Relation Between Abnormal Spontaneous Brain Activity and Altered Neuromuscular Activation of Lumbar Paraspinal Muscles in Chronic Low Back Pain

Abstract

ObjectiveTo investigate the neural mechanism underlying functional reorganization and motor coordination strategies in patients with chronic low back pain (cLBP). DesignA case-control study based on data collected during routine clinical practice. SettingThis study was conducted at a university hospital. ParticipantsFifteen patients with cLBP and 15 healthy controls. InterventionsNot applicable. Main Outcome MeasuresWhole brain blood oxygen level-dependent signals were measured using functional magnetic resonance imaging and amplitude of low-frequency fluctuation (ALFF) method to identify pain-induced changes in regional spontaneous brain activity. A novel approach based on the surface electromyogram (EMG) system and fine-wire electrodes was used to record EMG signals in the deep multifidus, superficial multifidus, and erector spinae. ResultsIn cLBP, compared with healthy groups, ALFF was higher in the medial prefrontal, primary somatosensory, primary motor, and inferior temporal cortices, whereas it was lower in the cerebellum and anterior cingulate and posterior cingulate cortices. Furthermore, the decrease in the average EMG activity of the 3 lumbar muscles in the cLBP group was positively correlated with the ALFF values of the primary somatosensory cortex, motor cortex, precuneus, and middle temporal cortex but significantly negatively correlated with the ALFF values of the medial prefrontal and inferior temporal cortices. Interestingly, the correlation between the functional activity in the cerebellum and the EMG activity varied in the lumbar muscles. ConclusionsThese findings suggest a functional association between changes in spontaneous brain activity and altered voluntary neuromuscular activation patterns of the lumbar paraspinal muscles, providing new insights into the mechanisms underlying pain chronicity as well as important implications for developing novel therapeutic targets of cLBP.