Department of Pharmacology and Physiology, University of Rochester, Rochester, New York, United States of America ; Department of Psychology and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
PLoS One. 2013 Dec 6;8(12):e82882. doi: 10.1371/journal.pone.0082882. eCollection 2013.
Previous research has yielded evidence for enhanced semantic priming in formal thought-disordered schizophrenia patients, a result that fits well with the hypothesis of disinhibited processes of spreading activation in this population.
The current study examined whether hyper priming among schizophrenia patients is an outcome of further spreading of activation of a node or a result of farther activation of nodes in the semantic network. We also try to shed light on the fate of this activation.
The present study tested this hypothesis by using semantic and identical priming in two different experiments. SOA (stimulus onset asynchrony) was manipulated (240 ms vs. 740 ms) within block. It is assumed that among healthy individuals, performance relies on a balance between activation and inhibition processes, contrary to in schizophrenic individuals. In order to examine this hypothesis, we compared formal thought-disordered schizophrenia patients, non thought-disordered schizophrenia patients, and healthy controls.
For thought-disordered schizophrenia patients, we found a large positive semantic effect and identical priming effect (129 ms and 154 ms, respectively) only with short SOA. SOA and type of priming did not modulate priming effects in the control groups.
This result supports the claim that there is a lack of inhibitory processes among thought-disordered patients. Hyper priming in the thought-disorder group may be an outcome of hyper activation followed by rapid decay below baseline threshold.
先前的研究为精神分裂症患者的正式思维障碍提供了增强语义启动的证据，这一结果与该人群中扩散激活的抑制过程假说相符。
本研究旨在检验精神分裂症患者的过度启动是节点的激活进一步扩散的结果，还是语义网络中节点的进一步激活的结果。我们还试图阐明这种激活的命运。
本研究通过在两个不同的实验中使用语义和相同的启动来检验这一假设。在块内操纵 SOA（刺激起始时距）（240ms 与 740ms）。与精神分裂症患者相反，人们认为健康个体的表现依赖于激活和抑制过程之间的平衡。为了检验这一假设，我们比较了形式思维障碍的精神分裂症患者、非思维障碍的精神分裂症患者和健康对照组。
对于思维障碍的精神分裂症患者，我们仅在短 SOA 时发现了较大的正语义效应和相同的启动效应（分别为 129ms 和 154ms）。SOA 和启动类型均未调节对照组的启动效应。
这一结果支持了思维障碍患者缺乏抑制过程的说法。思维障碍组的过度启动可能是过度激活后迅速衰减至基线阈值以下的结果。
