Neural correlates of heat-evoked pain memory in humans

Author:

Wang Liping12,Gui Peng1,Li Lei1,Ku Yixuan12,Bodner Mark3,Fan Gaojie4,Zhou Yong-Di256,Dong Xiao-Wei12

Affiliation:

1. Key Laboratory of Brain Functional Genomics, MOE and STCSM, Institute of Cognitive Neuroscience, East China Normal University, Shanghai, People's Republic of China;

2. NYU-ECNU Institute of Brain and Cognitive Science at NYU Shanghai and Collaborative Innovation Center for Brain Science, Shanghai, People's Republic of China;

3. MIND Research Institute, Irvine, California; and

4. Department of Psychology, Colorado State University, Fort Collins, Colorado

5. Department of Neurosurgery, Johns Hopkins University, Baltimore, Maryland;

6. Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland;

Abstract

The neural processes underlying pain memory are not well understood. To explore these processes, contact heat-evoked potentials (CHEPs) were recorded in humans with electroencephalography (EEG) technique during a delayed matching-to-sample task, a working memory task involving presentations of two successive painful heat stimuli (S-1 and S-2) with different intensities separated by a 2-s interval (the memorization period). At the end of the task, the subject was required to discriminate the stimuli by indicating which (S-1 or S-2) induced more pain. A control task was used, in which no active discrimination was required between stimuli. All event-related potential (ERP) analysis was aligned to the onset of S-1. EEG activity exhibited two successive CHEPs: an N2-P2 complex (∼400 ms after onset of S-1) and an ultralate component (ULC, ∼900 ms). The amplitude of the N2-P2 at vertex, but not the ULC, was significantly correlated with stimulus intensity in these two tasks, suggesting that the N2-P2 represents neural coding of pain intensity. A late negative component (LNC) in the frontal recording region was observed only in the memory task during a 500-ms period before onset of S-2. LNC amplitude differed between stimulus intensities and exhibited significant correlations with the N2-P2 complex. These indicate that the frontal LNC is involved in maintenance of intensity of pain in working memory. Furthermore, alpha-band oscillations observed in parietal recording regions during the late delay displayed significant power differences between tasks. This study provides in the temporal domain previously unidentified neural evidence showing the neural processes involved in working memory of painful stimuli.

Publisher

American Physiological Society

Subject

Physiology,General Neuroscience

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