Abstract
Previous studies have identified altered brain changes in chronic pain patients, however, it remains unclear whether these changes are reversible. We summarized the neural and molecular changes in patients with chronic pain and employed a meta-analysis approach to quantify the changes. We included 75 studies and 11 of these 75 studies were included in the activation likelihood estimation (ALE) analysis. In the 62 functional magnetic resonance imaging (fMRI) studies, the primary somatosensory and motor cortex (SI and MI), thalamus, insula, and anterior cingulate cortex (ACC) showed significantly decreased activity after the treatments compared to baseline. In the 13 positron emission tomography (PET) studies, the SI, MI, thalamus, and insula showed significantly increased glucose uptake, blood flow, and opioid-receptor binding potentials after the treatments compared to baseline. A meta-analysis of fMRI studies in patients with chronic pain, during pain-related tasks, showed a significant deactivation likelihood cluster in the left medial posterior thalamus. Further studies are warranted to understand brain reorganization in patients with chronic pain compared to the normal state, in terms of its relationship with symptom reduction and baseline conditions.
Highlights
Pain is a highly complex and individual experience, which elicits behavioral, chemical, and neuronal responses throughout the body
A reduced threshold and excessive responsiveness to pain in the nociceptive pathway is known as central sensitization, which is a type of brain reorganization caused by neural plasticity, which leads to increased pain sensitivity in chronic pain patients (Latremoliere and Woolf, 2009; Woolf, 2011)
We found a tendency of decreased functional activities and increased molecular activities in the sensory-discriminative and affective regions after the treatments than before the treatments of chronic pain, while other regions involved in reward and cognitive processes yielded inconsistent results across the studies
Summary
Pain is a highly complex and individual experience (https://www.iasp-pain.org/), which elicits behavioral, chemical, and neuronal responses throughout the body. A significant number of studies have identified brain regions involved in the processing of acute and chronic pain, using functional neuroimaging techniques They found an important role of the descending pain modulatory system, emotional circuitry, and learning, as well as anatomical and functional discrepancies in pain experience between healthy individuals and patients with chronic pain (Apkarian et al, 2005; Tracey and Mantyh, 2007; Henry et al, 2011; Bushnell et al, 2013). To summarize the body of evidence on the functional changes in patients with chronic pain, as compared to healthy participants, previous studies performed a meta-analysis using coordinate-based methods [e.g., activation likelihood estimation (ALE)]. Chronic pain is rather a complex experience which can alter many other functional networks such as corticolimbic (Baliki et al, 2012; Mansour et al, 2013), salience (Qiu et al, 2015), somatosensorymotor, and default mode networks (Baliki et al, 2008a, 2014; Becerra et al, 2014), as well as cross-network connectivity between the networks (Hemington et al, 2016; Cottam et al, 2018)
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