Effects of second-generation antipsychotic medication on smooth pursuit performance in antipsychotic-naive schizophrenia.

Effects of second-generation antipsychotic medication on smooth pursuit performance in antipsychotic-naive schizophrenia.
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DOI:
10.1001/archpsyc.65.10.1146
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发表时间:
2008-10
影响因子:
--
通讯作者:
Sweeney, John A.
Sweeney, John A.
中科院分区:
其他
文献类型:
--
作者:
Lencer, Rebekka;Sprenger, Andreas;Harris, Margret S. H.;Reilly, James L.;Keshavan, Matcheri S.;Sweeney, John A.

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对精神分裂症患者平滑追踪眼球运动参数的分析提供了有关介导运动感知、感觉运动转换和预测等认知过程的神经网络完整性的信息。尽管追踪眼球追踪缺陷在精神分裂症中已被广泛报道,但追踪反应的离散成分的完整性以及第二代抗精神病药物对其的影响尚未明确。旨在检查未接受抗精神病药物治疗的精神分裂症患者在使用第二代抗精神病药物治疗前后平滑追求表现的不同组成部分。 33 名未接受抗精神病药物治疗的精神分裂症患者进行了 3 种不同的平滑追踪范式,旨在评估追踪反应的特定组成部分。所有患者在接受利培酮或奥氮平治疗 6 周后重新进行测试。还对 39 名匹配的健康个体进行了测试。 13 名患者和 21 名健康参与者在 26 周和 52 周后重新进行了测试。追踪启动、维持增益(眼速与目标速度之比)以及追踪维持期间追赶眼跳的频率。在治疗之前,追踪难以预测的斜坡目标时的追踪增益往往会减少,追踪启动的延迟时间会加快,并且在预测追踪期间追赶扫视频率会增加。开始抗精神病治疗后,追踪增益随着斜坡目标的增加而减少,表明治疗中出现的感觉运动处理损伤。没有观察到预测追踪的变化。对亚组随访 1 年的探索性分析表明,这些影响在长期随访中持续存在,并在 1 年时部分正常化。缺陷与药物剂量和临床评级无关。在开始使用第二代抗精神病药物后,观察到感觉运动功能受损,这可能是由于它们对脑干感觉运动系统的血清素能拮抗作用所致。由额纹状体-小脑回路支持的预测机制不受治疗开始的影响,并且似乎能够在预测跟踪期间补偿治疗引起的感觉运动损伤。
Analyses of smooth pursuit eye movement parameters in patients with schizophrenia provide information about the integrity of neural networks mediating motion perception, sensorimotor transformation, and cognitive processes such as prediction. Although pursuit eye tracking deficits have been widely reported in schizophrenia, the integrity of discrete components of pursuit responses and the effect of second-generation antipsychotic medication on them are not well established. To examine different components of smooth pursuit performance in antipsychotic-naive patients with schizophrenia before and after treatment with second-generation antipsychotic medication. Thirty-three antipsychotic-naive patients with schizophrenia performed 3 different smooth pursuit paradigms designed to evaluate specific components of the pursuit response. All of the patients were retested after 6 weeks of treatment with risperidone or olanzapine. Testing was also performed with 39 matched healthy individuals. Thirteen patients and 21 healthy participants were retested after 26 and 52 weeks. Pursuit initiation, maintenance gain (ratio of eye velocity over target velocity), and frequency of catch-up saccades during pursuit maintenance. Prior to treatment, pursuit gain when tracking less predictable ramp targets tended to be reduced, latency of pursuit initiation was speeded, and catch-up saccade frequency was increased during predictive pursuit. After antipsychotic treatment initiation, pursuit gain decreased with ramp targets, indicating treatment-emergent impairments in sensorimotor processing. No changes were observed for predictive pursuit. Exploratory analyses in the subgroup with follow-up to 1 year revealed that these effects continued through long-term follow-up with some partial normalization at 1 year. Deficits were unrelated to drug dosage and clinical ratings. Impaired sensorimotor function was observed after initiation of second-generation antipsychotic medications, which may be explained by their serotonergic antagonism of brainstem sensorimotor systems. Predictive mechanisms supported by frontostriatal-cerebellar circuitry were not affected by treatment initiation and appear able to compensate for treatment-emergent sensorimotor impairments during predictive tracking.
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