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MeSH Review

Hyperkinesis

 
 
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Disease relevance of Hyperkinesis

 

Psychiatry related information on Hyperkinesis

 

High impact information on Hyperkinesis

 

Chemical compound and disease context of Hyperkinesis

  • OBJECTIVE: Tetrabenazine, a monoamine depleter and dopamine receptor blocker, is used to treat several hyperkinetic movement disorders [16].
  • RESULTS: At day 5, patients with serum valproate levels > or = 45 micrograms/ml were two to seven times as likely as patients with levels < 45 micrograms/ml to show 20% or greater improvement in scores on the manic syndrome subscale, the behavior and ideation subscale, elevated mood, increased activity, motor hyperactivity, and psychosis [17].
  • No consistent beneficial effects on the hyperkinetic movements, abnormal motor function, or ability to carry out normal activities were evident with gamma-vinyl GABA treatment [18].
  • The hyperkinesis is ameliorated by low doses of the psychostimulant D-amphetamine and can be rescued genetically by a transgene encoding SNAP-25, located within the Cm deletion [19].
  • Decreased glucose utilization of the striatum can underlie hyperkinetic movement disorders of various etiologies [20].
 

Biological context of Hyperkinesis

 

Anatomical context of Hyperkinesis

  • CONCLUSIONS: Heterogeneity of left ventricular wall thickening can be induced or magnified by dobutamine infusion even in subjects without coronary artery disease, with the inferior wall showing a lack of hyperkinesis, up to relative hypokinesis, in comparison with other myocardial regions [23].
  • The hypothesis is presented that phenytoin induces hyperkinesia by increasing dopaminergic and serotonergic activity in the basal ganglia, and that patients with preexisting basal ganglia damage are the most susceptible [24].
  • These results suggest that implantation of a GABA-releasing source may be an effective alternative to intrathalamic fetal-tissue grafts or lesions as an experimental approach to the treatment of hyperkinetic movement disorders [25].
  • This latter locomotor stimulant effect was suppressed by the dopamine antagonist, haloperidol (50 micrograms/kg, i.p.). Thus, the hypokinetic effect of 30 ng [D-Trp11]neurotensin is independent of dopamine transmission, whereas the hyperkinesia elicited by 750 ng proceeds via an increase in dopamine transmission in the nucleus accumbens [26].
  • Although a single solid graft of embryonic DA neurons can prevent progression of some lesioned-induced behavioral abnormalities such as LD-induced rotation and dystonia, it significantly increases hyperkinetic movements of the contralateral forelimb [27].
 

Gene context of Hyperkinesis

 

Analytical, diagnostic and therapeutic context of Hyperkinesis

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