Neuroscience 2001 Abstract
| Presentation Number: | 160.1 |
|---|---|
| Abstract Title: | <b>Dorsolateral prefrontal cortex activity regulates pain affect by modulating thalamic connectivity with the midbrain and limbic forebrain.</b> |
| Authors: |
Lorenz, J.*1
; Minoshima, S.2
; Casey, K. L.1
1Neurology, VAMC/Univ of Michigan, Ann Arbor, MI 2Radiology, Univ of Washington, Seattle, WA |
| Primary Theme and Topics |
Sensory Systems - Pain -- Thalamic and cortical regions and processing |
| Secondary Theme and Topics | Sensory Systems<br />- Pain Modulation<br />-- Neuropathic and inflammatory pain |
| Session: |
160. Pain: thalamic and cortical regions and processing I Poster |
| Presentation Time: | Sunday, November 11, 2001 1:00 PM-2:00 PM |
| Location: | Exhibit Hall G-9 |
| Keywords: | PET, Capsaicin, Frontal Cortex, C-fiber |
To address the role of the dorsolateral prefrontal cortex (DLPFC) in pain we used region of interest (ROI) and psychophysical data from a previous PET study where we observed a distinct negative correlation of DLPFC activity with the unpleasantness of capsaicin-induced heat allodynia (Lorenz et al. SFN abstract# 259.8, 2000). We analyzed the modulation that the DLPFC exerts on the connectivity between heat allodynia-specific ROI by computing inter-regional regressions separately for low and high DLPFC activity. We found that medial thalamic connectivity with the midbrain and limbic forebrain changes systematically during heat allodynia, dependent on DLPFC activity. Midbrain-thalamic connectivity was absent during high but marked during low DLPFC activity. In contrast, thalamic connectivity with the anterior insula and orbitofrontal cortex (OFC) was stronger during high compared to low DLPFC activity. Notably, positive correlations of insula and OFC activity with unpleasantness ratings were only present during low, but absent during high DLPFC activity. In contrast, midbrain activity only correlated positively with intensity ratings during high, but not low DLPFC activity. These results suggest that heat allodynia causes negative affect by strengthening midbrain-thalamic connectivity with limbic forebrain structures. These bottom-up mechanisms could trigger modulatory top-down mechanisms controlled by the DLPFC that dampens behavioral arousal and reduces negative affect induced by stimulation of sensitized C-nociceptors during protracted pain states.
Supported by Veteran Administration, NIH and Max Kade Foundation
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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