Brain activations during pain

Abstract

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.

Mental Health Comorbidities in Pediatric Chronic Pain: A Narrative Review of Epidemiology, Models, Neurobiological Mechanisms and Treatment

“…Therefore, it would appear that as an individual transitions from an acute to chronic pain state, activations within the brain move from primarily somatosensory regions to limbic regions, indicating a shift from primarily physical to emotional neural processing. These findings were recently corroborated by Jensen et al [153]. Using an activation likelihood estimate to analyze 138 independent data sets, they demonstrated that chronic pain patients were less likely to activate key nociceptive regions compared to healthy controls [153].…”

Cortical plasticity between the pain and pain-free phases in patients with episodic tension-type headache

“…The S1 is responsible for detecting the presence and magnitude of a pain stimulus and is involved in pain perception [27]. The ACC participates in the emotional-motivational aspect of pain [29]. Often working together with the ACC, the anterior insula is proposed to involve in the integration of polymodal sensory information as well as the integration of emotional and cognitive processes [29, 30].…”

“…Often working together with the ACC, the anterior insula is proposed to involve in the integration of polymodal sensory information as well as the integration of emotional and cognitive processes [29, 30]. A recent neuroimaging meta-analysis revealed common activations during pain for healthy subjects and patients with chronic pain in the ACC and the anterior insula regardless of modality, body part, or clinical experience [29]. This finding further supported the central role of the ACC and the anterior insula in human pain processing [29].…”

“…A recent neuroimaging meta-analysis revealed common activations during pain for healthy subjects and patients with chronic pain in the ACC and the anterior insula regardless of modality, body part, or clinical experience [29]. This finding further supported the central role of the ACC and the anterior insula in human pain processing [29]. Painful stimulation during the pain phase in ETTH patients contribute to these brain functional changes, which could further lead to the structural reorganization observed in our study.…”

Cortical Sensorimotor Processing of Painful Pressure in Patients with Chronic Lower Back Pain—An Optical Neuroimaging Study using fNIRS

“…However, the findings regarding maladaptive alterations in patients with CLBP are ambiguous. Some reports show decreased cortical activity in patients with CLBP during pain processing in regions such as the thalamus, S1, S2 and ACC (Peyron et al, 2000; Apkarian et al, 2005; Jensen et al, 2016). Others have found augmented cortical activity compared to healthy controls (HC) in S1, S2, cerebellum and parietal cortices (Giesecke et al, 2004) or the right insula, supplementary motor area (SMA) and posterior cingulate cortex (PCC; Kobayashi et al, 2009) after painful stimulation.…”