Chronic pain precedes disrupted eating behavior in low-back pain patients.

Chronic pain precedes disrupted eating behavior in low-back pain patients.
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慢性疼痛先于低背痛患者的饮食行为中断。

DOI:
10.1371/journal.pone.0263527
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发表时间:
2022
期刊:
影响因子:
3.7
通讯作者:
Geha P
Geha P
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Lin Y;De Araujo I;Stanley G;Small D;Geha P

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慢性疼痛与快感缺失和动机降低有关。这些行为改变与边缘脑的改变有关,并且可以解释疼痛患者肥胖风险增加的原因。然而,这些行为改变的机制以及它们与慢性疼痛发展的关联仍知之甚少。在此,我们研究了与疼痛消退的患者相比,腰痛患者在转变为慢性疼痛前后的饮食行为是如何受到影响的。此外,我们评估了在慢性疼痛患者中发生改变的高脂肪食物的享乐感知与该患者群体中伏隔核的特性之间的关系。我们假设,由于伏隔核在享乐性进食和脂肪摄入中已确立的作用以及它在慢性疼痛中逐渐显现的作用,它会直接参与疼痛患者对高脂肪食物的享乐性加工。因此,我们在基线和大约一年的随访中使用行为测定和脑结构成像对亚急性腰痛患者(SBP)和健康对照受试者进行了测试。我们还仅在一个时间点对慢性腰痛患者(CLBP)样本进行了研究。我们发现,在随访时康复的SBP患者(SBPr)和CLBP患者表现出饮食行为紊乱。相比之下,在随访时持续疼痛的SBP患者(SBPp)饮食行为正常。从神经学角度来看,只有SBPp和CLBP患者在高脂肪食物的享乐感知和伏隔核体积之间显示出强烈且直接的关系。这表明在先前研究中在SBPp患者中观察到的伏隔核改变可能在疾病早期保护他们免受享乐性饮食紊乱的影响。我们得出结论,饮食行为紊乱具体在疼痛慢性化之后出现,并伴有伏隔核的结构变化。
Chronic pain is associated with anhedonia and decreased motivation. These behavioral alterations have been linked to alterations in the limbic brain and could explain the increased risk for obesity in pain patients. The mechanism of these behavioral changes and how they set in in relation to the development of chronic pain remain however poorly understood. Here we asked how eating behavior was affected in low-back pain patients before and after they transitioned to chronic pain, compared to patients whose pain subsided. Additionally, we assessed how the hedonic perception of fat-rich food, which is altered in chronic pain patients, related to the properties of the nucleus accumbens in this patients’ population. We hypothesized that the accumbens would be directly implicated in the hedonic processing of fat-rich food in pain patients because of its well-established role in hedonic feeding and fat ingestion, and its emerging role in chronic pain. Accordingly, we used behavioral assays and structural brain imaging to test sub-acute back pain patients (SBP) and healthy control subjects at baseline and at approximately one-year follow-up. We also studied a sample of chronic low-back pain patients (CLBP) at one time point only. We found that SBP patients who recovered at follow-up (SBPr) and CLBP patients showed disrupted eating behaviors. In contrast, SBP patients who persisted in having pain at follow-up (SBPp) showed intact eating behavior. From a neurological standpoint, only SBPp and CLBP patients showed a strong and direct relationship between hedonic perception of fat-rich food and nucleus accumbens volume. This suggests that accumbens alterations observed in SBPp patients in previous works might protect them from hedonic eating disruptions during the early course of the illness. We conclude that disrupted eating behavior specifically sets in after pain chronification and is accompanied by structural changes in the nucleus accumbens.
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