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疼痛与无意识水平认知功能的相互调节作用及其神经机制
其他题名Behavioral and Neural Mechanisms for Pain and Unconscious Cognition Interaction
许杨
学位类型博士
导师罗非
2015-05
学位授予单位中国科学院研究生院
学位授予地点北京
学位专业心理学
关键词实验室诱发痛 慢性疼痛 认知损伤 失匹配负波 预期
摘要疼痛与认知功能相互紧密影响,疼痛(特别是临床的慢性疼痛)损伤认知功能,而另一方面,认知手段能够调节个体对疼痛的感知。然而不同的研究中疼痛对认知的影响的结果存在分歧,特别是实验室诱发痛的情况下,有些研究发现了疼痛对认知的损伤作用,而有些研究则没有发现疼痛的影响。因为认知功能本身受很多心理因素的调节,例如觉醒状态、动机水平等,为了排除这些因素,本研究从无意识的水平对疼痛和认知功能的相互作用进行考察。本论文主要考察了实验室诱发痛和临床慢性疼痛状态下,疼痛对认知的损伤作用,并探索其背后的神经机制,特别是脑网络在大尺度上结构的改变。此外,本论文也探索了将认知手段运用于对疼痛的调节的可能,以及个体特质对其调节作用的影响。
研究一通过冷压痛范式在实验室中诱发疼痛,记录健康被试在基线状态,疼痛状态以及恢复状态中的失匹配负波(MMN)。结果发现:首先,疼痛状态下MMN的波幅显著低于基线水平;其次,在疼痛状态下,MMN的波幅都与疼痛的强度显著负相关,即疼痛强度越大,则MMN的波幅越小;第三,疼痛的干扰作用并不是随着疼痛的消失而立即消失的,恢复期的MMN的平均波幅仍然低于基线状态,MMN的波幅随着恢复的时间的增加而增大。
研究二通过比较临床上慢性痛患者与健康被试,慢性痛患者在手术前后MMN的结果,以考察慢性痛状态对认知的影响。此外,研究二还考察了疼痛状态下MMN的额叶源和额叶源之间的功能连接以研究疼痛在更大尺度上对脑网络的影响。结果发现:首先,慢性痛患者在偏差刺激容易被探测时,MMN的波幅显著低于健康对照。当患者经过手术使疼痛症状缓解后,其额叶处的MMN的波幅显著增高,而健康对照组在两次检测中MMN没有发生显著的变化。其次,患者额叶处的MMN的波幅与其疼痛强度评分呈显著的负相关。第三,当偏差刺激易于探测时,慢性痛患者颞叶-额叶间的功能连接显著低于正常对照组。
研究三比较了慢性痛患者与健康被试,以及慢性痛患者在手术前后的静息态EEG信号。结果发现:首先,慢性痛患者在θ和β两个波段内功率谱密度显著高于健康对照组;在θ波段内的功能连接显著高于对照组。其次,以图论的方法分析神经结构的结果表明,慢性痛患者静息态的神经网络在θ和β 两个波段内具有更强的连接度和集聚系数,显示慢性痛患者的神经网络的小世界属性高于健康对照组。第三,神经网络的参数与临床症状之间的关联的结果表明,神经网络的连接度和集聚系数与对疼痛的反刍显著相关。最后,慢性痛患者静息态神经网络的各项异常的指标在疼痛症状缓解之后恢复正常水平。
研究四通过将不同的图片与高痛和低痛的刺激配对使被试通过图片对疼痛强度形成预期,考察这种预期对疼痛感知的调节作用。研究四中同时设置了阈上组和阈下组,进一步探索认知功能对疼痛的调节作用是否能发生在无意识的状态下。结果表明对疼痛强度的预期可以调节个体对疼痛的感知,个体对与高痛刺激配对的图片的评分高于中性图片,而与低痛刺激配对的图片评分低于中性图片,而这种作用可以发生在被试无意识的状态下。并且,当考察预期对疼痛调节作用与个体特质的关系时,结果发现无意识引发的预期效应与个体的特质焦虑显著负相关,而有意识的预期效应则不存在这种相关关系。
综上所述,本论文结合行为学和认知神经科学研究表明,疼痛状态损伤个体的认知功能,认知功能可以作为一个客观衡量疼痛状态的指标并且可以反映疼痛的恢复情况。同时,临床上也可以采用认知手段对疼痛进行调节。
其他摘要Pain and cognition are inherently associated with each other. Pain (especially chronic pain) could impair cognition. On the other hand, cognitive approach could modulate pain perception and thus act as an analgesic strategy. However, discrepant evidences are available for the interaction of pain and cognition especially in the experimental settings. In some studies, deteriorated cognition was found because of pain while there was no effect of pain in other studies. In the current study, the interaction between pain and cognition was investigated under unconscious level to rule out the effect of other psychological factors, like motivation and arousal. Moreover, previous works focused on the regional changes while ignored the large-scale network changes of the brain networks when investigating the underlying mechanism of the cognitive impairment resulted from pain. The current thesis investigated how pain impaired cognition in clinical and experiment settings. In addition, the present thesis also explored the use of cognitive modulation as an analgesic approach.
