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Journal of pain research · Jan 2011
Primary somatosensory cortex in chronic low back pain - a H-MRS study.
- Neena K Sharma, Kenneth McCarson, Linda Van Dillen, Angela Lentz, Talal Khan, and Carmen M Cirstea.
- Department of Physical Therapy and Rehabilitation Science.
- J Pain Res. 2011 Jan 1; 4: 143-50.
AbstractThe goal of this study was to investigate whether certain metabolites, specific to neurons, glial cells, and the neuronal-glial neurotransmission system, in the primary somatosensory cortex (SSC), are altered and correlated with clinical characteristics of pain in patients with chronic low back pain (LBP). Eleven LBP patients and eleven age-matched healthy controls were included. N-acetylaspartate (NAA), choline (Cho), myo-inositol (mI), and glutamine/glutamate (Glx) were measured with proton magnetic resonance spectroscopy ((1)H-MRS) in left and right SSC. Differences in metabolite concentrations relative to those of controls were evaluated as well as analyses of metabolite correlations within and between SSCs. Relationships between metabolite concentrations and pain characteristics were also evaluated. We found decreased NAA in the left SSC (P = 0.001) and decreased Cho (P = 0.04) along with lower correlations between all metabolites in right SSC (P = 0.007) in LBP compared to controls. In addition, we found higher and significant correlations between left and right mI (P < 0.001 in LBP vs P = 0.1 in controls) and between left mI and right Cho (P = 0.048 vs P = 0.6). Left and right NAA levels were negatively correlated with pain duration (P = 0.04 and P = 0.02 respectively) while right Glx was positively correlated with pain severity (P = 0.04). Our preliminary results demonstrated significant altered neuronal-glial interactions in SSC, with left neural alterations related to pain duration and right neuronal-glial alterations to pain severity. Thus, the (1)H-MRS approach proposed here can be used to quantify relevant cerebral metabolite changes in chronic pain, and consequently increase our knowledge of the factors leading from these changes to clinical outcomes.
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