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      Objective Pain Assessment: a Key for the Management of Chronic Pain

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          Abstract

          The individual and social burdens associated with chronic pain have been escalating globally. Accurate pain measurement facilitates early diagnosis, disease progression monitoring and therapeutic efficacy evaluation, thus is a key for the management of chronic pain. Although the “golden standards” of pain measurement are self-reported scales in clinical practice, the reliability of these subjective methods could be easily affected by patients’ physiological and psychological status, as well as the assessors’ predispositions. Therefore, objective pain assessment has attracted substantial attention recently. Previous studies of functional magnetic resonance imaging (fMRI) revealed that certain cortices and subcortical areas are commonly activated in subjects suffering from pain. Dynamic pain connectome analysis also found various alterations of neural network connectivity that are correlated with the severity of clinical pain symptoms. Electroencephalograph (EEG) demonstrated suppressed spontaneous oscillations during pain experience. Spectral power and coherence analysis of EEG also identified signatures of different types of chronic pain. Furthermore, fMRI and EEG can visualize objective brain activities modulated by analgesics in a mechanism-based way, thus bridge the gaps between animal studies and clinical trials. Using fMRI and EEG, researchers are able to predict therapeutic efficacy and identify personalized optimal first-line regimens. In the future, the emergence of magnetic resonance spectroscopy and cell labelling in MRI would encourage the investigation on metabolic and cellular pain biomarkers. The incorporation of machine learning algorithms with neuroimaging or behavior analysis could further enhance the specificity and accuracy of objective pain assessments.

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          Most cited references34

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          Theoretical perspectives on the relation between catastrophizing and pain.

          The tendency to "catastrophize" during painful stimulation contributes to more intense pain experience and increased emotional distress. Catastrophizing has been broadly conceived as an exaggerated negative "mental set" brought to bear during painful experiences. Although findings have been consistent in showing a relation between catastrophizing and pain, research in this area has proceeded in the relative absence of a guiding theoretical framework. This article reviews the literature on the relation between catastrophizing and pain and examines the relative strengths and limitations of different theoretical models that could be advanced to account for the pattern of available findings. The article evaluates the explanatory power of a schema activation model, an appraisal model, an attention model, and a communal coping model of pain perception. It is suggested that catastrophizing might best be viewed from the perspective of hierarchical levels of analysis, where social factors and social goals may play a role in the development and maintenance of catastrophizing, whereas appraisal-related processes may point to the mechanisms that link catastrophizing to pain experience. Directions for future research are suggested.
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            Network dysfunction after traumatic brain injury.

            Diffuse axonal injury after traumatic brain injury (TBI) produces neurological impairment by disconnecting brain networks. This structural damage can be mapped using diffusion MRI, and its functional effects can be investigated in large-scale intrinsic connectivity networks (ICNs). Here, we review evidence that TBI substantially disrupts ICN function, and that this disruption predicts cognitive impairment. We focus on two ICNs--the salience network and the default mode network. The activity of these ICNs is normally tightly coupled, which is important for attentional control. Damage to the structural connectivity of these networks produces predictable abnormalities of network function and cognitive control. For example, the brain normally shows a 'small-world architecture' that is optimized for information processing, but TBI shifts network function away from this organization. The effects of TBI on network function are likely to be complex, and we discuss how advanced approaches to modelling brain dynamics can provide insights into the network dysfunction. We highlight how structural network damage caused by axonal injury might interact with neuroinflammation and neurodegeneration in the pathogenesis of Alzheimer disease and chronic traumatic encephalopathy, which are late complications of TBI. Finally, we discuss how network-level diagnostics could inform diagnosis, prognosis and treatment development following TBI.
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              Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized by magnetoencephalography.

              Spontaneous magnetoencephalographic activity was recorded in awake, healthy human controls and in patients suffering from neurogenic pain, tinnitus, Parkinson's disease, or depression. Compared with controls, patients showed increased low-frequency theta rhythmicity, in conjunction with a widespread and marked increase of coherence among high- and low-frequency oscillations. These data indicate the presence of a thalamocortical dysrhythmia, which we propose is responsible for all the above mentioned conditions. This coherent theta activity, the result of a resonant interaction between thalamus and cortex, is due to the generation of low-threshold calcium spike bursts by thalamic cells. The presence of these bursts is directly related to thalamic cell hyperpolarization, brought about by either excess inhibition or disfacilitation. The emergence of positive clinical symptoms is viewed as resulting from ectopic gamma-band activation, which we refer to as the "edge effect." This effect is observable as increased coherence between low- and high-frequency oscillations, probably resulting from inhibitory asymmetry between high- and low-frequency thalamocortical modules at the cortical level.
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                Author and article information

                Contributors
                Role: Data CurationRole: InvestigationRole: MethodologyRole: Writing – Original Draft Preparation
                Role: ResourcesRole: SupervisionRole: Writing – Review & Editing
                Journal
                F1000Res
                F1000Res
                F1000Research
                F1000Research
                F1000 Research Limited (London, UK )
                2046-1402
                23 January 2020
                2020
                : 9
                : F1000 Faculty Rev-35
                Affiliations
                [1 ]Department of Anesthesiology, Chinese Academy of Medical Sciences & Peking Union Medical College Hospital, Beijing, China
                Author notes

                No competing interests were disclosed.

                Author information
                https://orcid.org/0000-0003-0243-9271
                Article
                10.12688/f1000research.20441.1
                6979466
                f5a55f26-ea4e-4d9e-8f9f-6ce4c56660ea
                Copyright: © 2020 Xu X and Huang Y

                This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 January 2020
                Funding
                The author(s) declared that no grants were involved in supporting this work.
                Categories
                Review
                Articles

                chronic pain,objective assessment,functional magnetic resonance imaging,electroencephalography

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