Disease relevance of Dyskinesia, Drug-Induced

• Another commonly encountered form of drug-induced dyskinesia is seen in patients with Parkinson's disease who are receiving levodopa [1].
• In that sensitization to the effects of repeated levodopa in this setting may be analogous to medication-induced dyskinesias in humans, our findings furthermore suggest that drugs which block D(3) function may be helpful in the treatment of dyskinesias, without necessarily exacerbating Parkinsonism [2].
• One patient in addition developed a florid orofacial dyskinesia, which resolved completely, as did the akinetic mutism, after withdrawal of cyclosporin [3].
• Further studies are warranted to determine the role of CCK in nitrile toxicity and drug-induced dyskinesia [4].
• Isolated orofacial dyskinesia: a methylphenidate-induced movement disorder [5].

Psychiatry related information on Dyskinesia, Drug-Induced

• Within hours after metoclopramide was given, she had hand tremor, akathisia, and truncal and orofacial dyskinesia [6].
• Pronounced oral dyskinesia developed in an elderly woman with advanced dementia who had been treated with buspirone for 3 days [7].
• Test compounds 5b, 5n and 5j were evaluated for nootropic activity in mice by examining the effect on transfer latency on elevated plus maze (EPM) in mice and compound 5c was tested for anti-catatonic activity in perphenazine-induced catatonia and anti-dyskinetic effects in reserpine induced orofacial dyskinesia in rats, respectively [8].

High impact information on Dyskinesia, Drug-Induced

• Medication-induced dyskinesias were reduced by 64% and were not observed off medication during chronic GDNF delivery [9].
• All remained predominantly responsive to levodopa, although with marked disability secondary to clinical fluctuations (short-duration responses) and medication-induced dyskinesias; all were receiving substantial doses of levodopa and 6 of the 8 patients were additionally receiving bromocriptine or pergolide [10].
• Both drugs significantly reduced dyskinetic movements: clonazepam had a stronger effect on orofacial dyskinesia, and phenobarbital was more effective for limbs and axial movements [11].
• AMPT and baclofen had similar influences on oral dyskinesia, resulting in reduced frequency, unchanged or slightly reduced amplitude, and increased duration of each movement [12].
• Paroxysmal tremor and orofacial dyskinesia secondary to a biopterin synthesis defect [13].

Chemical compound and disease context of Dyskinesia, Drug-Induced

• Assessment of striatal extracellular dopamine and dopamine metabolites by microdialysis in haloperidol-treated rats exhibiting oral dyskinesia [14].
• Oral dyskinesia associated with buspirone use in an elderly woman [7].
• Piracetam for drug-induced dyskinesia [15].
• Vacuous chewing movements, an animal analog of orofacial dyskinesia, were also recorded at several time points during haloperidol administration and throughout the dialysis sampling session [16].
• OBJECTIVES: To evaluate the effect of chronic quercetin treatment on haloperidol-induced orofacial dyskinesia [17].

Biological context of Dyskinesia, Drug-Induced

• Analysis of covariance (ANCOVA), controlling for age at first antipsychotic treatment, revealed a significant effect of 5-HT2C genotype on orofacial dyskinesia (OFD) scores (F=3.47, df 2, P=.03) [18].
• We investigated the role of oxidative stress in the pathophysiology of haloperidol (HP)-induced orofacial dyskinesia and evaluated the beneficial effect of Withania somnifera (Ws) root extract in the amelioration of HP-induced vacuous chewing movements (VCMs) and tongue protrusions in the rat model for TD [19].

Anatomical context of Dyskinesia, Drug-Induced

• Haloperidol treatment for 34 weeks increased the optical density of preproenkephalin messenger RNA in individual striatal neurons and enkephalin peptide in the neuropil, regardless of the level of oral dyskinesia produced [20].
• Sulpiride and clozapine (10 nmol/0.5 microl), sigma inactive/dopamine active atypical antipsychotic drugs with a much reduced risk for producing motor side effects in humans, were unable to elicit orofacial dyskinesias when microinjected into the facial or spinal trigeminal nucleus, oralis [21].
• Bilateral administration of endomorphin-1 in the globus pallidus of rats induced orofacial dyskinesia [22].
• Motor disorders affecting the orofacial musculature include bruxism, chronic orofacial muscle pain affecting the jaw and neck muscles and the involuntary waking period disorders such as orofacial dyskinesia, oral mandibular dystonia, tremor and others [23].

Gene context of Dyskinesia, Drug-Induced

• Among patients withdrawn from neuroleptics, those with an oral dyskinesia had significantly lower peak GH concentration 2.46 +/- 0.93 ng/ml) after apomorphine compared with those without (14.85 +/- 3.83 ng/ml) (P less than 0.05) [24].
• Effect of apomorphine on growth hormone and prolactin secretion in schizophrenic patients, with or without oral dyskinesia, withdrawn from chronic neuroleptic therapy [24].
• Important role of striatal catalase in aging- and reserpine-induced oral dyskinesia [25].
• OBJECTIVE: The objective of the present study was to elucidate the role of N-methyl-D-aspartate (NMDA) receptor involvement in neuroleptic-induced orofacial dyskinesia in rats [26].
• The present results suggest that NK3 receptor-active peptides might be symptom inducers in oral dyskinesia [27].

Analytical, diagnostic and therapeutic context of Dyskinesia, Drug-Induced

• 1. The effects of buspirone were studied on an animal model of tardive dyskinesia, i.e., the quantification of orofacial dyskinesia in rats repeatedly treated with reserpine [28].

References