In the study 1, mismatch negativity (MMN) was recorded in healthy human subjects to investigate the preconscious cognition under experimentally evoked pain. Cold-pressor test was used to produce tonic pain. MMN was elicited using a passive oddball paradigm and recorded in three conditions (baseline, pain, recovery). MMN amplitude was diminished under painful condition. There was a negative correlation between MMN amplitude and pain ratings under painful condition. In the recovery period, MMN amplitude was still diminished when compared with baseline and increased over time.
In the study 2, MMN was recorded during a frequency-deviant passive auditory oddball task at baseline and 7-10 days post-surgery in trigeminal neuralgia patients (TN) and healthy controls (HC). The ICA decomposition method was used to obtain a reliable MMN, and functional coupling analysis was performed to reveal changes in network activity. At baseline, MMN amplitude and functional connectivity between frontal and temporal MMN components was diminished in TN patients compared to HC subjects. Specifically, frontal MMN amplitude correlated with ratings of self-reported pain intensity in TN patients. After surgery-induced analgesia, TN patients showed significantly increased MMN. HC subjects, tested at the same time points, showed no changes.
In the study 3, large-scale structure of resting-state brain networks in patients with trigeminal neuralgia (TN) was examined. EEGs were recorded in TN patients and healthy controls (HC) at baseline and 7-10 days post-surgery when in a no-task, eye-closed condition. On an average, the TN patients exhibited higher spectral power over the θ and β band. Synchronization between all pairs of EEG electrodes was assessed using phase lag index (PLI). TN patients showed higher PLI over the θ band. PLI-weighted connectivity network were then analyzed using concepts from graph theory. TN patients showed increased connectivity degree and clustering coefficient. Moreover, positive correlations were found between structural changes (degree and clustering coefficient) and subjective pain ruminations. After surgery-induced analgesia, the power spectral, degree and clustering coefficient decreased to normal level.
In the study 4, high and low levels of thermal stimulation were paired with distinct visual cues, and expectancy effect which defined as the different ratings of the same moderate painful stimulation paired with different visual cues was tested to investigate whether expectation could modulate pain perception. Additionally, to investigate whether unconscious pain-related cue had expectancy effects on pain perception, subjects were separated into supraliminal group and subliminal group. Significant expectancy effect was found in both supraliminal and subliminal group. These results indicated that expectation could modulate subjective pain perception, even under unconscious condition. Furthermore, there was a significant negative correlation between expectancy effect and individual trait anxiety, which only observed in the subliminal but not in the supraliminal group.
In summary, the current thesis provide behavioral and neural evidence that both experimentally induced pain and chronic pain could impair cognitive function, and cognition may be a practical and objective tool for evaluating clinical pain severity as well as improvement or recovery. Meanwhile, the current thesis suggested that improved treatment strategies for pain with pain-related cognitive dysfunction and the use of cognitive modulations as an analgesic approach are two therapeutic goals in the future.
学科领域认知神经科学
语种中文
文献类型学位论文
条目标识符http://ir.psych.ac.cn/handle/311026/19738
专题健康与遗传心理学研究室
作者单位中国科学院心理研究所
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许杨. 疼痛与无意识水平认知功能的相互调节作用及其神经机制[D]. 北京. 中国科学院研究生院,2015.
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