme system, resulting in a dramatic decrease of circulating ethinyl estradiol. Available options are to increase the estrogen dose to as much as 100 mg, to substitute valproic acid for other anticonvulsants, or to augment ethinyl estradiol levels by oral administration of ascorbic acid, which increases the bioavailability of the steroid. During pregnancy, on the other hand, serum levels of anticonvulsants decrease by 30-40%.
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PMID:Sex hormones in stroke, chorea, and anticonvulsant therapy. 305 49

Paraballism in a 28-year old woman, associated with her 4 month intake of oral contraceptives, is described here. This constitutes only the 14th such case in the literature, and the only one in a pill user. The woman had pain in the head and neck when she first took the pill, Ovostat (1 mg lynestrenol, and 50 mcg ethinyl estradiol. Later she developed abnormal movements in the arms, neck and face. She was hospitalized in a psychiatric ward for depression, in response to the movements, and treated briefly with propanolol for palpitations. Her neurological findings were ballet-like movements of both arms, torsion movements of the neck, grimacing of the face, choreiform movements of both hands, and involuntary kicking while walking. The only other findings were an ejection murmur, and hypertrophied interventricular septum on the echocardiogram. When the pill was discontinued, the ballistic movements disappeared within days and the chorea within 2 weeks. The woman was discharged in a month with no complaints. A year later she bore her first child, with no return of abnormal movements.
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PMID:Oral contraceptive induced paraballism. 356 21

A left-handed 26-year-old woman was hospitalized in December 1984 for abnormal movements on the left side which had appeared abruptly 16 days earlier. Her medical history included neonatal anoxia with cyanosis and reanimation after a difficult delivery, and ophthalmic migraines. There were no previous rheumatismal or choreic episodes. The patient had taken a diphasic oral contraceptive (OC) containing 30 ng and 40 ng of ethinyl estradiol and 1 mg and 2 mg of norethisterone from 1976 to 1981 and had had a normal pregnancy and delivery in November 1983. In June 1984, 3 weeks after resuming use of the same pill, the patient began suffering violent migraines which persisted on a daily basis for 1 month. The abnormal movements of the left side were very broad at the outset. 3 days before hospitalization the OC was discontinued and the symptoms abated somewhat. On hospitalization, brusque, variable and arhythmic muscular jerks were visible on the face and left arm and leg. The left half of the body was hypotonic. The condition appeared to be hemichorea. A radioimmunologic test for synthetic steroid antihormone antibodies demonstrated the presence of anti-ethinyl estradiol antibodies at a level of 410 cpm, compared to the normal value of under 100 cpm. The electromyographic pattern was that of chorea. On discharge 12 days later the choreic movements had abated considerably after treatment with haloperidol 20 mg/day. 4 weeks after discontinuation of the OC and after discontinuation of the haloperidol, the abnormal muscular activity had disappeared; a neurologic examination 1 month later was normal. OCs have been proven responsible for some cases of chorea although the number of reported cases is small. Among hypotheses advanced to explain development of chorea are preexisting presence of unilateral lesions in the gray matter following a rheumatismal or viral episode or neonatal trauma which predisposes to a subsequent chorea induced by hormonal impregnation, or an immunologic action analogous to the mechanism of rheumatismal chorea.
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PMID:[Hemichorea and oral contraceptives]. 408 98

Estrogen was administered to male rats that had received unilateral injections of 6-hydroxydopamine into the striatum. Following this treatment, their duration of rotation increased in response to amphetamine. Estrogen treatment resulted in a corresponding increase in the number of striatal dopamine receptors. Therefore, both behavioral and biochemical evidence suggests that striatal dopamine function is influenced by peripherally administered estrogens. These results are relevant to the clinical cases of chorea associated with elevated concentrations of estrogen, which occur in pregnancy and during oral contraceptive use.
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PMID:Increased dopamine receptor sensitivity after estrogen treatment using the rat rotation model. 718 2

Estrogen have been reported in animal studies to both enhance and block central dopaminergic activity and in one clinical report to improve tardive dyskinesia. In the present study estrogen (Premarin, 2.5 mg per day) administration caused varying degrees of improvement in less than one-third of 21 patients with chorea due to Huntington's disease and tardive dyskinesia and had no effect in eight patients with dystonia. Estrogens appear to have an antidopaminergic effect in humans but poses only limited efficacy in the treatment of dyskinetic disorders.
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PMID:Estrogen treatment of dyskinetic disorders. 720 Feb 10

Movement disorders including Parkinson's disease (PD), Huntington's disease (HD), chorea, tics, and Tourette's syndrome (TS) display sex differences in disease susceptibility, disease pathogenesis, and clinical presentation. PD is more common in males than in females. Epidemiologic studies suggest that exposure to endogenous and exogenous estrogen contributes to these sex differences. There is extensive evidence that estrogen prevents dopaminergic neuron depletion induced by neurotoxins in PD animal models and therefore is neuroprotective. Estrogen may also decrease the efficacy of other neuroprotective substances such as caffeine in females but not males. Sex chromosomes can exert effects independent of sex steroid hormones on the development and maintenance of the dopamine system. As a result of hormone, chromosome and other unknown effects, there are sexual dimorphisms in the basal ganglia, and at the molecular levels in dopaminergic neurons that may lead to distinct mechanisms of pathogenesis in males and females. In this review, we summarize the evidence that estrogen and selective estrogen receptor modulators are neuroprotective in PD and discuss potential mechanisms of action. We also briefly review how sex differences in basal ganglia function and dopaminergic pathways may impact HD, chorea, and tics/Tourette's syndrome. Further understanding of these sex differences may lead to novel therapeutic strategies for prevention and treatment of these diseases.
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PMID:Sex differences in Parkinson's disease and other movement disorders. 2468 Oct 88