Kondo Masaki, Ikejiri Yoshitaka, Hanatani Takashi, Sumi Noriaki
Department of Psychiatry and Mental Health, Sumitomo Hospital.
Seishin Shinkeigaku Zasshi. 2010;112(1):23-30.
We report a schizophrenic patient with paroxysmal perceptual alteration (PPA) which disappeared completely on switching from the previous antipsychotic to aripiprazole (APZ). PPA is an attack characterized by hypersensitivity of perception mainly involving in the modality of visual sensation. The prevalence of PPA is about 4% in schizophrenia. It is regarded as a psychopharmacological symptom associated with antipsychotics, and a hypothesis regarding the cause has been proposed: PPA is caused by noradrenergic activation which compensates for the sudden incompetence of dopaminergic neural transmission in the context of chronic hypofunction of the dopamine system caused by antipsychotics. Since APZ maintains the dopaminergic nervous system in a steady state by its partial agonism of the D2 receptor, it is suggested that APZ could correct the chronic dysfunction of the dopamine system associated with PPA, explaining its resolution in this patient. Because APZ is positioned as a drug which relatively preserves tonic neurotransmission from the perspective of the tonic/phasic model of dopaminergic neurotransmission, an alternative hypothesis whereby a decrease in the tonic component might cause PPA can be proposed. Additionally, this patient experienced 'general restlessness' like akathisia shortly after we added a low dose of APZ to his formula, and we think that the symptom demands closer consideration on switching to APZ. Especially in chronic schizophrenic patients, PPA can be the main cause of a reduced quality of life, and treatment is essential. Switching to APZ should be a significant treatment option for PPA.
我们报告了一名患有阵发性感知改变(PPA)的精神分裂症患者,在从先前的抗精神病药物换用阿立哌唑(APZ)后,PPA完全消失。PPA是一种以感知超敏为特征的发作,主要涉及视觉感觉模态。PPA在精神分裂症中的患病率约为4%。它被认为是一种与抗精神病药物相关的精神药理学症状,并且已经提出了一个关于病因的假说:PPA是由去甲肾上腺素能激活引起的,这种激活在抗精神病药物导致多巴胺系统慢性功能减退的情况下,补偿了多巴胺能神经传递的突然无能。由于阿立哌唑通过其对D2受体的部分激动作用使多巴胺能神经系统维持在稳定状态,因此提示阿立哌唑可以纠正与PPA相关的多巴胺系统慢性功能障碍,这解释了该患者症状的缓解。因为从多巴胺能神经传递的紧张性/相位性模型的角度来看,阿立哌唑被定位为一种相对保留紧张性神经传递的药物,所以可以提出另一种假说,即紧张性成分的减少可能导致PPA。此外,在我们给他的用药方案中添加低剂量阿立哌唑后不久,该患者出现了类似静坐不能的“全身不安”,我们认为在换用阿立哌唑时,这种症状需要更仔细的考虑。特别是在慢性精神分裂症患者中,PPA可能是生活质量下降的主要原因,治疗至关重要。换用阿立哌唑应该是治疗PPA的一个重要选择。