Shifting brain circuits in pain chronicity

Abstract

The evaluation of brain changes to a specific pain condition in pediatric and adult patients allows for insights into potential mechanisms of pain chronicity and possibly long‐term brain changes. Here we focused on the primary somatosensory system (SS) involved in pain processing, namely the ventroposterolateral thalamus (VPL) and the primary somatosensory cortex (SI). We evaluated, using MRI, three specific processes: (a) somatotopy of changes in the SS for different pain origins (viz., foot vs. arm); (b) differences in acute (ankle sprain versus complex regional pain syndrome‐CRPS); and (c) differences of the effects of CRPS on SS in pediatric versus adult patients. In all cases, age‐ and sex‐matched individuals were used as controls. Our results suggest a shift in concurrent gray matter density (GMD) and resting functional connectivity strengths (rFC) across pediatric and adult CRPS with (a) differential patterns of GMD (VPL) and rFC (SI) on SS in pediatric vs. adult patterns that are consistent with upper and lower limb somatotopical organization; and (b) widespread GMD alterations in pediatric CRPS from sensory, emotional and descending modulatory processes to more confined sensory‐emotional changes in adult CRPS and rFC patterns from sensory‐sensory alterations in pediatric populations to a sensory‐emotional change in adult populations. These results support the idea that pediatric and adult CRPS are differentially represented and may reflect underlying differences in pain chronification across age groups that may contribute to the well‐known differences between child and adult pain vulnerability and resilience.

Biological and behavioral markers of pain following nerve injury in humans

“…This is supported by extracted features that show how inflammatory molecules relating to cell cycle and the stress response (Rosati et al, 2011) as well as brain regions implicated in sensory integration (superior longitudinal fasciculus (Herbet et al, 2018)) and the adaptation to chronic stressors such as pain (Caudate (Wunderlich et al, 2011)) were the highest correlated in the ankle injury cohort. Moreover, recently published work from our lab has shown that regions such as the inferior temporal gyrus and orbitofrontal cortex had a similar increase in acute neuropathic pain patients (Youssef et al, 2019). These same regions were found to further increase in chronic pain patients suggesting a potential for regions identified in this investigation to be implicated in the development of chronic pain.…”

Adaptive body awareness predicts fewer central sensitization‐related symptoms and explains relationship between central sensitization‐related symptoms and pain intensity: A cross‐sectional study among individuals with chronic pain

“…2 Neuroscience research suggests injuries and/or inflammatory processes may trigger change in pain processing in the peripheral and central nervous system (CNS), which is thought to contribute to the development and maintenance of chronic pain. [3][4][5][6][7] One proposed mechanism of the alterations in central pain processing is central sensitization (CS) defined as the amplification of neural signaling within the CNS that elicits pain hypersensitivity. [8][9][10] CS is thought be a predominant characteristic of fibromyalgia, chronic fatigue, irritable bowel syndrome, and chronic whiplash disorders.…”

A multistudy analysis reveals that evoked pain intensity representation is distributed across brain systems

“…This study assumes that there is a common configuration of brain activity that corresponds to pain representation, that it can be measured using BOLD fMRI, and that incremental reconfigurations of this activity correspond to proportional changes in subjective experience. However, distinct representations have been demonstrated for different types of pain including somatosensory and vicarious pain [ 45 ] and different kinds of clinical pain [ 46 , 47 ]. Further, BOLD fMRI is best at measuring the anatomical configuration of responses [ 48 ], but the absolute magnitude of evoked activity also encodes pain information [ 26 ].…”