@entity1090 and XXXX in the treatment of drug-resistant @entity161 and neuroleptic-induced supersensitivity @entity716 .

@entity1 @entity1088 @entity304 @entity935 @entity910 @entity161 @entity716 @entity1767 @entity1090
1. @entity716 ( @entity716 ) has emerged as a potential side effect of long-term neuroleptic therapy similar to @entity910 ( @entity910 ). 2. Six @entity161 @entity1 with @entity716 , considered to be drug-resistant, were treated with @entity1090 , while another 5 were treated with @entity1088 . 3. The 6 @entity1090 -treated @entity1 (all @entity1 ) were rated on the Clinical Global Impression Improvement Scale as at least very much improved. Among the 5 @entity1088 -treated @entity1 , all 4 @entity1 were found to have a marked response to @entity1088 , while the female @entity1 was judged to be minimally improved. 4. It is hypothesized that not only @entity910 but also @entity716 arise from destruction of cholinergic interneurons in the striatum as a consequence of prolonged neuroleptic administration. Thus, the drug-induced @entity304 , which was proposed as mediating the antipsychotic effect of @entity935 D2 blocking drugs, depends on the integrity of these cholinergic neurons. If these neurons are destroyed, drugs such as @entity1767 lose their therapeutic effect. 5. In contrast, atypical neuroleptics like @entity1088 and @entity1090 reduce @entity935 release in the striatum independently of prior production of extrapyramidal symptoms and, in this way, may be effective in @entity716 unresponsive to classical anti-D2 neuroleptics. 6. In the present sample of @entity1 , it is worth noting that @entity161 @entity1 were good responders to @entity1088 . In comparison, @entity1090 was found to be efficacious in @entity161 @entity1 .
