Disease relevance of Hypokinesia

• In adulthood, Ireb2(-/-) mice develop a movement disorder characterized by ataxia, bradykinesia and tremor [1].
• The recipients of GDNF displayed significant improvements in three of the cardinal symptoms of parkinsonism: bradykinesia, rigidity and postural instability [2].
• Parkinson disease (PD) is a common neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity, and postural instability, as well as by a clinically significant response to treatment with levodopa [3].
• The clinical features included asymmetric resting tremor, bradykinesia, and rigidity with a good response to levodopa and could not be distinguished from idiopathic Parkinson's disease [4].
• Affected members were examined both in Greece and in the United States. The clinical presentation consisted of asymmetric rigidity, resting tremor, bradykinesia, and postural instability, and symptoms were responsive to levodopa [5].

Psychiatry related information on Hypokinesia

• METHODS: The Unified Huntington's Disease Rating Scale (UHDRS) was administered to 127 subjects during their initial visit to the Huntington's Disease Center at the New York State Psychiatric Institute, where dystonia, chorea, bradykinesia, rigidity, and eye movements were rated [6].
• All 20 reported daytime somnolence (drowsiness, lethargy, or sleepiness), and one quazepam-treated patient also had hypokinesia [7].
• Dose-related EPS of dystonia and bradykinesia occurred in relation to decreased locomotor activity and reactivity to stimuli with haloperidol i.m. and p.o., which are features characteristically seen with traditional neuroleptics [8].
• Persistent sensitization of clonidine-induced hypokinesia following one exposure to a stressor: possible relevance to panic disorder and its treatment [9].
• Deficits in reaction times and movement times as correlates of hypokinesia in monkeys with MPTP-induced striatal dopamine depletion [10].

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

• A marked nigrostriatal dopamine deficiency, observed in 4 of the 5 patients, was sufficient to explain the parkinsonian features (especially bradykinesia) observed in patients with progressive supranuclear palsy [15].
• The syndrome is characterized by profound bradykinesia (slow movement), the full extent of which is reached 3 days after MPTP administration [16].
• We report 2 survivors of severe methanol poisoning who developed, apart from blindness, a Parkinson-like extrapyramidal syndrome characterized by reduced initiative, poor voice volume, masked facies, mild tremor, rigidity, and bradykinesia [17].
• Significant correlations were found between ratings of bradykinesia and the amount of abnormal reflex modulation in the wrist flexor [18].
• Microinjections of 10-23 microl of lidocaine produced striking improvements in bradykinesia, limb tremor and rigidity in three out of three patients [19].

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

• Findings from this study reveal that segmental or generalized left ventricular hypokinesia can develop in patients with hypertrophic cardiomyopathy in the absence of fixed coronary artery disease [25].
• Extensive dopamine (DA) depletion was observed in the caudate nucleus and putamen on the side ipsilateral to the injection and this was associated with contralateral tremor, rigidity, and bradykinesia [26].
• Their disease was characterized by autosomal dominant inheritance, bulging eyes, rigidity and spasticity of the lower extremities, dystonia, and bradykinesia [27].
• Neurosurgical treatment of Parkinson's disease (PD) frequently employs chronic high-frequency deep brain stimulation (DBS) within the internal segment of globus pallidus (GPi) and can very effectively reduce L-dopa-induced dyskinesias and bradykinesia, but the mechanisms are unknown [28].
• Tyrosine hydroxylase deficiency was diagnosed after determination of cerebrospinal fluid neurotransmitters and DNA analysis in a child with severe axial hypotonia and hypokinesia associated with dystonic and ballistic movements [29].

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

• Dobutamine stress echocardiography showed hypokinesia in five of these seven patients despite nonsignificant lesions at coronary angiography [35].
• Neurological examinations revealed modest hypokinesia for a maximum of 10 days after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the two more severely affected animals [36].
• SQ 29,548 improves reperfusion function and, thus by inference, thromboxane A2 may play a role in postischemic hypokinesia and some of its protective effects may occur during reperfusion [37].
• We describe here two patients who developed parkinsonism, with rest tremor and bradykinesia, after receiving cyclosporin A following allogeneic bone marrow transplantation [38].
• Lithium attenuates hypokinesia induced by immobilization stress in rats [39].

References