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Treatment of neurolept-induced tardive dyskinesia
被引:39
作者:
Jankelowitz, Stacey K.
[1
]
机构:
[1] Univ Sydney, Cent Clin Sch, Sydney, NSW 2006, Australia
来源:
NEUROPSYCHIATRIC DISEASE AND TREATMENT
|
2013年
/
9卷
关键词:
tardive dyskinesia;
treatment;
neuroleptic agents;
PLACEBO-CONTROLLED TRIAL;
DEEP BRAIN-STIMULATION;
SCHIZOPHRENIA SPECTRUM DISORDERS;
HYPERKINETIC MOVEMENT-DISORDERS;
GENETIC ASSOCIATION ANALYSIS;
VITAMIN-E TREATMENT;
OPEN-LABEL TRIAL;
1A2;
CYP1A2;
GENE;
DOUBLE-BLIND;
RECEPTOR GENE;
D O I:
10.2147/NDT.S30767
中图分类号:
R74 [神经病学与精神病学];
学科分类号:
摘要:
Tardive dyskinesia (TDK) includes orobuccolingual movements and "piano-playing" movements of the limbs. It is a movement disorder of delayed onset that can occur in the setting of neuroleptic treatment as well as in other diseases and following treatment with other drugs. The specific pathophysiology resulting in TDK is still not completely understood but possible mechanisms include postsynaptic dopamine receptor hypersensitivity, abnormalities of striatal gamma-aminobutyric acid (GABA) neurons, and degeneration of striatal cholinergic interneurons. More recently, the theory of synaptic plasticity has been proposed. Considering these proposed mechanisms of disease, therapeutic interventions have attempted to manipulate dopamine, GABA, acetylcholine, norepinephrine and serotonin pathways and receptors. The data for the effectiveness of each class of drugs and the side effects were considered in turn.
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页码:1371 / 1380
页数:10
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