|Alternative Title||Behavioral and Neural Mechanisms for Pain and Unconscious Cognition Interaction|
|Place of Conferral||北京|
|Keyword||实验室诱发痛 慢性疼痛 认知损伤 失匹配负波 预期|
|Other Abstract||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.
|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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