The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort

TLDR

Chronic pain patients frequently have comorbid depression, yet the influence of depressive symptoms on pain processing is not fully understood. This study investigated how depressive symptoms and major depressive disorder affect pain processing in fibromyalgia patients. Researchers compared quantitative sensory testing and fMRI responses to painful pressure stimuli with depression symptom severity and MDD status in these patients. Depression was not associated with sensory pain measures but was linked to heightened affective pain‑related brain activity, suggesting distinct neural pathways for sensory and affective pain and implying that treating depression may not reduce sensory pain intensity.

Abstract

Abstract Objective Individuals with chronic pain frequently display comorbid depression, but the impact of symptoms of depression on pain processing is not completely understood. This study evaluated the effect of symptoms of depression and/or clinically diagnosed major depressive disorder (MDD) on pain processing in patients with fibromyalgia (FM). Methods Results of quantitative sensory testing and neural responses to equally painful pressure stimuli (measured by functional magnetic resonance imaging [fMRI]) were compared with the levels of symptoms of depression and comorbid MDD among patients with FM. Results Neither the level of symptoms of depression nor the presence of comorbid MDD was associated with the results of sensory testing or the magnitude of neuronal activation in brain areas associated with the sensory dimension of pain (primary and secondary somatosensory cortices). However, symptoms of depression and the presence of MDD were associated with the magnitude of pain‐evoked neuronal activations in brain regions associated with affective pain processing (the amygdalae and contralateral anterior insula). Clinical pain intensity was associated with measures of both the sensory dimension of pain (results of sensory testing) and the affective dimension of pain (activations in the insula bilaterally, contralateral anterior cingulate cortex, and prefrontal cortex). Conclusion In patients with FM, neither the extent of depression nor the presence of comorbid major depression modulates the sensory‐discriminative aspects of pain processing (i.e., localizing pain and reporting its level of intensity), as measured by sensory testing or fMRI. However, depression is associated with the magnitude of neuronal activation in brain regions that process the affective‐motivational dimension of pain. These data suggest that there are parallel, somewhat independent neural pain‐processing networks for sensory and affective pain elements. The implication for treatment is that addressing an individual's depression (e.g., by prescribing an antidepressant medication that has no analgesic properties) will not necessarily have an impact on the sensory dimension of pain.