Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to investigate the degree of accuracy with which three groups of listeners could use perceptual analysis alone for identification of specific dysarthria types. The dysarthria types to be identified in this study were identical to those described by Darley, Aronson, and Brown (1969a): Flaccid, Spastic, Ataxic, Hypokinetic, Hyperkinetic Chorea, Hyperkinetic Dystonia, and Mixed. Each group demonstrated minimal success in the accurate identification of specific dysarthria types. Factors that possibly contributed to this poor success and potential implications are discussed.
 ...
PMID:Identification of dysarthria types based on perceptual analysis. 365 12

Clinico-neurophysiological study of the functional state of the nervous system was performed for persons who participated in elimination of the Chernobyl accident consequences in 1986, as well as for persons working in the 30 km zone. Mean age of the persons was 41. Vegetative dystonia syndrome was diagnosticated in 50% of examined subjects. The increased perception and pain thresholds, as well as the thresholds' asymmetry were determined in 30% of patients. The conduction velocity of sensory and motor nerves, as well as the neuromuscular transmission were normal. No substantial changes in parameters of the soleus H- and M-responses were detected. A decreased amplitude and increased latency of the evoked skin sympathetic potential were found indicating a decreased tone of the adrenergic sympathetic vasoconstrictors and cholinergic sudomotor fibres, that may be one of the pathogenic mechanisms of the sensory, vegetotrophovascular disorders for these subjects. Decreased activity of the sympathetic autonomic system causes permanent course of the vegetative dystonia syndrome and more seldom the parasympathetic autonomic paroxysms. A decreased tone of the sympathetic autonomic system may be due to the monoaminergic neuromediation inhibition (decreased noradrenaline and dopamine excretion for the same subjects), that can induce psychoemotional disorders, depression and sleep-wakeness cycle disorders.
 ...
PMID:[Some indicators of nervous system function in people exposed to harmful conditions of the Chernobyl accident]. 804 11

Inhibitory control of basal ganglia output to thalamocortical projection plays an important role in normal cortical activity in the current model of the basal ganglia motor circuit. Hypokinetic and hyperkinetic movement disorders of basal ganglia origin can be explained by excess or collapse of the basal ganglia output. An abundance of evidence indicates that parkinsonian akinesia results from hyperactivity of the basal ganglia output. Reversal of akinesia by lesions of the internal division of the globus pallidus (GPi) or its excitatory source, the subthalamic nucleus, agrees with this pathological schema. Ballism associated with subthalamic lesions, and dopa-induced dyskinesia are regarded as hyperkinetic disorders resulting from suppressed subthalamopallidal projection. Decreased firing rate in GPi was reported in both disorders. However, pallidotomy has recently been postulated to abolish both ballism and dopa-induced dyskinesia. A possible mechanism for the effect of GPi destruction in these hyperkinetic disorders may be blockade of the generation or conduction of phasic neuronal activities driving choreic movements. Symptomatologically, dystonia has aspects of both hypokinetic and hyperkinetic disorders. Overactivity of the premotor cortices, which receive projections from the basal ganglia via the ventral thalamus, was found both at rest and on movement in idiopathic dystonia. This abnormal cortical activity may arise from underactivity of basal ganglia output; however, the amelioration of dystonia with pallidotomy suggests a complex pathomechanism of the pallidothalamic system in dystonia.
 ...
PMID:[Pathophysiology of involuntary movements in adults]. 914 23

Three patients with sporadic amyotrophic lateral sclerosis (ALS) presented with a history of backward falls. Impaired postural reflexes and retropulsion accompanied clinical features of ALS. Hypokinesia, decreased arm swing, and a positive glabellar tap were noted in two of these three patients. Cognitive impairment, tremor, axial rigidity, sphincter dysfunction, nuchal dystonia, dysautonomia, and oculomotor dysfunction were absent. Brain MRI disclosed bilateral T2 weighted hyperintensities in the internal capsule and globus pallidus in one patient. Necropsy studies performed late in the course of ALS have shown degeneration in extrapyramidal sites-for example, the globus pallidus, thalamus, and substantia nigra. Clinically, backward falls and retropulsion may occur early in ALS. This may reflect extrapyramidal involvement.
 ...
PMID:Extrapyramidal involvement in amyotrophic lateral sclerosis: backward falls and retropulsion. 1040 93

We describe acute movement disorders in 92 children, aged 5 days to 15 years, from an Indian tertiary hospital. Eighty-nine children had hyperkinetic movement disorders, with myoclonus in 25, dystonia in 21, choreoathetosis in 19, tremors in 15, and tics in 2. Tetany and tetanus were seen in 5 and 2 children, respectively. Hypokinetic movement disorders included acute parkinsonism in 3 children. Noninflammatory and inflammatory etiology were present in 60 and 32 children, respectively. Benign neonatal sleep myoclonus in 16 and opsoclonus myoclonus syndrome in 7 accounted for the majority of myoclonus cases. Vitamin B12 deficiency in 13 infants was the most common cause of tremors. Rheumatic fever and encephalitis were the most common causes of acute choreoathetosis. Acute dystonia had metabolic etiology in 6 and encephalitis and drugs in 3 each. Psychogenic movement disorders were seen in 4 cases only, although these patients may be underreported.
...
PMID:Acute movement disorders in children: experience from a developing country. 2529 19

Disturbances in motor movement can have similar clinical presentations, albeit having different pathways and temporal onset. Hypokinetic movements present with rigidity, resting tremors, postural instability and bradykinesia, as seen in parkinsonism, while hyperkinetic movements typically present with chorea, ballismus, tic, athetosis and dystonia. Nonetheless, movement disorders are thought to be a continuum. Long-term therapy of parkinsonism with L-DOPA or dopamine (DA) agonists leads to late-onset dyskinesia - a hyperkinetic movement disorder, while patients with late-stage Huntington disease (HD) often develop non-DOPA responsive parkinsonism. In this paper, it is proposed that late-onset parkinsonism is driven by the overactivity of the nigrostriatal dopaminergic pathway. The excessive synthesis, storage, release, reuptake and degradation of dopamine in the presynaptic terminal and synaptic clefts lead to cellular stress and damage, resulting to progressive neuroapoptosis aggravated by pro-parkinsonism drugs used to treat hyperkinesia. Glutamate excitotoxicity may provide initial stress to neurons during early HD - but as the disease advances, lower glutamate levels are observed, making it less likely to cause the hypokinetic shift on its own. Over time, dopaminergic neurons are depleted and cholinergic influence to striatal GABA release is unopposed, leading to late-onset parkinsonism that is unresponsive to DOPA challenge, due to drastic DA neuron loss previously masked by the dominating choreic presentation. This paper thus provides a mechanism of action to a common clinical sequela and complication of long-term choreic diseases, whose pathophysiologic mechanism is presently lacking.
 ...
PMID:Cytosolic non-vesicular dopamine accumulation as the predominant mechanism for developing non-DOPA responsive parkinsonism in late-stage Huntington disease. 3146 19