Dorsolateral Prefrontal Cortex

背外侧前额叶皮质
  • 文章类型: Journal Article
    鞭打伤(WHI)的特征是颈部被迫弯曲/伸展,这种情况经常发生在机动车碰撞后。先前的研究表明,脑代谢物浓度的差异以及与慢性鞭打相关疾病(WAD)的神经性疼痛(NP)成分的相关性已在诸如前扣带皮质(ACC)之类的情感疼痛处理区域得到了证明。然而,在患有慢性WAD疼痛的这些皮质区域内代谢物浓度的差异的检测一直难以捉摸.在这项研究中,单体素磁共振波谱(MRS),遵循最新的MRSinMRS共识小组指南,在前扣带回皮质(ACC)进行,左背外侧前额叶皮质(DLPFC),和枕骨皮质(OCC)来量化有或没有神经性疼痛(NP)成分的慢性WAD个体中代谢物浓度的差异。
    使用DouleurNeuropathique4问卷(DN4)筛选健康个体(n=29)和慢性WAD参与者(n=29),并分为无(WAD-noNP,n=15)或具有NP成分(WAD-NP,n=14)。在ACC内的3TMRI扫描仪中的单个疗程后,用LCNmodel对代谢物进行定量。DLPFC,OCC。
    与WAD-noNP组相比,WAD-NP参与者表现出中等的疼痛强度和干扰。与WAD-noNP组相比,单体素MRS分析表明ACC中的谷氨酸浓度较高,而DLPFC中的总胆碱(tCho)较低。在OCC中未检测到群间代谢物差异。最佳拟合和逐步多元回归显示,归一化的ACC谷氨酸/总肌酸(tCr)(p=0.01),DLPFC正乙酰天冬氨酸(NAA)/tCr(p=0.001),和DLPFCtCho/tCr水平(p=0.02)预测了WAD-NP组中的NP成分(ACCr2=0.26,α=0.81;DLPFCr2=0.62,α=0.98)。正常的Glu/tCr浓度高于ACC中的WAD-noNP组(p<0.05),但不在DLPFC或OCC中。与WAD-noNP组相比,性别和年龄均不影响与WAD-NP成分相关的关键标准化代谢物浓度。
    这项研究表明,ACC内谷氨酸浓度升高与慢性WAD-NP成分有关,而较高的NAA和较低的tCho代谢物水平表明,在患有慢性WAD-NP成分的个体中,神经元-神经胶质信号传导和细胞膜功能障碍增加。
    UNASSIGNED: Whiplash injury (WHI) is characterised by a forced neck flexion/extension, which frequently occurs after motor vehicle collisions. Previous studies characterising differences in brain metabolite concentrations and correlations with neuropathic pain (NP) components with chronic whiplash-associated disorders (WAD) have been demonstrated in affective pain-processing areas such as the anterior cingulate cortex (ACC). However, the detection of a difference in metabolite concentrations within these cortical areas with chronic WAD pain has been elusive. In this study, single-voxel magnetic resonance spectroscopy (MRS), following the latest MRSinMRS consensus group guidelines, was performed in the anterior cingulate cortex (ACC), left dorsolateral prefrontal cortex (DLPFC), and occipital cortex (OCC) to quantify differences in metabolite concentrations in individuals with chronic WAD with or without neuropathic pain (NP) components.
    UNASSIGNED: Healthy individuals (n = 29) and participants with chronic WAD (n = 29) were screened with the Douleur Neuropathique 4 Questionnaire (DN4) and divided into groups without (WAD-noNP, n = 15) or with NP components (WAD-NP, n = 14). Metabolites were quantified with LCModel following a single session in a 3 T MRI scanner within the ACC, DLPFC, and OCC.
    UNASSIGNED: Participants with WAD-NP presented moderate pain intensity and interference compared with the WAD-noNP group. Single-voxel MRS analysis demonstrated a higher glutamate concentration in the ACC and lower total choline (tCho) in the DLPFC in the WAD-NP versus WAD-noNP group, with no intergroup metabolite difference detected in the OCC. Best fit and stepwise multiple regression revealed that the normalised ACC glutamate/total creatine (tCr) (p = 0.01), DLPFC n-acetyl-aspartate (NAA)/tCr (p = 0.001), and DLPFC tCho/tCr levels (p = 0.02) predicted NP components in the WAD-NP group (ACC r 2 = 0.26, α = 0.81; DLPFC r 2 = 0.62, α = 0.98). The normalised Glu/tCr concentration was higher in the healthy than the WAD-noNP group within the ACC (p < 0.05), but not in the DLPFC or OCC. Neither sex nor age affected key normalised metabolite concentrations related to WAD-NP components when compared to the WAD-noNP group.
    UNASSIGNED: This study demonstrates that elevated glutamate concentrations within the ACC are related to chronic WAD-NP components, while higher NAA and lower tCho metabolite levels suggest a role for increased neuronal-glial signalling and cell membrane dysfunction in individuals with chronic WAD-NP components.
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