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Query: UMLS:C0008489 (chorea)
 2,102 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review of the effects of sex steroids and oral contraceptives (OCs) on neurologic function in health and disease covers the following: sex steroids and their interaction with neural tissues; the human menstrual cycle and OCs; and sex hormones and OCs in human neurologic disease, i.e., stroke (thromboembolic cerebral infarction, subarachnoid hemorrhage, vascular malformations, and cerebral venous thrombosis), migraine, movement disorders, nervous system neoplasm, and the peripheral nerve. The various sex hormones may exert their effects on the nervous system directly or undergo conversion to more active metabolites. Interactions of sex hormones with neural substrates subserve numerous activities essential to both the well-being and perpetuation of the individual and the species. These interactions are key to the sexual differentiation of the brain, control of the brain-pituitary-gonad axis, and to the establishment of normal patterns of sexual and aggressive behavior in both sexes. Additionally, they play a role in temperature regulation (progesterone), caloric homeostasis (estrogen), and possibly sensory discrimination. The potent influences exerted by sex steroids on catecholamine and indoleamine turnover and the colocalization of labeled E2 within catecholamine and luteinizing hormone-releasing hormone (LHRH) positive perikarya suggest that many of the physiologic effects of sex steroids are mediated by modulation of specific monoaminergic and peptidergic pathways. Estrogens and aromatizable androgens also induce irreversible structural alterations in the rodent hypothalamus during the neonatal and peripubertal periods that are predominantly synaptogenic. In adult mammals, estrogens induce pathologic changes in the hypophysiotropic hypothalamus that may contribute to reproductive senescence in some species. Data from a series of retrospective and prospective studies have implicated OC use as an independent risk factor for the development of hemorrhagic and nonhemorrhagic stroke. Hormonal changes accompanying the pregnant state and the estrogen (and possibly progestogen) content of OCs may be predisposing factors in thromboembolic cerebral infarction, subarachnoid hemorrhage, cerebral venous thrombosis, and bleeding from intracranial and spinal vascular malformations. There are well-documented temporal associations of migrainous headache with specific phases of the menstrual cycle and the modifying influences of pregnancy, the menopause, and OC use. Also well established are relationships between endogenous and exogenous sex hormones and chorea. Fluctuating sex steroids also influence neuropsychiatric states, such depression and neuroendocrine disorders.
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PMID:Neurology of sex steroids and oral contraceptives. 302 81

Fernando and Chir 1st reported an association between chorea and oral contraceptives (OCs) in 1966. Differential diagnosis of chorea, in addition to Sydenham chorea, include Wilson disease; encephalitis; Huntington chorea; drug intoxication; benign familial chorea; pregnancy; systemic lupus erythematosus; Henoch-Schonlein purpura; polycythemia vera; hypocalcemia; hyperthyroidism; carbon monoxide poisoning; cerebral infarction, and; intracranial tumor. Chorea can also occur as an untoward side-effect of OC therapy, as shown by the case report of a 20-year old white woman. Chorea associated with OC therapy occur unilateraly but has also been bilateral in 37% of reported cases. 8 of 24 reported cases (33%) had a prior history of rheumatic fever - mean age of patient was 22 years (range, 16 to 40 years). The time between initiation of OC therapy and appearance of choreiform movements can vary from 6 days to 9 months, with a mean of 3 months. Time between discontinuation of OC therapy and cessation of symptoms vary from 3 days to 3 months, with a mean of 5 weeks. Speculations by various authors on the pathogenesis of chorea are described.
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PMID:Chorea associated with oral contraceptive therapy. 739 41

One of the clinical hallmarks of antiphospholipid syndrome is the development of neurological complications, namely cerebral ischaemia, chorea, multi-infarct dementia, amaurosis fugax, migraine and transverse myelitis. An animal model should include the development of measurable neurological deficits and evidence of cerebral infarction. Although there are a number of mouse models for fetal loss, there has been no convincing model for the neurological complications of the antiphospholipid syndrome. One explanation for the high frequency of neurological events in antiphospholipid syndrome is a vulnerability of the cerebral vasculature to the hypercoagulable state associated with the syndrome. A greater appreciation of the differences in the regulation of coagulation between the systemic and cerebral vasculatures may be key to understanding the apparent predilection for central nervous system involvement in the antiphospholipid syndrome.
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PMID:Models for central nervous system complications of antiphospholipid syndrome. 780 11

An association exists between antiphospholipid antibodies and chorea. As these antibodies are associated with thrombosis, it has been suggested that cerebral infarction might cause chorea. However, CT and MRI typically do not demonstrate focal basal ganglionic lesions in such patients and an autoimmune mechanism for chorea has also been proposed. We report a young woman with left hemichorea and dyspnea. She was found to have lupus anticoagulant, large aortic and tricuspid vegetations, and pulmonary emboli. CT and MRI showed a small lesion in the head of the right caudate. In the presence of a definite cardiac source for emboli (valvular vegetations) with embolic activity (pulmonary emboli), it is likely that this patient's hemichorea was caused by cardioembolic caudate infarction.
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PMID:Cardioembolic caudate infarction as a cause of hemichorea in lupus anticoagulant syndrome. 833 81

