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

Neuropeptide immunohistochemistry was used to test several hypotheses of the anatomical bases of chorea and rigidity-akinesia. To test the hypothesis that elevated concentration of striatal somatostatin causes chorea, we visually compared the density of striatal neurons containing somatostatin and neuropeptide Y in brains affected by choreic or rigid-akinetic Huntington's disease (HD). The density of these neurons was elevated in both rigid-akinetic and choreic HD specimens with an apparently normal total number of these neurons, indicating that elevated somatostatin concentration, by itself, does not lead to chorea. We tested the hypothesis that rigid-akinetic HD results from deficient dopaminergic nigrostriatal neurotransmission by examining tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra. In rigid-akinetic HD brains, there was no obvious reduction of nigral TH-IR neurons, indicating that rigid-akinetic HD is probably not due to loss of nigral dopaminergic neurons. Finally, we also examined the status of striatal projection neurons and found near total loss of all striatal neurons projecting to the lateral globus pallidus, medial globus pallidus, and substantia nigra in brains affected by rigid-akinetic HD in contrast to the preservation of neurons projecting to the medial globus pallidus in choreic HD. These results are consistent with the hypothesis that chorea results from preferential loss of striatal neurons projecting to the lateral globus pallidus and that rigid-akinetic HD is a consequence of the additional loss of striatal neurons projecting to the medial segment of the pallidum.
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PMID:Striatal and nigral neuron subpopulations in rigid Huntington's disease: implications for the functional anatomy of chorea and rigidity-akinesia. 197 18

Movement disorders are subdivided based on a variety of criteria. One useful and popular approach to movement disorders, based on clinical phenomenology, categorizes these disorders into two groups, those displaying a poverty of movement (akinesia) and those displaying excessive movement (hyperkinesia). This article discusses diagnosis and treatment of the latter. By necessity, certain hyperkinesias such as hyperexplexia, akathisia, and restless leg syndrome are omitted or only briefly discussed. The major hyperkinesias, dystonia, tremor, tics, chorea (including tardive dyskinesia and ballism), and myoclonus are reviewed and a guide to practical management emphasizing symptomatic treatment is presented.
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PMID:Treatment of hyperkinetic movement disorders. 218 Dec 68

The descriptive aspects of all types of movement disorders and their related syndromes and terminologies used in the literature are reviewed and described. This comprises the features of (a) movement disorders secondary to neurological diseases affecting the extrapyramidal motor system, such as: athetosis, chorea, dystonia, hemiballismus, myoclonus, tremor, tics and spasm, (b) drug induced movement disorders, such as: akathisia, akinesia, hyperkinesia, dyskinesias, extrapyramidal syndrome, and tardive dyskinesia, and (c) abnormal movements in psychiatric disorders, such as: mannerism, stereotyped behaviour and psychomotor retardation. It is intended to bring about a more comprehensive overview of these movement disorders from a phenomenological perspective, so that clinicians can familiarize with these features for diagnosis. Some general statements are made in regard to some of the characteristics of movement disorders.
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PMID:Clinical features of movement disorders. 662 43

The clinical motor symptoms of basal ganglia disease are explored in relation to possible functions of this region of the human brain. It is concluded that Parkinsonian akinesia, and the dyskinesias of chorea, hemiballism and torsion dystonia are likely to represent the critical abnormalities of motor action in human basal ganglia lesions. These motor disorders involve most muscles, all classes of movement, and the individual sequential components of movement, but spare the overall motor plan. It is suggested that Parkinsonian akinesia is due to putaminal dysfunction disrupting the normal automatic execution of learned motor plans. The dyskinesias of chorea, hemiballism and torsion dystonia are conceived as being due to dysfunction of other strio-pallidal regions superimposed upon the normal function of the motor strio-pallidal system.
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PMID:Motor disorders in basal ganglia disease. 671 9

