弱视和肝豆状核变性患者视觉认知功能损害机制的噪音与模型分析研究
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摘要
引入外部视觉噪音,测量视觉系统在受噪音干扰时对信号的检测能力是近年来在心理物理学研究中逐渐流行起来的实验方法。外部噪音的引入使得我们可以全面的研究视觉系统信号检测能力受到外部噪音影响的情况,从而得出信号检测阈值与外部噪音对比度之间的函数关系(TvC曲线)。在此基础之上,再通过模型分析求出视觉系统的一些内部组成成分,如内部加法噪音,内部乘法噪音,视觉模板效能,非线性传递因子等,从而进一步加深我们对视觉系统信号处理功能的了解。在本文中,我们运用引入外部噪音的方法,配以PTM模型分析,对弱视及肝豆状核变性患者视觉信号检测能力损害的机制进行了系统性分析,同时对弱视患者二阶运动信号的检测,以及肝豆状核变性患者知觉学习和分类学习之间的关系也作了相应研究。
     弱视是视觉发育敏感期异常视觉经验所导致的以空间视力损害为特征的一组视力不良综合征。其视功能损害涉及多个脑区并与皮层神经元空间特性的异常密切相关。我们共在8个噪音度(噪音对比度0-0.33)以及两个正确率(d’=1.09和d’=1.63)下分别测量了弱视患者与正常被试中央视野辨别Gabor信号朝向的对比度阈值。实验结果显示,在空间频率2.3c/d时,弱视的主要损害表现为在低噪音段的信号检测能力远弱于正常被试(弱视眼阈值比正常被试高169%),PTM模型分析显示这主要是由于弱视造成了视觉系统内部加法噪音的增高。弱视患者的成绩在高噪音段也表现出一定程度的受损(弱视眼阈值比正常被试高56%),这在PTM模型中表现为视觉模板的滤波能力相应的降低。且随着需检测信号的空间频率从1.5c/d逐渐增加至4.6c/d,弱视眼在高噪音段的损伤增加幅度要高于其在低噪音段的增加幅度,显示弱视视觉模板随空间频率的提高损害程度大于内部加法噪音的增加。此外,我们还发现弱视眼的乘法噪音和非线性系统与正常被试相比并未受到明显损害。
     在屈光参差性弱视患者对一阶运动和二阶运动信号的检测阈值测量实验中,我们在5个时间频率下分别测量了弱视眼与健康眼在未平衡载体(carrier)输入时与平衡载体输入后的二阶运动信号检测阈值。结果表明,与正常眼相比,弱视眼对未经载体平衡的二阶运动信号检测存在损伤,但其对比敏感度降低幅度(平均80%)小于其一阶信号降低幅度(平均150%);同时弱视眼对经过载体平衡的二阶运动信号的检测能力与健康眼相当。我们的实验结果说明,弱视眼对二阶运动信号的检测能力并未受到明显的损伤,其在未平衡载体时表现出的能力受损主要是来自于其对载体信号的一阶空间信号检测能力的损伤。
     肝豆状核变性又称Wilson病,是一种常染色体隐性遗传的铜代谢障碍疾病,由于铜在体内过度蓄积,损害肝、脑等器官而导致多种临床症状。肝豆状核变性患者大脑中的损害位点主要在基底节,通过对其进行知觉学习和分类学习实验,我们可以观察到两类学习处理过程与基底节的联系,并研究两类学习之间的相关性。我们的实验结果显示,肝豆状核变性患者的显性和隐性分类学习都受到损害,其成绩(显性分类达标正确率73.0%,隐性分类达标正确率65.3%)显著低于正常被试(显性分类达标正确率83.1%,隐性分类达标正确率72.7%),进一步证实了这两类分类学习过程都需要基底节的参与。同时在知觉学习任务中,患者在低噪音下的知觉学习能力与正常被试相比无显著性差异,而在高噪音下的知觉学习能力则有明显损伤(肝豆状核变性患者阈值降低2.21dB,正常被试阈值降低4.66dB),PTM模型分析显示肝豆状核变性患者视觉模板滤波能力降低,且此结果可能与基底节的损伤有关。此外我们还发现,高噪音下的知觉学习成绩与隐性分类学习有着显著性的相关,预示两类学习之间有着一些共同的神经机制。
     引入外部噪音进行建模分析,通过这种有效的研究方法我们可以获得更丰富的实验信息,帮助我们在更广泛的视觉研究工作中深入的了解其内在的机制。
Currently, external noise is frequently used by psychologists to measure the properties of a wide range of perceptual process. The basic idea of this methos is to estimate the amount of internal noise and characteristics of the perceptual processes by studying how performance in some task is affected by experimenter-manipulated external noise. In this paper, we apply the external noise method and a Perceptucal Template Model (PTM) to identify the mechanism of the visual deficit in amblyopia and Wilson's Disease patients. In addition, we also studied the detection threshold of second-order motion signal in amblyopia and the relationship of perceptual learning and category learning in Wilson's Disease patients.
     Amblyopia is a developmental visual disorder characterized by reduced vision in the absence of any detectable structural or pathological abnormalities that does not improve with refractive correction. In our experiment, amblyopic observers performed a Gabor orientation identification task in fovea with 8 level white external noises (contrast 0-0.33) added. Threshold versus external noise contrast (TvC) functions were measured at two performance criterion levels (d'=1.09 and d'=1.63). For a subset of observers, we also manipulated the center spatial frequency of the Gabor from spatial frequency 1.5-4.6 c/d. With PTM model analysis, we found that two independent factors contributed to amblyopic deficits: (1) increased additive internal noise, and (2) deficient perceptual templates. Whereas increased additive noise underlay performance deficits in all spatial frequencies, the degree of perceptual template deterioration increased with the center spatial frequency of the Gabor. In addition, we found that amblyopia did not affect the non-linear transducer and multiplicative noise.
     In the first-order and second-order motion detection experiments, we measured the sensitivity of first-order and second-order motion of sinusoidal grating signal in eight anisometropic amblyopes and ten normal observers. The measurement of second-order motion was performed in two conditions: with non-equated visible carrier and with equated visible carrier. The amblyopic eyes of amblyopes showed deficit in both perceptions of first-order and second-order motion with non-equated carrier, relative to their fellow eyes and to normal eyes. But with the equated carrier, we revealed the second order motion perception was normal for the amblyopic eyes, which means the deficit of second-order motion in amblyopic eye could be a sequence of its first-order detection loss.
     Wilson's disease (WD), hepatolenticular degeneration, is an autosomal recessively inherited disorder of copper metabolism. In this suty, we evaluated explicit and implicit category learning and perceptual learning in subjects with treated Wilson's disease and normal controls. The WD subjects exhibited deficits in both forms of category learning as well as perceptual learning in high external noise. However, their perceptual learning in low external noise was relatively spared. Furthermore, there were significant correlations between perceptual learning in high external noise and both forms of category learning, but perceptual learning in low external noise was not significantly correlated with either form of category learning. The results suggest that damages to brain structures in Wilson's disease that are important for category learning may lead to poor perceptual learning in high external noise, but may spare perceptual learning in low external noise; perceptual learning in high and low external noise environments may be served by different brain structures.
     With the method of systematic variations of environmental noise in signal detection task and quantification in a model analysis, increasing information can be acquired in our research experiments and new mechanisms of visual processing can be revealed in future.
引文
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