TY - JOUR
T1 - Somatosensory phenotype is associated with thalamic metabolites and pain intensity after spinal cord injury
AU - Widerström-Noga, Eva
AU - Cruz-Almeida, Yenisel
AU - Felix, Elizabeth R.
AU - Pattany, Pradip M.
N1 - Funding Information:
This work was funded by the US Department of Veterans Affairs Rehabilitation Research and Development Service (Merit Review 5023R), Craig Neilsen Foundation #164678 (normative data), and The Miami ProjecttoCure Paralysis. The authors have no financial or other relationships that inappropriately influenced this work. The sponsors had no involvement in the collection, analysis, and interpretation of data, nor in the writing or the decision to submit this article for publication.
PY - 2015/1
Y1 - 2015/1
N2 - Neuropathic 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.
AB - Neuropathic 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.
KW - Magnetic resonance spectroscopy
KW - Neuropathic pain
KW - Quantitative sensory testing
KW - Somatosensory phenotype
KW - Spinal cord injury
UR - http://www.scopus.com/inward/record.url?scp=84979860018&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84979860018&partnerID=8YFLogxK
U2 - 10.1016/j.pain.0000000000000019
DO - 10.1016/j.pain.0000000000000019
M3 - Article
C2 - 25599312
AN - SCOPUS:84979860018
VL - 156
SP - 166
EP - 174
JO - Pain
JF - Pain
SN - 0304-3959
IS - 1
ER -