Lisuride is a soluble ergolene derivative with endocrine effects similar to but more potent than those of bromocriptine. In nine subjects with idiopathic, postencephalitic, or drug-induced parkinsonism, lisuride at a dosage of 0.05 to 0.15 mg intravenously caused an immediate improvement in tremor, rigidity, akinesia, and postural deformity, but also caused chorea and orofacial dyskinesia. Improvement lasted 2 to 3 hours. Lisuride had little or no effect in a single patient with progressively supranuclear palsy. Oral lisuride therapy, 0.8 to 4.8 mg daily, had similar effects but occasionally caused reduced awareness and hallucinations.
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PMID:Lisuride in parkinsonism. 721 65

Patients with Huntington's disease exhibit poorer-quality handwriting, sometimes clinically exhibiting macrographia, an increase in the size of handwriting. To characterize deficits in handwriting of patients with Huntington's disease, we compared the writing of 12 young, 12 age-matched controls, and 12 patients with Huntington's disease. Subjects were asked to write the letter "l" four times, at a constant length, on a graphics tablet that sampled pen position at 200 Hz. Huntington's disease causes chorea (involuntary movement), akinesia (difficulty in initiating voluntary movement), and bradykinesia (slowness and difficulty in maintaining voluntary movement). To distinguish changes in handwriting quality due to involuntary movement from impairments of voluntary movement, handwriting samples with obvious choreic movements were analyzed separately from other handwriting samples. Several measures of quality of handwriting were considered, based on: the regularity and consistency of handwriting, the efficiency of movement trajectories, and the proportions of movement occurring at specific frequencies. Results suggested that Huntington's disease increases variability of movement parameters, and causes problems in producing smooth movements. Choreic movement was best characterized by the number of zero crossings in the velocity function relative to the prescribed number of writing strokes. We hypothesize that macrographia in Huntington's disease occurs when chorea predominates over bradykinesia. Comparisons were made between the handwriting of patients with Huntington's and Parkinson's diseases.
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PMID:Characteristics of handwriting of patients with Huntington's disease. 799 Aug 47

Basal ganglia have been known as a motor center because their lesions cause motor disturbances in involuntary movements such as chorea, ballism or akinesia in parkinsonism. The different types of involuntary movements are closely related to the underlying muscle tone. Mechanisms of bradykinesia or akinesia have been elaborated in physiological studies on Parkinson's disease and the significance of sensorimotor processing or attention arousal has been disclosed as a relevant factor of bradykinesia. Analysis of short-stepped gait, frozen gait or apraxia of gait, has claimed the frontal lobe and the striatum to be a locomotion center especially in humans (bipedal locomotion). Cognitive function of the basal ganglia has attracted attention particularly in the disorder of Parkinson's disease. Subcortical dementia, difficulty in formation or changes of concepts are encountered in advanced stages of Parkinson's disease. Whether cognitive functions in the frontostriatal system are primarily related to the motor function of the brain is an issue for future study.
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PMID:Historical review of research on functions of basal ganglia. 879 Oct 14

The pathophysiology of akinesia and chorea involve disruption of the motor basal ganglia circuit. This circuit begins with cortical output to the striatum, followed by projections from striatum to pallidum, pallidum to thalamus, and finally thalamus to cortex. Abnormal thalamic output to the frontal cortex, particularly the supplementary motor cortex, is responsible for chorea and akinesia. The substantia nigra and subthalamic nucleus are also important parts of this circuit. Chemical or pathological changes in these nuclei that lead to reduced thalamic outflow to the cortex are associated with parkinsonism. Most disorders affect the nigrostriatal dopaminergic projection. The overall consequence of loss of nigrostriatal dopamine is a loss of inhibitory input to the striatum. This feeds through the circuit resulting in reduced thalamic outflow. Local factors that may affect symptoms are the degree of dopamine loss, the involvement of ventral or dorsal parts of substantia nigra, effect on direct and indirect pallidal pathways, topographical representation of the body in the striatum, and the presence of parallel basal ganglia circuits serving cognition and mood. Ageing, dopa-responsive dystonia, juvenile dystonia-Parkinson syndrome and Parkinson's disease have different effects on the nigrostriatal tract. In Parkinson's disease the speed and regional variation in nigrostriatal dopamine loss are associated with a significant pre-symptomatic period, steady rate of progression and a particular topography of L-dopa dyskinesias.
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PMID:Functional neuropathology in Parkinson's disease. 938 99

