精神分裂症返回抑制的研究进展

20世纪中叶认知心理学兴起以后,注意作为心理活动的调节机制一直受到研究者的重视。自上世纪80年代至今,注意的研究经历了一个新的发展阶段,重要的一点是注意理论研究有新的突破,注意不再是被简单地理解为对所选择信息的激活,而是被看做对靶子和干扰项的双加工,包含激活和抑制的双过程。Neill（1977）的研究表明,没有被选择的刺激（干扰项）也可以得到加工,而且这种加工对随后该刺激成为下一次试验的靶子时有不利作用,Neill认为在注意的选择过程中,干扰项受到抑制,所以再次加工时其反应时变慢了,这就是后来被Tipper（1985）称之为的“负启动”现象。     

返回抑制及其在精神分裂症中的研究

人类视觉环境中的信息远远超过人脑处理能力,这就需要大脑提高搜索效率。返回抑制是在进化过程中形成的能力,在已经搜索过的位置上再出现目标时,人们的反应会减慢。从而忽略不重要的信息,对重要的信息更快地反应。这种现象一经发现,即成为认知科学研究的热点。而近20年来精神分裂症认知症状越来越引起临床医师的重视,返回抑制是认知功能中注意方面的重要抑制成分,能够量化检查,而且方法简便可行。研究精神分裂症返回抑制现象与正常人的差异,是精神分裂症认知症状方面的重要发现。     

糖耐量减低对男性精神分裂症患者注意功能及优势抑制的影响

目的:探讨糖耐量减低对男性精神分裂症患者注意功能及优势抑制的影响。方法:采用简易精神状态检查量表(MMSE)、数字广度测验、Stroop色词测验对30例糖耐量减低(IGT组)和30例糖耐量正常(NGT组)的男性精神分裂症患者进行认知功能评估。结果:IGT组Hb A1C、TG平均水平显著高于NGT组(P均0.05),IGT组Hb A1c达标百分比低于NGT组,IGT组高TG血症检出率高于NGT组;IGT组认知功能损害检出率高于NGT组,IGT组MMSE平均分显著低于NGT组,IGT组卡片C错误数、卡片C耗时数、SIE反应时显著高于NGT组,SIE正确数显著低于NGT组(P均0.05)。IGT组与NGT组顺背数字差异无统计学意义(P0.05),倒背数字IGT组显著低于NGT组(P0.05)。通过Logistics分析,年龄和病程对两组认知功能损害有显著影响(R2=0.85,P0.05)。结论:糖耐量减低影响男性精神分裂症患者的注意功能及优势抑制。     

慢性精神分裂症男性患者听觉刺激惊跳反射的初步研究

目的 探讨汉族人群精神分裂症患者是否存在听觉惊跳反射缺陷及抗精神病药的影响.方法 第1代药物组:服用第1代抗精神病药的慢性精神分裂症男性患者25例;氯氮平组:服用氯氮平的慢性精神分裂症男性患者25例;对照组:身体健康的男性25名;3组的年龄和受教育年限均匹配.对上述3组进行听觉刺激惊跳反射检测,并使用阳性和阴性症状量表(PANSS)评定精神分裂症患者的临床精神病理症状.结果 (1)第1代药物组惊跳反射的反应波幅(SR)[(553.6±516.9)mV]明显低于对照组[(942.0±447.3)mV,P=0.009],氯氮平组的SR[(755.9±439.4)mV]介于上述2组之间,但与2组间的差异均无统计学意义(P＞0.05);(2)第1代药物组惊跳反射的适应性(HAB)[(17.8±35.8)%]明显低于对照组[(44.9±28.9)%,P=0.027],氯氮平组的HAB[(22.9±34.1)%]介于上述2组之间,但与2组间的差异均无统计学意义(P＞0.05);(3)当时间间隔(LI)为120 ms时,第1代药物组的惊跳反射弱刺激抑制(prepulse inhibition,PPI)显著小于对照组(P=0.024),氯氮平组的PPI值介于上述2组之间,但与2组间的差异均无统计学意义(P＞0.05);LI为30 ms或60 ms时,3组间PPI的差异无统计学意义(P＞0.05);(4)第1代药物组和氯氮平组患者不同LI的PPI与其临床病理症状可能不存在相关(P＞0.05).结论 精神分裂症患者可能存在听觉惊跳反射弱刺激抑制的缺陷;氯氮平可能能部分改善精神分裂症患者对惊跳反射的脱抑制.     

