No evidence for accelerated brain aging in patients with chronic non-cancer pain

Abstract

Chronic pain is often associated with changes in brain structure and function, and also cognitive deficits. It has been noted that these chronic pain-related alterations may resemble changes found in healthy aging, and thus may represent accelerated or pre-mature aging of the brain. Here we test the hypothesis that patients with chronic non-cancer pain demonstrate accelerated brain aging compared to healthy control subjects. The predicted brain age of 59 patients with chronic pain (mean chronological age {+/-} standard deviation: 53.0 {+/-} 9.0 years; 43 women) and 60 pain-free healthy controls (52.6 {+/-} 9.0 years; 44 women) was determined using the software brainageR. This software segments the individual T1-weighted structural MR images into gray and white matter and compares gray and white matter images to a large (n = 2001) training set of structural images, using machine learning. Finally, brain age delta, which is the predicted brain age minus chronological age, was calculated and compared across groups. This study provided no evidence for the hypothesis that chronic pain is associated with accelerated brain aging (Welchs t-test, p = 0.74, Cohens d = 0.061). A Bayesian independent samples t-test indicated moderate evidence in favor of the null hypothesis (BF01 = 4.875, i.e. group means were equal). Our results provide indirect support for recent models of pain related-changes of brain structure, brain function, and cognitive functions. These models postulate network-specific maladaptive plasticity, rather than wide-spread or global neural degeneration, leading to synaptic, dendritic, and neuronal remodeling.