Background & Aims
Chronic nociception leads to brain reorganization in molecular and cellular level (1). Leads to Release of excitatory and inhibitory neurochemicals from glial cells, upregulation of ionotropic and metabolotropic receptors and the final outcomes are long term synaptic plasticity and central sensitization. These change reflected in altered functional connectivity (2,3). fMRI changes in previous studies denoted as, Increased activation in medial prefrontal cortex (medial PFC), cingulate cortex, amygdala and insula – both grey and white matter changes and decrease in grey matter volume in bilateral medial prefrontal cortex (mPFC) extending to the anterior cingulate cortex, the right mPFC extending to the orbitofrontal cortex(4,5).
Methods
Previous brain imaging studies in chronic nonspecific low back pain (cLBP) have been summarised in this meta-analysis. We carried out ALE based meta-analysis of resting functional brain imaging studies to identify the areas activated in cLBP patients. A total of 312 studies were selected after removing duplicates. Seventeen (553 cLBP patients, 192 activation foci) studies fulfilled the eligibility criteria and included in the ‘without stimulation’ group. Ten studies (353 cLBP patients, 125 activation foci) were selected in the’ with stimulation’ groups.
Results
Twelve statistically significant clusters are localized in the prefrontal cortex, primary somatosensory cortex, primary motor cortex, parietal cortex, anterior cingulate cortex, caudate, putamen, globus pallidus amygdala, occipital lobe, temporal lobe and associated white matter in “without stimulation’ group. Both the grey and white matter areas are activated. Statistically significant activation found in the both hemispheres and frontal, parietal, limbic, temporal, occipital, and sublobar regions . In ‘with Stimulation group’ seven statistically significant clusters were found in the frontal cortex, orbitofrontal cortex, premotor cortex, parietal cortex, claustrum and insula.
Conclusions
The statistically significant clusters indicate a probable imbalance in GABAergic modulation of brain circuits and dysfunction in the descending pain modulation system. This disparity in the pain neuro-matrix is the source of spontaneous and persisting pain in cLBP Descending pain modulation system should be the therapeutic target for management of cLBP.
References
1. Front Integr Neurosci. 2018;12:18, 2. Trends Neurosci. 2003 Dec;26(12):696–705, 3. J Pain Off J Am Pain Soc. 2009 Sep;10(9):895–926, 4. Semin Arthritis Rheum. 2015 Oct;45(2):229–37, 5. Clin J Pain. 2017 Nov;33(11):983–90