Chronic back pain is associated with decreased prefrontal and thalamic gray matter density

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: 6.34). 12/2004; 24(46):10410-5. DOI: 10.1523/JNEUROSCI.2541-04.2004
Source: PubMed


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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    • "However, the risk of chronic pain increases to nearly 50% with thoracotomies and amputations (Kehlet et al., 2006). As pain progresses from an acute origin, as from an injury or surgery, to a chronic condition, negative emotional states associated with chronic pain not only exacerbate physiological pain sensitivity (Borsook et al., 2013) but may also increase the incidence of comorbidities like depression, anxiety, anhedonia (e.g., the inability to experience pleasure), sleep disturbance, decision-making abnormalities, and even risk for suicide (Apkarian et al., 2004). In spite of its prevalence and impact on patients' lives and on society, chronic pain and comorbid affective disorders are still poorly managed and current therapies are often inadequate (Backonja et al., 2006, Finnerup et al., 2010). "
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    ABSTRACT: Chronic pain is an important public health problem that negatively impacts quality of life of affected individuals and exacts enormous socio-economic costs. Chronic pain is often accompanied by comorbid emotional disorders including anxiety, depression and possibly anhedonia. The neural circuits underlying the intersection of pain and pleasure are not well understood. We summarize recent human and animal investigations demonstrating that aversive aspects of pain are encoded in brain regions overlapping with areas processing reward and motivation. We highlight findings revealing anatomical and functional alterations of reward/motivation circuits in chronic pain. Finally, we review supporting evidence for the concept that pain relief is rewarding and activates brain reward/motivation circuits. Adaptations in brain reward circuits may be fundamental to the pathology of chronic pain. Knowledge of brain reward processing in the context of pain could lead to the development of new therapeutics for the treatment of emotional aspects of pain and comorbid conditions. This article is protected by copyright. All rights reserved.
    Full-text · Article · Jan 2016 · The Journal of Comparative Neurology
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    • "Prefrontal cortices, as DLPFC, processes attentional and memory components of noxious stimulation (Peyron et al., 2000). However, in other chronic pains the DLPFC showed an increase of GMC (Apkarian et al., 2004). BMS is often associated with depression and the DLPFC is likely a key area in depression, together with hippocampus and neighbouring areas. "
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    ABSTRACT: Burning Mouth Syndrome (BMS) is characterized by a burning sensation in the mouth, usually in the absence of clinical and laboratory findings. Latest findings indicate that BMS could result from neuropathic trigeminal conditions. While many investigations focus on the periphery, very few examine possible central dysfunctions. In order to highlight changes of the central system of subjects with BMS, we analysed the grey matter concentration in 12 subjects, with Voxel Based Morphometry. Data were compared with a control group (Ct). To better understand the brain mechanisms underlying BMS, the grey matter concentration of patients was also compared with those of dysgeusic patients (Dys). Dysgeusia is another oral dysfunction condition, characterized by a distorted sense of taste and accompanied by a reduced taste function. We found that a major part of the "pain matrix" presented modifications of the grey matter concentration in subjects with BMS. Six regions out of eight were affected (anterior and posterior cingulate gyrus, lobules of the cerebellum, insula/frontal operculum, inferior temporal area, primary motor cortex, dorsolateral pre-frontal cortex (DLPFC)). In the anterior cingulate gyrus, the lobules of the cerebellum, the inferior temporal lobe and the DLPFC, pain intensity correlated with the grey matter concentration. Dys also presented changes in grey matter concentration but in different areas of the brain. Our results suggest that a deficiency in the control of pain could be in part cause of BMS and that BMS and dysgeusia conditions are not linked to similar structural changes in the brain. This article is protected by copyright. All rights reserved.
    Full-text · Article · Jan 2016 · European Journal of Neuroscience
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    • "In the brain, preliminary evidence of pain-related structural changes was initially revealed by functional magnetic resonance imaging (fMRI) mostly concentrated on human adult brain. Imaging studies showing altered brain morphology and connectivity in multiple types of chronic pain conditions, such as chronic back pain[18]fibromyalgia[19]complex regional pain syndrome[20]and headache[21], have been reported. However, as most of these studies were conducted based on images with limited spatial resolution and temporal resolution, changes in local neural circuits of individual neurons and synapses in the brain are not clearly demonstrated. "
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    ABSTRACT: Damage in the periphery or spinal cord induces maladaptive plastic changes along the somatosensory nervous system from the periphery to the cortex, often leading to chronic pain. Although the role of neural circuit remodeling and structural synaptic plasticity in the 'pain matrix' cortices in chronic pain has been thought as a secondary epiphenomenon to altered nociceptive signaling in the spinal cord, progress in whole brain imaging studies on human patients and animal models has suggested a possibility that plastic changes in cortical neural circuits may actively contribute to chronic pain symptoms. Furthermore, recent development in two-photon microscopy and fluorescence labeling techniques have enabled us to longitudinally trace the structural and functional changes in local circuits, single neurons and even individual synapses in the brain of living animals. These technical advances has started to reveal that cortical structural remodeling following tissue or nerve damage could rapidly occur within days, which are temporally correlated with functional plasticity of cortical circuits as well as the development and maintenance of chronic pain behavior, thereby modifying the previous concept that it takes much longer periods (e.g. months or years). In this review, we discuss the relation of neural circuit plasticity in the 'pain matrix' cortices, such as the anterior cingulate cortex, prefrontal cortex and primary somatosensory cortex, with chronic pain. We also introduce how to apply long-term in vivo two-photon imaging approaches for the study of pathophysiological mechanisms of chronic pain.
    Full-text · Article · Jan 2016 · Korean Journal of Physiology and Pharmacology
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