what is the link between pain and depression? Frontiers in Behavioral Neuroscience. March 2014


What is the link between depression and pain? Patients with depression often experience unexplained painful somatic symptoms. Depression can reduce the pain threshold and sensitise pain perception. Chronic pain may lead to an altered emotional state and finally to depression. What is the neurobiology that link these experiences ?

Tereza Nekovarova et al explore this question in this article in the hypothesis  and theory section of the journal.

Pain experience is dependent on interaction between different elements that form the  “pain neuromatrix“. This matrix  is an integration of sensory, interoceptive, affective, and cognitive components. State of attention, anxiety, expectation, previous experience, learning, personality traits and cultural effects play their role in this.

In depression, it is considered that ‘default mode network’  ( consists of a set of regions in the cerebral cortex), which is important in the representation of a person’s mental state ( “internal mentation” and  “self-referential thoughts) is at fault. This is behind the increased self-focus in depression.It is also thought that abnormal default mode network connectivity might persist even after recovery.The default mode network functionally dissociates into two subsystems—connectivity in the posterior sub-network is normalized after antidepressant treat ment, whereas abnormal connectivity in the anterior sub-network persist. This might form the neural depressive scar and may become useful in predicting relapse.

Prolonged experience with chronic pain represents a form of emotional learning and this is accompanied by circuit shifting i.e.  from sensory to hedonic neuronal circuits . It is thought that the structural impairments that accompany chronic pain can also influence functions of the default mode network.Alterations of the default mode system, in chronic- pain patients, might influence brain mechanisms responsible for processing information unrelated to pain.

Authors argue that ‘default mode network’ could represent a nodal point that is common for both chronic pain and depression.

Stress  induces the release of glucocorticoids  that significantly impact hippocampal functions with the potential to enhance or suppress neuroplastic processes. Stress also leads to a reduction in brain derived neurotrophic factor (BDNF) in the hippocampus and increases it in the amygdala. Alterations in neurobiological properties  can result in faulty communication between the hippocampus, amygdala and cortex, which gives rise to disturbed processes of emotionality. Neurotrophins  can act as a pathogenic pain mediator and are known to be increased in several painful conditions.

Increased production of proinflammatory cytokines has repeatedly been described in depressive patients.Two individual studies (Müller et al., 2006; Nery et al., 2008) and one meta-analysis (Na et al., 2014) have shown that adjunctive celecoxib combined with antidepressants produced a rapid-onset antidepressant effect and was more effective than placebo combined with antidepressants. Antidepressants are shown to have nociceptive properties. for e.g.; fluoxetine  has anti-inflammatory properties. Depressed patients treated with antidepressants have shown to undergo a normalization of immune parameters. some studies suggest increase in longevity among cancer patients when treated with antidepressants.

Conclusion: Depression and chronic pain produce common negative neuroplastic changes in the 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.

Summary of the article

Common mechanisms of pain and depression: are antidepressants also analgesics? Tereza Nekovarova, Anna Yamamotova, Karel Vales, Ales Stuchlik, Jitka Fricova and Richard Rokyta. published: 25 March 2014 .Frontiers in Behavioral Neuroscience .

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