• Eva Widerström-Noga, Yenisel Cruz-Almeida, Elizabeth R Felix, and Pradip M Pattany.
• aResearch Service, Department of Veterans Affairs Medical Center, Miami, FL, USA bThe Miami Project to Cure Paralysis, Miller School of Medicine, University of Miami, Miami, FL, USA cDepartment of Neurological Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA dDepartment of Physical Medicine and Rehabilitation, Miller School of Medicine, University of Miami, Miami, FL, USA eNeuroscience Graduate Program (R50), Miller School of Medicine, University of Miami, Miami, FL, USA fDepartment of Radiology, Miller School of Medicine, University of Miami, Miami, FL, USA; Cruz-Almeida is now with Institute on Aging, Department of Aging and Geriatric Research, College of Medicine, University of Florida, Gainesville, FL, USA.
• Pain. 2015 Jan 1;156(1):166-74.

AbstractNeuropathic pain is one of the most difficult consequences of spinal cord injury (SCI). The clinical correlates of the underlying mechanisms responsible for neuropathic pain are not well understood, although methods such as quantitative somatosensory testing (QST) or brain imaging have been used to further a mechanism-based understanding of pain. Our previous SCI study demonstrated a significantly lower glutamate-glutamine/myo-inositol ratio (Glx/Ins) in the anterior cingulate cortex in persons with severe neuropathic pain compared with those with less severe neuropathic pain or pain-free, able-bodied controls, suggesting that a combination of decreased glutamatergic metabolism and glial activation may contribute to the development of severe neuropathic pain after SCI. The present study aimed to determine the relationships between somatosensory function below the level of injury and low thalamic Glx/Ins in persons with intense neuropathic pain after SCI. Participants underwent QST and a 3 Tesla proton magnetic resonance spectroscopy. A cluster analysis including SCI participants resulted in 1 group (n = 19) with significantly (P < 0.001) greater pain intensity (6.43 ± 1.63; high neuropathic pain [HNP], and lower Glx/Ins [1.22 ± 0.16]) and another group (n = 35) with lower pain intensity ratings (1.59 ± 1.52, low neuropathic pain [LNP], and higher Glx/Ins [1.47 ± 0.26]). After correcting for age, QST indicated significantly greater somatosensory function in the HNP group compared with the LNP group. Our results are consistent with research suggesting that damage to, but not abolition of, the spinothalamic tract contributes to development of neuropathic pain after SCI and that secondary inflammatory processes may amplify residual spinothalamic tract signals by facilitation, disinhibition, or sensitization.

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