PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1274963

Tardive dyskinesia.

K E Clyne·R Juhl
View original source ↗Export metadata ↓

Abstract

The etiology, pharmacology, treatment and possible prevention of tardive dyskinesia (TD) are discussed. This neurological disorder, characterized by involuntary movements of the lips, jaws and tongue, can occur as a result of short-term antipsychotic drug therapy, but usually occurs after long-term treatment. Phenothiazines, the thioxanthines, butyrophenones, dibenzoxazepines and dihydroindolines also posess the potential for inducing TD. Methods of treatment of TD with dopamine-depleting agents, dopamine-blocking agents and cholinomimetics are discussed. Despite the apparent effectiveness of some drugs in the treatment of TD, it should be kept in mind that most of the studies demonstrating drug effectiveness involved a small number of patients.

Explore related subjects

CholineDeanolDopamine AntagonistsHaloperidolHumansMethyldopaMovement DisordersPapaverineParasympathomimeticsReserpineTetrabenazineJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K E Clyne, R Juhl. 1976. Tardive dyskinesia.. https://pubmed.ncbi.nlm.nih.gov/1274963/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

1H NMR metabonomics of plasma lipoprotein subclasses: elucidation of metabolic clustering by self-organising maps.

(1)H NMR spectra of plasma are known to provide specific information on lipoprotein subclasses in the form of complex overlapping resonances. A combination of (1)H NMR and self-organising map (SOM) analysis was applied to investigate if automated characterisation of subclass-related metabolic interactions can be achieved. To reliably assess the intrinsic capability of (1)H NMR for resolving lipoprotein subclass profiles, sum spectra representing the pure lipoprotein subclass part of actual plasma were simulated with the aid of experimentally derived model signals for 11 distinct lipoprotein subclasses. Two biochemically characteristic categories of spectra, representing normolipidaemic and metabolic syndrome status, were generated with corresponding lipoprotein subclass profiles. A set of spectra representing a metabolic pathway between the two categories was also generated. The SOM analysis, based solely on the aliphatic resonances of these simulated spectra, clearly revealed the lipoprotein subclass profiles and their changes. Comparable SOM analysis in a group of 69 experimental (1)H NMR spectra of serum samples, which according to biochemical analyses represented a wide range of lipoprotein lipid concentrations, corroborated the findings based on the simulated data. Interestingly, the choline-N(CH(3))(3) region seems to provide more resolved clustering of lipoprotein subclasses in the SOM analyses than the methyl-CH(3) region commonly used for subclass quantification. The results illustrate the inherent suitability of (1)H NMR metabonomics for automated studies of lipoprotein subclass-related metabolism and demonstrate the power of SOM analysis in an extensive and representative case of (1)H NMR metabonomics.

Choline↗
PubMed2006

Metabolic imaging of atrophic muscle tissue using appropriate markers in 1H and 31P NMR spectroscopy.

INTRODUCTION: The purpose of this feasibility study was to demonstrate non-invasive metabolic imaging of human muscular atrophy using significant changes of NMR signals that are related directly or indirectly to fiber necrosis. METHODS: Single-voxel (1)H NMR spectroscopy and two-dimensional (31)P spectroscopic imaging on a 1.5-T whole-body scanner were used for in vivo mapping of areas of muscle damage in two cases of differently localized and pronounced atrophy. Spectral patterns affiliated with severe and intermediate stages of degeneration were compared to data of healthy control tissue to derive appropriate metabolic markers related to lipid infiltration or high-energy (31)P metabolism. RESULTS: Reliable detection of atrophic tissue was achieved by the following parameters: (1) liposclerotic turnover is related to a drastic reduction in the water/lipid (1)H signal intensity ratio (up to a factor of 74 compared to adjacent healthy tissue); (2) the (31)P resonance of phosphocreatine (PCr) is an adequate marker for differentiation of intact myocells with high-energy metabolism from regions dominated by terminal fiber necrosis (PCr signal vanished nearly completely or intensity was reduced by a factor of 3 in affected muscles). Metabolic images based on this signal allowed accurate non-invasive localization of atrophic tissue. CONCLUSION: The molecular information provided by NMR spectroscopy--previously only used with poor localization in atrophy studies--enables access to both the myocell-specific high-energy metabolism and the result of lipid infiltration allowing non-invasive mapping of degenerate tissue. The ability to investigate the results of these advanced levels of atrophy would also be useful for studies of more subtle degrees of denervation.

Choline↗