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1 f L-dopa and severe sensitivity reactions to neuroleptic drugs.
2 20%-40% of patients treated chronically with neuroleptic drugs.
3 r = 3 weeks) or stopped treatment with depot neuroleptic drugs.
4 and both gender and longterm responsivity to neuroleptic drugs.
5 and D4) is a target for typical and atypical neuroleptic drugs.
6 ain regions that are functionally altered by neuroleptic drugs.
7 zophrenia who do not respond to conventional neuroleptic drugs.
8 ute to their clinical advantage over typical neuroleptic drugs.
10 exacerbation of extrapyramidal effects with neuroleptic drugs and betel nut (Areca catechu); increas
11 chizophrenia who were and were not receiving neuroleptic drugs and normal control subjects were obtai
12 TS, but there is increasing interest in non-neuroleptic drugs, behavioural therapies, and surgical a
13 umans or experimental animals with classical neuroleptic drugs can lead to abnormal, tardive movement
14 val and exposure to either benzodiazepine or neuroleptic drugs do not account for the lack of marked
15 e stimuli and an alteration, correlated with neuroleptic drug dosage, in the functional coupling betw
18 rug, risperidone, and an older, conventional neuroleptic drug, haloperidol, in terms of the rate of r
19 y hepatic effects of chlorpromazine (CPZ), a neuroleptic drug known for years to induce intrahepatic
20 se changes are consistent with the idea that neuroleptic drugs lead to "compensation" and "adaptation
22 he comparison of the effects of 2 classes of neuroleptic drugs on regional brain functional activitie
23 awal are inadequate to escape the effects of neuroleptic drugs on regional cerebral glucose metabolis
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