Disease relevance of Dyskinesias

• CONCLUSIONS: In late-stage Parkinson's disease, pallidotomy significantly reduces levodopa-induced dyskinesias and off-period disability [1].
• Parkinsonism and tardive dyskinesia associated with long-term metoclopramide therapy [2].
• Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by progressive involuntary movements and dementia [3].
• When treatment began after the appearance of abnormal movements, cystamine extended survival, reduced associated tremor and abnormal movements and ameliorated weight loss [4].
• Abnormal involuntary movements were decreased on addition of lergotrile and reduction in levodopa while mental changes and orthostatic hypotension were increased [5].

Psychiatry related information on Dyskinesias

• Huntington's disease (HD) is a late-onset autosomal dominant neuropsychiatric disorder presenting in mid-adult life with personality disturbance and involuntary movements, cognitive and affective disturbance, and inexorable progression to death [6].
• These mice display abnormal movements and postures, indicating that NT3/TrkC-dependent sensor; neurons may play a primary role in proprioception, the sense of position and movement of the limbs [7].
• Tardive dyskinesia following haloperidol treatment in Tourette's syndrome [8].
• Paroxysmal dystonic choreoathetosis (PDC) is characterized by attacks of involuntary movements that last up to several hours and occur at rest both spontaneously and following caffeine or alcohol consumption [9].
• Propranolol-induced tardive dyskinesia in a patient with akathisia [10].

High impact information on Dyskinesias

• After improvement in the first year, dystonia and dyskinesias recurred in 15 percent of the patients who received transplants, even after reduction or discontinuation of the dose of levodopa [11].
• CONCLUSIONS: Early Parkinson's disease can be managed successfully for up to five years with a reduced risk of dyskinesia by initiating treatment with ropinirole alone and supplementing it with levodopa if necessary [12].
• A five-year study of the incidence of dyskinesia in patients with early Parkinson's disease who were treated with ropinirole or levodopa. 056 Study Group [12].
• More on metoclopramide and tardive dyskinesia [13].
• Prolactin levels in tardive dyskinesia [14].

Chemical compound and disease context of Dyskinesias

• Facilitation of levodopa-induced dyskinesias by dietary carbohydrates [15].
• In the past nine years, we have treated 11 patients who had an acute onset of hemiballismus believed to be the result of an acute vascular lesion with neuroleptic drugs (most frequently haloperidol) [16].
• Aggravation of tardive dyskinesia by phenytoin [17].
• Choline for tardive dyskinesia [18].
• Spinal-fluid homovanillic acid levels were increased in three patients, suggesting that altered dopaminergic feedback mechanisms may be involved in the pathophysiology of hemiballismus [16].
• SCH23390 also inhibited the development of dyskinesia and the induction of FosB/DeltaFosB [19].

Biological context of Dyskinesias

• These results support the view that pharmacologic attempts to stimulate GABA-mediated synaptic transmission may afford symptomatic relief to patients with tardive dyskinesia [20].
• Clinical pharmacology of levodopa-induced dyskinesia [21].
• Comparing the schizophrenia patients with and without TD, genotypes containing the gly allele (DRD3ser-gly and DRD3gly-gly genotypes combined) were significantly associated with dyskinesia (OR = 2.62, 95% CI 1.18-5.59, P = 0.02) [22].
• Further analysis using the ANCOVA statistic with a continuous measure of the TD phenotype (Abnormal Involuntary Movement Scale (AIMS) score) found that the AIMS scores were not significantly influenced by HTR2A polymorphisms, despite controlling for potential confounders such as age, gender and ethnicity (P > 0.05) [23].
• Tardive dyskinesia and substrates of energy metabolism in CSF [24].

Anatomical context of Dyskinesias

• In man consumption of choline increases in levels in the serum and cerebrospinal fluid; its administration is an effective way of treating tardive dyskinesia [25].
• Given the improvement in dystonic and hemiballistic movements in these patients after ablation of the sensorimotor portion of the internal segment of the globus pallidus, we suggest that pallidotomy can be an effective treatment for patients with dystonia and also for patients with medically intractable hemiballismus [26].
• Precision grip force of grasping movements and levodopa-induced dyskinesias was analyzed in 10 parkinsonian patients before and after 3 months of deep-brain stimulation of the subthalamic nucleus [27].
• Microelectrode recording was performed in the basal ganglia of 3 patients with generalized dystonia and 1 patient with hemiballismus secondary to a brainstem hemorrhage [26].
• No difference in mean putamen or caudate D1 or D2 receptor binding between the two patient subgroups was found, suggesting that dyskinesias are unlikely to arise from a primary disturbance of dopamine receptor availability [28].

Gene context of Dyskinesias

• Mice deficient for neurotrophin-3 (NT-3) and its receptor, encoded by the trkC gene, show abnormal movements caused by the loss of sensory proprioceptive neurons [29].
• We analyzed nine known polymorphisms of the DRD2 in 665 schizophrenic patients with European Caucasian ethnic background and compared the intensity of acute dystonia, extrapyramidal symptoms, akathisia, and tardive dyskinesia between carriers of different DRD2 genotypes [30].
• These data demonstrate that the lack of syntaxin 4 expression results in abnormal movement of GLUT8 in response to insulin, decreased insulin-stimulated glucose uptake, and increased apoptosis [31].
• Sixteen white schizophrenic patients who had developed tardive dyskinesia during long-term neuroleptic treatment were phenotyped with debrisoquine and genotyped by CYP2D6-specific DNA amplification and EcoRI restriction fragment length polymorphism analysis [32].
• BACKGROUND: Paroxysmal nonkinesigenic dyskinesia (PNKD) is a rare disorder characterized by attacks of involuntary movements brought on by stress, alcohol, or caffeine, but not by movement [33].

Analytical, diagnostic and therapeutic context of Dyskinesias

• The MPTP monkey is a well-characterized animal model of parkinsonism and provides an exceptional tool for the study of dyskinesias induced by dopamine-like agents [34].
• Each of these parameters (mental state, asterixis, TMT, EEG, and NH3) was improved significantly by neomycin-sorbitol and lactulose [35].
• Single clinical trials with each of the four modern agonists compared with levodopa show that as monotherapy the agonists delay the onset of involuntary movements, although at the expense of poorer treatment of motor impairments and disability and more dopaminergic adverse events [36].
• Melatonin treatment for tardive dyskinesia: a double-blind, placebo-controlled, crossover study [37].
• Levodopa-induced dyskinesias (LIDs) in patients with Parkinson's disease are considered to result from the severity of dopaminergic denervation in the striatum, which is an irrevocable phenomenon, and sensitization induced by long-term intermittent administration of levodopa [38].

References