In response to recent publications from pain neuroimaging experiments, there has been a debate about the existence of a primary pain region in the brain. Yet, there are few meta-analyses providing assessments of the minimum cerebral denominators of pain. Here, we used a statistical meta-analysis method, called activation likelihood estimation, to define (1) core brain regions activated by pain per se, irrelevant of pain modality, paradigm, or participants and (2) activation likelihood estimation commonalities and differences between patients with chronic pain and healthy individuals. A subtraction analysis of 138 independent data sets revealed that the minimum denominator for activation across pain modalities and paradigms included the right insula, secondary sensory cortex, and right anterior cingulate cortex (ACC). Common activations for healthy subjects and patients with pain alike included the thalamus, ACC, insula, and cerebellum. A comparative analysis revealed that healthy individuals were more likely to activate the cingulum, thalamus, and insula. Our results point toward the central role of the insular cortex and ACC in pain processing, irrelevant of modality, body part, or clinical experience; thus, furthering the importance of ACC and insular activation as key regions for the human experience of pain.
Supplemental Digital Content is Available in the Text.The minimum denominators of pain processing in the human brain were explored by means of activation likelihood estimation, suggesting that the insula and ACC are essential for the experience of pain.
aDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
bClinic of Diagnostic and Interventional Neuroradiology, RWTH Aachen University, Aachen, Germany
cMonell Chemical Senses Center, University of Pennsylvania, Philadelphia, PA, USA
dCogNAC, Department of Anatomy, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada
eCÉAMS, Research Center, Sacré-Coeur Hospital, Montréal, QC, Canada
fDepartment of Psychology, University of Pennsylvania, Philadelphia, PA, USA
Corresponding author. Address: Department of Clinical Neuroscience, Karolinska Institutet, Nobels väg 9, D3, 17176 Stockholm, Sweden. Tel.: +46702130811; fax: +468311101. E-mail address: email@example.com (K. B. Jensen).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
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Received October 06, 2015
Received in revised form January 03, 2016
Accepted January 25, 2016