精神分裂症患者住院时间与疗效的关系

目的:探讨精神分裂症患者住院时间与疗效的关系。方法:以10 d为间隔将235例精神分裂症患者按住院时间分为7~20 d、30 d、40 d、50 d、60 d及60 d组,在住院第1周和最后1周分别应用阳性和阴性症状量表(PANSS)及自知力和治疗态度问卷(ITAQ)评估病情及自知力;分析住院时间与疗效的关系。结果:235例患者平均住院时间为64.3 d;住院时间与出院时ITAQ总分(r=0.294)、PANSS总分(r=-0.407)、阳性症状分(r=-0.369)及PANSS总分减分率(r=0.377)、阳性症状分减分率(r=-0.369)的相关系数在7~30 d组最大;住院≥31 d后其疗效与30 d比较差异无统计学意义。结论:精神分裂症患者住院30 d后,疗效可能不会随着住院时间延长而显著改善。     

精神分裂症患者住院时间的影响因素分析

目的 分析精神分裂症患者住院时间的影响因素。方法 采用整群抽样方法，回顾2018年 1 月 1 日至 12 月 31 日在无锡市精神卫生中心住院精神分裂症患者的电子病历系统，收集基本资料和 临床资料，包括性别、年龄、工作、户口、监护人、住院付费方式、诊断分型、共病情况、住院次数、病程 及住院时间。采用无序多分类 Logistic 回归分析不同住院时间的影响因素。结果 共调查 1 063 例患 者，平均年龄（49.97±15.58）岁，以男性（566例，53.25%）、失业（943例，88.71%）、城镇户口（916例，86.17%）、 病程＞5年（809例，76.11%）、住院＞3次者（594例，55.87%）、偏执型分裂症（619例，58.23%）、共病躯体疾病 （590例，55.5%）居多，以医保支付住院治疗费用者895例（84.2%）。其中住院时间≤1个月占20.79%（221例）；＞ 1～3 个月占 34.34%（365 例）；＞ 3～＜ 12 个月占 11.00%（117 例）；≥ 12 个月占 33.87%（360 例）。回归分 析显示，男性（OR=1.913，95%CI：1.326～2.759；OR=2.835，95%CI：1.717～4.679；OR=4.341，95%CI： 2.782～6.772）、失业（OR=1.735，95%CI：1.082～2.780；OR=5.988，95%CI：2.376～15.087；OR=3.960， 95%CI：1.901～8.248）、医 保 付 费（OR=2.747，95%CI：1.820～4.145；OR=7.565，95%CI：3.502～16.342； OR=14.531，95%CI：6.430～32.839）是住院时间＞ 1～3 个月、＞ 3～＜ 12 个月和≥ 12 个月的共性影响因 素；无核心照料者（OR=2.087，95%CI：1.178～3.696；OR=4.173，95%CI：2.539～6.856）、住院次数＞ 3 次 （OR=1.775，95%CI：1.095～2.878；OR=4.272，95%CI：2.748～6.641）是住院时间＞ 3 个月的危险因素；年 龄≥ 50 岁（OR=2.290，95%CI：1.407～3.729）、病程＞ 5 年（OR=5.555，95%CI：2.749～11.228）、共病躯体疾 病（OR=2.034，95%CI：1.301～3.181）是住院时间≥ 12 个月的危险因素。结论 精神分裂症患者住院时 间普遍较长，男性、失业、医保付费、无核心照料者、住院次数＞ 3 次、病程＞ 5 年、年龄≥ 50 岁和共病躯 体疾病与住院时间延长及长期住院密切相关。     

青少年精神分裂症患者住院时间的影响因素

目的 探讨青少年精神分裂症患者住院时间的影响因素。方法 以收治本院的50例青少年精神分裂症患者（收集时间：2019年10月～2021年10月）为研究样本,回顾性调查患者人口学资料、临床资料、家属相关资料等,分析影响患者住院时间的相关因素。结果 留守、由家属陪护、家属对精神疾病态度不良、无医保、治疗无效、出现不良反应的患者其住院时间与非留守、无家属陪护、家属态度良好、治疗有效、无不良反应患者的住院时间存在统计学差异（P<0.05）;Logistic分析显示：留守、家属陪护、家属对精神疾病态度、医保、治疗效果、不良反应是影响患者住院时间的危险因素（P<0.05）。结论 影响青少年精神分裂症患者住院时间的主要因素为家属陪护、留守儿童、家属对精神障碍疾病态度不良、治疗无效、出现不良反应,进而对患者住院治疗及早期康复造成不良影响,临床需大力普及精神卫生知识,提供有效心理疏导,以减少不良影响因素。     

