Overlapping Chronic Pain and Depression: Pathophysiology and Management

Depression and chronic pain commonly coexist. Several biological hypotheses regarding pathophysiology of this phenomenon have been proposed. The role of activation of pro-inflammatory cytokines and abnormal glutamatergic neurotransmission has been widely studied in this context. Malfunction of descending 5-HT and nucleus accumbens (NAc) as well as dopaminergic neurons may also explain overlapping pathophysiology for pain and depression. Data from neuroimaging studies showed alterations in regions involved in pain perception and structures considered as a neural basis of depression. These regions include the anterior cingulate cortex (ACC), insular cortex (IC), amygdala, NAc, and prefrontal cortex. Besides their efficiency in depression, antidepressive drugs are also effective in the management of chronic pain. The usefulness of tricyclic antidepressants and serotonin-noradrenaline reuptake inhibitors (SNRIs) in neuropathic pain and functional somatic syndromes (fibromyalgia and irritable bowel syndrome) has been convincingly documented, whereas the superiority of antidepressants from different classes in treatment of painful physical symptoms (PPS) in depression is still a matter of debate.