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Mild inflammation may modify mental state and behaviour making chronic pain harder to treat

PainSci » bibliography » Lasselin et al 2016
updated
Tags: pain, systemic inflammation, anxiety, neat, etiology, pro, physiological vulnerability, risks, mind

Two pages on PainSci cite Lasselin 2016: 1. Anxiety & Chronic Pain2. Chronic, Subtle, Systemic Inflammation

PainSci notes on Lasselin 2016:

Forty-one patients with chronic pain (at least six months, many much longer) were tested for signs of systemic inflammation. They all had stable medications, and no major complications. Then they were provided with two kinds of behavioural treatments for several weeks, measuring their progress in several ways.

Unfortunately, no one did well: “No substantial overall effect of behavioral treatment on pain intensity and pain-related variables was found in the present study.” So that’s a sad result for these behavioural therapies.

However, there is a scrap of backwards good news here: the patients with more inflammation “were more resistant to the improvement in pain intensity and in psychological variables contributing to pain.” Note that the mechanism of that effect is probably not that inflammation directly makes pain harder to treat, but actually modifies mental state and behaviour and that makes the pain harder to treat.

The authors believe that this data tentatively “suggests that the inflammatory state may be one of the mechanisms of the persisting behavioral alterations in patients who do not respond to treatment, corresponding to previous studies on treatment resistant depression.”

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

The purpose of the present pilot study was to explore the moderating role of basal inflammation on the effects of behavioral pain treatment in 41 patients with long-standing pain. Baseline pro-inflammatory status moderated behavioral treatment outcomes: higher pre-treatment levels of Tumor Necrosis Factor (TNF)-α and Interleukin (IL)-6 were related to less improvement in pain intensity, psychological inflexibility and in mental health-related quality of life. The treatment outcomes improved in the subgroup that had low levels of pro-inflammatory cytokines at baseline, while the subjects with higher pro-inflammatory status did not. Altogether, results indicate that low-grade inflammation may influence the behavioral treatment outcomes and provide a possible explanation of the heterogeneity in treatment response.

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