LYCOS RETRIEVER
Thioridazine
built 633 days ago
Thioridazine is a typical low-potency neuroleptic that is slighly less potent than chlorpromazine. It has a halflife of 7 to 13 hours. (Other sources have 16 to 24 hours.) It has the advantage of a low incidence of early and late extrapyramidal side-effects (tardive dyskinesia). In this regard it is very similar to the atypical neuroleptic clozapine (Clozaril®). Thioridazine has ... intrinsic mild to moderate antidepressive properties. It has antiemetic properties.
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Thioridazine is a low-potency antipsychotic. Older antipsychotic medications (chlorpromazine, haloperidol), which do not meet specific criteria for “atypical” antipsychotics, are often referred to as typical antipsychotics. They are associated with the troubling side effect, EPS. However, it is commonly believed that in order for a drug to treat psychosis, it must block dopamine is some manner.
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Thioridazine has the potential to produce a serious side effect called tardive dyskinesia. This syndrome consists of involuntary, uncoordinated movements that may not disappear or may only partially improve after the drug is stopped. Tardive dyskinesia involves involuntary movements of the tongue, jaw, mouth or face or other groups of skeletal muscles. The incidence of tardive dyskinesia increases with increasing age and with increasing dosage of thioridazine. It may ... appear after thioridazine use has been discontinued. Women are at greater risk than men for developing tardive dyskinesia.
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Thioridazine has a wide therapeutic margin. At low and medium doses it relieves tension and anxiety, and acts against multiple symptoms (e.g. agitation, depression, sleep disturbances) of non-psychotic mental disorders. At higher doses, thioridazine is effective in controlling the symptoms of psychotic disorders.
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Thioridazine-containing ethyl cellulose (EC) microcapsules were prepared in the presence of gold nanoparticles via the W/O/W emulsification solvent-evaporation method. The gold nanoparticles have been verified as human safe and the nondestructive physisorption of thioridazine on gold nanoparticles was corroborated with the time-of-flight second ion mass spectrometry measurements. The morphology of the formed microcapsules (ETA, containing EC, Thioridazine and Au) changed substantially because of the presence of gold nanoparticles. In addition to a prolonged controlled release, these ETA microcapsules had an enhanced thioridazine encapsulation with an efficiency over one and half times that of the microcapsules (ET) containing no nanogold particles. While data of the release kinetics for ET microcapsules fitted the apparent first-order model, corresponding data for ETA microcapsules agreed better with the Higuchi model indicating a uniform distribution of thioridazine in the monolithic-type microcapsules.
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Thioridazine therapy should be initiated only by a specialist and only after the patient has failed to respond adequately to treatment with appropriate courses of at least two other suitable medicines. The patient should first be assessed for risk factors for arrhythmia (see above), and undergo an ECG to determine the QTc-interval and a check of serum potassium. Abnormal potassium levels should be corrected. If the patient is on interacting medicines, therapy must be adjusted to avoid these medicines or an alternative to thioridazine prescribed instead. Do not use thioridazine in patients with predisposing factors for arrhythmia or pre-existing QT-prolongation (QTc ≥ 500ms).
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