利培酮口服液治疗精神分裂症急性期对照研究

目的 探讨利培酮口服液治疗精神分裂症急性期的疗效和副作用.方法 以利培酮口服液与氟哌啶醇治疗精神分裂症急性期各30例作对照研究,采用简明精神症状量表（BPRS）及其各单项评分,不良反应量表（TESS）评定疗效及副反应.结果 利培酮组及氟哌啶醇组在入院后3 d临床疗效一致,无显著性差别（P＞0.05）,疗程30 d后利培酮口服液有效率93%,显效率73%,氟哌啶醇组有效率86%,显效率36%.利培酮口服液药物副反应明显较氟哌啶醇少（P＜0.01）.结论 两种药对治疗精神分裂症急性期均有确切疗效.利培酮口服液对症状的改善效果更好,两组BPRS总分：利培酮口服液组减分率P＜0.001,氟哌啶醇组减分率P＜0.01,两组药物总体疗效有显著性差异（P＜0.01）,且服药依从性好.     

奥氮平与氯丙嗪治疗精神分裂症急性期的对照研究

目的 比较奥氮平与氯丙嗪治疗精神分裂症急性期的疗效和安全性。方法 奥氮平组36例，剂量5—20mg／d；氯丙嗪组32例，剂量100-400mg／d。两组均以PANSS、CGI及TESS量表评定2周。结果两组总体疗效相当，奥氮平组PANSS兴奋激越因子减分在第5天（t=3．47，P〈0．05）、1周末（t=3．21，P〈0．05）及2周末（t=3．64，P〈0．05）优于氯丙嗪组。结论奥氮平治疗精神分裂症急性期的疗效肯定，起效较快，不良反应较小，且安全性良好。     

Auditory orienting and inhibition of return in schizophrenia: A functional magnetic resonance imaging study

Patients with schizophrenia (SP) exhibit deficits in both attentional reorienting and inhibition of return (IOR) during visual tasks. However, it is currently unknown whether these deficits are supramodal in nature and how these deficits relate to other domains of cognitive dysfunction. In addition, the neuronal correlates of this pathological orienting response have not been investigated in either the visual or auditory modality. Therefore, 30 SP and 30 healthy controls (HC) were evaluated with an extensive clinical protocol and functional magnetic resonance imaging (fMRI) during an auditory cuing paradigm. SP exhibited both increased costs and delayed IOR during auditory orienting, suggesting a prolonged interval for attentional disengagement from cued locations. Moreover, a delay in the development of IOR was associated with cognitive deficits on formal neuropsychological testing in the domains of attention/inhibition and working memory. Event-related fMRI showed the characteristic activation of a frontoparietal network (invalid trials > valid trials), but there were no differences in functional activation between patients and HC during either attentional reorienting or IOR. Current results suggest that orienting deficits are supramodal in nature in SP, and are related to higher-order cognitive deficits that directly interfere with day-to-day functioning.     

Delayed onset of inhibition of return in schizophrenia

Peripheral visual cues occuring before a subsequent target result in an almost immediate facilitatory and then a later inhibitory effect on target detection. In a detailed parametric investigation, the authors compared schizophrenic subjects (SCZ) and control subjects (CONT) to examine whether they showed any differences in the time course of these nonpredictive peripheral cuing effects. Subjects fixated a central position and made saccadic responses to visual targets. Targets were presented 10 degrees to the left or right of fixation and were preceded at various time intervals by visual cues. Targets occurred with equal probability in either the same position as the cue or in the opposite, uncued location, and 10 delay periods were used corresponding to stimulus onset asynchronies (SOAs) of 66, 79, 106, 133, 159, 226, 305, 505, 705, and 1000 ms. All subjects showed facilitation for short cue-target delays and inhibition of return (IOR) for longer delays. SCZ, however, showed an apparent shift in the time course of cuing effects in the form of a delayed onset of IOR. Using a task of reflexive orienting, these results support findings of a delayed rather than an absent inhibitory process in medicated SCZ.     

Deficient inhibition of return in chronic but not first-episode patients with schizophrenia

Background

Inhibition of return (IOR) has been tested in patients with schizophrenia with contradictory results. Some studies indicated that patients with schizophrenia have normal levels of IOR; however, other studies reported delayed or blunted IOR. Inconsistency in findings might be due to differences across studies in relevant aspects associated with disease, such as heterogeneity of the disorder, different medications, onset and severity of the illness. The present study was to explore different patterns of IOR in antipsychotic medication free first-episode schizophrenia and chronic schizophrenia.

