【罂粟摘要】全膝关节置换术前后膝关节骨性关节炎患者的丘脑神经代谢物改变情况
全膝关节置换术前后膝关节骨性关节炎患者的丘脑神经代谢物改变情况
贵州医科大学 高鸿教授课题组
翻译：任文鑫 修改/编辑：佟睿 审校：曹莹
残疾水平与“周围”（即膝关节）发现之间的弱联系表明，中枢神经系统的改变可能导致膝关节骨关节炎(KOA)的病理生理学 。在此，我们使用1H-磁共振波谱（MRS）评估了KOA患者全膝关节置换术（TKA）前后的大脑代谢物改变情况。使用PRESS序列（TE=30 ms, TR=1.7 seconds, voxel size= 15×15×15 mm）对术前34名KOA患者和13名健康对照组进行扫描。此外，13名患者在TKA手术后4.1±1.6（均数±标准差）周被重新扫描。当使用肌酸(Cr)标准化水平时，手术前KOA患者显示出比健康对照组更低的N-乙酰天门冬氨酸（NAA）（P＜0.001），更高的肌醇（mIns）（P＜0.001），和更低的胆碱（Cho）（P＜0.05）。mIns水平与疼痛严重程度评分呈正相关（r=0.37，P＜0.05）。除了Cho组的差异（P≥0.067），这些影响在使用水参考浓度时也达到统计学意义。TKA后的患者表现出NAA的增加（P＜0.01），而后恢复到健康对照组的水平（P＞0.05），与指标无关。此外，患者在手术后表现出Cr标准化的增加（P＜0.001），但不是水参照的mIns，这与NAA/Cr的增加成正比（r=0.61，P＜0.05）。由于mIns通常被认为是一种神经胶质标志物，我们的结果提示神经炎症在KOA疼痛和TKA后恢复中可能有双重作用。此外，手术后NAA的明显正常化，这是一个假定的神经元完整性的标志，可能暗示线粒体功能障碍，而不是神经退行性过程，是KOA的一个合理的病理生理机制。更广泛地说，我们的结果增加了越来越多的文献，表明一些与疼痛相关的大脑改变可以在外围手术治疗后被逆转。
Akila Weerasekeraa, Erin Morrisseya, Minhae Kima，et al.Thalamic neurometabolite alterations in patients with knee osteoarthritis before and after total
knee replacement.PAIN 162 (2021) 2014–2023.
Thalamic neurometabolite alterations in patients with knee osteoarthritis before and after total knee replacement
The weak association between disability levels and “peripheral” (ie, knee) findings suggests that central nervous system alterations may contribute to the pathophysiology of knee osteoarthritis (KOA). Here, we evaluated brain metabolite alterations in patients with KOA, before and after total knee arthroplasty (TKA), using 1H-magnetic resonance spectroscopy (MRS). Thirty-four presurgical patients with KOA and 13 healthy controls were scanned using a PRESS sequence (TE=30 ms, TR=1.7 seconds, voxel size=15×15×15 mm). In addition, 13 patients were rescanned 4.1 6 1.6 (mean±SD) weeks post-TKA. When using creatine (Cr)-normalized levels, presurgical KOA patients demonstrated lower N-acetylaspartate (NAA) (P＜0.001), higher myoinositol (mIns) (P＜0.001), and lower Choline (Cho) (P＜0.05) than 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 water-referenced 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. In addition, patients demonstrated postsurgical increases in Cr-normalized (P＜0.001), but not water-referenced 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 postTKA recovery. Moreover, the apparent postsurgical 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.
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