Basal ganglia have been known as a motor center because their lesions cause motor disturbances in involuntary movements such as chorea, ballism or akinesia in Parkinsonism. The different types of involuntary movements are closely related to the underlying muscle tone. Mechanisms of bradykinesia or akinesia have been elaborated in physiological studies on Parkinson's disease, and the significance of sensorimotor processing or attention, arousal has been disclosed as a relevant factor of bradykinesia. Cognitive functions of the basal ganglia have attracted attention, particularly in the disorder of Parkinson's disease. Subcortical dementia, difficulty in formation or changes of concepts, is encountered in advanced stages of Parkinson's disease. Whether cognitive functions in the frontostriatal system are primarily related to the motor function of the brain is an issue for future study.
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PMID:[Motor and cognitive functions of the basal ganglia]. 965 35

Common marmosets show parkinsonian motor deficits following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration and develop dyskinesias during chronic L-dopa exposure. The D1 agonists A-77636 [(1R, 3S) 3-(1'-adamantyl)-1-aminomethyl-3, 4-dihydro-5, 6-dihydroxy-1H-2-benzopyran HCl] and A-86929 [(-)-trans 9, 10-hydroxy-2-propyl-4, 5, 5a, 6, 7, 11b-hexahydro-3-thia-5-azacyclopent-1-ena[c]phenanthrene hydrochloride] possess potent antiparkinsonian activity in the MPTP-treated marmoset and we now assess their influence on L-dopa-induced dyskinesias. MPTP-treated marmosets with stable motor deficits were treated with L-dopa plus carbidopa for 28 days to induce dyskinesias. Subsequently, they received A-86929 for 10 days, initially at 0.5 micromol/kg and then at 1.0 micromol/kg for a further 5 days. Several months later, L-dopa 12.5 mg/kg plus carbidopa 12.5 mg/kg was given orally twice daily for 7 days, followed by A-77636 1 micromol/kg for 10 days, and then both A-77636 and L-dopa plus carbidopa were given concurrently for 3 further days. In these L-dopa-primed animals, A-86929 effectively reversed akinesia and produced dose-dependent dyskinesias which were significantly less intense than those produced by L-dopa administration. A degree of behavioral tolerance was encountered, but antiparkinsonian activity was preserved and elicited behaviour was free of hyperkinesis and stereotypy and more naturalistic than that seen with L-dopa. After a week of twice-daily L-dopa dosing, administration of the long-acting D1 agonist A-77636 initially dramatically enhanced locomotion and reproduced dyskinesia with prominent dystonia, but after repeated administration of A-77636, dyskinesia and in particular chorea, gradually disappeared. Tolerance to locomotor stimulation greater than with A-86929 occurred, although activity remained significantly above baseline levels. There was a marked reduction in L-dopa-induced climbing, stereotypy and hyperkinesis and behaviour more closely resembled that of normal unlesioned marmosets. Upon reintroduction of L-dopa concurrently with continued A-77636 administration, dystonic, but virtually no choreic dyskinesias appeared and behaviour was once again free of stereotypy and hyperkinesis, contrasting dramatically with the presence of these behaviours along with abundant chorea when L-dopa is given alone. These results show a lesser liability of A-86929 and A-77636 to reproduce dyskinesia in L-dopa-primed MPTP-lesioned subjects while maintaining effective antiparkinsonian activity and producing a more naturalistic motor response. The differential effects of A-77636 on chorea and dystonia, with suppression of chorea and stereotypy on co-administration with L-dopa, may reflect an altered balance of activity in the direct and indirect striatofugal pathways. These results suggest a possible role for D1 agonists in the treatment of Parkinson's disease.
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PMID:Actions of the D1 agonists A-77636 and A-86929 on locomotion and dyskinesia in MPTP-treated L-dopa-primed common marmosets. 1010 82


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