The effects of ketamine and risperidone on eye movement control in healthy volunteers.
The effects of ketamine and risperidone on eye movement control in healthy volunteers.
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DOI：
10.1038/tp.2013.109
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发表时间：
2013-12-10
影响因子：
6.8
通讯作者：
Ettinger U
中科院分区：
文献类型：
--
作者：
Schmechtig A;Lees J;Perkins A;Altavilla A;Craig KJ;Dawson GR;William Deakin JF;Dourish CT;Evans LH;Koychev I;Weaver K;Smallman R;Walters J;Wilkinson LS;Morris R;Williams SC;Ettinger U
非竞争性N-甲基-D-天冬氨酸受体拮抗剂氯胺酮可导致健康志愿者出现短暂性精神病样症状和眼部功能受损。本研究探讨了氯胺酮对眼科表现的不良影响是否可以被非典型抗精神病药利培酮逆转。在这项随机、双盲、安慰剂对照研究中，72名健康受试者进行了平滑追踪眼球运动（SPEM）、前视运动（PS）和反视运动（AS），同时被随机分配到四个药物组（静脉注射100 ng ml−1氯胺酮、2 mg口服利培酮、100 ng ml−1氯胺酮+2 mg口服利培酮、安慰剂）中的一个。给药未导致有害不良事件。氯胺酮可增加扫视频率，降低SPEM的速度增益（P均<0.01），但对PS和AS无明显影响（P均<0.07）。观察到利培酮对PS和AS的振幅增益和峰值速度的影响，表明与安慰剂相比，PS和AS的振幅增益和峰值速度降低（均P <0.04）。未发现氯胺酮与利培酮的相互作用（均P <0.26）。结果证实，氯胺酮给药产生的眼科表现缺陷部分类似于精神分裂症中所见。非典型抗精神病药利培酮不能逆转氯胺酮引起的病情恶化。这些发现不支持利培酮对精神分裂症模型系统中眼部生物标志物的认知增强潜力，并指出开发替代性能增强化合物以优化精神分裂症的药理学治疗的重要性。
The non-competitive N-methyl-D-aspartate receptor antagonist ketamine leads to transient psychosis-like symptoms and impairments in oculomotor performance in healthy volunteers. This study examined whether the adverse effects of ketamine on oculomotor performance can be reversed by the atypical antipsychotic risperidone. In this randomized double-blind, placebo-controlled study, 72 healthy participants performed smooth pursuit eye movements (SPEM), prosaccades (PS) and antisaccades (AS) while being randomly assigned to one of four drug groups (intravenous 100 ng ml−1 ketamine, 2 mg oral risperidone, 100 ng ml−1 ketamine plus 2 mg oral risperidone, placebo). Drug administration did not lead to harmful adverse events. Ketamine increased saccadic frequency and decreased velocity gain of SPEM (all P<0.01) but had no significant effects on PS or AS (all P⩾0.07). An effect of risperidone was observed for amplitude gain and peak velocity of PS and AS, indicating hypometric gain and slower velocities compared with placebo (both P⩽0.04). No ketamine by risperidone interactions were found (all P⩾0.26). The results confirm that the administration of ketamine produces oculomotor performance deficits similar in part to those seen in schizophrenia. The atypical antipsychotic risperidone did not reverse ketamine-induced deteriorations. These findings do not support the cognitive enhancing potential of risperidone on oculomotor biomarkers in this model system of schizophrenia and point towards the importance of developing alternative performance-enhancing compounds to optimise pharmacological treatment of schizophrenia.
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