Neither pain, nor depression exist as independent phenomena per se, they are highly subjective inner states, formed by our brain and built on the bases of our experiences, cognition and emotions. Chronic pain is associated with changes in brain physiology and anatomy. It has been suggested that the neuronal activity underlying subjective perception of chronic pain may be divergent from the activity associated with acute pain. We will discuss the possible common pathophysiological mechanism of chronic pain and depression with respect to the default mode network of the brain, neuroplasticity and the effect of antidepressants on these two pathological conditions. The default mode network of the brain has an important role in the representation of introspective mental activities and therefore can be considered as a nodal point, common for both chronic pain and depression. Neuroplasticity which involves molecular, cellular and synaptic processes modifying connectivity between neurons and neuronal circuits can also be affected by pathological states such as chronic pain or depression. We suppose that pathogenesis of depression and chronic pain shares common negative neuroplastic changes in the central nervous system (CNS). The positive impact of antidepressants would result in a reduction of these pathological cellular/molecular processes and in the amelioration of symptoms, but it may also increase survival times and quality of life of patients with chronic cancer pain.
Keywords: chronic pain, depression, antidepressants, default mode network, neuroplasticity, stress, cytokines
Citation: Nekovarova T, Yamamotova A, Vales K, Stuchlik A, Fricova J and Rokyta R (2014) Common mechanisms of pain and depression: are antidepressants also analgesics? Front. Behav. Neurosci. 8:99. doi: 10.3389/fnbeh.2014.00099
Received: 29 December 2013; Accepted: 09 March 2014;
Published online: 25 March 2014.
Edited by:Tomiki Sumiyoshi, National Center of Neurology and Psychiatry, Japan
Copyright © 2014 Nekovarova, Yamamotova, Vales, Stuchlik, Fricova and Rokyta. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Anna Yamamotova, Department of Normal, Pathological and Clinical Physiology, Third Faculty of Medicine, Charles University in Prague, Ke Karlovu 4, 120 00 Prague, Czech Republic e-mail: firstname.lastname@example.org