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Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. Journal of Neuroscience, 24, 10410-10415

Department of Physiology and Institute of Neuroscience, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience (Impact Factor: 6.75). 12/2004; 24(46):10410-5. DOI: 10.1523/JNEUROSCI.2541-04.2004
Source: PubMed

ABSTRACT 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.

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    • "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). "
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    • "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). "
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    • "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). "
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