Neurophysiology of the cortical pain network: revisiting the role of S1 in subjective pain perception via standardized low-resolution brain electromagnetic tomography (sLORETA).
Multiple studies have supported the usefulness of standardized low-resolution brain electromagnetic tomography (sLORETA) in localizing generators of scalp-recorded potentials. The current study implemented sLORETA on pain event-related potentials, primarily aiming at validating this technique for pain research by identifying well-known pain-related regions. Subsequently, we pointed at investigating the still-debated and ambiguous topic of pain intensity coding at these regions, focusing on their relative impact on subjective pain perception. sLORETA revealed significant activations of the bilateral primary somatosensory (SI) and anterior cingulate cortices and of the contralateral operculoinsular and dorsolateral prefrontal (DLPFC) cortices (P < .05 for each). Activity of these regions, excluding DLPFC, correlated with subjective numerical pain scores (P < .05 for each). However, a multivariate regression analysis (R = .80; P = .024) distinguished the contralateral SI as the only region whose activation magnitude significantly predicted the subjective perception of noxious stimuli (P = .020), further substantiated by a reduced regression model (R = .75, P = .008). Based on (1) correspondence of the pain-activated regions identified by sLORETA with the acknowledged imaging-based pain-network and (2) the contralateral SI proving to be the most contributing region in pain intensity coding, we found sLORETA to be an appropriate tool for relevant pain research and further substantiated the role of SI in pain perception.


CONCLUSIONS
Because the literature of pain intensity coding offers inconsistent findings, the current article used a novel tool for revisiting this controversial issue. Results suggest that it is the activation magnitude of SI, which solely establishes the significant correlation with subjective pain ratings, in accordance with the classical clinical thinking, relating SI lesions to diminished perception of pain. Although this study cannot support a causal relation between SI activation magnitude and pain perception, such relation might be insinuated.
Nir
Rony-Reuven
RR
Laboratory of Clinical Neurophysiology, Department of Neurology, Rambam Health Care Campus, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Lev
Rina
R
Moont
Ruth
R
Granovsky
Yelena
Y
Sprecher
Elliot
E
Yarnitsky
David
D
D000293:Adolescent; D000328:Adult; D001921:Brain / Q000503:physiopathology; D001931:Brain Mapping / Q000379:methods; D002540:Cerebral Cortex / Q000503:physiopathology; D004569:Electroencephalography / Q000379:methods*; D055590:Electromagnetic Phenomena; D005071:Evoked Potentials / Q000502:physiology*; D005260:Female; D006179:Gyrus Cinguli / Q000503:physiopathology; D006801:Humans; D008297:Male; D009482:Neurophysiology; D010146:Pain / Q000503:physiopathology*; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold / Q000502:physiology; D017397:Prefrontal Cortex / Q000503:physiopathology; D012044:Regression Analysis; D013003:Somatosensory Cortex / Q000503:physiopathology*; D014054:Tomography; D055815:Young Adult