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Background: Early evidence suggests human assumed central sensitization (HACS) is present in some people with acute low back pain (LBP). Factors influencing individual variation in HACS during acute LBP have not been fully explored. We aimed to examine the evidence for HACS in acute LBP and the contribution of brain-derived neurotrophic factor (BDNF), clinical, psychological and demographic factors to HACS., Methods: Participants with acute LBP (<6 weeks after pain onset, N = 118) and pain-free controls (N = 57) from a longitudinal trial were included. Quantitative sensory testing including pressure and heat pain thresholds and conditioned pain modulation, BDNF serum concentration and genotype and questionnaires were assessed., Results: There were no signs of HACS during acute LBP at group level when compared with controls. Sensory measures did not differ when compared between controls and LBP participants with different BDNF genotypes. Two LBP subgroups with distinct sensory profiles were identified. Although one subgroup (N = 60) demonstrated features of HACS including pressure/heat pain hypersensitivity at a remote site and deficient conditioned pain modulation, pain severity and disability did not differ between the two subgroups. Variation in sensory measures (~33%) was partially explained by BDNF genotype, sex, age and psychological factors., Conclusions: This study confirms that HACS is present in some people with acute LBP, but this was not associated with pain or disability. Further, no relationship was observed between BDNF and HACS in acute LBP. More research is needed to understand factors contributing to individual variation in sensory measures in LBP., Significance: Human assumed central sensitization (HACS) is present in acute low back pain (LBP) but factors contributing to individual variation are not fully explored. This study investigated the relationship between factors such as brain derived neurotrophic factor (BDNF) and HACS in acute LBP. Our findings indicate that HACS was present in specific LBP subgroups but BDNF was unrelated to HACS. Combinations of BDNF genotype, demographic and psychological factors explained a small proportion of the variation in sensory measures during acute LBP., (© 2022 European Pain Federation - EFIC ®.)

Acute muscle pain has both motor and sensory consequences, yet the effect of muscle pain on the primary sensory (S1) and motor (M1) cortices has yet to be systematically evaluated. Here we aimed to determine the strength of the evidence for (1) altered activation of S1/M1 during and after pain, (2) the temporal profile of any change in activation and (3) the relationship between S1/M1 activity and the symptoms of pain. In September 2015, five electronic databases were systematically searched for neuroimaging and electrophysiological studies investigating the effect of acute experimental muscle pain on S1/M1 in healthy volunteers. Demographic data, methodological characteristics and primary outcomes for each study were extracted for critical appraisal. Meta-analyses were performed where appropriate. Twenty-five studies satisfied the inclusion criteria. There was consistent evidence from fMRI for increased S1 activation in the contralateral hemisphere during pain, but insufficient evidence to determine the effect at M1. Meta-analyses of TMS and EEG data revealed moderate to strong evidence of reduced S1 and corticomotor excitability during and following the resolution of muscle pain. A comprehensive understanding of the temporal profile of altered activity in S1/M1, and the relationship to symptoms of pain, is hampered by differences in methodological design, pain modality and pain severity between studies. Overall, the findings of this review indicate reduced S1 and corticomotor activity during and after resolution of acute muscle pain, mechanisms that could plausibly underpin altered sensorimotor function in pain. WHAT DOES THIS REVIEW ADD?: We provide the first systematic evaluation of the primary sensory (S1) and motor (M1) cortex response to acute experimental muscle pain in healthy volunteers. We present evidence from a range of methodologies to provide a comprehensive understanding of the effect of pain on S1/M1. Through meta-analyses we evaluate the strength of evidence concerning the direction and temporal profile of the S1/M1 response to acute muscle pain., (© 2016 European Pain Federation - EFIC®)

Background: Lateral epicondylalgia (LE) is a musculotendinous condition characterized by persistent pain, sensorimotor dysfunction and motor cortex reorganization. Although there is evidence linking cortical reorganization with clinical symptoms in LE, the mechanisms underpinning these changes are unknown. Here we investigated activity in motor cortical (M1) intracortical inhibitory and facilitatory networks in individuals with chronic LE and healthy controls., Methods: Surface electromyography was recorded bilaterally from the extensor carpi radialis brevis (ECRB) muscle of 14 LE (4 men, 41.5 ± 9.9 years) and 14 control participants (4 men, 42.1 ± 11.1 years). Transcranial magnetic stimulation of M1 was used to evaluate resting and active motor threshold, corticomotor output, short- (SICI) and long-latency intracortical inhibition (LICI) and intracortical facilitation (ICF) of both hemispheres., Results: In individuals with LE, SICI (p = 0.005), ICF (p = 0.026) and LICI (p = 0.046) were less in the M1 contralateral to the affected ECRB muscle compared with healthy controls. Motor cortical threshold (rest: p = 0.57, active: p = 0.97) and corticomotor output (p = 0.15) were similar between groups. No differences were observed between individuals with LE and healthy controls for the M1 contralateral to the unaffected ECRB muscle., Conclusions: These data provide evidence of less intracortical inhibition mediated by both GABAA and GABAB receptors, and less intracortical facilitation in the M1 contralateral to the affected ECRB in individuals with LE compared with healthy controls. Similar changes were not present in the M1 contralateral to the unaffected ECRB. These changes may provide the substrate for M1 reorganization in chronic LE and could provide a target for future therapy., What Does This Study Add: Lateral epicondylalgia (LE) is a common musculoskeletal condition characterized by elbow pain and sensorimotor dysfunction. The excitability and organization of the motor cortical representation of the wrist extensor muscles is altered in LE, but the mechanisms that underpin these changes are unknown. evidence of less intracortical inhibition mediated by both GABAA and GABAB receptors, and less intracortical facilitation mediated by NMDA receptors, in the M1 contralateral to the affected extensor carpi radialis brevis muscle in chronic LE compared with healthy controls. Altered activity in intracortical networks may contribute to altered motor cortex organization in LE and could provide a potential target for future treatments., (© 2016 European Pain Federation - EFIC®)