Although central nervous system involvement is an important manifestation of systemic lupus erythematosus (SLE), chorea is a relatively uncommon complication. A strong association between chorea and the presence of antiphospholipid antibodies (aPLs) has been reported in patients with SLE, lupus-like disease, or primary antiphospholipid syndrome. We describe a patient with lupus nephritis and cerebral infarction, who subsequently developed recurrent hemichorea associated with increased aPLs levels. A 7-year-old boy suffered from lupus nephritis and a left middle cerebral artery infarction associated with aPLs. He subsequently experienced two episodes of right hemichorea associated with increased aPLs levels without any evidence of further neurological lesions by brain computed tomography or magnetic resonance imaging. The previous left cerebral artery infarction might have increased the susceptibility of the left basal ganglia to the effects of aPLs that contributed to the development of the right hemichorea in this patient.
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PMID:Hemichorea with antiphospholipid antibodies in a patient with lupus nephritis. 1474 Feb 86

A 73-year-old woman was admitted with dry mouth, polyposia, polyuria, hyperglycemia (611 mg/dl) and positive urine ketone bodies. Blood glucose levels decreased gradually after initiation of insulin injections. The patient was discharged, but developed involuntary movement of the right extremities on the following day. At that time, her blood glucose levels were 54 mg/dl. Four days later, she was admitted to our Neurology Ward because the movement worsened. On admission, choreic involuntary movements were severe in the right extremities and slight in the left extremities. Urine ketone bodies were negative, but HbA1c had elevated to 11.7%. Although a brain CT did not detect any abnormal density areas, we suspected that the patient had cerebral infarction of the basal ganglia or the parietal lobe on the left side, or of the subthalamic nucleus on the right side because choreic involuntary movements were more prominent on the right side. Anti-platelet therapy was performed, but the involuntary movements persisted. A T1-weighted image of brain MRI, performed on the 4th day after hospitalization, detected abnormal high intensity areas in the bilateral putamens. The abnormal area in the left putamen was more prominent. This MRI finding was consistent with that of diabetic chorea-ballism. Surface electromyography demonstrated the simultaneous appearance of grouping discharges in the biceps and triceps muscles of the right arm. We diagnosed the patient as having diabetic chorea based on the MRI findings, and discontinued anti-platelet therapy. MRI should be performed as soon as possible in diabetic patients with acute-onset chorea-ballism which occurs on one side or predominantly on one side in order to differentiate diabetic chorea-ballism from cerebral infarction.
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PMID:[Choreic involuntary movement that occurred during therapy for diabetes mellitus]. 1844 98

We present seven cases of movement disorders encountered in patients with AIDS at a national referral centre over a 4 year period. These include cases of chorea athetosis due to cerebral toxoplasmosis, progressive multifocal leucoencephalopathy, cerebral infarction due to Herpes zoster infection and hypoglycaemia secondary to pentamidine therapy, wing beating tremor as a result of primary cerebral lymphoma, and two cases of drug induced akinetic rigid syndrome.
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PMID:Movement disorders in AIDS: Infective, neoplastic and iatrogenic causes. 1859 Sep 97

Generalized chorea caused by unilateral cerebral infarction has rarely been reported. A 58-year-old woman presented involuntary movement in her all extremities after acute cerebral infarction on her right anterior cerebral artery territory. The involuntary movements were diagnosed as generalized chorea. We didn't find any cause of generalized chorea except the acute cerebral infarction. Here, we described the case of generalized chorea after unilateral cerebral infarction discussing the possible mechanisms.
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PMID:Generalized chorea induced by an unilateral anterior cerebral artery territorial infarction. 2486 51

It is not unusual to observe hemichorea in patients with diabetes mellitus, with origins attributable to recent ischemia. Our patient was a 66-year-old female with diabetes mellitus who suddenly developed right hemichorea, mild muscle weakness of the right upper extremity, ideational apraxia, and acalculia. Her blood glucose was 600 mg/dL, and HbA1c was 13.3%. After the patient underwent head magnetic resonance imaging (MRI), a new cerebral infarction was observed in the left frontal lobe, and treatment was started with edaravone and cilostazol. At the same time, insulin treatment was also started for hyperglycemia. The acalculia and ideational apraxia improved approximately 1 week after treatment initiated, and the hemichorea also decreased. ECD-SPECT was performed on admission, and it was observed that blood flow was decreased in the left frontal lobe and striatum, but increased in the thalamus; two weeks later on follow-up ECD-SPECT, blood flow had increased slightly in the left forebrain and striatum, while it had decreased slightly in the thalamus. This suggests that the cause of hemichorea was related to ischemia. When the activity of the pallidum is impaired, it is presumed that the inhibitory activity towards the thalamus weakens and the thalamic cells become over-excited, causing chorea.
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PMID:Hemichorea in a diabetes mellitus patient following acute ischemic stroke with changes in regional cerebral blood flow. 2574 12