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MeSH Review

Hypokinesia

 
 
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Disease relevance of Hypokinesia

 

Psychiatry related information on Hypokinesia

 

High impact information on Hypokinesia

  • Among 20 patients completing a six-month trial, there was a significant (P less than .01) reduction in rigidity, tremor, bradykinesia, gait disturbance, and total score when lergotrile was added to levodopa plus carbidopa [11].
  • Nigrostriatal dopaminergic deficits and hypokinesia caused by inactivation of the familial Parkinsonism-linked gene DJ-1 [12].
  • Animals derived from crosses of Ink4d- null with Kip1-null mice exhibited bradykinesia, proprioceptive abnormalities, and seizures, and died at about 18 days after birth [13].
  • Abnormal movements such as rigidity and hypokinesia (hypokinetic-rigid syndrome) are an important hallmark and may orientate to PC deficiency when associated with severe lactic acidosis [14].
  • Abnormal movements (high-amplitude tremor and hypokinesia) and bizarre ocular behavior were the most common findings, whereas epilepsy was infrequent [14].
 

Chemical compound and disease context of Hypokinesia

 

Biological context of Hypokinesia

  • Clinical trials have shown longterm graft survival and therapeutically valuable improvements with decreased L-dopa dose and time spent in the "off"-phase, and reduced rigidity and hypokinesia [20].
  • Increased methylation reactions may play a role in the etiology of PD, because it has been observed recently that the CNS administration of S-adenosyl-L-methionine (SAM), the methyl donor, caused tremors, hypokinesia, and rigidity; symptoms that resemble those that occur in PD [21].
  • The results affirm the site-specific response of TGF-beta2 gene expression in rats, and suggest that the cortical and trabecular bone osteopenia associated with hypokinesia in rats may be associated with a deficit in osteoblastic and osteocytic TGF-beta2 level [22].
  • A hypothesis was tested whether the increased T4 and T3 levels result from a decreased fecal excretion of these compounds due to presumably increased food intake during the first day of hypokinesia, but it was found that the intake of food and water on the first day was the same as on subsequent days [23].
  • These results suggest, that the liver and adipocyte insulin receptors of flight rats did not respond to the increased plasma insulin levels by "down regulation". The determination of plasma corticosterone levels showed that in flight rats and animals exposed to antiorthostatic hypokinesia the plasma hormone levels are significantly elevated [24].
 

Anatomical context of Hypokinesia

 

Gene context of Hypokinesia

  • Knock-out IRP1 and IRP2 mice have shown that in latter mice brain iron accumulation precedes the neurodegeneration, ataxia and bradykinesia observed in these animals [30].
  • After a two-week hypokinesia G6P-DH, A1, LDH activities and ATP, ADP, AMP concentrations decreased, whereas other estimated parameters did not differ from the control levels [31].
  • These results are consistent with inappropriate overactivity of striatofrontal projections and impaired activity of motor executive areas in idiopathic torsion dystonia and may explain the simultaneous dystonic posturing and bradykinesia evident in these patients [32].
  • Adjustment of stimulation parameters in GPi DBS may have the potential to optimize the motor response in HD, improving chorea without aggravating bradykinesia [33].
  • Absence of the murine dopamine D2 receptor gene (drd2) produces bradykinesia and hypothermia [34].
 

Analytical, diagnostic and therapeutic context of Hypokinesia

References

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  13. Postnatal neuronal proliferation in mice lacking Ink4d and Kip1 inhibitors of cyclin-dependent kinases. Zindy, F., Cunningham, J.J., Sherr, C.J., Jogal, S., Smeyne, R.J., Roussel, M.F. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
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  19. Lidocaine and muscimol microinjections in subthalamic nucleus reverse Parkinsonian symptoms. Levy, R., Lang, A.E., Dostrovsky, J.O., Pahapill, P., Romas, J., Saint-Cyr, J., Hutchison, W.D., Lozano, A.M. Brain (2001) [Pubmed]
  20. Health-related quality of life following bilateral intrastriatal transplantation in Parkinson's disease. Hagell, P., Crabb, L., Pogarell, O., Schrag, A., Widner, H., Brooks, D.J., Oertel, W.H., Quinn, N.P., Lindvall, O. Mov. Disord. (2000) [Pubmed]
  21. Substantia nigra degeneration and tyrosine hydroxylase depletion caused by excess S-adenosylmethionine in the rat brain. Support for an excess methylation hypothesis for parkinsonism. Charlton, C.G., Mack, J. Mol. Neurobiol. (1994) [Pubmed]
  22. Transforming growth factor-beta2 mRNA level in unloaded bone analyzed by quantitative in situ hybridization. Zhang, R., Supowit, S.C., Hou, X., Simmons, D.J. Calcif. Tissue Int. (1999) [Pubmed]
  23. Changes of iodothyronine levels in plasma after acute and long term hypokinesia (unforced restriction) in rats. Langer, P., Földes, O., Macho, L., Kvetnanský, R. Endocrinol. Exp. (1981) [Pubmed]
  24. The effect of space flight on the board of the satellite Cosmos 2044 on plasma hormone levels and liver enzyme activities of rats. Macho, L., Fickova, M., Nemeth, S., Svabova, E., Serova, L., Popova, I. Acta astronautica. (1991) [Pubmed]
  25. Progression of hypertrophic cardiomyopathy into a hypokinetic left ventricle: higher incidence in patients with midventricular obstruction. Fighali, S., Krajcer, Z., Edelman, S., Leachman, R.D. J. Am. Coll. Cardiol. (1987) [Pubmed]
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  28. Microstimulation-induced inhibition of neuronal firing in human globus pallidus. Dostrovsky, J.O., Levy, R., Wu, J.P., Hutchison, W.D., Tasker, R.R., Lozano, A.M. J. Neurophysiol. (2000) [Pubmed]
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  32. Overactive prefrontal and underactive motor cortical areas in idiopathic dystonia. Ceballos-Baumann, A.O., Passingham, R.E., Warner, T., Playford, E.D., Marsden, C.D., Brooks, D.J. Ann. Neurol. (1995) [Pubmed]
  33. Bilateral globus pallidus stimulation for Huntington's disease. Moro, E., Lang, A.E., Strafella, A.P., Poon, Y.Y., Arango, P.M., Dagher, A., Hutchison, W.D., Lozano, A.M. Ann. Neurol. (2004) [Pubmed]
  34. A Ser311Cys mutation in the human dopamine receptor D2 gene is associated with reduced energy expenditure. Tataranni, P.A., Baier, L., Jenkinson, C., Harper, I., Del Parigi, A., Bogardus, C. Diabetes (2001) [Pubmed]
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