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Treatment-resistant schizophrenia characterised by dopamine supersensitivity psychosis and efficacy of asenapine

机译:治疗抗性精神分裂症其特征是多巴胺超敏感性精神病和aseanapine的疗效

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摘要

Dopamine supersensitivity psychosis (DSP) frequently arises with long-term antipsychotic treatment and accounts for a significant proportion of treatment-resistant schizophrenia. The mechanism underlying DSP is thought to be a compensatory increase in dopamine receptor density in the striatum caused by long-term antipsychotic treatment. Previous animal studies have reported that antipsychotics increase serotonin 5-HT2A receptor density in the striatum and that 5-HT2A receptor blockers suppress dopamine-sensitive psychomotor activity, which may be linked to the pathophysiology of DSP. In this paper, we describe a patient who was hospitalised with treatment-resistant schizophrenia. Following treatment with high-dose antipsychotic polypharmacy for 10 weeks, the patient experienced worsening of psychotic and extrapyramidal symptoms. The patient was then started on second-generation antipsychotic asenapine while other antipsychotics were tapered off, resulting in improvement of these symptoms. Retrospectively, we presumed that the high-dose antipsychotic polypharmacy caused DSP, which was effectively treated by the potent 5-HT2A receptor antagonism of asenapine.
机译:多巴胺超敏感性精神病(DSP)经常出现长期抗精神病治疗和占治疗抗性精神分裂症的显着比例。 DSP的机制被认为是长期抗精神病治疗引起的纹状体中多巴胺受体密度的补偿性增加。以前的动物研究报道,抗精神病药增加纹状体中的血清素5-HT2A受体密度,并且5-HT2A受体阻滞剂抑制多巴胺敏感性活性活性,这可能与DSP的病理生理学相关联。在本文中,我们描述了与治疗抗性精神分裂症住院的患者。在用高剂量抗精神来的复疗治疗10周后,患者患有精神病和外氮瘤症状的恶化。然后在第二代抗精神病药物上开始患者,而其他抗精神病药逐渐减少,导致这些症状的改善。回顾性地,我们假设高剂量抗精神来的多酚疾病导致DSP,其有效地由aseanapine的强效5-HT2A受体拮抗作用治疗。

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