A computational model unifies apparently contradictory findings concerning phantom pain.

A computational model unifies apparently contradictory findings concerning phantom pain.
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DOI:
10.1038/srep05298
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发表时间:
2014-06-16
期刊:
影响因子:
4.6
通讯作者:
Wagner H
Wagner H
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Boström KJ;de Lussanet MH;Weiss T;Puta C;Wagner H

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截肢常常会导致痛苦的幻觉,其发病机制尚不清楚。在实验结果的支持下,提出了一个解释模型,该模型将初级体感皮层(S1)的适应不良重组确定为幻痛的原因。然而,最近发现幻肢随意运动期间的 BOLD 活动与幻肢疼痛等级呈正相关,从而产生了持续表征模型。在本研究中,我们开发了一种生理上真实的计算模型来解决相互矛盾的发现。模拟结果表明,与幻痛较弱的情况相比,幻痛较强的情况下幻痛运动期间的重组量和皮质活动水平均有所增强。这些结果表明,幻痛、适应不良的重组和持续表征可能都是由相同的潜在机制引起的,该机制是由传入神经传导障碍的伤害性通道的自发活动异常增强所驱动的。
Amputation often leads to painful phantom sensations, whose pathogenesis is still unclear. Supported by experimental findings, an explanatory model has been proposed that identifies maladaptive reorganization of the primary somatosensory cortex (S1) as a cause of phantom pain. However, it was recently found that BOLD activity during voluntary movements of the phantom positively correlates with phantom pain rating, giving rise to a model of persistent representation. In the present study, we develop a physiologically realistic, computational model to resolve the conflicting findings. Simulations yielded that both the amount of reorganization and the level of cortical activity during phantom movements were enhanced in a scenario with strong phantom pain as compared to a scenario with weak phantom pain. These results suggest that phantom pain, maladaptive reorganization, and persistent representation may all be caused by the same underlying mechanism, which is driven by an abnormally enhanced spontaneous activity of deafferented nociceptive channels.
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