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)

Ischemic disorders of brain blood circulation caused by brain artery thrombosis due to antiphospholipids-induced anticoagulopathy are main neurological appearances of primary antiphospholipid syndrome (PAPS). A number of neurological disorders in patients with PAPS are the result of primary involvement of the brain and peripheral nervous system. We analyzed the spectrum of neurological non-ischemic PAPS manifestations in 125 patients (102 female, 23 male, mean age--37.5 +/- 11.3 years) with definite PAPS. These manifestations included headache (67%), epileptic seizures (23%), chorea (15%), optic neuropathy (9%), peripheral neuropathy (6%), multiple sclerosis like syndrome (MSLS) (8%), acute psychosis (2%), myasthenic syndrome (1%), non-vascular parkinsonism (1%). In the development of non-ischemic PAPS manifestations, antiphospholipids as well as other antibodies produced as a result of immune disregulation (antibodies to acetylcholine receptors in myasthenic syndrome, antineuronal antibodies in MSLS) may have pathogenic significance. In some cases a role of infection involved in PAPS manifestation cannot be ruled out.
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PMID:[Non-ischemic neurological manifestations in patients with primary antiphospholipid syndrome]. 1579 37

Antiphospholipid syndrome can be associated with several neurological manifestations. The most common symptom is headache. It has also been associated with cognitive dysfunction, probably due to ischemia. A high prevalence of antiphospholipid antibodies has been found in patients with epilepsy and in transverse myelitis. The most common thrombotic manifestation is stroke. Venous thrombosis can also be found, yet it is less frequent. A stroke in a young person obliges to rule out the antiphospholipid syndrome. The neurological manifestations can mimic multiple sclerosis. Thus, determination of antiphospholipid antibodies is recommended in the study of patients with atypical manifestations of multiple sclerosis. Other manifestations associated with antiphospholipid antibodies include chorea, neurosensorial deafness, Guillain-Barre syndrome, and psychotic disorders.
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PMID:[Neurological manifestations of the antiphospholipid syndrome]. 1587 82

Neurological, including cecbrovascular, disorders frequently emerge in primary antiphospholipid syndrome (PAS). Clinical peculiarities of PAS were studied in 113 patients with cerebrovascular disturbances. Its had mainly ischemic patogenesis. Structure of cerebrovascular disorders was as follows: stroke (33% cases), transient ischemic lesions (10%), its combination (57%), thrombosis of brain venous sinuses (3%), vascular dementia (27%). Besides it were found epileptic seizures, peripheral neuropathy, headache, chorea and some symptoms of myasthenia, parkinsonism, multiple sclerosis and psychotic disorders. In all cases antibodies to phospholipids have been detected. Secondary prophylaxis includes regular use of anticoagulants and small doses of aspiriny.
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PMID:[Primary antiphospholipid syndrome and cerebrovascular disturbances]. 1595 34

Neurological disturbances frequently emerge in antiphospholipid syndrome (APS). One hundred and twenty four patients (100 women, 24 men, mean age 37.5 +/- 11.3 years) with primary APS (PAPS), including 76 patients with Sneddon's syndrome and positive antibodies to phospholipids (aPL), have been studied. A structure of neurological disturbances was as follows: ischemic lesions of cerebral blood flow (LCBF) which comprised stroke and transient LCBF (91%); thrombosis of brain venous sinuses (3%); epileptic seizures (24%); headache (65%); chorea (15%); visual neuropathy (9%); peripheral neuropathy (6%); multiple-sclerosis-like syndrome (10%); myasthenia syndrome (1%); syndrome of parkinsonism of non-vascular genesis (1%) and psychotic disorders (2%). 84% patients had main systemic APS symptoms (fetal loss, thrombosis), which preceded neurological appearances in 78% cases. All the patients had aPL: aPL to cardiolipin (aCL) and/or lupus coagulant (LC) and/or aPL to phosphatidyl serine, phosphatidyl inositol, phosphatidyl ethanolamine. In some patients, aCL titres ranged from positive to negative values and LC was not consistently detected. Thus, the presence of clinical symptoms of PAPS including neurological disturbances demands an investigation of different aPL types as well as a replicate study for immunological confirmation of PAPS.
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PMID:[Neurological appearances of primary antiphospholipid syndrome]. 1598 22

Tetrabenazine, a dopamine-depleting agent first synthesized half a century ago, was initially developed for the treatment of schizophrenia. Although psychotic disorders have since been treated more successfully with other neuroleptic medications, many studies have shown this drug to be effective in the treatment of hyperkinetic movement disorders (hyperkinesias). Hyperkinesias are neurologic disorders characterized by abnormal involuntary movements such as chorea associated with Huntington's disease, tics in Tourette's syndrome and stereotypies in tardive dyskinesia. Recently, clinical trials investigating tetrabenazine for the treatment of chorea associated with Huntington's disease found the drug to be safe and efficacious, making approval by the US Food and Drug Administration for this indication a distinct possibility.
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PMID:Tetrabenazine in the treatment of hyperkinetic movement disorders. 1646 7

We described a 32-year-old woman with Huntington's disease (HD) who presented with severe chorea, psychosis and cognitive abnormalities. We started risperidone at 2 mg p.o./d and increased to 4 mg p.o./d after six weeks. Psychotic and motor symptoms were markedly improved. Since there was no change in cognitive functions, we added memantine at 5 mg p.o./d and gradually increased the dose to 20 mg p.o/d after five weeks. We continued risperidone and memantine for nearly six months. The patient did not show any progression of cognitive symptoms or motor abnormalities. We did not observe any psychotic symptoms.
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PMID:Clinical experience with risperidone and memantine in the treatment of Huntington's disease. 1691 37

