Abstract| Volume 22, ISSUE 5, P601, May 2021

Thalamic Neurometabolite Alterations in Patients with Knee Osteoarthritis Before and After Total Knee Replacement

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      The weak association between disability levels and “peripheral” (i.e., knee) findings suggests that central nervous system alterations may contribute to the pathophysiology of knee osteoarthritis (KOA). Here, we evaluated brain metabolite alterations in KOA patients, before and after total knee arthroplasty (TKA), using 1H-magnetic resonance spectroscopy (MRS). Thirty-four pre-surgical KOA patients and 13 healthy controls were scanned using a PRESS sequence (TE=30ms, TR=1.7s, voxel size=15 × 15 × 15mm). Additionally, a subset of patients (n=13) were re-scanned 4.1±1.6 (mean±SD) weeks post-TKA. When using Creatine (Cr)-normalized levels, pre-surgical KOA patients demonstrated lower N-acetylaspartate (NAA) (p≤0.01) and higher myoinositol (mIns) (p≤0.001), compared to healthy controls. The mIns levels were positively correlated with pain severity scores (r=0.37, p<0.05). These effects reached statistical significance also using absolute concentrations, except for the Cho group differences (p≥0.067). Post-TKA, patients demonstrated an increase in NAA (p<0.01), which returned to the levels of healthy controls (p>0.05), irrespective of metric. Additionally, patients demonstrated post-surgical increases in Cr-normalized (p<0.001), but not absolute, mIns, which were proportional to the NAA/Cr increases (r=0.61, p<0.05). Because mIns is commonly regarded as a glial marker, our results are suggestive of a possible dual role for neuroinflammation in KOA pain and post-TKA recovery. Moreover, the apparent post-surgical normalization of NAA a putative marker of neuronal integrity might implicate mitochondrial dysfunction, rather than neurodegenerative processes, as a plausible pathophysiological mechanism in KOA. More broadly, our results add to a growing body of literature suggesting that some pain-related brain alterations can be reversed after peripheral surgical treatment. 1R01NS094306-01A1.
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