Brain Activation in Chronic Nonspecific Low Back Pain : A Systematic review and ALE Meta-analysis
Pain, a protective mechanism turns into a pathologic response when it becomes chronic. Recent evidences are pointing towards neuroplastic brain changes as the primary factor for the persisting pain in chronic nonspecific low back pain (cLBP). To summarise the previous fMRI studies, a coordinate-based ALE meta-analysis of resting functional brain imaging studies is carried out to identify the clusters activated in the brain in cLBP. Literature survey: PubMed, Scopus and Sleuth were searched for studies with resting functional whole-brain imaging in cLBP. Till October 2020; 258, 238, and 7 studies were found respectively after search. The activity pattern was documented in without stimulation and with stimulation groups. The risk of bias was assessed by Joanna Briggs Institute critical appraisal checklist for analytical cross-section studies. Total seven (224 cLBP patients, 110 activation foci) and six studies (106 cLBP patients, 66 activation foci) were selected among 277 studies for metanalysis in the without stimulation and with stimulation group respectively. In the without stimulation group 8 statistically significant clusters were found. The clusters are distributed in the prefrontal cortex, primary somatosensory cortex, and primary motor cortex, anterior cingulate cortex, insular cortex, putamen, claustrum, amygdala, and associated white matters in both hemispheres. On the other group, 3 statistically significant clusters were found in the frontal cortex, Parietal cortex, and Insula. In the with stimulation group, significant lateralization was observed and most of the clusters were in the right hemisphere. The white matter involvement was more in the with stimulation group (78.62% Vs 38.21%). The statistically significant clusters found in this study indicate a probable imbalance in GABAergic modulation of brain circuit and dysfunction in descending pain modulation system. This disparity in pain neuro-matrix is the source of spontaneous and persisting pain in cLBP.