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Tardive dyskinesia definition

The critical question concerns the neurotoxic potential of HP in the human. Since the development of drug induced tardive dyskinesias often requires months or even years of drug exposure (Gerlach and Casey 1988 Casey 1991), the demonstration of toxin-induced lesions in experimental animals may be difficult. Furthermore, in view of the dramatic species selectivity of MPTP (Singer et al. 1987 Giovanni et al. 1994a, 19946), the absence of a detectable anatomical lesion in HP- or HPTP-treated rodents may not provide a definitive answer to the question... [Pg.96]

The drug exerts its distinet eentral actions to suppress tremor as well as rigidity that are gainfully employed therapeutically in Parkinsonism. It is also employed for the treatment of extrapyramidal dyskinesia but certainly not tardive dyskinesia which is caused due to the administration of various potent tranquillizers, namely reserpine, chlorpromazine (CPZ) ete. It may be worthwhile to mention here that the drug fails to cause any sort of central stimulation Q.e., a definite plus point), and instead produces the characteristic sedative effect normally seen amongst the antihistaminics. [Pg.560]


See other pages where Tardive dyskinesia definition is mentioned: [Pg.116]    [Pg.218]    [Pg.100]    [Pg.189]    [Pg.209]    [Pg.379]    [Pg.2439]    [Pg.2455]    [Pg.580]    [Pg.1213]   
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Tardive dyskinesias

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