The role of the brain in chronic pain conditions remains speculative. We compared brain morphology of 26 chronic back pain (CBP) patients to matched control subjects, using magnetic resonance imaging brain scan data and automated analysis techniques. CBP patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Pain-related characteristics were correlated to morphometric measures. Neocortical gray matter volume was compared after skull normalization. Patients with CBP showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10-20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3 loss of gray matter for every year of chronic pain. Regional gray matter density in 17 CBP patients was compared with matched controls using voxel-based morphometry and nonparametric statistics. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic CBP. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.
"The Human Brain in Chronic Pain: Anatomy Approximately 10 years ago, we discovered regional anatomical brain abnormalities that correlated with intensity and duration in patients with chronic back pain (CBP) (Apkarian et al., 2004). This initial observation is now replicated across many clinical pain conditions that primarily show regional decreases in gray matter density, although there is also some evidence for increased density in a subset of pain populations as well (May, 2008; see recent meta-analyses: Cauda et al., 2014; Smallwood et al., 2013). "
"Anatomical and physiological evidence supports its role in pain perception (Devoize et al., 2011). The modulatory function of the PFC in pain is further illustrated by its role in placebo analgesia, and it has been reported that the PFC undergoes anatomical and functional reorganization during chronic pain conditions (Apkarian et al., 2004; Metz et al., 2009). Indeed, neural imaging studies in humans demonstrated enhanced neural activities (BOLD signal) in the PFC in chronic pain states (Apkarian et al., 2005; Moisset and Bouhassira , 2007), and in an arthritis model of persistent pain, deactivation of the PFC through increased inputs from the basal lateral amygdala has been reported (Ji and Neugebauer, 2011; Ji et al., 2010). "
"Morphometric magnetic resonance imaging (MRI) demonstrated gray matter atrophy in the dorsolateral PFC (Apkarian et al., 2004a). Functional MRI showed that, in chronic pain patients, experimental noxious stimuli cause decreased activity in brain regions identified for acute pain (Peyron et al., 2000; Apkarian et al., 2005) and increased activity in regions that are not part of the spinothalamic pathway, mainly the PFC and related subcortical structures (Apkarian et al., 2005). "
[Show abstract][Hide abstract] ABSTRACT: Previous reports documented abnormalities in cognitive functions and decision-making (DM) in patients with chronic pain, but these changes are not consistent across studies. Reasons for these discordant findings might include the presence of confounders, variability in chronic pain conditions, and the use of different cognitive tests. The present study was aimed to add evidence in this field, by exploring the cognitive profile of a specific type of chronic pain, i.e., chronic low back pain (cLBP). Twenty four cLBP patients and 24 healthy controls underwent a neuropsychological battery and we focused on emotional DM abilities by means of Iowa gambling task (IGT). During IGT, behavioral responses and the electroencephalogram (EEG) were recorded in 12 patients and 12 controls. Event-related potentials (ERPs) were averaged oﬄine from EEG epochs locked to the feedback presentation (4000 ms duration, from 2000 ms before to 2000 ms after the feedback onset) separately for wins and losses and the feedback-related negativity (FRN) and P300 peak-to-peak amplitudes were calculated. Among cognitive measures, cLBP patients scored lower than controls in the modified card sorting test (MCST) and the score in this test was significantly influenced by pain duration and intensity. Behavioral IGT results documented worse performance and the absence of a learning process during the test in cLBP patients compared to controls, with no effect of pain characteristics. ERPs findings documented abnormal feedback processing in patients during IGT. cLBP patients showed poor performance in the MCST and the IGT. Abnormal feedback processing may be secondary to impingement of chronic pain in brain areas involved in DM or suggest the presence of a predisposing factor related to pain chronification. These abnormalities might contribute to the impairment in the work and family settings that often cLBP patients report.
Frontiers in Psychology 11/2014; 5. DOI:10.3389/fpsyg.2014.01350 · 2.80 Impact Factor
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