Methods

Forty two patients with first-episode schizophrenia, 44 patients with chronic schizophrenia, and 38 healthy controls were included in the study. All subjects went through a covert orienting of attention task with seven stimulus onset asynchrony (SOA) intervals (400 ms, 500 ms, 600 ms, 700 ms, 800 ms, 1200 ms and 1500 ms).

Results

Compared with healthy controls, the magnitude and onset of IOR in first-episode patients with schizophrenia were intact. However, in patients with chronic schizophrenia, there was an attenuated cuing effect especially at SOA 700 ms; in addition, there was a robust IOR until at SOAs 800 ms or above. Moreover, the illness duration and the number of psychotic episodes were significantly correlated with the validity effect at SOAs 400 ms and 600 ms.

Conclusion

Our study suggests that deficient IOR presents in chronic but not in first-episode patients with schizophrenia. IOR deficit in schizophrenia may begin during the course of illness and deteriorate over the course of illness. Our findings are consistent with the neurodegenerative model of schizophrenia.     

Auditory orienting and inhibition of return in schizophrenia: A functional magnetic resonance imaging study

Background

The brain mechanisms of cognitive-behavioral therapy (CBT), a highly effective treatment for pediatric obsessive-compulsive disorder (OCD), are unknown. Neuroimaging in adult OCD indicates that CBT is associated with metabolic changes in striatum, thalamus, and anterior cingulate cortex. We therefore probed putative metabolic effects of CBT on these brain structures in pediatric OCD using proton magnetic resonance spectroscopic imaging (¹H MRSI).

Method

Five unmedicated OCD patients (4 ♀, 13.5 ± 2.8) and 9 healthy controls (7 ♀, 13.0 ± 2.5) underwent MRSI (1.5 T, repetition-time/echo-time = 1500/30 ms) of bilateral putamen, thalamus and pregenual anterior cingulate cortex (pACC). Patients were rescanned after 12 weeks of exposure-based CBT. The Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS) of OCD symptoms was administered before and after CBT.

Results

Four of 5 patients responded to CBT (mean 32.8% CY-BOCS reduction). Multiple metabolite effects emerged. Pre-CBT, N-acetyl-aspartate + N-acetyl-aspartyl-glutamate (tNAA) in left pregenual anterior cingulate cortex (pACC) was 55.5% higher in patients than controls. Post-CBT, tNAA (15.0%) and Cr (23.9%) in left pACC decreased and choline compounds (Cho) in right thalamus increased (10.6%) in all 5 patients. In left thalamus, lower pre-CBT tNAA, glutamate + glutamine (Glx), and myo-inositol (mI) predicted greater post-CBT drop in CY-BOCS (r = 0.98) and CY-BOCS decrease correlated with increased Cho.

Conclusions

Interpretations are offered in terms of the Glutamatergic Hypothesis of Pediatric OCD. Similar to ¹⁸FDG-PET in adults, objectively measurable regional MRSI metabolites may indicate pediatric OCD and predict its response to CBT.     

The time course of information-processing deficits in schizophrenia

A visual backward masking task was used to specify the time course of the information-processing dysfunction in 19 schizophrenic patients and 15 matched control patients using novel interstimulus intervals. The authors found that the information-processing deficit in schizophrenic subjects occurred at interstimulus intervals of greater than 60 msec and less than 500 msec. These data are compared with the results of evoked-potential and other psychophysiological studies. The visual-processing impairment is specific and time-linked rather than a reflection of the effects of gross psychopathology or medication in schizophrenic individuals.     

The time course of visual backward masking deficits in schizophrenia

Schizophrenia, it has been hypothesized, is linked to a deficiency in the magnocellular portion of the visual system. Abnormal backward masking has been invoked as support for this hypothesis. The rationale for linking backward masking to the magnocellular system is the hypothesis that fast responses in the magnocellular systems catches up with, and then inhibits slower responses in the parvocellular system. However, the latency difference between the magno- and parvocellular systems is at most 20 ms. Magnocellular abnormalities as a result would be expected to manifest themselves only at relatively short stimulus onset asynchronies (SOAs) or interstimulus intervals (ISIs). The present study examines this implication. It is found that a substantial number of investigations have uncovered abnormal masking at SOAs or ISIs of 300 ms or larger, and some even at ISIs as large as 700 ms. It is difficult to reconcile abnormalities at these SOAs and ISIs with magno-parvocellular latency differences of 20 ms or less. It is concluded that the abnormal masking does not support the existence of a magnocellular deficiency in schizophrenia.