Delusional parasitosis (DP) is a psychotic condition in which a person has the unshakeable and mistaken belief (delusion) and/or aberrant perception (hallucination) of being infested with parasites. The disorder will be usually classified in a primary DP-group without a detectable cause (so-called pure forms), while secondary DP-groups are associated with general organic conditions, psychiatric illnesses and drugs (substance induced). Etiology and pathophysiology of DP remain however unknown. In the present paper we hypothesize for the first time a decreased striatal dopamine transporter (DAT)-functioning (corresponding with an increased extracellular dopamine-level) as etiologic condition for DP (primary and secondary groups). The DAT as key regulator of the dopamine-reuptake in the human brain is well known (regulation of the extracellular dopamine concentration). It is a presynaptic plasma membrane protein highly dense represented in the striatum. The hypothesis of a decreased DAT-functioning as etiologic condition by DP is revealed in case reports which show that DAT-inhibitors, such as cocaine, pemoline, methylphenidate and other amphetamine-derivatives can induce the clinical expression of DP. Several other associated causes of secondary DP-groups (medications, parkinson, chorea huntington, multiple system atrophy, diabetes, cerebrovascular diseases, alcoholism, traumatic brain injury, hyperuricemia, human immunodeficiency virus, iron deficiency, schizophrenia, depression) suggest that the clinical expression of DP may be related to a decreased striatal DAT-functioning (blocking, reduced ligand binding, reduced density, reduced activity). Our examined DP-cases (2-females) show means of magnetic resonance imaging a structurally damaged striatum. Furthermore, we presume that by the primary DP-group, the physiologically age-related decline of the DAT-density is pathologically elevated. Based on this hypothesis we show in the present paper the relation between DP and decreased striatal DAT-functioning, trying to give a new insight into the pathophysiologically mechanism involved. The hypothesis provides supporting evidence that increased levels of extracellular dopamine in the striatum of DP-patients is likely to be the result of decreased DAT-functioning and not increased rates of release. The hypothesis can be investigated simply by dopamine transporter imaging in patients with DP.
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PMID:Delusional parasitosis and the dopamine transporter. A new insight of etiology? 1713 47

Thyroid hormones are of primary importance for the perinatal development of the central nervous system, and for normal function of the adult brain. These hormones primarily regulate the transcription of specific target genes. They increase the cortical serotonergic neurotransmission, and play an important role in regulating central noradrenergic and GABA function. Thyroid deficiency during the perinatal period results in mental retardation. Hypothyroidism of the adults causes most frequently dementia and depression. Other less common clinical pictures include myxoedema coma, dysfunction of cerebellum and cranial nerves. Hypothyroidism also increases predisposition of stroke. Peripheral diseases frequently include polyneuropathy, carpal tunnel syndrome, myalgic state, and rarely myokymia. Nearly all the hyperthyroid patients show minor psychiatric signs, and infrequently psychosis, dementia, confusion state, depression, apathetic thyrotoxicosis, thyrotoxic crisis, seizures, pyramidal signs, or chorea occur. The peripheral complications may be indicated by chronic thyrotoxic myopathy, infiltrative ophthalmopathy, myasthenia gravis, periodic hypokalemic paralysis and polyneuropathy. Generalized resistance to thyroid hormone was confirmed in a number of patients with attention deficit-hyperactivity disorder. Significantly elevated antithyroid antibody titers characterize Hashimoto's encephalopathy. This condition is a rare, acute - subacute, serious, life threatening, but steroid-responsive, relapsing-remitting, autoimmune disease.
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PMID:[Some neurologic and psychiatric complications in endocrine disorders: the thyroid gland]. 1734 50

The X-linked McLeod neuroacanthocytosis syndrome strongly resembles Huntington's disease and has been reported in various countries world-wide. Herein, we report two Chilean brothers with predominant psychiatric features at disease onset including schizophrenia-like psychosis and obsessive compulsive disorder. Molecular genetic analysis revealed a small deletion in the XK gene (938-942delCTCTA), which has been already described in a North American patient of Anglo-Saxon descent and a Japanese family, presenting with seizures, muscle atrophy or chorea yet absence of psychiatric features. These findings argue against a founder effect and indicate a profound phenotypic variability associated with the 938-942delCTCTA deletion. Our report supports the inclusion of McLeod syndrome in the differential diagnosis of Huntington's disease as well as acute psychosis in male subjects.
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PMID:Phenotypic variability of a distinct deletion in McLeod syndrome. 1746 88

Neuropsychiatric (NP) manifestations are found in approximately 25% of children and adolescents with pediatric SLE (pSLE). In 70% of those, NP involvement will occur within the first year from the time of diagnosis. Headaches (66%), psychosis (36%), cognitive dysfunction (27%) and cerebrovascular disease (24%) are the most common presentations. The support of a psychiatrist is often required. Anti-phospholipid antibodies are associated with distinct NP disease entities and may be implicated in the pathogenesis of several manifestations of NP-pSLE including chorea, cerebrovascular disease and seizures. The role of novel auto-antibodies and imaging modalities is currently explored. The treatment of NP-pSLE is not based on prospective studies; however, an immunosuppressive combination therapy consisting of high doses of prednisone and a second line agent such as cyclophosphamide or azathioprine is commonly suggested for children with NP-pSLE. The role of novel therapies is currently studied. The outcome of children with NP-pSLE is relatively good. The overall survival is 95-97%, 20% of children experience a disease flare during childhood and 25% have evidence of permanent neuropsychiatric damage.
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PMID:Neuropsychiatric involvement in pediatric systemic lupus erythematosus. 1771 89


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